LYMPHOMA A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Lymphoma: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-84022-9 1. Lymphoma-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on lymphoma. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes&Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON LYMPHOMA .............................................................................................. 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Lymphoma..................................................................................... 7 E-Journals: PubMed Central ....................................................................................................... 66 The National Library of Medicine: PubMed ................................................................................ 83 CHAPTER 2. NUTRITION AND LYMPHOMA................................................................................... 131 Overview.................................................................................................................................... 131 Finding Nutrition Studies on Lymphoma ................................................................................. 131 Federal Resources on Nutrition ................................................................................................. 141 Additional Web Resources ......................................................................................................... 141 CHAPTER 3. ALTERNATIVE MEDICINE AND LYMPHOMA ............................................................ 143 Overview.................................................................................................................................... 143 National Center for Complementary and Alternative Medicine................................................ 143 Additional Web Resources ......................................................................................................... 182 General References ..................................................................................................................... 184 CHAPTER 4. DISSERTATIONS ON LYMPHOMA .............................................................................. 185 Overview.................................................................................................................................... 185 Dissertations on Lymphoma ...................................................................................................... 185 Keeping Current ........................................................................................................................ 188 CHAPTER 5. CLINICAL TRIALS AND LYMPHOMA ......................................................................... 189 Overview.................................................................................................................................... 189 Recent Trials on Lymphoma ...................................................................................................... 189 Keeping Current on Clinical Trials ........................................................................................... 210 CHAPTER 6. PATENTS ON LYMPHOMA ......................................................................................... 213 Overview.................................................................................................................................... 213 Patents on Lymphoma................................................................................................................ 213 Patent Applications on Lymphoma............................................................................................ 238 Keeping Current ........................................................................................................................ 269 CHAPTER 7. BOOKS ON LYMPHOMA ............................................................................................. 271 Overview.................................................................................................................................... 271 Book Summaries: Federal Agencies............................................................................................ 271 Book Summaries: Online Booksellers......................................................................................... 272 The National Library of Medicine Book Index ........................................................................... 280 Chapters on Lymphoma ............................................................................................................. 281 CHAPTER 8. MULTIMEDIA ON LYMPHOMA .................................................................................. 283 Overview.................................................................................................................................... 283 Video Recordings ....................................................................................................................... 283 Audio Recordings....................................................................................................................... 284 Bibliography: Multimedia on Lymphoma .................................................................................. 284 CHAPTER 9. PERIODICALS AND NEWS ON LYMPHOMA ............................................................... 287 Overview.................................................................................................................................... 287 News Services and Press Releases.............................................................................................. 287 Newsletter Articles .................................................................................................................... 291 Academic Periodicals covering Lymphoma................................................................................ 294 CHAPTER 10. RESEARCHING MEDICATIONS................................................................................. 295 Overview.................................................................................................................................... 295 U.S. Pharmacopeia..................................................................................................................... 295 Commercial Databases ............................................................................................................... 297 Researching Orphan Drugs ....................................................................................................... 297
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APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 303 Overview.................................................................................................................................... 303 NIH Guidelines.......................................................................................................................... 303 NIH Databases........................................................................................................................... 305 Other Commercial Databases..................................................................................................... 309 The Genome Project and Lymphoma ......................................................................................... 309 APPENDIX B. PATIENT RESOURCES ............................................................................................... 315 Overview.................................................................................................................................... 315 Patient Guideline Sources.......................................................................................................... 315 Associations and Lymphoma...................................................................................................... 325 Finding Associations.................................................................................................................. 326 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 329 Overview.................................................................................................................................... 329 Preparation................................................................................................................................. 329 Finding a Local Medical Library................................................................................................ 329 Medical Libraries in the U.S. and Canada ................................................................................. 329 ONLINE GLOSSARIES................................................................................................................ 335 Online Dictionary Directories ................................................................................................... 335 LYMPHOMA DICTIONARY ...................................................................................................... 337 INDEX .............................................................................................................................................. 429
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with lymphoma is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about lymphoma, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to lymphoma, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on lymphoma. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to lymphoma, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on lymphoma. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON LYMPHOMA Overview In this chapter, we will show you how to locate peer-reviewed references and studies on lymphoma.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and lymphoma, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “lymphoma” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •
Infective Endocarditis in a Patient with Hodgkin's Lymphoma: A Case Report Source: Special Care in Dentistry. 14(2): 57-60. March-April 1994. Summary: A common sequela of certain malignancies is nonbacterial thrombotic endocarditis (NBTE), a phenomenon in which sterile fibrin/platelet aggregates are deposited onto normal cardiac valves. These verrucae represent a predisposing factor for the initiation of infective endocarditis following a bacteremia. In this article, the authors present a case history which is highly suggestive of infective endocarditis that occurred as a result of multiple odontogenic abscesses in a patient with Hodgkin's lymphoma. The case illustrates the important role that the dentist can play in the management of cancer patients. The authors emphasize a holistic concept of medical care in which the dentist is an integral member of the health-care team. 35 references. (AA-M).
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Inflammatory Bowel Disease is Not Associated with an Increased Risk of Lymphoma Source: Gastroenterology. 121(5): 1080-1087. November 2001. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 32887-4800. (800) 654-2452. Website: www.gastrojournal.org. Summary: Previous studies of the risk of lymphoma in inflammatory bowel disease (IBD) patients have provided conflicting results. This study examines the risk of Hodgkin's and non Hodgkin's lymphoma among patients with inflammatory bowel disease. The authors performed a retrospective cohort study using the General Practice Research Database. Inflammatory bowel disease patients were matched to randomly selected controls on age, sex, and primary care practice. Lymphoma rates were also compared with published age and sex specific rates. The study included 6,605 patients with Crohn's disease; 10,391 with ulcerative colitis (UC); and 60,506 controls followed for an average of 3.7, 3.9, and 4.4 years, respectively. The incidence of lymphoma was not increased in patients with IBD. In subgroup analyses, an increased risk was not observed among patients with Crohn's disease or UC. Compared with IBD patients not treated with azathioprine or 6MP, the relative risk of lymphoma among the 1,465 IBD patients treated with these medications was 1.27. The authors conclude that patients with IBD do not have an increased risk of lymphoma as compared with the general population. Although the authors cannot completely rule out a modest increased risk of lymphoma with azathioprine of 6MP therapy, an increased risk was not observed in this cohort. 4 tables. 48 references.
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Non-Hodgkin's Lymphoma and Periodontitis. A Case Report Source: Journal of Periodontology. 71(3): 504-509. March 2000. Contact: Available from American Academy of Periodontology. Suite 800, 737 North Michigan Avenue, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: This article describes an unusual case of extranodal non Hodgkin's lymphoma that developed in the maxillae (upper jaw) associated with localized severe periodontitis in a 64 year old Caucasian male. The lymphoma was diagnosed less than 2 years following routine periodontal surgery and 8 weeks after the extraction of hopeless teeth in the associated area. Two months following the extractions, the patient experienced pain and swelling in the maxillary right edentulous (without teeth) area, mimicking an abscess, and reported for emergency care. An expansile lesion measuring 2.0 by 2.5 centimeters in diameter was noted on radiographic (x ray) examination to extend into the right maxillary sinus. A definitive biopsy diagnosis of high grade, small, non cleaved, diffuse non Hodgkin's lymphoma of the right posterior maxillae was established. The patient was subsequently treated by a combination of radiation, chemotherapy, and bone marrow transplantation. The maxillary tissues healed uneventfully, and the patient has been closely observed for approximately 5 years without symptoms or recurrence of the lymphoma. The authors conclude that this case highlights the need for careful debridement of extraction sockets associated with severe periodontitis and argues for the routine submission of extracted teeth with adjacent soft tissue for microscopic analysis, to assist in the early diagnosis of potentially life threatening malignancies (cancers). 5 figures. 1 table. 13 references.
•
Gingival Overgrowth as the Initial Paraneoplastic Manifestation of Hodgkin's Lymphoma in a Child. A Case Report Source: Journal of Periodontology. 72(1): 107-112. January 2001.
Studies
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Contact: Available from American Academy of Periodontology. 737 North Michigan Avenue, Suite 800, Chicago, IL 60611-2690. (312) 573-3220. Fax (312) 573-3225. Summary: This article presents a case of gingival (gum) overgrowth, premature root resorption, and alveolar bone loss, which preceded the diagnosis of a stage IV B Hodgkin's lymphoma (HL) in a 9 year old boy. The child presented complaining of gingival pain which first appeared 3 months prior. Clinical examination revealed inflamed, hyperplastic (overgrown) gingiva, while x ray shoed premature root resorption and alveolar bone loss. Medical work up was significant for cervical (neck) lymphadenopathy. Gingival biopsy, followed by lymph node resection, was performed twice. Histological examination of both gingival biopsies disclosed a mixed inflammatory infiltrate, while classical Hodgkin's lymphoma of the nodular sclerosis type was diagnosed from the second lymph node biopsy. Chemotherapy was instituted. Remission of the lymphoma was observed with concomitant regression of the gingival overgrowth. 8 figures. 23 references. •
Benefits from Elimination of Helicobacter Pylori Infection Include Major Reduction in the Incidence of Peptic Ulcer Disease, Gastric Cancer, and Primary Gastric Lymphoma Source: Preventive Medicine. 23(5): 712-716. September 1994. Summary: This article reports on a research study in which the author reviewed the accumulated data showing that successful treatment of Helicobacter pylori (H. pylori) infection results in healing of gastritis and cure of peptic ulcer disease. The author stresses that current data suggest that by elimination of H. pylori, it may be possible to prevent most gastric carcinomas and primary gastric lymphomas. The author concludes that H. pylori infection is a major public health problem and elimination or prevention of H. pylori infection will result in a tremendous reduction in medical costs, morbidity, and mortality. 1 table. 38 references. (AA-M).
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Protective Effect of Gluten-Free Diet Against Development of Lymphoma in Dermatitis Herpetiformis Source: British Journal of Dermatology. 134(3): 363-367. September 1996. Contact: Available from Blackwell Science, Ltd. Journal Subscriptions, P.O. Box 88, Oxford, England OX2 0NE. Phone (44) 1865 206180. Fax (44) 1865 206219. Summary: This article reports on a retrospective study of 487 patients with dermatitis herpetiformis (DH). The study showed that lymphoma developed in eight patients (the expected incidence being 0.21). All lymphomas occurred in patients whose dermatitis herpetiformis had been controlled without a gluten-free diet (GFD) or in those who had been treated with a GFD for less than 5 years. The results suggest that GFD plays a protective role against lymphoma in DH and give further support for advising patients to adhere to a strict GFD for life. 2 tables. 22 references. (AA-M).
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Disturbances in Oral and Dental Structures in Patients with Pediatric Lymphoma After Chemotherapy: A Preliminary Report Source: Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 87(3): 317-321. March 1999. Contact: Available from Mosby, Inc. 11830 Westline Industrial Drive, St. Louis, MO 63146-3318. (800) 453-4351 or (314) 453-4351.
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Summary: This article reports on a study undertaken to evaluate the effects of chemotherapy on oral and dental structures and craniofacial growth in 30 survivors of childhood lymphoma (cancer). Eruption status, root malformations, premature apexification (closure of the tooth root), agenesis (lack of a tooth or teeth), crown anomalies, soft tissue abnormalities, gingival and periodontal status, enamel defects and discolorations, and craniofacial growth status of the subjects were documented and compared with findings in 20 healthy children who served as controls. Statistically significant differences between the study and control groups were found for plaque index, enamel hypoplasia, discolorations, and agenesis. The authors conclude that antineoplastic therapy and or childhood cancer can result in a higher prevalence of various malformations in teeth. Children treated in the early years of their lives displayed the most severe dental defects, suggesting that immature teeth are at a greater risk of developmental disturbances than fully developed teeth. 1 figure. 3 tables. 22 references. (AA-M). •
Primary Care Approach to Cutaneous T-Cell Lymphoma, A Source: Nurse Practitioner. 25(4): 82,85-86,88,91-92,94,98. April 2000. Summary: This journal article provides health professionals with information on the epidemiology, clinical manifestations, diagnosis, staging, and treatment of cutaneous T cell lymphoma (CTCL). This malignant lymphoma comprises a group of diseases typified by a proliferation of malignant T lymphocytes. Approximately 1,000 new cases of CTCL are definitively diagnosed each year. CTCL has four phases: premycotic, infiltrative, tumor, and erythrodermic. CTCL, represented primarily by mycosis fungoides and Sezary syndrome, has several clinical variants. Mycosis fungoides can begin in the patch, plaque, or tumor stage, or in a combination. Less commonly, its initial presentation is erythrodermic. Because the initial appearance of CTCL can be subtle and the histopathologic evidence nonspecific, the disease is commonly misdiagnosed as a common dermatologic condition such as chronic eczema. Misdiagnosis can severely affect treatment and prognosis. Therapeutic options may be adjusted for disease stage. The first two stages of CTCL, IA and IIA, may be treated with topical steroids, retinoids, psoralen plus ultraviolet A (PUVA) therapy, extracorporeal photochemotherapy, single agent chemotherapy, interferon, electron beam radiation, or combination therapy. Therapeutic options for stage IIB include combination therapy of mechlorethamine and PUVA therapy, interferon, retinoids, and photopheresis; multidrug systemic chemotherapy; and radiation therapy. Stage III or Sezary syndrome may be treated with photopheresis, systemic chemotherapy, total skin electron beam irradiation, and combination drug therapy. The final stage is treated with multidrug chemotherapy. Clinicians must be able to recognize this disease and know when to include it in the differential diagnosis. 3 figures, 5 tables, and 13 references. (AA-M).
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AIDS - Associated Non - Hodgkin Lymphoma Source: The Lancet; Vol. 337, no. 8745. Contact: Lancet Ltd., 655 Ave of the Americas, New York, NY, 10010-5107, (212) 6333800. Summary: This reprint of a journal article discusses non-Hodgkin lymphoma associated with Acquired immunodeficiency syndrome (AIDS). It says that the authors investigated the epidemiology of such lymphoma by analyzing data from cases reported to the Centers for Disease Control and Prevention (CDC) through June 30, 1989. During this period, 2,824 cases of non-Hodgkin lymphoma were reported, with the condition
Studies
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about 60 times more prevalent in Persons with AIDS (PWA's) than in the general U.S. population. These cases included immunoblastic lymphoma, primary lymphoma of the brain, and Burkett's lymphoma. Statistics on their prevalance are presented, and associated risk factors discussed. Each type was twice as common in whites as in Blacks, and in men as in women. Epidemiological data suggest that while infectious agents, such as Epstein-Barr virus, may be associated with the development of the lymphomas, there was probably no single cause for all types.
Federally Funded Research on Lymphoma The U.S. Government supports a variety of research studies relating to lymphoma. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to lymphoma. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore lymphoma. The following is typical of the type of information found when searching the CRISP database for lymphoma: •
Project Title: LYMPHOMA
ADHESION
MOLECULES
IN
HUMAN
LEUKEMIA
AND
Principal Investigator & Institution: Mcintyre, Bradley W.; Professor; Immunology; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2001; Project Start 01-SEP-1993; Project End 31-DEC-2003 Summary: (adapted from the investigator's abstract) The broad, long term objective of this proposal is to understand the role of adhesion molecules in the pathogenesis of lymphoid malignancies. This proposal will focus on the regulatory and functional mechanisms of integrins that control cell adhesion and the processes of cell migration and localization. The major hypotheses of this proposal are (1) although levels of integrin expression have obvious implications in the development of cancer, it is the alterations in the regulation of integrin receptor function that result in the major pathophysiological consequences, and (2) unique regulatory alterations will characterize distinctly differentiated normal lymphocyte subpopulations and malignant lymphocytes with different histopathological sybtypes and grades. The major observations that provide much of the foundation of this proposal are (1) integrin-mediated adhesion of lymphoid cells is subject to a regulatory cycle of "off" and "on" signals, (2) integrin triggering induces the rapid morphological changes in lymphocytes that result in pseudopodial extension and motility, and (3) normal resting lymphocytes, normal activated lymphocytes, indolent non-Hodgkin's lymphoma cells, chronic lymphocytic 2
Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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leukemia, and acute lymphoblastic leukemia cells all apparently have different alterations in these processes. The specific aims will employ a combination of quantitative cellular adhesion and spreading assays, digital color microscopy, biochemical assays, and immunochemical techniques to analyze the roles of different structural and signal transduction molecules in the initiation and maintenance of integrin-mediated adhesion, pseudopodial extension, and transendothelial migration. The health relatedness of this research is that an understanding of normal integrin regulation versus that found in disease states and function may have diagnostic or prognostic value to the clinician and will lay the foundation for the development of novel therapeutic methods for controlling the growth and metastasis of leukemia and lymphoma cells, potentially allowing normal integrin functions to be maintained. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AIDS CONSORTIUM
ASSOCIATED
MALIGNANCIES
CLINICAL
TRIALS
Principal Investigator & Institution: Krown, Susan E.; Professor; Sloan-Kettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 30-SEP-1995; Project End 31-JUL-2004 Summary: Memorial Sloan-Kettering Cancer Center is applying to continue as a Clinical Trials Member of the AIDS-associated Malignancies Clinical Trials Consortium (AMC). Our qualifications include: (1) A strong record of scientific and administrative contributions to the AMC since its inception in 1995; (2) Broad experience in the development and performance of innovative clinical trials, laboratory investigations and AIDS patient care relevant to the objectives of the AMC; (3) Expertise in infectious diseases required for the care of patients with AIDS- associated malignancies; (4) An extensive referral network that will facilitate accrual; (5) A well-developed clinical, laboratory and data management infrastructure and resources to support collection of tumor tissue and biological fluids for the AIDS Malignancy Banks; and, (6) A commitment to making AMC trials our highest priority. Particular strengths of our group include extensive experience in the early phase testing and evaluation of cytokines and cytokine modulators in cancer and AIDS; an active program for development and diagnostic and therapeutic applications of monoclonal antibodies in cancer; expertise in the development of novel therapeutic approaches for primary CNS lymphoma; expertise in the design, performance and analysis of phase I drug trials; and, experience in the diagnosis, treatment and monitoring of patients with HPV-associated anogenital squamous malignancies. Members of our group have been leaders in the analysis of prognostic factors in AIDS-associated KS and NHL and in the development of criteria for evaluating and staging AIDS-associated cancers, and have developed several innovative clinical trials for AIDS-associated malignancies that are in progress or being developed for future implementation through the AMC. In sum, our scientific and clinical resources make us uniquely positioned to continue to contribute to the collaborative clinical trials effort that has been developed in the AMC over the past 3 years. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AIDS CONSORTIUM
ASSOCIATED
MALIGNANCIES
CLINICAL
TRIALS
Principal Investigator & Institution: Kaplan, Lawrence D.; Professor of Medicine; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122
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Timing: Fiscal Year 2001; Project Start 30-SEP-1995; Project End 31-JUL-2004 Summary: This proposal is for continued funding for the UCSF/Northern California AIDS Malignancies Consortium site. In this proposal for grant renewal the consortium consists of San Francisco General Hospital, University of California San Francisco, Mt. Zion Cancer Center, Kaiser Permanente Medical Center, Pacific Hematology/Oncology Associates, The UC-Davis Medical Center, and The University of Hawaii/AIDS Clinical Research Program for The State of Hawaii. This group of institutions will function as a single participating member of the National Cancer Institute AIDS Malignancies clinical trials consortium for the purpose of enrolling patients with HIV associated malignancies onto clinical trials of novel agents. The six institutions will work together as one unit with a full time data manger for the San Francisco group who will be dedicated to the consortium and will travel to each of the participating sites as necessary for the monitoring of patients on consortium clinical trials. The UC Davis and The University of Hawaii groups will have their own part-time data managers. The Clinicians will interact closely with the San Francisco General Hospital AIDS Immunobiology Laboratory under the direction of Dr. Michael McGrath who will perform necessary laboratory studies on lymphoma specimens and will collect specimens for the NCI-AIDS Malignancies Tissue Repository for which he is the Principal Investigator. In addition, the San Francisco General Hospital General Clinical Research Center (GCRC), which has been actively involved in a variety of clinical trials in HIV disease, will be available for both inpatient and outpatient drug administration and collecting of pharamokenetic specimens as required. This group has a high level of expertise in conducting clinical trials in patients with HIV associated malignancies and consists of clinicians with specialized areas of expertise in management of Kaposi's Sarcoma, non-Hodgkin's lymphoma, and anogenital neoplasias. Clinical trials proposed for consortium studies include a polyamine analog designed to target proliferating macrophages in AIDSlymphoma, the use of Toremifene with liposomal doxorubicin for treating KS, and a study of an HPV-16 vaccine for treatment of anal neoplasia. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: AIDS MALIGNANCY CONSORTIUM Principal Investigator & Institution: Sparano, Joseph A.; Montefiore Medical Center (Bronx, Ny) Bronx, Ny 104672490 Timing: Fiscal Year 2001; Project Start 20-SEP-1999; Project End 31-JUL-2004 Summary: This application for membership in the AIDS Malignancy Consortium is submitted by Dr. Joseph A. Sparano on behalf of Montefiore Medical Center (including the Moses Division and Weiler Division) and a consortium of four other institutions, including Jacobi Medical Center, North Central Bronx Hospital, Bronx Lebanon Hospital, and Long Island Jewish Medical Center. At Montefiore Medical Center (MMC) alone, 111 patients with HIV-associated malignancies have been enrolled on clinical trials under Dr. Sparano s direction over the past 8 years. The prevalence of HIV infection in the Bronx, the community served by five of the six hospitals in this consortium, is among the highest in the nation. Of the 1.2 million residents of the Bronx, it is estimated that about 30,000 are knowingly (16,000) or unknowingly (14,000) HIVinfected. This community is served not only by hospital-based HIV specialty care clinics, but also by over 30 community-based clinics affiliated with MMC or Bronx Lebanon Hospital (BLH). BLH also has an active community outreach program. Approximately 5900 patients receive primary HIV care by the consortium institutions. Moreover, among consortium institutions, it is estimated that each year there are approximately 110 patients newly diagnosed with HIV-associated and AIDS-associated cancers each
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year, including 46 patients wit systemic lymphoma, 14 patients with primary CNS lymphoma, and 50 patients with Kaposi s sarcoma. MMC has extensive experience in clinical trials in cancer and AIDS research. It is the University Hospital of the Albert Einstein College of Medicine (AECOM), and as such is the clinical arm of the NCIdesignated Comprehensive Cancer Center at AECOM. Each year, over 100 clinical protocols are active, over 400 patients are enrolled on clinical trials, and about 55 percent of those enrolled on clinical trials are either African- American or Latino. MMC is also a member of the Eastern Cooperative Oncology Group. At ECOG s last audit of MMC s clinical trials performance and data management in 1997, MMC was rated as excellent to outstanding by ECOG. New York State- designated AIDS centers are based at MMC and BLH, and MMC, BLH, and Jacobi Medical Center participate in the CPCRA. MMC and its partners are therefore ideally suited to become productive members of AMC because of its large patient base, its considerable experience in cancer clinical trials, and the scientific leadership that has been demonstrated by its principal investigator. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANTI VIRAL THERAPEUTIC FOR EBV MALIGNANCIES Principal Investigator & Institution: Faller, Douglas V.; Professor and Director; None; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2001; Project Start 07-FEB-2001; Project End 31-JAN-2003 Summary: Epstein-Barr Virus is a common and worldwide pathogen. While exposure usually results in a self-limited lymphoproliferative syndrome, infectious mononucleosis, the virus is causative, or associated with, a number of malignancies. The latent virus is detected in 2 endemic tumors: 95% of African Burkitt's lymphoma, and 90-100% of nasopharyngeal carcinoma. Many B-lymphomas, some T-lymphomas, and approximately 50% of Hodgkin's lymphomas have also been found to contain latent EBV. 40% of lymphomas arising in AIDS, and nearly all lymphomas arising in transplant recipients (post-transplant-associated lymphoproliferative disease (PT-LPD) harbor EBV. PT-LPD is especially difficult to treat unless the immunosuppression can be reversed, and is typically refractory to radiation therapy and chemotherapy. Similar to herpes simplex virus and varicella-zoster virus, EBV encodes a thymidine kinase (TK) enzyme. In a rate-limiting step, the viral TK converts nucleoside analogues to their monophosphate form, eventually leading to premature termination of the nascent DNA and cell death. Latently-EBV-infected B-cells and epithelial cells, including tumor cells, do not express TK. We have found that exposure of these cells to the experimental drug Arginine Butyrate results in induction of TK expression. Preliminary in vitro studies demonstrated that induction of EBV-TK in patient-derived tumor cells by Arginine Butyrate is possible, and that these previously-resistant cells are rendered susceptible to Ganciclovir (GCV) therapy. We have years of clinical experience in the administration of Arginine Butyrate to adults and children in studies to induce fetal hemoglobin as therapy for sickle cell anemia and thalassemia. We hypothesized that treatment of patients with EBV- associated tumors with arginine butyrate (to induce the EBV-TK) and GCV (to eliminate EBV-TK expressing cells) might be an effective, nontoxic therapy. We have treated eight patients with Arginine Butyrate plus ganciclovir in an FDAregistered pilot study with documented responses in the majority of patients, and no adverse outcomes related to this regimen. Our Specific Aims are: (1) To determine if treatment with Arginine Butyrate plus Ganciclovir will result in clinical responses in a significant proportion of patients with EBV-associated lymphomas and lymphoproliferative disease (LPD); (2) To determine toxicity or side effects of the combination therapy; and (3) To determine if tumor specimens and cell lines derived
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from patients demonstrate the same response to Arginine Butyrate and Ganciclovir (with respect to TK gene induction and synergistic susceptibility) as the EBV(+) cell lines we have studied to date. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANTIVIRAL MEDIATED APOPTOSIS OF NON HODGKIN'S LYMPHOMA Principal Investigator & Institution: Harrington, William J.; Professor; Medicine; University of Miami-Medical Box 248293 Coral Gables, Fl 33124 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2003 Summary: (Applicant's Abstract) The applicant has found that certain high grade Herpes virus associated lymphomas are sensitive to anti-viral mediated apoptosis in vitro and in vivo. Epstein-Barr Virus positive Burkitt's lymphoma and Human Herpes Virus Type 8 related Primary Effusion Lymphomas undergo apoptosis when cultured in the presence of Azidothymidine (AZT) or AZT and Interferon Alpha (IFN Alpha). He has investigated the mechanisms by which this therapy causes apoptosis in these lymphoma subtypes. He has found that incubation of Burkitt's lymphoma cells with AZT results in upregulation of CD95 and apoptosis. Primary Effusion Lymphoma requires Interferon Alpha to potentiate AZT mediated apoptosis. He has also found that Interferon Alpha induces the death receptor ligands, TRAIL and Fas Ligand in B cell lymphomas. In contrast to Burkitt's lymphoma and Primary Effusion Lymphoma, EBV positive large cell immunoblastic lymphomas and Epstein-Barr virus negative lymphomas were resistant to AZT and Interferon Alpha. These initial findings indicate that some lymphomas might be selectively sensitive to anti-viral therapy. In susceptible lymphomas, AZT and Interferon Alpha mediated apoptosis does not occur solely through Fas/Fas-Ligand interaction and likely involves activation of additional mechanisms of apoptosis. The applicant will investigate the role of viral and cellular pro- and anti-apoptotic proteins in blocking or facilitating AZT and Interferon Alpha induction of apoptosis in primary lymphoma specimens and cell lines developed from these tumors. A mechanism of inducing apoptosis in aggressive lymphomas would benefit patients with these diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ARSENIC TRIOXIDE TREATMENT OF LYMPHOPROLIFERATIVE DISORD Principal Investigator & Institution: Waxman, Samuel; Wiener Professor/ Medical Director; Medicine; Mount Sinai School of Medicine of Nyu of New York University New York, Ny 10029 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2004 Summary: As2O3, given by an intravenous infusion empirically designed in China, has become a new therapeutic agent of choice in the treatment of refractory acute promyelocytic leukemia (APL). It is an unusual agent since it is effective in APL patients that are chemotherapy-resistant and at the apparent therapeutic concentration of 1-2 M induces clinical remission with minimal myelotoxicity. Similar to all trans retinoic acid, As203 may be uniquely effective in treating APL since it can induce both differentiation and apoptosis in APL cells in vitro and in vivo. Whether As203 can be extended as a cancer treatment remains to be determined. We elected to extend the use of As203 to lymphoproliferative disorders (LPD). Anecdotal, unpublished reports from China and more recent case reports in the United States suggest that As203 may be an effective
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Lymphoma
treatment of LPD. Consistent with this is our observation that As203 (1-2 M) treatment of cell lines and primary cultures of LPD (B-cell lymphoma, CLL, ALL, multiple myeloma but not T-cell lymphoma) causes significant growth inhibition and, in some cells, measurable apoptosis similar to NB4 cells (t(15:17) APL cell line). As303 is also appealing since it effectively inhibits growth and induces apoptosis in malignant cells with mutant p53, in lymphoma cells with t(14:18) that overexpress Bcl-2 and does not demonstrate cross resistance to taxol and doxorubicin in P388 lymphoma cells expressing MDR-1. As203 probably has multiple effects that contribute to the induction of cell death dependent on dose, cell type or cellular environment. In vitro, As203 in some cells increases H202 accumulation which acts on the mitochrondria to induce caspase dependent apoptosis. However, these observations made in vitro should be interpreted with caution since cellular levels of glutathione and H202 may be artifactually altered in tissue culture media and are likely to differ from that of cells in vivo. Little is known about the consequence of in vivo exposure of 1-2 M As203 and its effect on human malignant cells. We will compare and contrast in vitro and in vivo effects of As203 treatment of LPD cell lines and primary cultures of LPD cells obtained from animals and patients. These materials will be used: 1) to evaluate the importance of the intracellular redox profile and accumulation of H202 and arsenic to As203-induced growth inhibition and apoptosis; 2) to characterize the cellular responses to As203 at mRNA level using cDNA microarray in LPD cells obtained from patients treated with As203; 3) to design combination therapies in vitro and in vivo to improve the sensitivity of LPD cells to As203; 4) we have designed a phase II pilot study to evaluate 0.25 mg/kg/day As203 (2-1/2 higher concentration than used in APL) in the treatment of patients with relapsed and refractory indolent LPD. The study is designed to identify potential surrogate markers of As203 activity. Should our laboratory study identify agents or schedules that enhance the response to As203, we will use them to appropriately modify the initial phase II pilot study. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BIMP3 IN ANTIGEN RECEPTOR SIGNALING AND MALT LYMPHOMA Principal Investigator & Institution: Mcallister-Lucas, Linda M.; Pediatrics & Communicable Dis; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2003; Project Start 25-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): The Bimps (BcI10 Interacting MAGUK Proteins) are a newly described family of signaling proteins that activate the pro-survival transcription factor, NF-kappaB. Bimps belong to the larger MAGUK (Membrane Associated Guanylate Kinase) family, a class of proteins composed of multiple distinct protein/protein interaction domains that function as molecular scaffolds in assembling multiprotein complexes at the plasma membrane. Bimps bind to and operate upstream of Bcl10, an NF-kappaB signaling molecule that is known to be an essential mediator of lymphocyte proliferation in response to antigen. The genes encoding Bcl10 and its downstream binding partner, MALT1, are each targets of recurrent chromosomal translocation in mucosa associated lymphoid tissue (MALT) lymphoma, suggesting that perturbation of the Bcl10-mediated NF-kappaB signaling pathway can promote lymphomatous transformation. Our preliminary data suggest that the Bimp proteins function to link surface receptor signaling and subsequent protein kinase C (PKC) activation to Bcl10-mediated induction of NF-(B. We hypothesize that the lymphocyte specific Bimp isoform, Bimp3, functions as a scaffold to assemble the signaling
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molecules that are required for Bcl10/MALT1-mediated NF-(B activation in response to lymphocyte antigen receptor stimulation. Furthermore, we hypothesize that disruption of the normal mechanisms by which the antigen receptor and Bimp3 regulate Bcl10 and MALT1 activity, as a consequence of chromosomal translocation, contributes to the pathogenesis of MALT lymphoma. In order to test these hypotheses, we propose three specific aims: 1) Determine if Bimp3, Bcl10 and MALT1 participate in a common NF-(B signaling pathway in lymphocytes with known antigen receptor-related signaling molecules; 2) Delineate the function of the individual protein/protein interaction domains within the Bimp3 structure, and 3) Characterize the physiological role of Bimp3 by generating and analyzing mice deficient in Bimp3. The career development program outlined in this proposal will build upon the investigator's prior research experience and will also provide the opportunity to master new laboratory techniques, to interact with a new mentor and team of collaborators, and to participate in additional didactic training in immunology, mouse genetics and bioinformatics. This training experience will ultimately lead to transition to the status of independent investigator. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BIOLOGIC MODIFIER THERAPIES IN AIDS MALIGNANCIES Principal Investigator & Institution: Shah, Manisha H.; Comprehensive Cancer Center; Ohio State University 1960 Kenny Road Columbus, Oh 43210 Timing: Fiscal Year 2002; Project Start 30-SEP-1995; Project End 31-JUL-2004 Summary: This application is a five year competing renewal for the AIDS Malignancy Consortium (AMC) grant currently awarded to Michael A. Caligiuri, M.D. at The Ohio State University (OSU). During the past four years of this award, the PI was an active participant in the AMC Lymphoma Working Group and the AMC Laboratory Working Group. The PI successfully competed for correlative science awards for two AMC clinical trials, and the PI currently chairs one AMC clinical protocol that uses a biologic response modifier in HIV non Hodgkin's lymphoma (NHL). Two additional clinical studies are currently under development by the PI for the AMC: The first is a randomized trial of low dose interleukin (IL) 2 following first induction therapy in HIV NHL. This study will likely be performed in collaboration with industry and AIDS malignancy sites in Europe. The letter of intent (LOI) was reviewed by the AMC and a protocol has been submitted to the AMC. The second study submitted by the PI is a phase II study assessing the anti-tumor activity of anti-CD20 monoclonal antibody against patients with posttransplant lymphoproliferative disorder (PTLD). PTLD will now be incorporated into the AMC agenda as an immunodeficiency lymphoma, and this will be the first such protocol within the AMC. The LOI as been approved by the AMC and the protocol has been submitted. Despite these intellectual contributions, the accrual of OSU and its former affiliate, Roswell Park Cancer Institute, was poor, ranking approximately 8th among 13 primary AMC sites. Therefore, in order to address this weakness, the PI has now affiliated with four new sites, each with a high patient volume of HIV-1+ patients and patients with AIDS malignancies, and each a new member to the AMC. The PI is no longer affiliating with Roswell Park. These four new sites include the University of Maryland Cancer Center, The Brady Memorial Hospital of Emory University, Saint Vincent's Comprehensive Cancer Center in New York, and a consortium of three hospitals in Australia that function under a common clinical research group called the National Center for HIV Epidemiology and Clinical Research (NCHECR). The NCHECR evaluates and treats the vast majority of HIV-1 and AIDS malignancy patients for all of Australia. Each of the OSU- affiliated sites has unique strengths. Some centers have large inner city populations with high volumes of women
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Lymphoma
and minority patients, while other centers have extremely strong histories of phase I-III cooperative group trials or unique laboratory expertise. Collectively, this new group of OSU-affiliated sites should bring several strengths to the AMC, most notably an increase in accrual to AMC protocols for HIV NHL and HIV Kaposi's sarcoma. A budget has been structured to provide a minimal baseline of support for each affiliated site to get protocols approved by Institutional Review Boards and to begin to screen patients for study. However, after an initial accrual of four patients per site, the funding of each site becomes tied to their ability to accrue patients. Collectively, this application provides enhanced strength in intellectual contributions and patient accrual for the AMC, compared to our previous application. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: C MYC EXPRESSION DURING ALV LYMPHOMAGENESIS Principal Investigator & Institution: Ruddell, M Alanna.; Staff Scientist; Fred Hutchinson Cancer Research Center Box 19024, 1100 Fairview Ave N Seattle, Wa 98109 Timing: Fiscal Year 2001; Project Start 15-MAY-1996; Project End 31-MAY-2004 Summary: (Adapted from the investigator's abstract) Avian leukosis virus (ALV) rapidly induces metastatic bursal lymphomas in lymphoma-susceptible chicken strains, after clonal expansion of B cells harboring a proviral c-myc gene integration within transformed follicles. Pulse-chase labelling measurements of proliferation and bursal emigration will examine how c-myc overexpression induces rapid expansion of these transformed follicles. The same analysis will determine why transformed follicles from lymphoma-resistant chicken strains fail to expand and form tumors. Transplantation of bursal progenitors overexpressing exogenous myc from retroviral vectors will test whether this resistance results from reduced ALF LTR-driven myc expression, or altered target cell response to myc expression. Immunohistochemical studies of the effects of myc in lymphoma-susceptible birds revealed angiogenesis at early stages within c-myc or v-myc-transformed follicles and tumors. The angiogenic activity induced by myc overexpression in B cells will be characterized using in vitro and in vivo assays of endothelial proliferation, migration, and vessel growth. Angiogenesis will be manipulated during bursal lymphomagenesis by transplantation of bursal progenitors expressing myc and/or angiogenic inhibitors from retroviral vectors, to determine whether inhibition of angiogenesis prevents early growth of myc-transformed follicles or their ability to form metastatic lymphomas. Bursal lymphocytes overexpressing myc show increased vascular endothelial growth factor (VEGF) production. The contribution of this endothelial growth factor to myc-induced angiogenesis will be assessed by overexpressing or underexpressing VEGF in B cells. The effects of VEGF overexpression in low myc B cell lines will be characterized by endothelial proliferation, migration, and angiogenesis assays, and bursal progenitors overexpressing VEGF will be assessed for their ability to induce angiogenesis in vivo. The VEGF gene will be deleted from mycoverexpressing B cell lines by homologous recombination, to determine whether this reduces angiogenic activity in vitro, and formation of angiogenic tumors in vivo. These studies will give insight to the role of myc- and VEGF-induced angiogenesis during the generation of lymphomas. Findings from the experimental model will be applied to studies of angiogenesis in human lymphomas and other cancers involving de-regulated c-myc expression, to determine whether myc-induced angiogenesis contributes to the common association of myc overexpression with human cancers. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CALGB INSTITUTIONAL GRANT Principal Investigator & Institution: Clamon, Gerald H.; Internal Medicine; University of Iowa Iowa City, Ia 52242 Timing: Fiscal Year 2003; Project Start 01-APR-1988; Project End 31-MAR-2009 Summary: (provided by applicant): The University of Iowa has been a member of CALGB since 1986. Accrual at the main member hospital is approximately 100 patients per year and approximately 20 more patients are accrued at two affiliates. Over the past 5 years, we have authored or co-chaired studies in non-small cell lung cancer, in chemoprevention of lung cancer, in experimental therapeutics for 506U78, and for omega-3 fatty acids in cancer cachexia. Administratively, Dr. Gerald Clamon has been vice chair of the Membership Committee and Dr. Raymond Hohl has been vice chair of the Institutional Performance Evaluation Committee (IPEC). In addition, Dr. Clamon is on the Respiratory Committee and is the liaison to the Cancer Control and Health Outcomes Committee, Dr. Hohl is on the Leukemia Committee and is the liaison to the Pharmacology and Experimental Therapeutics (PET) Committee, Dr. Brian Link is on the Lymphoma Committee, and Dr. Badrinath Konety is on the GU Committee. Dr. Nancy Rosenthal is reviewing slides for the Hematopathology Committee for a lymphoma trial, Dr. Shivanand Patel reviews cytogenetics for the Leukemia Committee, and Dr. Michael Vannier is serving on a new committee to evaluate new technologies in the imaging of tumors. New translational research at the University of Iowa has lead to the development of two new promising anti-cancer therapies. The HU 1D10 antibody developed in the laboratory of Dr. George Weiner at the University of Iowa has completed Phase I trials at the University of Iowa and demonstrated activity against lymphoma. The CpG oligodeoxynucleotide developed at the University of Iowa in the lab or Dr. Arthur Krieg is now completing Phase I trials at the University of Iowa. A pilot study of Pneumovax plus GM-CSF is being completed at the University of Iowa. This should lead to a phase III trial within CALGB and potentially improve success with vaccinations of the immune suppressed cancer patient. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CANCER AND LEUKEMIA GROUP B Principal Investigator & Institution: Shea, Thomas C.; Professor of Medicine; Medicine; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2003; Project Start 01-JUN-1991; Project End 31-MAR-2006 Summary: (provided by applicant): This application represents the second competitive renewal of the CALGB institutional grant submission from the University of North Carolina at Chapel Hill (UNC-CH) and its affiliates. UNC-CH has been a member of CALGB since 1986. Our accrual has been maintained at approximately 40 treatment cases (including 6-10 minority accruals/year) plus companion studies. We also maintain an affiliate network responsible for another 60-90 accruals/year while maintaining excellent data quality control. Moreover, our institution now has broad leadership participation in the Group in Breast, Cancer Prevention and Control, GI, Lymphoma, Molecular Pathology, Radiation Oncology, and is the research base for a UNC based Minority Initiative Program and a VCU based Minority CCOP. Moreover, our leadership efforts in the Group have also continued to expand. We now enjoy the distinction of having one committee chair, five committee vice-chairs, seven committee or working group core or liaison members, eight modality committee members, one Executive Committee member, two members of the Board of Directors, five
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administrative committee members and seven protocol principal investigators. Members from UNC and its affiliates have held 56 positions on various scientific, administrative, and leadership committees of CALGB during the past 5 years. Additional faculty at UNC-CH will expand our commitment and Group leadership in the Breast, Surgery, GU, GI, Lymphoma and PET committees (F. Detterbeck, M. Graham, C. Sartor, L. Carey, J. Mohler, R. Pruthi, B. O'Neil, R. Orlowski, P. Watkins, and C. Dees). We therefore believe that this application reflects the growing and crucial contribution that UNC-CH investigators provide to the Group in leadership, science and service as well as our continued efforts to increase accrual through affiliate members while maintaining rigorous control of quality data submission. We respectfully submit that this application demonstrates both the current value of this institution to the Group and the contributions that: the membership of UNC-CH and its affiliates will continue to provide CALGB over the next five years. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CANCER AND LEUKEMIA GROUP B Principal Investigator & Institution: Perry, Michael A.; Internal Medicine; University of Missouri Columbia 310 Jesse Hall Columbia, Mo 65211 Timing: Fiscal Year 2001; Project Start 01-APR-1979; Project End 31-MAR-2003 Summary: (adapted from the applicant's abstract): The University of Missouri-Ellis Fischel Cancer Center (UM/EFCC) wishes to continue its participation in the clinical, translational, and basic research programs of the Cancer and Leukemia Group B (CALGB), as it has since 1969. The institutions in this grant include the UM/EFCC, our affiliated Harry S. Truman Veterans Administration Hospital, adjacent to the University Hospital, our sister medical school, the University of Missouri-Kansas City, and our CGOP affiliates, Missouri Hematology Associates of Columbia, Missouri Baptist Medical Center and St. Luke's Hospital of Saint Louis. (A new affiliate, the Kirksville College of Osteopathic Medicine, has been approved, but is not yet functional). Members of the UM/EFCC and our affiliates contribute to the group through participation on disease and modality committees, administrative committees, and through the protocol development process, serving as core committee members who originate the ideas behind studies, protocol chairs, and investigators who place patients on studies. Historically, UM/EFCC has been a major contributor to Respiratory Committee studies, and to a lesser extent, breast cancer studies. The recruitment of surgical oncologists to the center has resulted in an increase in gastrointestinal cancer studies. All leukemia and lymphoma patients are also considered for protocol participation. The research design involves the production of a protocol or treatment plan. The initial idea may arise from an individual or derive from a meeting of one of the CALGB disease committees (Breast, Gastrointestinal, Lung, Leukemia, Lymphoma, Prostate) or from a modality committee (Pharmacology and Experimental Therapeutics, Radiation Therapy, Surgery, and Psycho-oncology). The protocol is discussed, modified if necessary, and approved by the participating modality committees, and then by the Executive Committee. The final protocol is then submitted to the National Cancer Institute for approval. Following any additional changes the study is sent to the institutional Review Boards of the participating hospitals, and after approval implemented. Patients are then enrolled, treated, and followed until accrual goals are met at which time the protocol is closed. The results are then tabulated, statistically analyzed, and subsequently published. Sequential studies build upon the results of prior completed trials. The group also participates in CALGB Prevention Studies and all possible studies are activated to meet patient needs and enhance accrual.
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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CANCER AND LEUKEMIA GROUP B--MINNESOTA ONCOLOGY GROUP Principal Investigator & Institution: Peterson, Bruce A.; Medicine; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, Mn 554552070 Timing: Fiscal Year 2001; Project Start 01-APR-1979; Project End 31-MAR-2003 Summary: (adapted from the applicant's abstract): The University of Minnesota has been a participating member of the Cancer and Leukemia Cooperative Group B (CALGB) for the clinical studies of hematologic malignancies and solid tumors since August 1973. The Minnesota Oncology Group consists of established investigators from the Department of Medicine, the Department of Therapeutic Radiology, the Department of Laboratory Medicine and Pathology, the Department of Surgery, and the Department of Pediatrics/School of Public Health with extensive expertise in clinical cancer research, including clinical trials, bone marrow transplantation, immunology, cytogenetics, pathology and epidemiology. The Minnesota Oncology Group participates in the CALGB in order to pool its intellectual, technical and clinical resources with other academic institutions to expedite progress in clinical cancer research. The specific aims of this proposal include: (1) to contribute to and participate in the scientific endeavors of CALGB; (2) to reach our accrual potential and then to maintain patient accrual at that increased level; (3) to assist in the administrative and organizational matters of CALGB. The methods of study are through the clinical research protocols established by the CALGB. The clinical material provided by the Minnesota Oncology Group is composed primarily of patients with leukemia, lymphoma, breast cancer, gastrointestinal cancer and lung cancer, and participation is in the entire range of trials, including bone marrow transplantation and phase I drug testing. Major scientific positions held by Minnesota participants are the Chair of the Lymphoma Committee and Vice-Chair of the Pathology Committee for Hematologic Malignancies. In addition, 10 participants are members of various scientific core committees and a major group service in leukemic research is centered at Minnesota. The Minnesota Oncology Group is active in administrative activities with the Chair of the Constitution Committee and membership on the Institutional Performance Evaluation Committee (Standards, Ethics and Peer Review Committee), Membership Committee, Data Audit Committee and the Board of Directors. The objective of this research program is to participate in inter-institutional clinical research to resolve unanswered and important questions in the therapy and biology of malignant diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CANCER SUBTRACTION
VIRUS
DISCOVERY
BY
COMPUTATIONAL
Principal Investigator & Institution: Meyerson, Matthew L.; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2003; Project Start 24-SEP-2003; Project End 31-JUL-2006 Summary: (provided by applicant): We have developed a new method to discover microbial causes of human disease, sequence-based computational subtraction. In this method, sequences from diseased tissue are compared to the human genome computationally, and the filtered sequences are highly enriched for non-human nucleic acids. I propose to apply computational subtraction to search for viruses that cause lymphomas associated with immunodeficiency, most notably post-transplant
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lymphoproliferative disorder and HIV-associated lymphoma. First, I propose to use specimens of post-transplant lymphoproliferative disorder, known to be positive for Epstein-Barr virus, to refine our methods for library generation and sequencing. In particular, we would like to test the use of normalization, subtraction, and concatenation techniques. Once we have improved these techniques, I plan to focus on searching for novel viruses in immunodeficiency-associated lymphomas of unknown etiology. We plan to generate cDNA libraries from immunodeficiency-associated lymphoma biopsy specimens, to sequence a sampling of these libraries, and then to subtract the sequences computationally and experimentally against the human genome. Filtered sequences will be tested further for specific association with lymphoma using the polymerase chain reaction. Should we successfully identify novel lymphoma-associated sequences, we will then attempt to generate molecular clones of the entire putative viruses and begin to characterize the protein products of their genomes. Computational subtraction is a broadly applicable method. While we will begin our pathogen discovery projects in cancer, our methods will be broadly applicable to many human diseases. These include auto-immune diseases and inflammatory diseases, as well as uncharacterized epidemics, whether natural or bio-terrorist in origin. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LYMPHOMA
CASE-CONTROL
STUDY
OF
PESTICIDES
AND
T(14;18)
Principal Investigator & Institution: Chiu, Brian C.; Preventive & Societal Medicine; University of Nebraska Medical Center Omaha, Ne 681987835 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2004 Summary: (provided by applicant): A population-based, case-control study of nonHodgkin's lymphoma (NHL) was conducted in Nebraska between 1983 and 1986. This NCI's study collected extensive information on agricultural exposures. Herein, an ancillary molecular study is proposed to determine the role of pesticides in the occurrence of t(14;18) chromosomal translocation in this case-control study. An association between NHL and pesticides has been observed repeatedly, but not consistently. Results of epidemiologic studies of pesticides and NHL may be obscured by the aggregate evaluation of cases that are etiologically diverse. The t(14;18) is the most common cytogenetic abnormality, and t(14;18)-mediated constitutive overexpression of BCL2 protein is an important early event in NHL pathogenesis. The current proposal will classify NHL cases according to t(14;18) status to identify agricultural risk factors that may be specifically associated with t(14;18)-positive or negative pathogenic mechanisms. The specific aims are to 1) obtain paraffin-embedded tumor blocks for NHL cases; 2) determine the presence of the t(14;18) translocation; and 3) investigate pesticides for their association with t(14;18)-positive NHL or t(14;18)negative NHL. The hypothesis is that pesticides act specifically along a t(14;18)dependent pathway, resulting in stronger associations with t(14;18)-positive than t(14;18)-negative NHL. The research design is a molecular case-control study. Tumor blocks will be obtained from the Lymphoma Registry Tissue Bank for all NHL cases in the original case-control study (about 270-290 tissue blocks will be available). Fluorescence in-situ hybridization (FISH) analysis will be used to determine the presence of the t(14;18) translocation. Results from FISH analyses will be used to classify NHL cases into t(14;18)-positive NHL or t(14;18)-negative NHL. Logistic regression models will be used to calculate the odds ratios for t(14;18)-positive NHL and t(14;18)negative NHL associated with various groups and types of pesticides. The low-term
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objective is to improve understanding of the disease process which may ultimately lead to improved prevention of NHL in the general population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: COGNITIVE EFFECTS OF CANCER CHEMOTHERAPY Principal Investigator & Institution: Ahles, Tim A.; Professor; Psychiatry; Dartmouth College 11 Rope Ferry Rd. #6210 Hanover, Nh 03755 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2006 Summary: APPLICANT'S Cognitive deficits associated with cancer treatment can have a dramatic effect on patients' quality of life and have been recognized as a problem by the President's Cancer Panel (1999) and the National Coalition for Cancer Survivorship as a challenge facing people with cancer. The present application is an extension of work completed by researchers at Dartmouth with a supplement from the Office of Cancer Survivors to the Norris Cotton Cancer Center Core grant (Grant No. P30CA23 108, supplement) entitled "Cognitive Impact of Systemic Chemotherapy in Long-Term Survivors of Breast Cancer and Lymphoma." Survivors who were greater than 5 years post-diagnosis and disease free were administered a battery of standardized neuropsychological and psychological tests. The results demonstrated that survivors who had been treated with systemic chemotherapy scored significantly lower in overall neuropsychological functioning as compared to survivors who had been treated with local therapy only. In this next phase of research, we propose to prospectively study the cognitive deficits experienced by breast cancer and lymphoma patients treated with their first course of systemic chemotherapy versus local surgery or non-CNS radiation. Patients will be assessed at pre-treatment and 6, 12 and 24 months post-diagnosis with a standardized battery of neuropsychological and psychological tests. The primary hypothesis is that patients treated with systemic chemotherapy will demonstrate greater decrements in performance from pre- to post-treatment on standardized measures of neuropsychological functioning as compared to patients treated with local therapy only after controlling for important confounding variables such as age, education, and psychological state. Secondarily, we will evaluate the associations between cognitive functioning and other factors that may effect cognition in cancer patients including genetic markers (APOE status), metabolic factors, menopausal status (pre- vs. postmenopausal at diagnosis), and use of tamoxifen (breast cancer only). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: COMBINED CYTOKINE-MONOCLONAL ANTIBODY THERAPY LYMPHOMA Principal Investigator & Institution: Porcu, Pierluigi; Internal Medicine; Ohio State University 1960 Kenny Road Columbus, Oh 43210 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 31-AUG-2008 Summary: This application is a synthesis of didactic training in clinical research, translational immunology and clinical protocol development. Its focus is the study of cytokine-induced modulation of innate immunity in combination with monoclonal antibody (mAb) therapy as a novel immunotherapeutic approach in lymphoma. Its goals are to discover the role played by specific innate immune effector cell subsets in the anti-lymphoma activity of mAbs in vivo and to learn how in vivo modulation of effector cell subsets with cytokines, such as interleukin-2 (IL-2), might enhance the clinical effectiveness of mAbs. The applicant is an Assistant Professor of Internal Medicine at The Ohio State University (OSU) with extensive training in basic cancer
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laboratory research, cytokine biology, and medical oncology, with a strong concentration in lymphoma. For his academic career development, the applicant has chosen the arena of clinical research in hematological malignancies, with a specific focus in lymphoma. OSU has assembled a cadre of outstanding investigators with expertise in clinical cancer research, particularly in the area of hematological malignancies, providing an excellent environment for career development. The mentor for this application is a recognized leader in the study of the immune system and its role in the pathogenesis and therapy of lymphoma, and has an extensive track record of training successful physician-scientists. This proposal presents two specific aims: Specific Aim 1: To participate in a NIH K30- funded Clinical Research Curriculum (CRC) specifically designed for the development of clinical investigators at OSU. Specific Aim 2: Based on extensive pre-clinical observations made in the mentor's laboratory, the applicant will complete a Phase I and initiate a Phase II study of rituximab (anti-CD20 monoclonal antibody) and interleukin-2 (IL-2) in relapsed B-cell lymphoma. Correlative science studies in Specific Aim 2 will focus on the study of NK-cells, Fcgamma receptors, ADCC, and pharmacokinetics, with the goal of elucidating the interactions between the innate immune system and rituximab that are relevant to the clinical anti-lymphoma activity of rituximab. These studies will advance our knowledge about the role of the innate immune system in the therapy of lymphoma and may lead to a broader use of cytokine-mAb combinations in the therapy of cancer. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CONTROL OF MYC TRANSCRIPTION IN HIGH GRADE LYMPHOMA Principal Investigator & Institution: Boxer, Linda M.; Associate Professor; Medicine; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 15-APR-1996; Project End 31-JAN-2006 Summary: (Adapted from the applicant's abstract) We proposed to study the mechanism of activation of c-myc at a molecular level in human lymphoma tissue and in mouse model of the translocation. The goal is to reach a better understanding of the mechanisms of malignant transformation. 1. Completion of the characterization of the regulatory elements in the murine and human immunoglobulin heavy chain (IgH) enhancers that deregulate c-myc transcription. We will continue to identify the regulatory elements that are required for activation of c-myc, including increased transcription and P2 to P1 promoter shift. 2. Identification of the regions of the c-myc promoter that are required for the interaction with the IgH enhancers for maximun transcriptional activity and the promoter shift. Study of the mechanisms involved. 3. Determination of the mechanisms of transcriptional silencing of the normal c-myc allele in Burkitt's lymphoma. 4. Construction of a mouse model of the c-myc-IgH translocation. We will target the active sites of the IgH enhancers to the murine c-myc gene to recreate the Burkitt's translocation. 5.Development of strategies to interfere with c-myc transcription that is driven by the IgH enhancers. We have shown that several NF-kB sites are critical for deregulated c-myc expression, and we will first target the function of NF-kB. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CYTOKINE THERAPY OF CUTANEOUS T CELL LYMPHOMA Principal Investigator & Institution: Rook, Alain H.; Dermatology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104
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Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: Cutaneous T-cell lymphoma (CTCL) is a clonally-derived, skin-invasive malignancy of CD4+ T-lymphocytes with the phenotype of mature helper T-cells. Our previous work has demonstrated that the Sezary form, or typically leukemic form of CTCL, is characterized by prominent immunologic defects including depressed cellmediated immunity. We have also demonstrated increased production of T-helper type 2 (Th2) cytokines (IL-4, IL-5) and deficient production of Th1 cytokines (IL-2 and interferon gamma [IFN gamma]) by their peripheral blood cells (PBMC) as well as detecting IL-4 and IL-5 mRNA within lesional skin but not normal skin of patients with all stages of CTCL. A marked defect in IL-12 production in CTCL has also been noted, which may also play a role in depressed cell-mediated immunity. Because evidence exists for an antitumor T-cell response and since IL-12 is pivotal in stimulating cytotoxic T-cells, we have completed a phase I trial of IL-12 conducted in our GCRC to treat CTCL. Our data indicate that IL-12 has marked therapeutic activity. This K24 translational grant should permit the P.I. greater time to focus on understanding the in vivo mechanisms of action of IL-12 and other therapeutically active cytokines by studying 1) skin immune cells, 2) cytokine expression, and 3) extent of apoptosis within active skin lesions prior to and during IL-12 therapy and correlate this with lesion regression. We will also characterize the effects of IL- 12 to inhibit growth and induce apoptosis of the purified malignant CD4+ T-cells and determine if there is in vitro synergism with the therapeutically active agent, IFN alpha. We will also examine IL-12 receptor expression prior to and prospectively during therapy to determine if downmodulation of receptors accounts for tolerance to the clinical effects of IL-12. Since our preliminary data indicate that IFN alpha upregulates IL-12 receptor expression on the peripheral blood cells of CTCL patients, we will determine if interferons in vitro can enhance IL-12 receptor expression during therapy as a potential marker of a more efficacious protocol using both IL-12 and IFN alpha. The results of these studies will further improve our understanding of the mechanisms of action of IL- 12 and other cytokines and will assist in targeting a more potent combination of agents which can suppress clonal growth and correct abnormal antitumor immunity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DAILY LOW-DOSE IL-2 AUGMENTS ANTI-CD20 ANTIBODY THERAPY Principal Investigator & Institution: Eisenbeis, Charles F.; Internal Medicine; Ohio State University 1960 Kenny Road Columbus, Oh 43210 Timing: Fiscal Year 2002; Project Start 19-AUG-2002; Project End 31-JUL-2007 Summary: (provided by applicant): The anti-CD20 antibody, rituximab, is effective as a single agent for the treatment of human B-cell lymphomas. Despite a 50% response rate in intermediate grade lymphomas, the complete response rate is low, and no patients are cured of their disease. The mechanism of rituximab's activity against lymphoma remains unclear; almost all of the existing data is from in vitro studies using lymphoma cell lines, and suggests that rituximab functions through antibody- dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), direct induction of apoptosis, or a combination of these mechanisms. We have utilized a murine model of a spontaneously arising human malignant lymphoproliferation to study the mechanism of rituximab's cytotoxic activity in vivo. In this model, severe combined immune deficient (SCID) mice are engrafted with human peripheral blood leukocytes (hu-PBLs) via intraperitoneal injection (the hu-PBL-SCID model). If PBL from selected normal EpsteinBarr virus (EBV)-seropositive donors are injected, all mice develop lethal EBV-derived
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Lymphoma
lymphoproliferative disease (EBV-LPD) within 8-12 weeks. This EBV-LPD is CD20+, is of human origin, and arises in the midst of engrafted normal human immune effector cells including CD8+ T cells and NK cells. In this model, rituximab is capable of eradicating established EBV-LPD, but only in mice pretreated with daily low-dose interleukin-2 (IL-2). The mechanism by which IL-2 promotes the cytotoxic function of rituximab is unknown, and is the focus of this proposal. A leading hypothesis is that IL2 exerts its effect through the modulation of activating and inhibitory Fc-gamma receptors (Fc-gamma- R), either on the tumor itself, or on required immune effector cells, thus leading to more effective ADCC. In the first aim we will determine the immune effector subset(s) necessary for the therapeutic effect of rituximab and daily low-dose IL-2. In the second aim, we will characterize the effect of IL-2 on the differential expression of Fc-gamma-RI, Fc-gamma-RII, and Fc-gamma-RIII on human and murine immune effector subsets, and determine the functional relevance of murine Fc-gamma-R molecules for the protective effect of rituximab and IL-2 therapy. For the third aim we will characterize the effect of daily low-dose IL-2 therapy on EBV-LPD tumors and their susceptibility to ADCC, apoptosis, and cell-mediated cytotoxicity. Insight gained from these studies should be applicable to the treatment of a variety of human malignancies for which antibody therapy currently exists, and may lead to further optimization of such therapies in the future. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DESIGN AND EFFICACY OF ANTI LYMPHOMA DNA VACCINE Principal Investigator & Institution: Ghosh, Swapan K.; Life Sciences; Indiana State University 217 N 6Th St Terre Haute, in 47809 Timing: Fiscal Year 2000; Project Start 01-AUG-2000; Project End 31-JUL-2004 Summary: The overall objective is to understand mechanisms of action of scFv plasmid DNA vaccines that encode the idiotype (Id) ,i.e., the variable regions of heavy (VH) and light chains (VL) of the clonotypic immunoglobulin (Ig) of a murine B-cell lymphoma 2C3, and evaluate efficacy in terms of protection against the 2C3 tumor and the nature of immune responses evoked. Vaccination with Ig protein or scFv plasmid DNA usually induces humoral responses with limited prophylactic efficacy. With the 2C3 tumor, repeated immunizations using irradiated cells evoke both CTLs (cytotoxic T lymphocytes) and protective immunity. In contrast, similar immunization with purified secreted Ig is less effective, and results in indolent tumors. Furthermore, 2C3-Id- specific CTLs also occur at the early stages, but decline at late stages of tumor growth. The scFv plasmids are expected to overcome problems associated with protein immunogens by consistently producing only Id determinants of an Ig and thereby provoking memory immune cells. The question is whether scFv plasmids, to be effective, express cytosolic, secreted or membrane forms of the idiotype. To facilitate this study, we developed: (1) a prototype scFv construct encoding cytosolic VH- VL of 2C3 Ig based on the nucleotide sequences of both heavy and light chains; (2) a permanent transfectant P815A4, that expresses both intact scFv as well as CTL-recognized idiopeptides; (3) PCR, ELISA and cellular methodologies; (4) Id-specific CTL lines; and (5) anti-Id antibody reagents. With these tools, we will address the following: Design and construct a series of scFv producing plasmids that express distinct variants of the 2C3 idiotype. These variants will differ in the structure of the scFv itself, as well as in the subcellular localization of the scFv molecule (cytoplasmic, membrane-bound, or secreted); (2) Characterize the expression and mechanism of presentation of the above scFv variants after in vitro transfection into two different antigen-presenting cells: P815, and A20; and (3) Determine the in vivo effects of these scFv variants on the nature, magnitude and
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specificity of humoral and cellular (CTL) immune responses and on host survival rates against tumor challenge. We expect that these studies will provide understanding of molecular features of immunoglobulin idiotype that can be successfully exploited to design CTL- inducing antitumor responses. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DEVELOPMENT OF NEW PEPTIDE-PEPTIDE NUCLEI ACID CONJUGATES: FOR IMAGING OF BCL-XL Principal Investigator & Institution: Lewis, Michael R.; University of Missouri Columbia 310 Jesse Hall Columbia, Mo 65211 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: (Revised Abstract) (provided by applicant): The overall goal of the proposed research is to develop new radiolabeled peptide-peptide nucleic acid (peptide-PNA) constructs for molecular imaging of proto-oncogene expression in cancer. The hypotheses to be addressed in this application are 1) that overexpression of bcI-XL in non-Hodgkin's lymphoma (NHL) can be detected in vivo by radiolabeled antisense PNAs conjugated to peptides for intracellular delivery, and 2) that in vivo imaging of bcI-XL overexpression correlates with poor response to conventional chemotherapy in canine lymphoma patients. The bcI-XL gene is a member of a new category of cellular oncogenes involved in blocking tumor cell apoptosis, which is a major cytotoxic response to chemotherapy and radiotherapy. Furthermore, bcl- XL overexpression is involved in blocking anoikis, or anchorage-dependent apoptosis, and may play a role in tumor invasion and metastasis. The objective of this research application is to synthesize peptide-antisense-PNA conjugates labeled with the diagnostic imaging radiometal 111In and evaluate these radiopharmaceuticals for bcl- XL mRNA targeting in vitro and in vivo. These goals will be accomplished by synthesizing new bcI-XL antisense PNAs conjugated to peptides for intracellular delivery (Specific Aim 1), evaluating the bcI-XL mRNA binding properties of the peptide-PNA conjugates by Northern blot analysis (Specific Aim 2), performing in vitro cell uptake, internalization, efflux, and fluorescence microscopy studies of the peptide-PNA conjugates in bcI-XL -positive and -negative lymphoma cell lines in culture (Specific Aim 3), performing biodistribution and microSPECT imaging studies in SCID mice bearing human NHL xenografts, in order to select the optimal tumor targeting conjugate (Specific Aim 4), and evaluating the optimal 111In- labeled anti-bcI-XL peptide-PNA construct by performing gamma scintigraphy studies in canine lymphoma patients receiving conventional chemotherapy, in order to determine whether in vivo bcI-XL imaging correlates with treatment outcome (Specific Aim 5). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DNA LYMPHOMAGENESIS
PK
IN
RADIATION
DAMAGE
REPAIR
AND
Principal Investigator & Institution: Li, Gloria C.; Member, Attending Biophysicist; Sloan-Kettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 01-AUG-1998; Project End 31-MAY-2003 Summary: DNA-dependent protein kinase DNA-PK is a serine-threonine kinase that consists of a 465-kDA catalytic subunit, DNA-PKcs, and a 70 kDA and an 86-kDa heterodimeric DNA-targeting component, Ku70 and Ku80. Based on our recent pilot studies of Ku70- /- and Ku80-/- mice and earlier studies of SCID mice by others, it is postulated that each of the three components of DNA-PK may have distinct yet
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overlapping roles. The proposed studies aim at a test of this hypothesis and the elucidation of the physiological roles of the individual components of DNA-PK in DNA double- strand break (DSB) repair and V(D)J recombination, in lymphocyte development and lymphomagenesis. There are two specific aims. Specific Aim 1 focuses on the physiological role(s) of the individual subunits in DSB repair, V(D)J recombination and lymphocyte development. We plan to generate mutant mice and cell lines deficient in one or more of these polypeptides, and use them to deduce the roles of individual components of DNA-PK during T-and B-cell development, and in the repair of radiation-induced DSB and the associated effects on radiation sensitivity. In addition, we will examine the effect of low (non-lethal) does of ionizing radiation on V(D)J recombination in these mutant mice and evaluate whether T- and B-cell development can be restored by X- irradiation and whether such restoration enhances the development of lymphoma. Specific Aim II focuses on the role(s) of Ku70, Ku80 and DNA-PKcs in lymphomagenesis and tumorigenesis. We will test a hypothesis, inferred from our preliminary studies, that the loss of Ku70 enhances illegitimate recombination and leads to the development of lymphoma. Using various mutant mice and cell lines, spontaneous tumor development and tumor induction by ionizing radiation will be studied in vivo, and neoplastic transformation in vitro. In addition, the induction of chromosome damage (chromosome aberrations and sister chromatid exchanges) with and without X-irradiation will be examined with a view to understand the roles of the individual subunits of DNA-PK in the maintenance of genomic stability. The proposed study should add new information and insight regarding the physiological functions of DNA-PK and its individual subunits in programmed gene rearrangement and the maintenance of genomic stability. Furthermore, our studies should verify whether there is a role of Ku70 in lymphomagenesis, and specifically whether Ku70 may be considered as a candidate tumor suppressor gene. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EBV ASSOCIATED HEAD AND NECK CANCERS Principal Investigator & Institution: Robertson, Erle S.; Associate Professor; Microbiology and Immunology; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-MAY-2006 Summary: Epstein-Barr virus (EBV) infects most of the world's population, is the etiological agent of Infectious mononucleosis, and is also associated with a number of malignancies including Burkitt's Lymphoma, Nasopharyngeal Carcinoma, Oral Hairy Leukoplakia, Hodgkin's Lymphoma, Adult T-Cell Lymphomas and Lymphoproliferative Diseases in AIDS patients. In vitro, EBV infects and growth transforms B-lymphocytes so that they proliferate continually into lymphoblastoid cell lines (LCLs). In these infected B-lymphocytes, EBV expresses a repertoire of latent genes. EBNA2, EBNA3A and 3C and LMP1 are essential for B lymphocyte transformation. The increase in the number of immune compromised patients in the population due to other factors like co-infection with other viral agents and genetic defects has led to an increase in the ability of EBV strains to undergo recombinantion. We propose that immune suppression provides an opportunity for selection and emergence of new EBV strains through intertypic recombination that are more potent in their ability to transform and induce proliferation of infected human cells. In this study we will investigate carcinomas and lymphomas from head and neck patients who are immunecompromised. We will specifically target samples positive for EBV based on the aggressiveness of the tumors and the immune status of the patients. The EBV genome
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will be analyzed for the possibility of intertypic strains of the virus from type I and type II EBV having a greater potency of transforming human B-cells. Additionally, we will create cell lines (LCLs) using the virus from these tumors to further analyze the genomes and determine the gene expression patterns of these intertypic viruses and characterize the activation markers of LCLs induced by infection with the intertypic recombinants. Finally, the new strains will be analyzed for determination of their infectivity, virulence and transformation potency. These studies will generate information for determining the potential emergence of new EBV strains in a population of immunocompromised patients with head and neck cancers and lymphomas. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EBV BASED STRATEGIES FOR AIDS RELATED MALIGNANCIES Principal Investigator & Institution: Kenney, Shannon C.; Professor; Medicine; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2001; Project Start 13-FEB-1995; Project End 31-JAN-2003 Summary: AIDS patients frequently develop central nervous system (CNS) lymphomas, for which there is currently no effective treatment. These AIDS-related CNS lymphomas all carry the Epstein-Barr virus (EBV) genome and express the EBV protein, EBNA 1. The ubiquitous presence of EBV in the AIDS- related CNS lymphomas presents unique opportunities for targeting these malignant cells for destruction using gene therapy approaches. In addition, gene therapy strategies which distinguish between proliferating (tumor) versus nonproliferating (neuronal) cells, and which have already been shown to cure glioblastomas in animal models, may likewise be useful in the treatment of CNS lymphomas. In these studies, we propose to use a recently developed SCID mouse model of CNS lymphoma to develop a variety of gene therapy approaches for the potential treatment of CNS lymphomas in AIDS. In our first specific aim, we will exploit the presence of EBV in AIDS-related CNS lymphomas and insert the "suicide" gene HSV-TK (herpes simplex virus thymidine kinase), which confers ganciclovir sensitivity to cells, into a retroviral vector under the control of the EBV element, oriP. OriP, which contains both an origin of replication and a transcriptional enhancer element, requires the EBV protein EBNA 1 for function. In our second specific aim, we will insert the HSV-TK gene (under the control of the EBNA 1 dependent oriP enhancer element) into a plasmid vector and use the molecular-conjugate method to deliver DNA. The molecular conjugates will include a peptide containing the CD21 ligand (expressed on B cells) to specifically deliver the HSV-TK DNA only to tumor cells. In our third specific aim, we will attempt to induce lytic destruction of the EBV-infected lymphoma cells by using gene therapy to over-express the EBV immediate-early protein, BZLF1. Over-expression of BZLF1 is known to induce lytic EBV infection and consequent lysis of the host cell. In the final specific aim, we will examine the ability of defective HSV mutants to lyse EBV-transformed B cells in vitro, and cure EBV-induced CNS lymphomas in vivo. The studies proposed will not only be important in the development of an animal model system for AIDS-related CNS lymphomas, but should provide critical information regarding which therapeutic approaches are most promising for eventual human trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EBV SPECIFIC THERAPY OF LYMPHOMA USING DENDRITIC CELLS Principal Investigator & Institution: Dhodapkar, Madhav V.; Assistant Professor; Lab/Cell Physiol & Immunology; Rockefeller University New York, Ny 100216399 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2004 Summary: Epstein Barr virus (EBV) is a ubiquitous gamma herpes virus associated with the development of several B lymphoproliferative diseases including lymphoma in human immune deficiency virus (HIV) infected individuals. Cellular immunity plays a critical role in the control of EBV and other viral infections. However it has been difficult to boost this arm of the immune response using current approaches in humans. Dendritic cells (DCs) are specialized antigen presenting cells (APCs) capable of generating strong anti-viral immune responses. Our hypothesis is that Dcs will be effective adjuvants for the generation of EBV specific immune response for therapy and prevention of lymphoma in HIV infected individuals. Maturation of DCs ex vivo leads to an increase in their potency in vitro. We have recently demonstrated that a single injection of antigen bearing mature DCs, but not unpulsed DCs or antigens alone, generated broad CD4 and CD8+ve T cell immunity in healthy volunteers. These data provide the first controlled evidence of immunogenicity of DCs in humans. We will now examine the strength and durability of the T immunity using newer quantitative assays. In studies proposed herein, we will next determine the magnitude of EBV specific memory using DCs as APCs and EBV specific effector CTL response using newer sensitive assays (ELISPOT and MHC-tetramer binding) in patients with HIV infection, as compared to normal hosts. Using the ELISPOT assay, we will also examine the nature of CD4+ve T cell immunity to EBV in these populations. These studies will serve as a baseline for future immune therapeutic trials to boost EBV and HIV specific immune responses. Recent studies in our laboratory have demonstrated that DCs can acquire exogenous antigen from apoptotic cells and generate CD8+ CTLs. There fore we will examine if DCs are able to acquire antigen from apoptotic EBV infected cells, as a potentially novel strategy for generating EBV specific CTL responses in patients. The long term goals are to use DCs as adjuvants to boost EBV and HIV specific immune response in patients with HIV associated lymphoma. The proposed studies and career development plan will provide the necessary laboratory experience to complement the PI s prior expertise in clinical oncology research and lay the foundation for career as a physician-scientist in tumor immunology. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: EPSTEIN BARR VIRUS INDUCED GENOMIC INSTABILITY Principal Investigator & Institution: Sixbey, John W.; Professor; Microbiology and Immunology; Louisiana State Univ Hsc Shreveport P. O. Box 33932 Shreveport, La 71103 Timing: Fiscal Year 2001; Project Start 05-APR-1995; Project End 31-MAR-2006 Summary: (provided by the applicant): The Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus that, despite the life-time rapport typically achieved with its human host, can be associated with benign (infectious mononucleosis) and malignant (Burkitt's lymphoma, Hodgkin's lymphoma, primary central nervous system lymphoma) lymphoproliferative diseases. The overall objective of this grant is to understand molecular mechanisms by which EBV causes disease and their inter-relatedness to modes of viral persistence in the memory B lymphocyte reservoir. Physiologic signaling via the B cell antigen receptor (surface immunoglobulin) has major implications for the fate of any infected B cell, leading to cell proliferation and differentiation or, conversely,
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apoptosis. Because we showed up-regulation of recombinase activating genes RAG1 and RAG2 upon EBV infection of mature B cells, we now hypothesize that virus diversifies the B cell antigen receptor through induction of secondary immunoglobulin gene rearrangements as a means of assuring adequate survival signaling in infected cell progeny. Renewed V(D)J recombination outside the selective environment of bone marrow or germinal centers has potential pathogenic consequences that include autoimmunity, lymphoproliferation and chromosomal damage. The specific aims to test our hypothesis are: 1) to determine if secondary rearrangements of immunoglobulin variable region genes occur as a consequence of RAG induction by Epstein-Barr virus; 2) to determine if RAG1 and RAG2 are expressed in human peripheral blood lymphocytes in vivo as a consequence of acute EBV infection; 3) to analyze EBV DNA integration as a marker of illegitimate recombination prompted by viral induced RAG expression; 4) to determine the mechanism by which RAG1 and RAG2 are up regulated by latency protein EBNA1. The use of recombinant EBV expressing green fluorescent protein allows rapid selection of infected cells now capable of expressing RAG; concurrent analysis by flow cytometry for altered surface immunoglobulin; detection by PCR of broken DNA ends or excision circles that are byproducts of V(D)J recombination; and subsequent analysis for chromosomal abnormalities from aberrant RAG. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EXPRESSION LYMPHOMAS
PROFILING
OF
PROGRESSED
FOLLICULAR
Principal Investigator & Institution: Elenitoba-Johnson, Kojo Seys John.; Associate Professor; Pathology; University of Utah 200 S University St Salt Lake City, Ut 84112 Timing: Fiscal Year 2001; Project Start 14-JAN-2000; Project End 31-DEC-2002 Summary: (adapted for the investigator's abstract) The incidence of non-Hodgkin's lymphoma (NHL) has been rising more rapidly than that of most other cancers, and accounts for approximately 53,000 new cases of cancer annually. The most dramatic increases have been in the category of diffuse large cell lymphomas, which are aggressive neoplasms with short median survival. Diffuse large B-cell lymphoma (DLBCL) may arise de novo, or as the end result of histologic progression from a preexisting low grade B-cell lymphoma. Accumulating experimental evidence suggests that secondary genetic alterations such as p53 gene mutations or inactivation of the p16INK4A gene in low-grade follicular lymphomas (LGFCL) are associated with histologic transformation to DLBCL. Prior studies have only examined one or a few possible genes that may be implicated in lymphoma progression. It is the investigators hypothesis that multiple molecular aberrations may accompany histologic transformation from LGFCL into DLBCL. They propose to employ microarray analysis in the determination of the important molecular changes associated with histologic progression, by studying matched pairs of LGFCL and DLBCL occurring in the same patient. They shall verify clonal identity in the two tumors by immunoglobulin heavy chain gene PCR analysis, and establish the presence of the characteristic t(14;18) translocation in both samples in order to ensure that both neoplasms originate from a follicular lymphoma. The microarray technology permits the simultaneous study of the expression status of multiple genes and will provide insights into the common patterns of gene dysregulation that contribute to lymphoma progression. Elucidation of these molecular aberrations will allow the delineation of distinct progressed lymphoma subgroups, the identification of molecular prognostic factors, and the development of novel therapeutic targets that are directed at the specific molecular aberrations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FUNCTIONAL/GENOMIC ANALYSIS OF CUTANEOUS T CELL LYMPOMA Principal Investigator & Institution: Kupper, Thomas S.; Professor and Chair; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-AUG-2006 Summary: Mycosis fungoides is the most common form of Cutaneous T Cell Lymphoma, which is in turn the most common adult non-Hodgkin's T cell lymphoma. When the disease is correctly diagnosed in its earliest stages, several treatments are available to arrest disease progression. However, when the diagnosis is made in later stages (e.g., > Stage II), long-term survival is unusual. Current treatments for CTCL are effective primarily when disease is limited clinically to skin; therapies for disease that clinically involves lymph node, peripheral blood, and other organs is largely palliative. There are large deficiencies in our ability to diagnose and treat this non-Hodgkins lymphoma. Moreover, our understanding of the biology of this disease is at best primitive. In the last decade, our understanding of how memory T cells mediate immunosurveillance in different tissues has grown exponentially. Memory T cells that home to skin utilize specific cell surface molecules to exit blood into skin, including CLA, CCR4, and LFA-1. This occurs constitutively, as normal skin contains many such cells, but is greatly facilitated by inflammation, which up-regulates the ligands of the above molecules. Our preliminary data and that of others compel us to state the hypothesis that CTCL is a malignancy of CD4+ skin homing memory T cells. Against this background, we propose the following Specific Aims. To improve our ability to diagnose and treat CTCL, we propose to fully characterize, both functionally and phenotypically, the molecules on MF T cells that are involved with T cell trafficking. We propose that CTCL that involves skin only will express high levels of CCR4 and CCR10 and relatively little CCR7 an L selectin. Conversely, T cells in CTCL that involves lymph nodes will express L selectin, CCR7, and LFA-1 the trinity of homing molecules required for entry into lymph node from blood. Finally, we will test the hypothesis that leukemic CTCL cells do not respond well to skin derived chemokines normally involved in skin homing. In a second specific aim, we seek to generate new hypotheses about the biology of CTCL, by using whole genome microarray approaches to human CTCL cells and normal T cells. Taken together, we believe that these studies will improve the accuracy of both diagnosis and prognosis in this disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GENETIC ANALYSIS OF CHEMICALLY INDUCED LYMPHOMAS IN MICE Principal Investigator & Institution: Conti, Claudio J, Dvm.; Biologist & Professor; Carcinogenesis; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2001; Project Start 23-MAY-2001; Project End 31-MAR-2005 Summary: (provided by applicant): The outbred SENCAR stock of mice has been a useful model for dissecting out the multistage nature of cancer development as well as the critical mechanisms involved in skin tumorigenesis. More recently several inbred strains derived from the SENCAR stock have been developed. These strains display different sensitivities to two-stage carcinogenesis and, in particular, some of them show a dissociation between the susceptibility to papilloma development and their malignant conversion into Squamous Cell Carcinomas (SCC). Interestingly we have recently shown that the treatment of young SENCARB/Pt mice with N-methyl-N-nitrosourea
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(MNU) results in the induction of a high incidence (> 90 percent) of thymic lymphomas occurring between 4 and 6 months after MNU injection. In contrast SSIN mice were not susceptible to MNU induced thymic lymphomas supporting the idea that the differential susceptibility to chemical carcinogenesis between SSIN and SENCARB/Pt is not restricted to the skin model and therefore, these strains constitute a powerful tool for the mechanistic studies of the underlying genetic basis of resistance and susceptibility to chemical carcinogenesis. Specific Aim 1: To establish a genetic mode or the susceptibility to chemically induced thymic lymphomas using SSIN (resistant) and SENCARB/Pt (susceptible) strains. The long-term objective of this project is to identify the putative resistance/susceptibility gene/s that play a role in the differential behavior against chemical carcinogenesis in these two SENCAR-derived inbred strains and investigate their possible mechanisms of action. Using a backcross we have previously identified a region on mouse chromosome 14 containing a putative susceptibility gene for skin tumor progression. We are now proposing to use the lymphoma model to investigate whether lymphoma susceptibility is controlled by the same locus and follows the same genetic models than that observed in the skin model. Specific Aim 2: To identify the gene/s involved in the differential susceptibility to MNU carcinogenesis by positional cloning. We will develop a high-resolution linkage map and a physical map of the region/s harboring gene/s involved in MNU-induced thymic lymphoma susceptibility using intercross mice between the wild derived MBT/Pas strain and SENCARB/Pt. We will continue with approaches to isolate at least the more relevant gene by positional cloning, and positional candidate routes. Specific Aim 3: To investigate the extent of the susceptibility of SENCARB/Pt to environmental carcinogens. So far, we have shown differences in susceptibility in lymphomas and progression of skin cancer. The purpose of this specific aim is to investigate if SENCARB/Pt mice have also a higher susceptibility to chemically induced mammary carcinomas and UV induced skin carcinomas. Specific Aim 4: To investigate whether genomic instability plays a major role in the phenotypic differences between SSIN and SENCARB/Pt strains against chemical carcinogenesis. We have the hypothesis that the differences in susceptibility to chemical carcinogenesis between these strains are related to the different levels of genomic instability displayed. Using a new PCP technique we will be able to evaluate the degree of genomic instability and if this hypothesis is substantiated we will investigate probable mechanisms involved in this phenomena. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETIC MECHANISMS OF B CELL LYMPHOMA Principal Investigator & Institution: Chaganti, Raju S.; Member and Professor, William E. Snee c; Sloan-Kettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 30-SEP-1997; Project End 31-JUL-2004 Summary: The goal of this Program Project is in-depth analysis of normal and deregulated function of two novel genes recently cloned by us from IG gene-associated chromosome translocations in diffuse lymphoma with a large cell component (DLLC), clinically the most significant form of NHL. One, BCL6, is a zinc finger transcription factor mapped to chromosome band 3q27. BCL6 is altered by rearrangement in its 5' non-coding region in about 30% of DLLC and about 50% of follicular lymphomas (FL). Recent studies showed that in about 70% of DLLC and about 50% of FL, the BCL6 gene is also altered by multiple, often bi-allelic, mutations clustering in its %' non-coding region. These mutations are somatic in origin and independent of rearrangement by chromosome translocation. Our goals for BCL6 studies are represented by three projects in this Program Project which address the following issues: (1) mechanism,
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consequence, and role in NHL development of BCL6 and cytokine signaling, and (3) POK proteins in ontogenesis, lymphopoiesis, and lymphomagenesis. BCL8 has just been identified by virtue of its rearrangement with IGH gene in a DLLC by way of a chromosome translocation. It maps to 15q11-13. The goal of the final project in this Program Project is to investigate the structure and function of normal BCL8 and the mechanism and consequence of its alteration to NHL development. The studies proposed are designed to gain insights into the normal and abnormal function of BCL6 and BCL8 genes. Such insights are essential to understand the roles of these genes in normal mammalian development and human tumorigenesis. The four projects will be aided by an Administrative Core and a Mouse Molecular Pathology Core. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: GENETIC PATHWAY TO IGH TRANSLOCATIONS IN LYMPHOMA Principal Investigator & Institution: Willerford, Dennis M.; Associate Professor; Medicine; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-JAN-2000; Project End 31-DEC-2004 Summary: Non-hodgkin s lymphomas are an important cause of cancer morbidity and mortality in the United States. The majority of these tumors arise in the B cell lineage and carry chromosome translocations involving the immunoglobulin loci. Expression of oncogenes in the vicinity of the breakpoint is deregulated, thereby contributing to cellular transformation. Lymphoid cells normally undergo somatic rearrangement of V, D, and J gene segments of antigen receptor loci, and there is evidence that this tissuespecific oncogenic mechanism represents aberrant V(D)J recombination. We have observed that mice with a combination of the scid mutation and targeted inactivation of the DNA-damage checkpoint gene p53 uniformly develop high-grade B cell lymphomas at 6-13 weeks of age. The majority of these tumors carry a t(12;15) which appears to involve the IgH locus on chromosome 12. Mutation of Rag-2 suppresses t(12;15) lymphomas in scid p53-/- mice, demonstrating that initiation of V(D)J recombination is a required element in the oncogenic pathway. Thus, we have identified for the first time a genetic pathway involving V(D)J recombinase, which leads reproducibly to a lymphoma-associated Ig locus translocation. The long-range goal of our investigation is to understand elements of the V(D)J recombination process which suppress the generation of chromosome translocations. Such tumor suppressors may be subverted in conditions which predispose to lymphoma development, such as inherited conditions, toxin exposure, infections, including EBV, and immunodeficiencies. We propose to clone translocation breakpoints, identify putative oncogenes and study why some oncogene loci are susceptible as translocation targets. Factors regulating the efficiency of aberrant V(D)J recombination, such as mutations in recombinase compnents or in genes mediating cellular responses to DNA damage are studied, and the mechanism of p53mediated tumor suppression is investigated. By understanding the mechanisms which act to prevent translocations during lymphocyte gene rearrangement, we hope to develop models for testing the mechanism of lymphomagenic agents, including studies of how immune responses may contribute to tumor development. Ultimately, strategies to prevent lymphoma development in groups at increased risk may emerge. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: GROWTH REGULATION AND THERAPY OF LEUKEMIAS AND LYMPHOMAS Principal Investigator & Institution: Bondada, Subbarao A.; Professor; Microbiology Immunology, and Molecular Genetics; University of Kentucky 109 Kinkead Hall Lexington, Ky 40506 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2008 Summary: The overall goal of this program project is to understand the molecular mechanisms underlying leukemia and lymphoma development and to devise novel therapeutic strategies to control lymphoid neoplasms. There are four highly interactive projects that progress from basic studies to clinically applicable therapeutic strategies with a delicate balance between in vitro and in vivo model systems. Project 1: Cell Cycle Progression of Normal and Malignant B Cells: Dr. Snow will study the role of cell cycle regulators in the ability of CD40 to synergise with BCR to induce cell cycle progression in normal B cells. They will determine the basis of the diverse response patterns of three subgroups of B cell lymphomas to CD40 signaling and the in vivo relevance of such CD40 signaling for B lymphoma growth using transgenic mice. Porject 2: Role of egr-1 gene in the growth regulation of normal B cells and B cell lymphoma: Dr. Bondada will study the basis of B cell receptor induced down regulation of the immediate early gene, egr-1 and its relation to lymphoma growth inhibition using BKS-2, a B cell lymphoma. The importance of egr-1 for B cell development and B lymphoma growth will be studied in transgenic mice that express a dominant negative form of the egr-1 protein. Project 3: Biological chaaracterization of human leukemic stem cells (LSC): Dr. Jordan will examine the novel concept that LSC are the basis of relapse of drug treated leukemias. The growth requirement of LSC will be characterized. Modulation of pro and antiapoptotic genes will be explored to control leukemic cell growth. Project 4: Graft-versustumor (GVT) activity of syngeneic/allogeneic graft versus host disease (GVHD): Dr. Bryson will determine the cellular mechanisms involved in GVHD and in GVT reaction. They will test the hypothesis that cyclosporin A induced oxidative stress directly participates in the induction of SGVHD. Cellular basis of the lack of memory in GV7responses will be studied. Support for three Cores, a transgenic and genetically defined animal facility, histopathology and administrative core, is requested to support the rsearch in this PO1 application. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: HHV-8 IN PRIMARY EFFUSION LYMPHOMAS Principal Investigator & Institution: Koeffler, H P.; Cedars-Sinai Medical Center Box 48750, 8700 Beverly Blvd Los Angeles, Ca 90048 Timing: Fiscal Year 2001; Project Start 15-FEB-1997; Project End 31-JAN-2002 Summary: (Applicant's Description) Kaposi s sarcoma associated herpes virus/human herpesvirus 8 (HHV-8) is found in Kaposi's sarcoma (KS) and primary effusion lymphomas (PEL). The applicant has the largest collection of frozen PEL samples and their DNA and RNA. Also, he has established an EBV-negative, PEL cell line (KS-1) that produces large quantities of HHV-8 which can actively infect other cells. Armed with these tools, the applicant will: 1) determine the spectrum of HHV-8-related disorders and determine which hematopoietic cells are permissive for HHV-8 infection. The tissue bank of 3,800 lymphoproliferative disorders, of which 722 are from HIV-infected individuals, will allow him to determine which disorders contain HHV-8 sequences. Also, the hematopoietic cell types permissive for HHV-8 infection will be determined, including macrophages and dendritic cells. 2) Identify and study cytokines produced by
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HHV-8-infected lymphocytes and determine the effect of cytokines and other agents on growth of HHV-8 infected cells. Using the KS-1 cell line and matched HHV-8 infected lymphoma lines, the applicant will determine cytokines produced by the cells and identify cytokines that stimulate growth of the cells and determine if autocrine loops exist. 3) Define the modulation of HHV-8 expression in lymphoid cells, especially from open reading frame-72 (ORF-72, cylin D-like homolog) and correlate these results with their modulation of growth and apoptosis. The applicant s KS-1 and other HHV-8 infected lymphoma cell lines will be exposed to active compounds and their expression of ORF-72, -73, -74, -75 can be correlated with their alterations in clonal growth, apoptosis and apoptosis-related proteins. Additional studies of ORF-72 will determine its protein partners, kinase activity, and ability to deregulate the cell cycle. Selective molecular biology studies will also be performed on PEL cells: A) determine their cytogenetic abnormalities, B) examine for their alterations of selected tumor suppressor genes, and C) perform allelotyping of PEL to determine DNA regions that contain altered tumor suppressor genes. In summary, the unique cell line, its ability to infect other cells and the large tumor bank will allow in-depth analysis of HHV-8 related lymphomas. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IMMUNOGENETICS OF NON-HODGKIN LYMPHOMA SURVIVAL Principal Investigator & Institution: Cerhan, James R.; Associate Professor; Mayo Clinic Rochester 200 1St St Sw Rochester, Mn 55905 Timing: Fiscal Year 2002; Project Start 16-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): Non-Hodgkin Lymphoma (NHL) incidence and mortality have been increasing over the past 50 years, and these trends are largely unexplained. The five-year survival rates are 50% overall, and appear to have changed little over the last several decades. For NHL, a compelling hypothesis is that survival may be related to the host immune status, which is in part influenced by functional polymorphisms in genes encoding cytokines and chemokines central to immune function and regulation. The role for host immunogenetic susceptibility in overall survival from NHL is largely unexplored. We propose to systematically test the hypothesis that genes with functional, common variant polymorphisms involved in immune function and regulation are associated with overall survival from NHL. Our specific aims are: 1) to evaluate the association of polymorphisms in selected immunerelated genes from four key pathways on NHL survival that include genes encoding inflammatory and regulatory cytokines (IL-1A IL-1B IL-1RN TNFalpha), Th1/Th2 cytokines (LTA, INFgamma IL-4, IL-4RA IL-6 iL-JO, IL-13), innate immunity (MPO, ICAM-1) and chemokines (IL-8, SDF-1, CCR2, CCR5); 2) to evaluate whether any effects are independent of other NHIL prognostic factors (e.g., age, stage, ECOG performance status, extranodal site involvement, and serum LDH), and treatment modality; and 3) to evaluate whether any effects are specific for diffuse large B-cell lymphoma or the combination of follicular and small lymphocytic lymphoma. To achieve these aims, we will develop a prognostic cohort using 364 HIV-negative NHL patients who participated in a population-based case-control study in Iowa. The patients were aged 20-74 years when first diagnosed from 1998-2000. We will abstract treatment and other clinical/laboratory prognostic data from the medical record. We will follow all of these patients by both passive and active means through mid-2006 (a minimum of 6.5 years) in order to identify all deaths (including cause of death) and disease recurrences. Genotyping will be conducted in conjunction with the investigators at the National Cancer Institute. The association of genotype frequencies with NEIL survival will be
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evaluated using standard survival analysis approaches, and we have sufficient statistical power to detect clinically meaningful hazard ratios. In summary, we will evaluate innovative translational hypotheses regarding the immunogenetic determinants of NEIL survival in order to better understand disease pathogenesis, treatment response, and disease prognosis among patients from the community. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: IMPROVED QUANTITATIVE GA-65 SPECT IMAGING Principal Investigator & Institution: Moore, Stephen C.; Associate Professor; Brigham and Women's Hospital 75 Francis Street Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 09-JAN-1998; Project End 31-DEC-2002 Summary: (Adapted from Applicant's Abstract): The goal of the proposed research is to improve the acquisition, reconstruction, and extraction of quantitative information from Ga-67 SPECT data, and to assess these improvements to the imaging system using taskdependent criteria. Gallium has proven to be a useful nuclear medicine tracer for imaging certain tumors, and it is known that gallium avidity is correlated with histopathologic tumor grade. Imaging Ga-67, however, is challenging because it emits many high-energy photons. Quantitative estimates of Ga-67 tumor uptake are degraded by three principal sources of error: a location-dependent bias caused by imperfect correction for photon scatter and nonuniform attenuation, a size-dependent bias due to blurring by the nonstationary detector response function, and stochastic variability arising from Poisson noise in the acquired data. The proposed research will address these challenges by (1) optimizing for Ga-67 imaging several methods of correcting images for the effects of scatter and attenuation in the patient, (2) modifying for Ga-67 SPECT methods that have previously been developed for estimating activity within volumes of interest using a priori boundary information from registered CT images, and (3) designing a new collimator, tailored for Ga-67 quantitation in body imaging. These aspects of the imaging system will be optimized and evaluated on the basis of performance in several quantitative imaging tasks. The tasks to be considered, prototypes of tumor quantitation in the chest and abdomen, will involve estimation of activity concentration and size of lesions located in anatomically realistic backgrounds. For each of these tasks, Cramer-Rao lower bounds on variance or mean-squared error will be computed to determine the best possible performance for different correction methods, while maximum-likelihood or Bayesian parameter estimation will be used to measure best realized performance. Volume-of-interest activity estimation with resolution recovery will be used to assess clinically realizable performance. The investigators will measure, by simulation and phantom experiment, the improvements in performance in these tasks, and compare the results with theoretical bounds on performance. They will also consider clinical classification tasks related to non-Hodgkin s lymphoma. It is expect that the proposed imaging system improvements will lead to more accurate staging of lymphoma patients and, consequently, improved patient care due to enhanced capability to follow the progression of disease, choose the best treatment, and monitor the response to therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: LYMPHOID TRANSFORMATION WITH HUMAN HERPESVIRUS 8 K1 Principal Investigator & Institution: Samaniego, Felipe C.; Assistant Professor; Clinical Cancer Prevention; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030
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Timing: Fiscal Year 2003; Project Start 13-SEP-2003; Project End 31-AUG-2006 Summary: (provided by applicant): In this K22 award application, the PI describes plans for career development through a comprehensive research plan to define the role of HHV-8 K1 in lymphocytes and lymphoma. The PI has generated data showing that the K1 gene codes for a transmembrane protein with an immunoreceptor tyrosine-based activation motif (ITAM). K1 stimulates NF-kappaB activity and K1 expression in transgenic mice induces lymphoma development. Lymphoma cells expressing K1 became resistant to apoptosis that is induced by fas antibody. Equipped with the reagents and models described, the PI will be able to complete the proposed studies showing the role of K1 in lymphocyte signaling and possible transformation. The hypothesis to be tested is that K1 expression in lymphocytes and lymphoma cells stimulates NF-kappaB signaling and other pathways, leading to the transformation of lymphocytes and development of lymphoma. Specific Aim 1. To establish whether K1 expression is associated with the development of lymphoma. New lines of transgenic mice will be developed and the resulting lymphomas characterized. Specific Aim 2. To delineate the signaling pathway of K1 in lymphoma cells and lymphocytes. Using dominant negative constructs and specific active blocking reagents that target NFkappaB, NFAT, or AP-1, the pattern of K1 signaling will be determined. ITAM deleted K1 and other constructs will be used to identify K1's signaling pathway. Specific Aim 3. To determine whether K1 suppresses apoptosis. Early mediators of fas-dependent apoptosis will be characterized through monitoring of caspase activation. K1 can induce lymphocyte signaling that may constitute the early steps leading to lymphocyte transformation. By analyzing K1 signaling in lymphocytes and its long-term expression in transgenic mice, we will determine K1's role in mediating cell signaling and lymphoma development. By carrying out the plans in this application, the PI will show how a viral gene participates in inducing lymphoma and offer insights into therapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LYMPHOMA TRANSPLANTS
THERAPY
USING
MIXED
PROGENITOR
Principal Investigator & Institution: Strober, Samuel; Professor of Medicine; Medicine; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 08-JUN-2001; Project End 31-MAY-2005 Summary: The goal of the proposed research is to effectively treat the BCL1, B cell lymphoma, in mice using an in allogeneic bone marrow transportation regimen that will not only eliminate tumor cells without graft versus host disease (GVHD), but also allow for satisfactory immune reconstitution of hosts lacking a thymus. Immune reconstitution of MHC-haplotype matched humans given bone marrow or hematopoietic progenitor transplants for treatment of malignancy remains a major problem. In order to facilitate immune reconstitution of CD4+ and CD8* T cells in lethally irradiated BALB/c x C57BL/6 hosts, we will add a newly identified committed T cell progenitor (CTP) to allogeneic C57BL/6 transplants that include purified hematopoietic stem cells (HSC) for hematopoietic reconstitution and purified marrow CD8' T cells for tumor cell killing without GVHD. Hosts will be euthymic or thymectomized. The CTP have been shown to rapidly reconstitute the CD4+ and CD8' T cells of irradiated athymic nude mice via an extrathymic pathway. Hosts will be monitored for survival, tumor cell elimination chimerism, GVHD, and reconstitution of mature CD4' and CD8' T cells. The function of the latter cells will be determined by assaying protection against murine cytomegalovirus infection, antibody responses to sheep red blood cells, and delayed type hypersensitivity responses to ovalbumin. In addition, donor-type chimeric cells
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will be studied for tolerance to host alloantigens. Purified populations of donor cells will be obtained by cytometry to identify and sort HSC, CTP, and CDS' T cells. Chimerism and presence of tumor cells will be measured by immunofluorescent staining and flow cytometric analysis such that chimeric cells derived from each of the three injected donor cells can be identified. GVHD will be monitored by clinical signs, survival, and histopathology. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LYMPHOMAGENESIS Principal Investigator & Institution: Choi, Yong S.; Laboratory Director; Ochsner Clinic Foundation 1514 Jefferson Hwy New Orleans, La 70121 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2005 Summary: A number of lymphoma including follicular cell, Burkitt's, and diffuse large cell lymphoma are known to originate from lymphoid tissues. Although the pathobiology of malignant B cells has been studied extensively, the role of the germinal center (GC)-microenvironment in lymphomagenesis has not been investigated in the molecular term. The GC is an unique microenvironment where antigen-activated B cells undergo clonal selection by proliferation and apoptosis, selecting memory B cells. At the same time, the genetic events such as somatic mutation and Ig-isotype switching occur, producing high-affinity antibodies. B cell lymphoma originate as a consequence of the genetic mobility and mutability. Follicular dendritic cell (FDC) is a stromal cell located inside but not outside of the GC. Furthermore, most of the GC-B cells die by apoptosis unless rescued by FDC. FDC provides the signals for survival and proliferation of GC-B cells and lymphoma cells in the early stage of lymphomagenesis. The objective is to characterize the function of FDC in B cell lymphomagenesis in the molecular term. Specific Aims are to identify the FDC-signaling molecules, using the FDC-specific monoclonal antibodies and a mammalian cell expression vector, and to characterize the function of the FDC-molecules in lymphomagenesis in vivo. The molecular identification of the FDC signaling molecule will help us understand the unique role of the stromal cells in blast transformation of lymphoma cells. In addition, it will facilitate the development of the therapeutic monoclonal antibodies and antagonists which block the propagation of lymphoma cells. Furthermore, our in vivo experimental model will be useful in discovering the target genes for the anti-cancer drugs. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: MAPPING AND CLONING TRANSLOCATION BREAKPOINTS Principal Investigator & Institution: Rowley, Janet D.; Blum-Riese Distinguished Serv Professor; Medicine; University of Chicago 5801 S Ellis Ave Chicago, Il 60637 Timing: Fiscal Year 2001; Project Start 08-JUN-2000; Project End 31-MAY-2005 Summary: (adapted from the applicant's abstract) Malignant cells from human leukemia and lymphoma have a very high frequency of chromosome abnormalities, especially translocations. Careful cytogenetic analysis has defined the breakpoints in recurring chromosome rearrangements, and this has been the major tool leading to identification of genes critically involved in leukemia and lymphoma. Mapping and cloning chromosome translocation breakpoints in leukemia, lymphoma and sarcoma have been one of the most efficient ways to discover new genes that are important in malignant transformation of hematopoietic cells. Although most of the common recurring rearrangements in leukemia have been cloned, the mapping and cloning of rare rearrangements continues to provide a wealth of biologically relevant information. The
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long-term goal of this project is to identify new genes involved in leukemia and lymphoma. The strategy will be to use translocation breakpoints to identify the chromosome location of the involved genes using defined genomic probes and fluorescence in situ hybridization (FISH). Samples containing malignant cells will be analyzed from two groups. The first group will be patients known to have rearrangements of MLL, TEL, or AML1 (Specific Aim 1). These three genes are very important in human acute leukemia as well as in other hematologic diseases. They have been shown to be involved in translocations with many other genes. Cloning these partner genes has identified a large number of previously unknown genes that play a role in transformation of hematopoietic cells. The second group includes patients with breakpoints in 11q, 12p, and 21q whose breaks do not involve MLL, TEL or AML1 (Specific Aim 2). The breakpoints of rearrangements in these three regions will be mapped using FISH to determine whether any of them cluster in a particular location. For translocations in which neither partner gene is known, probes that are split will be identified to determine the involved gene. DNA probes appropriate for the genes will be used to determine whether these "new" genes are involved in other rearrangements in samples that have the same breakpoint. Various cDNA selection strategies will be used to clone the involved gene as well as the partner gene. This research will identify genes involved in leukemogenesis and based on past results, most of these will be novel genes whose identification will enrich our understanding of the complex genetic changes involved in malignant transformation of hematopoietic cells. Identification of these genes has provided a very valuable resource for clinical medicine because they are used to improve the diagnostic precision with which the genotype of the malignant cells can be determined. Moreover, particular cytogenetic abnormalities have very great prognostic implications so that patients are stratified for treatment based on the karyotype of their malignant cells. The more translocations we can identify, the more complete will be our diagnostic tests. Especially with the advent of DNA chip technology, we could screen for all of the fusion genes and the prognostic implications of even rare rearrangements could be determined. In the future, when we have sufficient understanding of the biology of these genes, we can hope to develop genotypic specific treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MODELING AND DOSIMETRY FOR RADIOLABELED ANTIBODY THERAPY Principal Investigator & Institution: Sgouros, George; Associate Member; SloanKettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 01-APR-1995; Project End 31-JAN-2003 Summary: Overall objective: Develop and implement treatment planning approaches for optimizing radio-immunotherapy (RIT). The emphasis during the first period of funding was on developing analytical tools for achieving this objective. The emphasis in this application is on applying these tools in the analysis and optimization of novel and emerging RIT. Specific Aims: 1. Calculate the expected therapeutic impact of prescribing, for each patient, the amount of unlabeled (cold) antibody (Ab) given in RIT of non-Hodgkin's Lymphoma; define a protocol for obtaining the optimum amount. 2. Using models of normal tissue histology for microdosimetry calculations, estimate expected normal tissue toxicity with alpha- emitter RIT; predict appropriate doseescalation schedules for alpha- emitter RIT for minimal disease. 3. Continue support and development of techniques and software related to 3-D and patient-specific internal dosimetry. Background & Methods: 1. 131I-anti-Bl Ab has yielded durable complete
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responses in patients with otherwise untreatable non-Hodgkin's Lymphoma/ Currently, 131I-anti-Bl is preceded by a fixed amount of cold anti-Bl for all patients. This is thought to improve targeting by saturating rapidly accessible, non-tumor antigen sites. Total tumor burden will be estimated from CT and SPECT of 131I-anti-Bl patients. Absorbed dose and dose volume-histograms of several index tumors will be calculated to evaluate correspondence with response. Retrospective analyses will be conducted to see if "underdosing" (too little Ab relative to tumor burden) led to reduced response and "overdosing" to increased toxicity. 2. Alpha emitters are ideal for eradicating minimal or micrometastatic disease due to their short range and high energy. These properties also make it difficult to predict normal organ toxicity. Mathematical models of organ histology will be developed and used for microdosimetry calculations to evaluate toxicity in RIT trials directed against micrometastases. 3. The dosimetery methodologies developed under this grant have been implemented in a software package called 3D-ID (3d-Internal Dosimetry). This software has been provided to, and used by, several outside investigators in on-going collaborations. Aim 3 will make it possible to continue upgrading and adding features to this software and also to continue investigating new, dosimetry-related, techniques for treatment planning. Summary: Completion of the aims will (1) markedly improve what is likely to become a prevalent therapy for NonHodgkin's Lymphoma and (2) will provide fundamental information for designing clinical trials of a novel and emerging approach for eradicating minimal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR CLASSIFICATION OF B-CELL LYMPHOMA Principal Investigator & Institution: Chan, Wing C.; Professor of Pathology; Pathology and Microbiology; University of Nebraska Medical Center Omaha, Ne 681987835 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-MAR-2004 Summary: Tumors derived from the same cell type and having similar morphology may nevertheless have a distinctly different clinical behavior and response to therapy. Differences in the genetic lesions in these tumors, as reflected by their gene expression profiles, will provide insight into the mechanisms underlying the divergent clinical spectrum that is observed. Comparative genomic hybridization (CGH) and spectral karyotyping (SKY) are highly complementary novel techniques that examine the entire genome for genetic abnormalities and can supplement and extend conventional cytogenetic studies. In addition, the recently - developed high-density cDNA microarray technology is a very promising method for displaying the pattern of gene expression in tumor tissues. These powerful technologies with their associated informatic systems are now available for translational research. In order to evaluate the information generated by these technologies, an adequate number of well-characterized tumors with detailed clinical data must be available. We propose a multi-institutional, comprehensive molecular analysis of a large series of B-cell non-Hodgkin's lymphoma (NHL). The molecular data obtained will be correlated with the clinical and pathologic information in the extensive databases kept at our institutions to identify clinically and biologically distinct subsets of B- NHL. When unique molecular profiles of clinical and biological significance are identified, we will then define which components within each profile are essential determinants of the clinical features and outcome. Specific confirmatory assays for the expression of key genes, and the cytogenetic abnormalities involving these genes, will be performed. Our longer term goal is to use this information to design a simpler and less expensive microarray for diagnostic use. This "diagnostic chip" could provide rapid molecular characterization of every B-NHL at presentation for optimal treatment decisions and prognostication. We also anticipate the identification of new
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and significant genetic alterations that will contribute to our understanding of the key events in neoplastic transformation and tumor progression. The insights gained from this project may also identify novel targets for preventive and therapeutic interventions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LYMPHOMA
MOLECULAR
EPIDEMIOLOGY
OF
AIDS-ASSOCIATED
Principal Investigator & Institution: Martinez-Maza, Otoniel M.; Professor; Obstetrics and Gynecology; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024 Timing: Fiscal Year 2002; Project Start 30-SEP-1997; Project End 31-MAY-2005 Summary: (Provided by the applicant): Non-Hodgkin' s B cell lymphoma (AIDSlymphoma) is seen in greatly-elevated frequency in HIV-infected people, not only in North America and Europe, but worldwide. In this proposal, studies are presented to elucidate the molecular epidemiology of AIDS-lymphoma. The proposed studies will utilize the resources of the Multicenter AIDS Cohort Study of the Natural History of AIDS (MACS). In prior studies supported by this award, elevated levels of various immune system molecules that are associated with B cell activation, including IL6 and IL10, sCD23, sCD27, sCD44, and IgE, were seen prior to the clinical detection of AIDSlymphoma. Notably, there were clear differences in the patterns of expression of such B cell-stimulatory molecules seen in different subtypes of AIDS-lymphoma (Burkitt's/SNCCL vs. other subtypes), suggesting that there are differences in the character of the immune dysfunction that precedes the development of different subsets of these cancers. In addition to this, in very recent work we saw that a single-nucleotide polymorphism (SNP) in the IL10 promoter (-592 C/C), which is known to result in increased expression of IL10, was associated with the development of AIDS-lymphoma. These findings are of great significance, since few risk factors have been identified for AIDS-lymphoma. The specific aims of the proposed studies are to determine: I ) if enhanced B cell stimulation, elevated immunoglobulin isotype switch activity, detectable c-myc:Ig gene translocations, and/or detectable circulating B cells with a germinal center-like phenotype, precede the development of AIDS- lymphoma, 2) if SNPs in the genes encoding B cell-stimulatory cytokines (IL6, IL10, TNFalpha, LTalpha, RANTES) are associated with an elevated risk for the development of AIDS-lymphoma, and 3) if subjects who have a genotype that has been seen to be associated with a decreased risk for developing AIDS-lymphoma (CCR5 delta-32 heterozygotes, SDF-1 3'UTR 801 G/G SNP, or IL10 promoter -592 A/A or A/C SNP) show lower levels of B cell activation. The accomplishment of these specific aims will add valuable new information to our understanding of the molecular epidemiology of AIDS-lymphoma, as well as the role of immune dysfunction in the generation and growth of this cancer. This information could form the foundation for future studies on the pathogenesis of AIDS-lymphoma, and may lead to new screening techniques able to detect AIDSlymphoma earlier in the course of tumor development, allowing for earlier and more effective clinical intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: MOLECULAR MECHANISMS OF CD30+ LYMPHOMA GROWTH Principal Investigator & Institution: Podack, Eckhard R.; Professor and Chairman; Microbiology and Immunology; University of Miami-Medical Box 248293 Coral Gables, Fl 33124
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Timing: Fiscal Year 2001; Project Start 01-FEB-1999; Project End 31-DEC-2002 Summary: CD30 has long been recognized as a unique antigen on lymphomas of T or B origin of immature to the fully differentiated state. CD30 moreover has been found to be associated with disease progression in anaplastic large cell lymphoma. CD30 is expressed as a disease marker in allergic conditions and CD30 expression is associated with progression of HIV disease, with Epstein-Bar virus infection and transformation and with HTLV associated lymphomas. Finally, CD30 over-expression is found in Omenn's syndrome, a severe combined immunodeficiency of unknown etiology, characterized by high Il-5 levels, eosinophilia and IgE production. CD30 signaling functions via TRAF proteins have recently been elucidated. Similar to other members of the TNF-R family of receptors, CD30 signals have a dual role for activation, proliferation and anti-apoptosis; or for apoptosis. CD30 expression itself is favored by a TH2 environment and suppressed by Ifn-gamma. It is postulated and will be tested in this application that CD30 expressed on lymphomas provides a selective advantage to lymphomas or other CD30 positive cells through its co- stimulatory activity, by promoting proliferation and increasing resistance to apoptosis. This hypothesis will be examined 1. by analyzing pathways regulating TRAF2 activity which is primarily responsible for anti apoptotic signals through Jun-N-terminal kinase (JNK) and NFkappaB activation; 2. by CD30-L gene ablation to eliminate CD30-L triggered CD30 signals and signaling by CD30 induction on ongoing immune responses to tumors in vivo and in vitro. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LYMPHOMA
MONOCLONAL
ANTIBODY
THERAPY
FOR
FOLLICULAR
Principal Investigator & Institution: Friedberg, Jonathan W.; Medicine; University of Rochester Orpa - Rc Box 270140 Rochester, Ny 14627 Timing: Fiscal Year 2003; Project Start 01-SEP-2003; Project End 31-AUG-2008 Summary: (provided by applicant): As both basic laboratory research and clinical research become increasingly complex, development of novel therapeutic strategies for patients with B-cell malignancies requires collaborative efforts between clinical researchers and basic scientists. During the proposed funding period, a formal didactic program, dedicated team of mentors with a history of training investigators, and a supportive, enthusiastic environment should allow the applicant to achieve an independent research career as such a "translational" investigator in the field of lymphoma therapy. Patients with advanced stage follicular non-Hodgkin's lymphoma (NHL) are generally accepted to be incurable with conventional treatment, and the median survival has not changed significantly in the past thirty years. Novel approaches with minimal toxicity are therefore needed. Rituximab, a chimeric CD20 monoclonal antibody, has significant, albeit limited activity as a single agent for treatment of follicular NHL. Immunostimulatory DNA oligonucleotides (ISS) are novel compounds that have pleotropic immunological effects, including enhancement of antigen presentation and costimulatory molecule expression, stimulation of dendritic cell maturation, and induction of cytokines resulting in enhanced antibody-dependent cellmediated cytotoxicity (ADCC). Through these effects on both the adaptive and innate immune response, ISS have significant promise as synergistic agents with monoclonal antibody therapy such as dtuximab, with minimal added toxicity. Given a favorable safety profile, and evidence of biologic activity in an ongoing phase I study of ISS (1018) with rituximab, this project proposes to test the efficacy of rituximab in combination with 1018 ISS in a phase II study for patients with relapsed follicular NHL Detailed
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analysis of the immunological effects of this combination both in vivo and in vitro, including evaluation of effector cell number and function, dendritic cell maturation, and changes in the tumor microenvironment, will allow optimization of this rational combination for further clinical development. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NOVEL HUMAN ANTI-CD19 ANTIBODIES FOR LYMPHOMA THERAPY Principal Investigator & Institution: Ma, Dangshe; Progenics Pharmaceuticals, Inc. 777 Old Saw Mill River Rd Tarrytown, Ny 10591 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2005 Summary: (provided by applicant): Non-Hodgkin's lymphoma (NHL) is the fifth most common type of cancer in the United States. Approximately 300,000 people are currently living with NHL in the U.S. and an estimated 53,900 new cases will occur in 2002. The 5% annual increase in incidence is the fastest for any human cancer. The therapeutic utility of unmodified monoclonal antibodies (mAbs) and radiolabeled mAbs against the B-cell antigen CD20 is demonstrated by the recent FDA approvals of these agents for the treatment of relapse and refractory B-cell NHL. Although response rates are high, complete cures are rare and the median duration of response is only 1-2 years. Consequently, there is an urgent need for new therapies to prevent or combat disease relapse. CD19 is a 95-kD membrane glycoprotein found on nearly all of B-cell lymphomas, chronic lymphocytic leukemias (CLL), and acute lymphoblastic leukemias (ALL). CD19 is not expressed on mature plasma cells, hematopoietic stem cells, or normal tissues outside the B-lineage. The CDI9 protein is not shed into the circulation and is maintained on tumors despite loss of CD20 expression following anti-CD20 therapy. Taken together, the expression profile of CD19 makes it a highly attractive target for immunotherapy of B-cell neoplasms. Our recent studies in mouse models of human lymphoma demonstrated that CD19 offers clear advantages over CD20 as a target for radioimmunotherapies that employ both traditional and highly innovative radionuclides. The profound anti-tumor effects observed in these studies provide compelling proof-of-principle for CD19-directed therapies. However, our studies employed murine CD19 mAbs that have foreseeable limitations for use in humans. A fully human mAb that recognizes CD19 with high affinity and specificity would be an ideal candidate for therapy. We propose development of novel, fully-human anti-CD19 mAbs using mice that are transgenic for the human immunoglobulin gene locus. The mAbs will be evaluated for specificity and anti-tumor properties in vitro in both unlabeled form and when labeled with novel alpha- and beta-emitting therapeutic isotopes. The most promising immunotherapeutic agents will be critically evaluated for their therapeutic potential using the best available animal models of human lymphoma. Success in the project would provide strong impetus to rapidly advance the most promising agents into development for human clinical testing. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NOVEL MONOCLONAL ANTIBODY THERAPIES FOR LYMPHOMA Principal Investigator & Institution: Leonard, John P.; Assistant Professor of Medicine; Medicine; Weill Medical College of Cornell Univ New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 01-SEP-2001; Project End 31-AUG-2006 Summary: (provided by applicant): Development of novel therapeutic strategies in lymphoma and other B-cell malignancies requires collaborative efforts between clinical
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researchers and basic scientists. There is a clear need for individuals with skills in patient care, clinical trial design, and basic science principles who can bridge the gap between the bench and the bedside in the conception, development and evaluation of new treatments in these and other forms of cancer. As the principal investigator in this project, Dr. Leonard is dedicated to further his research activities and undergo further mentored training for his career development to fill this long term role. In order to attain the necessary skills, the strategy is to follow an educational and research path including: 1) Previous bench laboratory work in hematopoiesis and gene therapy 2) Didactic and mentored training in clinical trial design with Drs. Joseph Bertino and David Nanus, as well as through several institutional resources including the General Clinical Research Center and the Weill Graduate School of Medical Sciences of Cornell University 3) Investigator-initiated monoclonal antibody therapeutic trials for non-Hodgkins lymphoma using I-131 Anti-B1 antibody (tositumomab), epratuzumab, and HulD10 either alone or in combination with chemotherapy or other biologics in the management of untreated or relapsed disease as outlined in Specific Aims 1, 2, and 3. Dr. Leonard has focused in novel monoclonal antibody therapies for lymphoma in this proposal given the rapid emergence of this class of agents as well tolerated and effective new treatments, with a critical need for further exploration into their optimal settings for clinical use. Following this five year comprehensive program, he will attain the independent clinical research skills to work with basic science collaborators to lead a translational research program in the development of other novel treatments for lymphoma. It is also expected that this work will significantly contribute to the care of patients with these and other B-cell malignancies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: NOVEL THERAPEUTIC STRATEGIES IN LEUKEMIA AND LYMPHOMA Principal Investigator & Institution: Griffin, James D.; Professor; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 15-JUN-1996; Project End 31-MAR-2002 Summary: Although most leukemias and lymphomas respond to conventional and high dose therapy, only a small fraction of adults with these diseases are cured. Since most of these tumors can be induced into a complete remission, the major impediment to their cure is the persistence of resistant, minimal residual disease. Over the last decade, the members of this Program have investigated oncogenes, growth regulation, surface molecules, and set up animal models and attempted to address this issue by administering increasingly intensified treatments with only modest improvement in outcome, yet these approaches have been complicated by severe toxicities including myelodysplasia. Although we have translated our basic laboratory studies to the clinic by purging tumor cells from autologous marrow, detecting minimal residual disease, and administering immunotoxins as primary therapy and agents to treat minimal residual disease, most of our patients still relapse. Therefore, to address these issues, we have joined together in a PROGRAM PROJECT to develop novel, non-overlapping treatment strategies which can be added to present treatment approaches in the hope of eradicating residual resistant disease. We believe that the generation of leukemia/lymphoma therapies will continue to come from laboratory studies aimed at understanding the pathogenesis and the molecular and biological characteristics of these diseases. To achieve our goals, we have assembled a team of basic scientists, immunologists, clinical scientists, and oncologists who bring to the Program expertise in a wide range of areas. The central hypothesis of this Program Project is to determine
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how tumor cells evade the immune system, cytotoxic therapy, and immunotherapies. To this end, we plan to study how these neoplastic cells grow; how they interact with the immune system, why the immune system fails to recognize and reject most human leukemias and lymphomas; how to detect minimal residual disease; how to optimally use autologous bone marrow transplantation without damaging hematopoietic stem cells, ad how to harness the immune system to develop novel immunotherapies. We expect these studies to demonstrate specific defects in antigen presentation, antigen recognition, and T cell responses. Our therapeutic objectives will be to attempt to repair one or more of the defective components of the immune system by gene transfer, cytokine therapy, and cell based immunotherapies. By translating basic laboratory studies to the clinic, we hope both improve outcome and decrease toxicity for patients who suffer with these dreaded diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: N-RAS SIGNALING IN TUMORIGENESIS AND PHYSIOLOGY Principal Investigator & Institution: Pellicer, Angel G.; Professor; Pathology; New York University School of Medicine 550 1St Ave New York, Ny 10016 Timing: Fiscal Year 2001; Project Start 01-JAN-1984; Project End 31-DEC-2003 Summary: (adapted from Investigator's abstract) This continuation application investigates the role of N-ras in signal transduction, its role in thymic lymphoma development and the analysis of tumor suppressor genes that cooperate with ras in tumor formation. The grounds for that analysis have been laid out during the previous grant period, during which Dr. Pellicer obtained N-ras transgenic lines carrying the overexpressed normal gene (N-rasN) or the oncogene (N- rasT), knockout N-ras mice (KONras), and has identified the frequent involvement of the INK4b locus(p15) in tumors derived from these mouse strains. These experiments permitted the identification of a specific response to PMA+ ionomycin treatment in KONras derived cells, prompting the proposal of a series of experiments to elucidate where in the pathway this signal becomes N-ras specific, and which domain in the molecule is responsible for the specificity. The observation, that there is an increased lymphoma yield when N-rasT mice are crossed with KONras mice compared to mice wild type for N-ras suggests that the normal allele has a blunting effect on the action of the oncogenic allele. To explore the differences between the N-rasT and the wild type, the effects of increasing amounts of normal allele on the effects of oncogenic N-ras will be measured in vivo and in vitro. The biochemical effects of this competition, the affinity of both NRas isoforms for their targets and the inhibitory effect of NF1 will also be measured. Results have been obtained indicating that the INK4b locus is involved in the development of thymic lymphomas. To understand the role of this locus in lymphoma development, the impact of ras genes on cell cycle regulators will be investigated in vivo, using the transgenic lines. The recent identification of a new molecule derived from the INK4b locus, p10, opens the way to investigate the role of p10 in lymphoma development versus p15, and the mechanism of action of p10 will be studied and its role in vivo analyzed. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: NYUMC-AIDS-RELATED MALIGNANCY CONSORTIUM Principal Investigator & Institution: Takeshita, Kenichi; Dermatology; New York University School of Medicine 550 1St Ave New York, Ny 10016 Timing: Fiscal Year 2001; Project Start 30-SEP-1995; Project End 31-JUL-2002
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Summary: This proposal is for New York University Medical Center (NYUMC) to continue to participate as a member of the NCI-sponsored AIDS- associated Malignancies Clinical Trials Consortium (AMC). The specific aims of this proposal are: 1) To help design, develop and participate in multicenter Phase I and II clinical trials using novel agents and/or innovative approaches for the treatment of patients with AIDS-associated malignancies; 2) To provide well characterized tissue specimens to the recently established AIDS Malignancies Bank (AMB) including: cryopreserved tumor tissue, sera, peripheral blood mononuclear cells (PBMC), bone marrow, and other body fluids from individuals with AIDS-related Neoplasms such as Kaposi's sarcoma (AIDSKS), non- Hodgkin's lymphoma (NHL), Hodgkin's Disease (HD), multicentric angiolymphoproliferative hyperplasia (Castleman's Disease), anogenital or cervical dysplasia and carcinomas. These permanently stored specimens would be made available to other members of the AMC and other investigators in the research community at large for future clinical, epidemiologic, virologic and molecular biological research. NYUMC is an NCI-designed Cancer Center. NIAID supported AIDS- Treatment Evaluation Unit (ATEU), and an NIH sponsored Center for AIDS Research (CFAR) to which patients from the greater New York area are referred. NYUMC has served as a major referral center for HIV-infected individuals from the greater New York area. We continue to see a substantial number of patients with AIDS- related malignancies. Investigators at our institution have an established track record for patient accrual and the performance of clinical treatment trials in a well supported setting. Because of the decrease in patients with AIDS-related malignancies seen in the USA, attributed in part to the use of combination, highly active, antiretroviral therapy (HAART), we have recently enlisted the referral of appropriate patients from investigators at Beth Israel and Northshore Hospitals to participate in the AMC trials performed at the NYUMC. A newly formed health management organization (HMO) which will care for more than 10,000 HIV/AIDS clients on Medicaid in NYC has also agreed to refer suitable patients to our AMC clinical trials. Scientists and physicians at NYUMC are dedicated to basic and clinical research on the etiology, pathogenesis and treatment of HIV-disease, especially AIDS-KS, AIDS-NHL and anogenital neoplasia during the past 17 years including participation in the AMC trials since its inception in 1995. These studies have contributed to the development of potentially innovative approaches for the treatment of these neoplastic disorders, which tend to be more aggressive and difficult to manage in AIDS patients. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: OPTIMIZING RADIOIMMUNOTHERAPY FOR NON HODGKIN'S LYMPHOMA Principal Investigator & Institution: Gopal, Ajay K.; Medicine; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 21-AUG-2000; Project End 31-JUL-2005 Summary: I am a physician-scientist committed to patient-oriented research involving radioimmunotherapy (RIT) for the treatment of non- Hodgkin's lymphoma (NHL). My immediate career development plans include specialized clinical research training in biostatistics, epidemiology, and clinical trial design at the School of Public Health at the University of Washington (UW), as well as didactic and mentored instruction in ethical aspects of clinical research, Quality of Life assessment, and research group involvement at the UW and Fred Hutchinson Cancer Research Center. The overall scientific objectives of this project are to expand and optimize RIT for the treatment of relapsed non-Hodgkin's lymphoma by (1) determining the toxicities and efficacy of
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Lymphoma
myeloablative I-131- anti-CD20 antibody (Ab) combined with cyclophosphamide and etoposide and autologous stem cell transplantation (ASCT) in a Phase II trial for patients (pt) with relapsed NHL, (2) investigating the feasibility, tolerability, and potential efficacy of single agent myeloablative I-131-anti-CD20 Ab followed by ASCT in pt greater than or equal to 60 years old with relapsed NHL in a Phase I/II study, (3) assessing the quality of life (QOL) and neurocognitive function (NCF) of high dose RIT on pt treated in aims 1 and 2, and (4) performing pre-clinical and clinical studies of biological agents with minimal toxicity (cytokines and retinoids) to further augment the efficacy of anti-CD20 antibody therapy. We hypothesize that targeting radiation specifically to B cell lymphomas with I-131-anti-CD20 antibodies will augment the efficacy and decrease the toxicity of therapy compared with transplant regimens containing nonspecific external beam total body irradiation (TBI). We further postulate that I-131-anti-CD20 targeted RIT will improve the post- transplant QOL and NCF compared to those of pt transplanted with traditional conditioning regimens containing TBI (which deliver greater than or equal to 12 Gy to the brain). We anticipate that the tolerable toxicity of single agent I-131-anti-CD20 + ASCT (established in previous trials) will allow us to safely extend this potentially curative therapy to elderly pt who may not otherwise be eligible for stem cell transplantation. Finally, we hypothesize that augmenting CD20 antigen expression on malignant B cells with cytokines such as GMCSF and enhancing anti-CD20 Ab mediated apoptosis with retinoic acid derivatives will amplify the cytotoxicity of both unmodified and radiolabeled anti-CD20 Ab. We anticipate that these interventions will ultimately enhance the prognosis for patients with relapsed lymphoma by increasing the response and survival rates, while simultaneously minimizing toxicities. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: OVERCOMING TUMOR IMMUNE EVASION STRATEGIES IN HODGKIN'S LYMPHOMA Principal Investigator & Institution: Rooney, Cliona M.; Associate Professor; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-AUG-2007 Summary: (provided by applicant): The malignant B-lineage Reed-Sternberg (H-RS) cells in about half of all cases of Hodgkin lymphoma express Epstein-Barr virus (EBV) antigens, rendering this tumor highly attractive for cytotoxic T-lymphocyte (CTL) immunotherapy. However, these tumor-associated viral antigens are either subdominant (LMP1 and LMP2) or not presented to the immune system (EBNAI and BARFO). The H-RS cells also express molecules that are inhibitory to CTL, such as TGFbeta, the chemoattractant TARC and Fas-ligand that can comprise immunotherapy even when immune epitopes are effectively presented to CTLs. The studies proposed here seek to overcome these immune evasion tactics by redirecting immune responses to the LMP2 viral antigen, using LMP2a-transduced dendritic cells, and by genetically modifying CTLs in vitro so that they will resist the inhibitory effects of TGF-beta and Fas ligand. The latter aim will rely on a transgenic dominant-negative TGF-beta type 2 receptor expressed on CTLs and the adenoviral RID protein, which should render CTLs resistant to inhibition by TGF-beta and killing through Fas ligand-receptor interactions. Our preliminary studies suggest that there may be few T helper epitopes in LMP2. Since persistence in vivo is dependent on the availability of help, we will also explore the possibility that EBNA1, expressed as a retrogen in dendritic cells (using technology developed in project 4) will reactivate EBNA1-specific CD4+ T cells that can provide cognate help for LMP2-specific CTL as well as broaden the cytotoxic repertoire of the
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tumor specific CTL by reactivating CD4+ EBNA1-specific CTL. The hypotheses underlying these aims will be tested both in vitro and in vivo (Phase l/ll trials in patients with post-transplant or relapsed EBV-positive Hodgkin Lymphoma). Upon successful completion of the project, we will have learned whether our experimental modifications are safe in patients and whether they will render CTLs resistant to several of the immune evasion strategies commonly used by tumor cells. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: P16 AND CELL SENESCENCE AND ONCOGENESIS Principal Investigator & Institution: Diaz, Manuel O.; Professor; Medicine; Loyola University Medical Center Lewis Towers, 13Th Fl Chicago, Il 60611 Timing: Fiscal Year 2001; Project Start 15-JAN-1997; Project End 31-DEC-2002 Summary: (Applicant's Abstract) The tumor suppressor gene INK4A (MTS1, CDK41, CDKN2) codes for p16, an inhibitor of the G1 cyclin-dependent kinases CDK4 and CDK6. Deletion or inactivation of this gene is a frequent event in the oncogenic process. P16 is expressed at very low levels in most normal cells, including lymphoid cells and their precursors, but it is up-regulated by unknown mechanisms before senescence. The applicant proposes that p16 up-regulation partially mediates the irreversible cell cycle arrest of senescence, and that deletion or inactivation of INK4A allows progression of a neoplastic clone that has growth arrested at senescence. Inactivation of INK4A by gene deletion, point mutation, and DNA methylation has been reported in neoplastic cells. On the basis of the applicant's previous results, he postulates that in some neoplastic cells suppression of p16 expression can also be achieved by post-transcriptional downregulation. The specific aims of this project are: 1) To study the role of p16 in senescence and oncogenesis through expression of p16 from transfected expression vectors, and down-regulation of its expression by antisense strategies. 2) To study the mechanisms of p16 regulation in normal senescent cells and neoplastic cells. 3) To study the posttranscriptional down-regulation of p16 in leukemia and lymphoma cell lines. 4) To measure the prevalence of post-transcriptional down-regulation of INK4A in primary leukemias and lymphomas. During oncogenesis, cell immortalization is an essential step to achieve full malignant transformation. P16 participates in the control of cell senescence. Therefore, it is important to understand its role and transcriptional regulation in senescent and immortal cells. Since in some lymphoma and ALL cell lines INK4A expression is inhibited at a post-transcriptional level, it is important to determine if this phenomenon is relevant to oncogenesis in primary tumors. If the posttranscriptional down-regulation of p16 is relevant, we should try to understand its mechanism to explore the possibility of manipulating it for therapeutic purposes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PATHOPHYSIOLOGY OF PRIMARY EFFUSION LYMPHOMA Principal Investigator & Institution: Whelan, John P.; Massachusetts General Hospital 55 Fruit St Boston, Ma 02114 Timing: Fiscal Year 2002; Project Start 01-SEP-2002; Project End 31-MAY-2007 Summary: (provided by applicant): Infection with the Kaposi's sarcoma-associated herpesvirus (KSHV) is common around the world and affects more than half of all HIVinfected individuals. This newly described virus has been implicated in virtually all cases of primary effusion lymphoma (PEL), an unusual but universally deadly complication of AIDS and organ transplantation. PEL is unique among B cell lymphomas in that these cells accumulate suspended in the pleural, pericardial or
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Lymphoma
peritoneal cavities of the body. The reason for this tropism is completely unknown. In preliminary experiments we have shown that multiple PEL lines express a novel and uniform chemokine receptor phenotype not previously reported for other lymphomas or normal B lymphocytes. PEL cells demonstrate directed movement in response to chemokines for which they bear the appropriate receptors. Acellular effusions from PEL patients cause specific attraction of PEL cells in vitro, a finding that is amplified and confirmed in a new mouse model we developed for lymphocyte migration to the peritoneal cavity. Furthermore, this phenotype can be imparted to a non-PEL lymphoma cell line by transfecting genes from the latency program of KSHV. We hypothesize that chemokine-driven directed migration attracts and sequesters KSHVinfected PEL cells in the body cavities, and that expression of KSHV latency genes may be responsible for establishing this unique tropism. Thus, PEL homing may represent a novel target for interrupting the virus-associated development and progression of this high-grade lymphoma. The goal of this proposal is to further elucidate what role KSHV plays in the body cavity tropism of PEL cells, to determine whether the process is chemokine-related, and to identify the molecular components of the homing process. These studies constitute part of a training program that will build on the investigator's previous immunology experience by expanding his facility with virologic principles and molecular biology techniques through coursework, intense interaction with a dedicated mentor and monitoring committee, and scientific partnership with collaborators, and an outstanding research environment. This award will substantially advance the candidate's goal of developing an independent basic science research program in a university setting while contributing new training in infectious disease and oncology to the development of new perspectives on the inflammatory diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PEDIATRIC ONCOLOGY GROUP Principal Investigator & Institution: Link, Michael P.; Professor; Pediatrics; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2001; Project Start 01-JAN-1983; Project End 31-DEC-2002 Summary: The overall goal of this research proposal is for Stanford University, the University of Arizona, and the Kaiser Permanente Medical Centers of the South San Francisco Bay Area to continue their active involvement in Pediatric Oncology Group research activities. Stanford faculty and the University of Arizona faculty have already assumed key leadership positions in POG and have or have had major roles in the scientific and administrative aspects of the Group. Further, Stanford, the University of Arizona, and Kaiser have maintained excellent performance ratings in their participation in POG studies and have received commendations for the large numbers of evaluable patients placed on therapeutic protocols. Specifically: l) We plan to continue to enter patients on appropriate POG studies where they exist. The number of patient entries from Stanford has increased each year as appropriate POG studies become available. We anticipate that between 65 and 80 patients will be entered on front-line therapeutic studies each year from Stanford in addition to patients who will be entered from the affiliates; in addition, 40-50 patients or more will be entered on POG non-therapeutic studies. 2) We anticipate that the activities of individual investigators from Stanford and the University of Arizona will continue and increase during the period of this research proposal. Currently, our faculty serve as study coordinators for front- line therapeutic studies in lymphoma and leukemia, and they have coordinated and analyzed data from recently closed protocols in osteosarcoma, lymphoma, leukemia, and Ewing's sarcoma. Our faculty also serve key scientific and administrative
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roles as Group Vice Chair, Disease and Discipline Committee Chairmen and CoChairmen, as members of Disease and Discipline Core Committees, and as members of the Executive Committee. Thus, our faculty are in position to influence the future direction of the scientific activities of POG. 3) We anticipate that involvement of Stanford faculty in the laboratory scientific activities of POG will continue. The laboratories of Drs. Link and Cleary have served as immunology reference laboratories and molecular biologic reference laboratories for leukemia studies of POG. 4) We anticipate that non-POG related laboratory and clinical research conducted at Stanford University and its affiliates will become increasingly relevant to POG activities. Some of these activities have already been incorporated into POG laboratory and therapeutic studies and others are targeted for incorporation into future POG studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PILOT--LEUKEMIA/LYMPHOMA TRANSPLANTATION
AND
BONE
MARROW
Principal Investigator & Institution: Ferrara, James L.; Professor of Internal Medicine and Pedia; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, Mi 481091274 Timing: Fiscal Year 2001; Project Start 30-SEP-1988; Project End 31-MAY-2006 Summary: The Leukemia/Lymphoma-BMT (LL-BMT) Program is an interdisciplinary program with 37 members from nine departments with over $3.5 million in annual direct research support. The chief scientific aims of the Program are: to devise novel treatments for leukemia, lymphoma and related hematologic disorders using immunotherapeutic approaches with or without concurrent stem cell transplant; to understand the immunobiology of allogeneic BMT in order to reduce its toxicity and increase its; and to understand hematopoietic stem cell biology with the ultimate goal of stem cell gene modification for therapeutic purposes. This program was recently organized to integrate more fully research activities related to clinical therapies of malignant hematologic diseases. This integration is exemplified by numerous intraprogrammatic conferences, tumor boards and clinical research projects incorporating multiple disciplines. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: POK PROTEINS IN ONTOGENESIS, LYMPHOPOIESIS, AND LYMPHOMAGENESIS Principal Investigator & Institution: Pandolfi, Pier P.; Professor; Sloan-Kettering Institute for Cancer Res New York, Ny 10021 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-JUL-2003 Summary: POK (POZ and Kruppel) proteins are characterized by the presence of a C2H2 Zinc finger motif, typified by the Drosophila gap gene Kruppel, and the POZ (Poxvirus and Zinc finger) domain, initially identified in a Zinc finger protein named ZID where it was shown to facilitate protein- protein interactions. Two members of the POK family of transcription factors, BCL-6 (for B Cell Lymphoma 6) and PLZF, have already been found implicated in the pathogenesis of tumors affecting the lymphohemopoietic compartment. The BCL6 gene was identified by virtue of its involvement in translocations associated with Non-Hodgkin's lymphoma. We have recently isolated a new member of the POK family, which we have named LRF1 (for Lymphoma Related Factor 1), that is coexpressed and physically interacts with BCL6. The focus of this proposal is to elucidate the role of the BCL6 and LRF1 POK proteins in development
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and lymphopoiesis, and to clarify how BCL6 and LRF1 functions relate to lymphomagenesis with the following Specific Aims: 1. To define, in knock out mice, the role of BCL6 and LRF1 in ontogenesis. Using homologous recombination technology, we have successfully disrupted the BCL6 gene in mouse Embryonic Stem (ES) cells, and mice homozygous for the mutation have been generated and are being characterized. Using a similar approach, we will disrupt the LRF1 gene. Mice or embryos homozygous for the LRF1 inactivating mutation will be generated and studied. We will define the developmental role of these genes by characterizing the embryonic or adult phenotype resulting from their inactivation. 2. To elucidate, in knock out mice and null ES cell lines, the role of BCL6 and LRF1 in lymphopoiesis. We will specifically analyze lymphopoiesis and B cell function in BCL6 and LRF1 mutants. Different experimental approaches will be undertaken depending on whether mice lacking the LRF1 gene are viable or on the stage of embryonic development at which they die. In parallel, we have produced BCL6 null ES cells and we will produce LRF1 null ES cells and study the capacity of these cells to differentiate towards lympho-hemopoietic precursors in vitro and in vivo in RAG-/complementation assays. Finally, we will interbreed BCL-/- and LRF1-/- mice in order to generate and characterize the hemopoietic phenotype of the double mutants. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: POLYADENYLATION FACTORS IN B-CELLS, LYMPHOMA & MYELOMA Principal Investigator & Institution: Milcarek, Christine A.; Professor; Molecular Genetics & Biochem; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2003; Project Start 15-FEB-2000; Project End 31-JAN-2008 Summary: (provided by the applicant): The mRNA 3'-end processing reaction has been shown to play an important role in modulating Ig heavy chain poly(A) site use in B-cell development. This proposal focuses on defining the mechanisms of action of hnRNPF and H/H', auxiliary polyadenylation factors, and how they operate to influence poly(A) site choice during the induction of myeloma/plasma and lymphoma/memory B cells. We propose the following: Aim 1. To define the role of hnRNP F in binding RNA and blocking 3' end processing in cells. A. We will test the hypothesis that specific domains of hnRNP F are responsible for its RNA binding and inhibition of 3' end processing. B. We will test the hypothesis that the differences between hnRNP F and the closely related proteins hnRNP H/H', in the carboxyl-terminal region and between RNA binding domains 2 and 3, are responsible for the differing biological effects of these molecules on 3' processing. C. We will test the hypothesis that specific phosphorylation of CTD will enhance the competition between hnRNP F and CstF-64. AIM 2. We will test the hypothesis that differential loading of 3'-end processing factors occurs both along the Ig heavy chain gene and during different stages of B-cell development. AIM 3. We will test the hypothesis that over-expression of hnRNP F in authentic plasma cells will suppressIg heavy chain secretion by reducing the amount of secretory specific mRNA. AIM 4. We hypothesize that the increased expression of PC4 we have seen in plasma cells influences 3'-endformation by interacting directly with CstF-64.The experiments described in this proposal attempt to find differences in cells that may serve as markers to identify memory, naive, and plasma B-cells as well as to understand the molecular events that determine how memory an/or B-cells may be activated to differentiate into plasma cells. Understanding plasma cell development is important for vaccine development to eradicate infectious diseases, mediating allergic responses and autoimmune diseases, and limiting tumor growth. Understanding the control of
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polyadenylation is important for understanding and possibly controlling aspects of cell growth, differentiation and malignancy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: POPULATION STABILITY IN TUMOR DORMANCY Principal Investigator & Institution: Scheuermann, Richard H.; Director; Pathology; University of Texas Sw Med Ctr/Dallas Dallas, Tx 753909105 Timing: Fiscal Year 2001; Project Start 01-AUG-1998; Project End 31-MAY-2003 Summary: Tumor dormancy, a state in which a malignant tumor becomes quiescent, has been well documented for several human cancers. An important implication of dormancy is that under certain circumstances a malignant tumor can be brought under growth restraint. The mouse BCL1 lymphoma system provides an experimental model in which dormancy can be reproducibly established and investigated. Previous work indicates that dormancy is induced in this system through signal transduction pathways originating from membrane immunoglobulin (mIg). In vitro, engagement of mIg induces cell cycle arrest (CCA), cell cycle progression and apoptosis, and the activation of the Lyn and Syk tyrosine kinases. In addition, the lymphoma cell population remains constant both in long term cultures and in dormant animals, indicating that cell cycle progression must be balanced by cell death. Our working hypotheses are that i) activation of Lyn is important for the CCA response and Syk for the apoptotic response; ii) cell cycle progression and apoptosis are interconnected in these cells; iii) this connection results in an asymmetric cell division in which one daughter cell dies while the other continues to progress through the cell cycle; iv) this balance is essential for tumor dormancy in vivo. The specific aims of this project are: 1. To determine the relationship between CCA, cell cycle progression, apoptosis and population stability in anti-Ig-treated lymphoma cultures. 2. To determine if the balance between growth and death that results in long term population stability in culture is achieved by an overall balance between two stochastic processes in the population or as directed process involving asymmetric cell division. 3. To alter Syk and Lyn kinase activities in BCL1.3B3 and determine effects on CCA, cell cycle progression, apoptosis and population stability in vitro. 4. To determine how alterations in Syk and Lyn kinase activities affect the induction, maintenance and escape of dormancy in vivo. The long term objectives of our studies are - to identify signal transduction cascades controlling apoptosis and cell cycle progression, to determine the relationship between these processes and in vivo tumor growth (especially tumor dormancy, a relatively unexplored clinical problem), and to use this knowledge for the design of improved therapeutic approaches. In addition, the possibility that population stability is dictated by asymmetric cell division balancing growth and death is novel and has important implications for understanding tumor growth control and normal population homeostasis at a fundamental level. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: POSITIVE AND NEGATIVE REGULATORY PATHWAYS IN LYMPHOMA Principal Investigator & Institution: Ford, Richard J.; Chief; Molecular Pathology; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2003; Project Start 25-JUN-2003; Project End 31-MAY-2008 Summary: (provided by applicant): Non-Hodgkin's Lymphomas (NHL) are common tumors of the human immune system, primarily of B cell lineage (NHL-B) that have been showing significant unexplained increases in incidence for the last three decades.
50
Lymphoma
Unlike normal B-lymphocytes aggressive forms of NHL-B show rapid, dysregulated B lymphocyte growth characteristics, while retaining typical B cell immuno-phenotypes, including expression of characteristic CD40 and SIg. cell surface receptors. Normal B cells, involved in inflammatory, or other immune functions, transduce signals to activate and release, the key transcription factor, NF-kappaB from its cytoplasmic inhibitor; but aggressive NHL-B cells, such as Large B cell Lymphomas (LBCL), show constitutive expression of nuclear NF-kappaB. Our studies have shown that this is accomplished by continually maintaining an assembled, scaffold-like, signaling platform as a concatenate molecular aggregate, called a Signalosome within a lipid raft microdomains, contained within or subjacent to the lymphoma cell membrane. We have developed a hypothetical model of aggressive NHL-B cell pathophysiology that envisions dysregulation of the CD40 mediated signaling pathways as the major mechanism controlling tumor cell growth and other parameters of malignancy. The CD40 Signalosome appears to be initiated through autochthonous production and cognate ligand binding of CD154 (CD40L, gp39) to the CD40 receptor on the lymphoma cell surface. Our studies have indicated that the necessary and sufficient conditions for CD154 expression seem to differ in NHL-B cells from normal activated T lymphocytes, suggesting that the neoplastic lymphocytes show dysregulated gene expression and signaling pathways to mediate autonomous tumor cell growth. Constitutive expression of NF-kappaB in NHLB can be down-regulated by treatment with specific antibodies or antisense oligos to CD40 or CD154, that disrupt the integrity of the CD40 Signalosomes, resulting in the inhibition of lymphoma cell growth, and the induction of lymphoma cell death in vitro. In this proposal, we will study the molecular characteristics of the CD40 Signalosome, by isolating and sequencing the component proteins of the canonical CD40/NFkB pathway contained within the signalosome, and demonstrate the signaling capabilities of this macromolecular structure. We will also study the signaling pathways controlling gene expression of the CD40 ligand, CD154, that we believe is intimately involved with driving the signalosome pathway, to ascertain the mechanism of its "ectopic" expression, as well as its possible role the aggressive growth pattern and resistance to cell death shown by aggressive NHL-B. In addition to these abnormalities involving lymphoma cell proliferation and cell viability, NHL-B cells also show aberrant expression of the TGF-beta/SMAD-SNO/SKI system, that is responsible for negative growth regulation in normal B lymphocytes (as well as many other functions in most cell types). Our preliminary studies have shown that abnormalities in SNO/SKI gene expression are involved in abrogating the negative regulatory influence of this signaling system in NHL-B that also appears to be linked to the CD40/NFkB system in NHL-B. Our studies will further examine the role of this system in potentiating the biologic, and possibly the clinical aggressiveness of these lymphoid tumors, and explore whether inhibition of the dysregulatory elements in this pathway can have therapeutic potential. We believe that our CD40 Signalosome model will provide an important "roadmap" into the important control mechanisms involved in NHL-B, that can be used for developing new therapeutic approaches for this very important group of human lymphoid neoplasms. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PRETARGETED RIT TO TREAT NON-HODGKIN'S LYMPHOMA Principal Investigator & Institution: Fritzberg, Alan R.; Neorx Corporation 410 W Harrison St Seattle, Wa 98119 Timing: Fiscal Year 2001; Project Start 15-JAN-2001; Project End 31-DEC-2002 Summary: The objective of the proposed research is to develop a therapeutic agent based on pretarget radioimmunotherapy that is superior to the current treatments of
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non-Hodgkin's B-cell lymphoma in terms of therapeutic efficacy and non-target organ toxicity. Fusion proteins of a single chain antibody and streptavidin (scFv/SA) will be developed that are reactive with CD2O and target in a lymphoma xenograft animal model. Two candidate scFv/SA constructs will be genetically modified (e.g., with changes to the linker region) for the purpose of improving the expression, purification, and/or biochemical characteristics. Additional fusion constructs will be generated from selection of a human Fab/phage display library on CD2O-positive peripheral blood lymphocytes. All scFv/SA candidates will be evaluated for meeting set criteria for E. coli expression level, purification yield, immunoreactivity and CD2O cell binding, biotin binding affinity, and targeting ability in a lymphoma xenograft animal model. These characteristics should be sufficient to warrant further Phase II efforts directed toward cGMP scale-up and formulation development for clinical trials. PROPOSED COMMERCIAL APPLICATIONS: The application of radioimmunotherapy toward the treatment of non- Hodgkin's lymphoma (NHL) has been constrained by dose limiting toxicity to the radiosensitive bone marrow. Antibody pretargeting provides a method to specifically deliver significantly greater doses to tumor sites without serious toxicities. A large number of patients with NHL are candidate's for this treatment. These patients represent a sizable market opportunity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: LYMPHOMAS
PRETARGETING
RADIOIMMUNOTHERAPY
OF
CD20+
Principal Investigator & Institution: Press, Oliver W.; Professor of Medicine; Fred Hutchinson Cancer Research Center Box 19024, 1100 Fairview Ave N Seattle, Wa 98109 Timing: Fiscal Year 2002; Project Start 01-JAN-1998; Project End 31-JUL-2007 Summary: (provided by the applicant): Preliminary clinical trials have demonstrated that radiolabeled anti-CD2O monoclonal antibodies can achieve remissions in 65-90 percent of lymphoma patients failing chemotherapy. However, most patients treated with conventional radiolabeled antibodies (RAb) subsequently relapse and die of recurrent lymphoma. The objective of this research proposal is to optimize radioimmunotherapy (RIT) of B cell lymphomas utilizing two-step pretargeting amplification strategies to improve the efficacy and decrease the toxicity of conventional RIT. Two separate pretargeting approaches will be investigated, one using streptavidin (SA) and radioactive biotin and the second employing molecularly engineered bispecific anti-CD20 x anti-ligand antibodies which bind covalently to radiolabeled ligands. First, we will compare the biodistributions, toxicities and efficacies of anti-CD2O, anti-CD22, and anti-DR antibody-SA conjugates pretargeted to lymphoma xenografts in an athymic mouse model, followed by radiobiotin administration. Second, we will investigate the pharmacokinetics, biodistributions, toxicities, and efficacies of 2 molecularly engineered recombinant tetravalent single chain antibody-SA fusion proteins ([scFv]4-SA) and compare them to standard synthetic antibody-SA chemical conjugates. Third, we will compare the relative merits of 4 genetically engineered SA mutant molecules with native SA for pretargeting protocols in combination with either biotin or a synthetic divalent bis-biotin targeting molecule. These streptavidin mutants will afford a unique opportunity to test the effect of SA avidity on tumor penetration as delineated in the "binding site barrier" hypothesis. Fourth, we will evaluate the pharmacokinetics, biodistributions, toxicities, and efficacies of novel molecularly designed bispecific antiCD2O x anti-ligand Abs which possesses a molecularly engineered binding pocket capable of binding covalently to synthetic radiolabeled electrophilic ligands. These bispecific anti-CD2O x anti-ligand Abs will be compared directly to the SA-biotin
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Lymphoma
pretargeting approach in lymphoma xenograft models. We hypothesize that the pretargeting strategies defined in this proposal will improve the tumor-to-normal organ ratios of absorbed radiation compared with conventional RIT, allowing improvement in response rates and response durations with less toxicity than is currently feasible. We hypothesize that pretargeting will eliminate the necessity of administering myeloablative doses of 131I-anti-CD20 Ab with hematopoietic stem cell rescue to achieve maximal response rates and survival rates. We anticipate rapid translation of the results of these preclinical experiments into our clinical RIT program for human Non-Hodgkin's lymphomas. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PROGRESSION OF T CELL LYMPHOMA LINES TO IL2 INDEPENDENCE Principal Investigator & Institution: Tsichlis, Philip N.; Professor/Director; Microbiology and Immunology; Thomas Jefferson University Office of Research Administration Philadelphia, Pa 191075587 Timing: Fiscal Year 2001; Project Start 01-JUL-1992; Project End 31-JAN-2002 Summary: (adapted from the investigator's abstract) The Gfi-1 proto-oncogene is activated by provirus integration in T cell lymphoma lines selected for IL-2 independence in culture and in primary retrovirus-induced thymomas and collaborates with c-myc and pim-1 in oncogenesis. Gfi-1 encodes a zinc finger protein with six C2H2 type, C-terminal zinc finger motifs. The investigator s recent studies have shown that Gfi-1 is a 55 kD nuclear protein that binds DNA in a sequence specific manner and functions as a position and orientation independent active transcriptional repressor. Repressor activity depends on a novel twenty amino acid N-terminal repressor domain, coincident with a nuclear localization motif. The sequence of the Gfi-1 repressor domain is related to the sequence of the repressor domain of Gfi-1B, a Gfi-1 related protein, and to sequences at the N-termini of the insulinoma-associated protein, IA-1, the homeobox protein Gsh-1 and the vertebrate members of the Snail-Slug protein family. Among the genes repressed by Gfi-1 are p21WAF1, encoding a cyclin dependent kinase inhibitor, and Bax, an inducer of apoptosis, both of which are upregulatd by the tumor suppressor gene p53. Gfi-1 mediated repression is associated with inhibition of cell death and abrogation of the G1 checkpoint induced by IL-2 withdrawal in T cells. Induction of Gfi1 may therefore contribute to T-cell activation and tumor progression by promoting cell cycle progression and by increasing cell viability. The Gfi-1 related protein Gfi-1B is expressed transiently during primitive embryonic hematopoiesis. In adult animals it is expressed in the less differentiated B and myeloid cells. Gfi-1B also represses expression of p21 and inhibits myeloid cell differentiation. He now proposes to examine the role of Gfi-1 and Gfi-1B in cell cycle progression, apoptosis, hematopoietic cell differentiation and oncogenesis, and to characterize functionally the Snail-Gfi-1 (SNAG) repressor domain. The long term objective of this project is to use Gfi-1 and Gfi-1B as probes to explore the biology of the hematopoietic system and the pathobiology of neoplasia with emphasis on cell cycle progression differentiation and apoptosis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: PROPERTIES OF LYMPHOID TUMOR CELLS IN VIVO AND IN VITRO Principal Investigator & Institution: Tsiagbe, Vincent K.; Pathology; New York University School of Medicine 550 1St Ave New York, Ny 10016
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Timing: Fiscal Year 2001; Project Start 01-MAY-1976; Project End 31-DEC-2002 Summary: The host T cell germinal center (GC) derived B lymphoma cell interaction will be examined. A central question to be answered about the lymphomagenesis in SJL mice is: What causes the high mtv-29 encoded vSAg transcription and how does it relate to the GC origin of these lymphomas (RCS)? The 5' LTR of mtv-29 in liver and RCS DNA will be sequenced to determine whether the 5'LTR is defective in all cells or only in RCS cells to explain that the vSAg initiation site is in the end region mtv-29. Regulation of the expression of this vSAg will be studied by using transection of reporter constructs and looking for specific binding factors for regions in mtv-29, expressed in RCS and normal GC but not in other B cells. The mechanism of the growth promotion in vivo will be studies, including the fate of vbeta16+ T cells in c57L mice will be analyzed. The vbeta16 T cell representation in PBL of mice with developing primary lymphomas will be followed and the effect of anti-vbeta16 on tumor growth in vivo evaluated. Attempts will be made to identify secondary oncogenic events that cause continued proliferation and a lack of differentiation in e lymphoma cells. It will be determined whether RCS, normal isolated GC and NJ101 cells differ in resistance to spontaneous and glucocorticosteroid induced apoptosis. The expression of several oncogenes in morphologically abnormal and normal GCs from bcl-2 transgenic and normal SJL mice will be studies. To evaluate whether the phenomenon of ~reverse immune surveillance~ may be applicable to humans, CD4+ T cell infiltrates in human GC-derived lymphomas will be examined for Vbeta or Va TCR patterns that might reflect monoclonal responses to specific Ag or v beta restricted responses to a SAg. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION OF REPLICATION AND LATENCY BY EBV EBNAS Principal Investigator & Institution: Hayward, S D.; Professor; Pharmacology; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 01-APR-1986; Project End 31-JAN-2008 Summary: (provided by applicant): Epstein-Barr virus (EBV) is a gamma herpesvirus that causes infectious mononucleosis and is associated with a variety of human lymphoid and epithelial cancers. Immunocompromise is a risk factor for EBV associated disease with malignancies such as post-transplant lymphoproliferative disease arising in transplant patients and central nervous system lymphoma and a proportion of systemic lymphomas being EBV associated in AIDS patients. EBV is also associated with Burkitt' s lymphoma, nasopharyngeal carcinoma, nasal T cell lymphoma, and a subset of Hodgkin' s lymphomas and gastric carcinomas. After primary infection an individual will remain latently infected with EBV and it is this life-long reservoir of latently infected cells that is a factor in the development of subsequent malignant disease. EBV infection of B cells in culture leads to the outgrowth of immortalized B cell lines and EBNA2 is one of the EBV encoded proteins essential for this process. EBNA2 alters cellular gene expression by targeting a DNA binding protein, CBF1/RBPJk, and switching CBF1 repressed promoters to an activated state. In its targeting of CBF1, EBNA2 mimics activated Notch signaling. A recently recognized ORF present in the EBV BARTs encodes a protein, RPMS, that also interacts with the Notch pathway, in this case negatively regulating Notch activity. The goal of this research program is to understand the contribution of EBNA2 to EBV driven B cell immortalization and the role of RPMS in latency maintainance and in EBV associated epithelial malignancies. The Specific Aims are: [1] To examine EBNA2 mediated cell survival activities by generating an EBV mutant defective for Nur77 binding and further characterizing the EBNA2-Nur77 interaction and its consequences. [2] To identify and compare the
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Lymphoma
downstream targets of EBNA2 and NotchIC. Primary B cells and EBV negative B cell lines will be infected with lentivirus vectors expressing EBNA2 or NotchIC and with EBV EBNA2 mutant viruses and the changes induced in cell gene expression will determined using gene array technologies. [3] To examine RPMS function and the regulation of RPMS stability. The contribution of phosphorylation to RPMS protein turnover and proteosomal targeting will be examined and the potential role of RPMS anti-Notch activity in epithelial tumor development will be probed. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATION/GLUCOSE HOMEOSTASIS/LYMPHOMA
METAB/LYMPHOCYTE
Principal Investigator & Institution: Elstrom, Rebecca L.; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 09-SEP-2002; Project End 31-JUL-2007 Summary: (provided by applicant): This proposal delineates the principal investigator's plan for development of a career in academic Hematology. The candidate has demonstrated a commitment to research and a long-standing interst in blood-rated diseases, and is completing an academic fellowship in Hematology/Oncology. The University of Pennsylvania and, specifically, the mentorship of Dr. Craig Thompson, Scientific Director of the Abramson Family Cancer Research Institute, provides a stimulating and supportive environment for creative thought and rigorous scientific development. In multicellular organisms, extracellular signals are required to maintain survival in normal tissues. One way which these signals prevent programmed cell death in lymphocytes is through the promotion of nutrient uptake and cellular metabolism. Interference with these processes results in programmed cell death. Further-more, malignant tissues utilize glucose abnormally, and we hypothesize that this results from bypass of growth factor signals allowing unregulated glucose uptake and metabolism. The proposed experiments will address both the mechanism of extracellular signalmediated regulation of glucose metabolism in normal lymphocytes and its disruption in lymphoma. The specific aims include: 1) Study of the regulation of glucose uptake and metabolism in normal human lymphocytes, 2) Determination of the role of Akt in glucose metabolism and its cooperation with Myc and Bc1-XL in transformation in transgenic mice, and 3) Evaluation A the mechanism of increased glycolysis in lymphoma. With the input and participation of an advisory committee including Dr. Abass Alavi, Chief of Nuclear Medicine and Dr. Stephen J. Schuster, assistant professor of Hematology and Director of the Lymphoma Program at the University of Pennsylvania Cancer Center, this program provides a clear plan for the development of the candidate's projected academic career. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF EPSTEIN-BARR VIRUS IN BURKITT LYMPHOMA Principal Investigator & Institution: Sample, Jeffery T.; Associate Professor; St. Jude Children's Research Hospital Memphis, Tn 381052794 Timing: Fiscal Year 2003; Project Start 30-SEP-1996; Project End 31-MAR-2008 Summary: (provided by applicant): The long-term objective of the work supported by this grant is to define the role of Epstein-Barr virus (EBV) in Burkitt lymphoma (BL), a B-cell tumor that occurs in geographically distinct regions, and which is also associated with immunosuppression as a consequence of HIV infection and AIDS. The underlying hypothesis of this grant is that EBV contributes directly to BL, despite lack of expression
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of the known viral transforming genes within the tumor cells. This is supported by the observation that the tumorigenic potential of the BL cell line Akata is dependent on EBV infection and at least two viral gene products the EBV small RNAs EBER-1 and EBER-2. The contribution of the EBER RNAs to tumorigenic potential, however, is partial relative to that conferred by EBV infection as a whole, indicating that additional viral genes expressed during infection of BL cells are important. The immediate goals of the proposed work are to define the mechanistic contributions of the EBER RNAs and other EBV gene products to the tumorigenic potential of BL cells and to lymphomagenesis itself. Three specific aims are proposed. Under Aim 1, we will identify the cellular targets of the EBER RNAs and define the mechanisms through which they are regulated. We will address two potential mechanisms of EBER function that are suggested by previous experimental observations. The first is that the EBER RNAs function in posttranscriptional gene silencing through direct RNA:RNA interactions with cellular gene RNAs. The second, based on known interactions of the EBERs with components of the cellular translational machinery, is that the EBERs regulate translation of specific cellular mRNAs. Under Aim 2, we will define the contributions of proteins encoded by the EBV BamHI rightward transcripts (BARTs) to BL-cell tumorigenic potential, and in particular whether any of these proteins are responsible for the enhanced survival conferred upon BL cells by EBV that is attributed to viralenforced down-regulation of the c-MYC proto-oncoprotein under growth-limiting conditions. Under Aim 3, we will assess the importance of EBV genes expressed in BL cell lines to actual lymphomagenesis using the murine model of BL, the Emu-myc transgenic mouse, in which expression of the c-myc proto-oncogene, as in BL, is constitutively overexpressed in B lymphocytes. Specifically, we will express the EBV genes within the B cells of these mice to determine whether this accelerates c-Mycinduced lymphomagenesis, and if so, we will identify the genetic and biochemical basis for this contribution to lymphoma. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE OF HERV-K18 SUPERANTIGEN IN EBV LYMPHOMAGENESIS Principal Investigator & Institution: Sutkowski, Natalie A.; Pathology; Tufts University Boston Boston, Ma 02111 Timing: Fiscal Year 2003; Project Start 30-SEP-2003; Project End 31-AUG-2006 Summary: (provided by applicant): More than 90% of adults are latently infected throughout their lifetime with the ubiquitous herpesvirus Epstein-Barr virus (EBV). While EBV infection is usually asymptomatic during childhood, it is estimated that half of first-time infected adolescents or adults develop infectious mononucleosis, a disease characterized by polyclonal B cell activation and massive expansion of T cells. EBV is an oncogenic virus; it is associated with Burkitt's lymphoma, Hodgkin's disease and nasopharyngeal carcinoma. At least 1% of organ and bone marrow transplant recipients develop EBV+ lymphomas; and EBV lymphoproliferative disorders are common in AIDS patients. The tumors are often associated with vast T cell infiltrates. The SCID/hu mouse is well accepted as an animal model for EBV lymphomagenesis, because SCID mice adoptively transferred with EBV seropositive PBMC from healthy human donors develop EBV+ B cell lymphomas at a high rate. These tumors are strictly T cell dependent and can be prevented by blocking the B-T interaction. We have recently established that EBV transactivates a human endogenous retrovirus, HERV-K18, that encodes a superantigen, which strongly activates T cells. This is the first described report of a pathogen inducing a host cell superantigen. We propose that HERV-K18 Env superantigen activated T cells contribute to EBV lymphomagenesis. This proposal seeks
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Lymphoma
to test whether blocking the superantigen driven T cell response prevents tumorigenesis in the SCID/hu lymphoma mouse model. We propose to block T cell activation by: I. developing monoclonal antibodies specific for the HERV-K18 superantigen; II. blocking CD28/ICOS costimulation; III. induction of T cell anergy; and IV. ligation of immunoinhibitory receptor PD-1. Since several other herpesviruses are associated with superantigen or superantigen-like activity, these experiments may have broad-reaching implications for herpesvirus biology. Overall, these studies represent a completely new approach towards understanding the potential role of T cells in herpesvirus oncogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ROLE TRANSFORMATION
OF
SMRT
DOWN-REGULATION
IN
NHL
Principal Investigator & Institution: Coignet, Lionel J.; Roswell Park Cancer Institute Corp Buffalo, Ny 14263 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2007 Summary: (provided by applicant): Molecular analysis of chromosomal abnormalities has allowed the identification of many genes directly involved in the pathogenesis of lymphoid malignancies. However, in non-Hodgkin's lymphoma (NHL), the development of the full neoplastic phenotype depends on the acquisition of multiple genetic events including concurrent activation of synergistic "dominant" oncogenes and loss of tumor suppressor gene functions. NHLs often present complex karyotypes that may prevent complete analysis. To overcome this difficulty, many transformed NHL cell lines have been established. Others and we have identified chromosome 12q24 as a recurrent breakpoint in mature lymphoid malignancies of both T- and B-cell lineage and have recently mapped the gone encoding SMRT to 12q24.3. We observed that SMRT is altered in all transformed NHL cell lines/patients tested at the genomic, transcript and protein levels. We propose that SMRT plays an important role in NHL. This implies that SMRT acts as a tumor suppressor gene. To test this hypothesis, we propose the following Specific Aims: 1-To perform a retrospective study of a large series of transformed and non-transformed patient samples by FISH, LOH and immunohistochemistry, to expand upon our observation of transformed lymphoma phenotype and deletion of one SMRT allele. 2- To study the mechanisms by which SMRT regulates apoptosis and cell survival in SMRT-deficient NHL cells. For this purpose, we will study variation of expression of a set of genes involved in cell survival and of the different caspases (and their activation) upon SMRT-restoration-driven apoptosis. The ultimate goal of this aim is to identify future investigative area for potential (new) therapeutic approaches to induce apoptosis in SMRT-deficient NHL cells. 3- To establish a cause: effect relationship between SMRT down-regulation and the NHL transformation process. For this purpose, we will use an antisense strategy to down-regulate SMRT in different normal and low-grade transgenic mice hematopoietic environment. Confirmation of the role of SMRT in NHL transformation and in apoptosis could potentially allow development of new diagnostic and prognostic tools as well as new therapeutic strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SFGH AIDS MALIGNANCY BANK Principal Investigator & Institution: Mcgrath, Michael S.; Associate Professor; Medicine; University of California San Francisco 500 Parnassus Ave San Francisco, Ca 94122
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Timing: Fiscal Year 2001; Project Start 01-AUG-1998; Project End 31-MAY-2002 Summary: (Applicant's Description) The AIDS Malignancy Bank was established in 1994, and since 1995 has been composed of five sites: UCSF, UCLA, George Washington University, SUNY-Brooklyn, and Ohio State University. The AMB is a national resource that reflects the history of the malignancies of HIV disease in specimens. Because scientists in the AMB are themselves actively involved in studies of the p a t hogenesis of AIDS-related malignancies, the AMB is responsive to therapeutic and scientific advances in HIV disease. Currently, the AMB contains 12,688 individual specimens in 43 different categories. These fluid, cell, and tissue specimens, along with associated clinical information, are a v ailable to qualified researchers worldwide. To due, 18 different investigators have received over 900 specimens after critical evaluation of their Letters of Intent (LOIS) by an independent Research and Evaluation Decision Panel (REDP) of experts in the field. This current recompetition proposal combines information from all AMB member sites, as well as reporting accomplishments, future plans, goals and budget projections from individual sites. The key AMB goals are: 1) to establish an Operations Center that will maintain the national database, coordinate activities of the AMB sites, and interface with external sources of specimens such as the AIDS-related Malignancy Consortium and the Women's Interagency HIV Study, ind the scientific community; 2) to expand the AMB to serve as the specimen repository for large oncological clinical and epidemiological consortia, ultimately leading to procurement of their specimens; 3) to increase visibility and broaden the use of the AMB by investigators; and 4) to f u rther develop individual member site programs to increase specimen acquisition. UCSF has provided more than 600 specimens to nine investigators from its specialized Bank. The UCSF AMB will continue to utilize its wellestablished network of clinicians and pathologists to obtain specimens for the Bank. The strengths of the UCSF Bank include: a) a large lymphoma banking program, including contributions from the largest lymphoma epidemiology study ever performed; b) an anogenital malignancy program; and c) an aggressive multi-site autopsy acquisition program. In the current proposal, efforts will be made to acquire specimens in categories underrepresented in the national AMB, as well as international specimens and a complete set of lymphoma specimens linked to an epidemiology database. The SFGH Operations Office will continue to coordinate the local infrastructure and maintain the local AMB database. In addition, a national AMB Operations Center will be established at UCSF and will be responsible for coordinating the efforts of all the participating AMB sites. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SMALL MOLECULE MICROARRAYS FOR INTRACELLULAR PROTEINS Principal Investigator & Institution: Lam, Kit S.; Professor and Chief; Internal Medicine; University of California Davis Sponsored Programs, 118 Everson Hall Davis, Ca 95616 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2006 Summary: (provided by applicant): This project involves the application of the "onebead one-compound" encoded small molecule combinational library method and chemical microarray technique to study functional proteomics. Five enormous libraries of small molecule ligands (a total of over 1 million compounds) will be generated and screened against whole cell extracts derived from a B lymphoma cell line (Ramos). Billions of possible molecular interactions will be examined concurrently. Beads containing compounds that bind to cellular proteins or protein complexes will be isolated and the compound chemical structure determined by our novel decoding
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Lymphoma
method. Selected small molecule ligands will be resynthesized on Sepharose beads and used as affinity matrix to capture the binding proteins or protein-complexes. The identity of the bound proteins will then be determined by protein separation and mass spectroscopy. Based on the chemical structure of these ligands, a small molecule microarray (approximately 1000 compounds) will be developed to probe the functional state of the whole cell extract. Our hypothesis is that with the above experimental scheme, we can systematically select a finite number of small molecule ligands and use them as capturing agents to probe the functional state of a B lymphoma cell. We further hypothesize that some of the ligands that bind to unique protein targets in lymphoma cell can be used as lead compounds for the development of anti-lymphoma agents. Once validated in a large number of lymphoid malignant cell lines, peripheral blood lymphocytes, and a limited number of primary malignant lymphoid tissues, this microarray technology can be applied to biopsy specimens obtained from a large number of patients with lymphoid malignancies. This technique, if successful, can readily be applied to other cancer types as well. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SMOKING, ALCOHOL AND NHL: AN INTERLYMPH-BASED ANALYSIS Principal Investigator & Institution: Zheng, Tongzhang; Head, Division of Environmental Health s; Epidemiology and Public Health; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2004 Summary: (provided by applicant): Over the past several decades, incidence rates of non-Hodgkin's lymphoma (NHL) have increased dramatically throughout the world among both men and women. However, few concrete risk factors for NHL have been identified. Cigarette smoking and alcohol consumption have been proposed as two factors that could potentially impact the risk of NHL. Understanding the role of these behaviors in the etiology of NHL is critical due to the population prevalence of these exposures. In 2000, 23.3 percent of adults in the US reported current cigarette smoking, and 48.4 percent of adults reported current, regular consumption of alcohol. However, epidemiologic studies that have investigated the impact of cigarette smoking and alcohol on the risk of NHL have yielded inconsistent results due to relatively small sample sizes. Several epidemiologic studies have suggested that the risk of NHL from cigarette smoking and alcohol consumption varies by disease subtype and by the type of alcohol consumed. However, individual epidemiologic studies have been limited in their ability to consider the impact of risk factors on NHL by alcohol type and disease subtype because of small sample sizes. Considering the prevalence of cigarette smoking and alcohol consumption and the uncertainty surrounding the relationship between these exposures and risk of NHL, there exists an urgent need to assess the impact of smoking and drinking on NHL using a larger sample size. The International Consortium of Investigators Working on Lymphoma Epidemiologic Studies (InterLymph) was established to facilitate the cooperation between large, epidemiologic studies of NHL, providing us with a unique opportunity to explore the relationships between smoking, alcohol, and NHL. Therefore, we propose to conduct a pooled analysis of data from several population-based case-control studies that are a part of InterLymph. Due to the recent establishment of InterLymph, the proposed pooled analysis represents the first opportunity to benefit from this international collaboration. The primary specific aim of this pooled analysis is to determine if the risk of NHL is associated with cigarette smoking and alcohol consumption, and whether this risk
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varies by disease subtype and type of alcohol. This InterLymph-based pooled analysis will include three population-based case-control studies with similar study design, resulting in a total of 3,592 histologically-confirmed, incident cases and 4,333 population-based controls, from six SEER sites. The increased sample size that will result from the collaboration of several large, epidemiologic studies will enable us to have sufficient statistical power to examine the strength and consistency of the associations between smoking, alcohol, and NHL. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SYMPTOMS OF TRANSPLANT PATIENTS NEAR THE END OF LIFE Principal Investigator & Institution: Anderson, Karen O.; Anesthesiology/Crit Care; University of Texas Md Anderson Can Ctr Cancer Center Houston, Tx 77030 Timing: Fiscal Year 2001; Project Start 15-FEB-2000; Project End 31-JAN-2004 Summary: (Adapted from the Applicant's Abstract): Increasing numbers of patients face the end-of-life following technologically advanced medical interventions. Cancer patients receiving autologous blood or marrow transplantations are a good example of this category of patients who face mortality after advanced clinical care. We know little of what happens to these patients at the end of their lives, such as their symptom patterns, emotional status, and when or whether a decision is made to transition to palliative care. The specific objectives of the proposed research are: (1) to assess the symptoms of metastatic breast cancer, high risk non-Hodgkin's lymphoma, and multiple myeloma patients who will die during the year following transplantation in order to identify changes in symptoms and symptom patterns that predict the end-oflife; (2) to determine the relationships among symptoms, functional status, quality of life, and length of survival post-transplant; and (3) to evaluate the efficacy of an IVR system in improving symptom assessment, symptom management, and quality of life for metastatic breast cancer, high risk non-Hodgkin's lymphoma, and multiple myeloma patients after transplantation, and a randomized clinical trial to evaluate the efficacy of an IVR system to monitor and triage the symptoms of patients during the posttransplantation period. The phase I descriptive study will enroll 110 patients with metastatic breast cancer, high risk non-Hodgkin's lymphoma, or multiple myeloma who are scheduled for autologous transplantations. The patients will complete pre-transplant measures of symptoms, quality of life, and functional status. Physical, affective, and cognitive symptoms will be monitored during the patients' hospitalization. Following discharge, the patients' symptoms will be assessed using the IVR system until death or the end of the first post-transplant year. In the phase II study, 154 patients with metastatic breast cancer, high risk non-Hodgkin's lymphoma, or multiple myeloma who are scheduled for transplants will be randomly assigned to the experimental (IVR assessment plus triage) or control (IVR assessment only) condition. The symptom data of patients in the experimental condition will be provided to their M.D. Anderson physicians and nurses during the first 30 days after discharge from the hospital. After patients return to their home communities, the IVR system will continue to assess the symptoms of patients in the experimental group and will provide the symptom information directly to the patients' local physicians. Outcome variables will include the patients' symptom intensities and frequencies, functional status, and quality of the end of life. It is predicted that patients in the experimental condition who die during the year will demonstrate better symptom management and quality of the end of life than patients in the control condition. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SYNERGISTIC LYMPHOMAS
CHEMO
RADIOIMMUNOTHERAPY
FOR
B
Principal Investigator & Institution: Johnson, Timothy A.; Medicine; University of Washington Seattle, Wa 98195 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: The long-term objectives of this proposal are 1) to improve therapy for nonHodgkin's lymphoma using combinations of radioimmunotherapy and chemotherapy and 2) to discern the intracellular mechanisms responsible for the synergistic cytotoxicity mediated by these two therapeutic modalities. Preliminary data demonstrate marked synergism in vitro between Iodine-131-radiolabeled anti-CD20 antibody and nucleoside analogs; moderate synergism with topoisomerase inhibitors; and non synergism with cisplatin or 4-hydroxycyclophosphamide. The specific aims of this proposal are four-fold. First, we will test the hypothesis that nucleoside analogs are a more potent class of radiosensitizing drugs for use with I-131-anti-CD20 antibodies than other drug classes using human-derived lymphoma cell lines in vitro. Conclusions will be confirmed in three different in vitro cytotoxic assays, including a clonogenic outgrowth assay, and data will be analyzed by a rigorous isobolographic methodology. Second, we will investigate the mechanisms involved in the potent synergism observed with the nucleoside analogs by assaying well-established effects of the analogs, including the induction of apoptosis, the enhancement of radiation- induced DNA damage, and the incorporation of nucleoside analog into repair DNA. Third, we will investigate the role of Fs-dependent apoptosis in the synergism between anti-CD20 radioimmunotherapy and nucleoside analogs. Fas-dependent and Fas-independent signaling will be studied in experiments employing specific anti-Fas receptor and antiFas ligand blocking antibodies, soluble protein inhibitors of the caspase proteins, and immunoblotting of activated forms of caspase 3 (CPP32), caspase 8 (FLICE), and poly(ADP-ribose) polymerase. Fourth, the most promising combinations of radiolabeled anti-CD20 antibody and chemotherapy will be tested for efficacy in two mouse tumor xenograft models, including a subcutaneous tumor model in nude mice and a disseminated tumor model in SCID mice. The proposed studies will be performed in the laboratory of Dr. Oliver Press at the University of Washington. The large patient base and intense focus on the treatment of lymphomas and other hematologic malignancies at both the University of Washington and the Fred Hutchinson Cancer Research Center and the expertise of the radioimmunotherapy group at these institutions will facilitate rapid translation of promising combinations of radioimmunotherapy and chemotherapy into clinical trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: T CELL DEVELOPMENT & LYMPHOMAGENESIS IN TRANSGENIC MICE Principal Investigator & Institution: Peng, Xiao-Cong; Oklahoma Medical Research Foundation Oklahoma City, Ok 73104 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-DEC-2001 Summary: This application is submitted by an individual with previous research experience in toxicology and clinical training in pathology. The applicant is committed to pursue a career as a physician scientist focusing on molecular pathology. It is therefore necessary for the applicant to receive further training in molecular biology and immunology. The applicant will be mentored by Dr. Xiao-Hong Sun at New York University School of Medicine. The proposed research project attempts to address the
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mechanism by which the basic helix-loop-helix (bHLH) transcription factors, E proteins, control T cell development and prevent T cell lymphomagenesis. The crucial roles of E proteins in T cell development and tumor suppression has recently been demonstrated in Dr. Sun's laboratory by using a transgenic mouse model, in which the Id1 gene, encoding a natural dominant- negative inhibitor of all E proteins, is expressed specifically in the T cell lineage. T cell development in these mice is blocked at the progenitor stage and T cell lymphoma appears in adult mice at a high frequency. To elucidate the underlying mechanisms, I hypothesize that excessive apoptosis of differentiating T cells prevents the accumulation of viable differentiating T cells, and thus dramatically reduces the cellularity in the thymus. I propose that the reasons for the aberrant apoptosis may be due to inappropriate V(D)J recombination of the T cell receptor (TCR) genes such as the incorrect timing at which recombination occurs and the inefficiency at which the rearranged fragments are joined. The inappropriate recombination events may then trigger DNA-damage mediated apoptosis. Increased apoptosis may also take place as a result of the failure to support progenitor cell survival during early stages of differentiation. To test this hypothesis, I will cross the Id1 transgenic mice with RAG 1-/-, p53-/- or bc12 transgenic mice, which will prevent inappropriate recombination, impair DNA-mediated apoptosis and enhance cell survival, respectively. T cell development and lymphomagenesis in these hybrid mice will then be analyzed in comparison with the Id1 transgenic mice as well as RAG1-/-, p53-/- or bc12 transgenic mice. In this proposal, I have also outlined experiments investigating the mechanisms concerning lymphoma development and progression. I belief that knowledge that I will acquire regarding normal T cell development will shed light on the mechanism of lymphomagenesis. It is interesting to determine if the block of T cell development and the predisposition of lymphoma share any common mechanisms. Through these studies, I plan to acquire the knowledge and skills in the fields of molecular biology and immunology and develop my own independent research program. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THERAPEUTIC VACCINATION FOR LYMPHOMA W DENDRITIC CELLS Principal Investigator & Institution: Levy, Ronald; Professor; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2002; Project Start 01-JUN-2002; Project End 31-MAY-2007 Summary: (provided by the applicant): In this project we will develop a vaccine approach using dendritic cells for the treatment of malignant B cell lymphoma. We will build on our prior experience with dendritic cells in which immunoglobulin idiotype from each patient's tumor was used as the antigen and in which safety, immune responses and anti-tumor effects were documented. We will now develop a similar approach in which whole tumor cells will be used as the antigen source and dendritic cells, or exosomes derived from such cells, will be used as the delivery vehicle. This will allow vaccination against the entire constellation of tumor antigens expressed by the lymphoma cell, including immunoglobulin idiotype. We anticipate that such an approach would elicit a broader and more potent anti-tumor immune response. We will begin with animal models and in vitro human systems, in which we will determine the optimum methods for induction of appropriate immune responses. In the animal models the goal will be to induce protection against the growth of the lymphoma. In the human system the goal will be to induce autologous cytotoxic T cell responses against patients' own tumors. The most effective method will then be employed in a human
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clinical trial in patients with lymphoma who have failed conventional therapy. Through the use of dendritic cells or exosomes expressing a wide range of autologous tumor epitopes, we hope to develop a highly effective and broadly applicable vaccine for lymphoma. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TRANSLATIONAL THERAPEUTIC STRATEGIES FOR LOW GRADE LYMPHOMA Principal Investigator & Institution: Freedman, Arnold S.; Associate Professor; DanaFarber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 10-MAY-2000; Project End 31-MAR-2002 Summary: Few, if any, patients with advanced stage follicular low grade NHL (FL) are cured with conventional treatment strategies. Following relapse the majority of these patients still respond to re-institution of treatment, however most will ultimately succumb to their disease. Over the past 10 years, we and others have attempted to cure relapsed and newly diagnosed patients with FL using ABMT. Although a subgroup of these patients clearly benefit from this approach, a significant percentage of patients relapse and/or experience complications of this procedure. The objective of this proposal is to attempt to study the biology of follicular lymphoma and attempt to translate these observations to the clinic to improve outcome while minimizing toxicity. It is presently unknown which biologic parameters govern the sensitivity of subpopulations of FL cells to treatment. Clinical, we observe extraordinary heterogeneity with regard disease presentation, rate of tumor progression, and heterogeneity of response to treatment. We propose to examine two major areas with regard to the biologic of FL. Second, to understand at a molecular level, why subpopulations of FL cells are resistant to treatment in vitro and then potentially in vivo. Therefore, the primary goal of this Project will be to identify which signals regulate follicular lymphoma growth and resistance to treatment. To this end, we propose three Specific Aims. First, we plan to continue our ongoing treatment protocols which focus ont he use of myeloablative therapy and anti-B cell mAb treated autologous hematopoietic stem cell support and immunotoxin therapy of minimal residual disease. Moreover, we plan to pilot new translational strategies including intensification of induction and ablative therapy, synergy of immunotoxins with chemotherapy, and treatment of minimal residual disease with immunotoxins, cytokines, and immunization based treatment strategies. Second, we plan to develop and optimize systems to growth FL cells in culture to study the heterogeneity of this neoplasm. Once technology is optimized, we plan to determine which microenvironment influences affect FL cell growth and survival, and which molecular signals regulate these observation. Third, we plan to examine the expression of survival genes in FL and to determine whether these molecules are responsible for the observed resistance. Again, attempts to modulate these pathways might provide translational strategies to alter treatment. The success of this Project is highly interdependent on determining which patients have minimal residual disease in the marrow or in the patient and methods to treat minimal residual disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TREATMENT AND OUTCOME OF AIDS-RELATED LYMPHOMA Principal Investigator & Institution: Diamond, Catherine A.; Medicine; University of California Irvine Irvine, Ca 926977600 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2007
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Summary: Non-Hodgkin's lymphoma (NHL) is an increasing cause of death among people with acquired immunodeficiency (AIDS) due to declining rates of opportunistic infection (OI) with the use of highly active antiretroviral therapy (HAART). While the prognosis of AIDS- related NHL has been poor in the past, HAART may improve outcomes. Specific Aims: 1) We will identify NHL patients with and without AIDS from the population-based cancer registry using a rapid case ascertainment method. 2) We will describe HIV-specific patient and treatment characteristics of AIDS-NHL patients and distinguish which factors influence prognosis. 3) We will describe tumor characteristics and cancer treatment in NHL patients with and without AIDS and distinguish which oncologic features influence prognosis. 4) We will determine how the use of HAART influences the International Prognostic Index (IPI) and form an original prognostic model. Research Design: Using rapid case ascertainment, we will contact all AIDS-NHL cases reported in a two-year period to the cancer registry for Orange, San Diego, and Imperial Counties and a sample of non- AIDS NHL cases matched on age, sex and race/ethnicity reported during the same two-year period. We will perform interviews and chart reviews on NHL patients to collect information on biologic factors that influence prognosis such as such as NHL site, stage, and pathologic grade as well as patient-specific features such as race/ethnicity, performance status, and health care access. We will gather data on HIV-specific features including CD4 cell count, HIV viral load, HIV risk factors, and use of HAART for NHL patients with AIDS. We will compare survival, development of co-morbidities/OI, and quality of life (QOL) between NHL patients with and without AIDS over a three-year follow-up period between AIDS patients who receive HAART and those who do not. Lastly, we will determine how the use of HAART influences the IPI and develop a prognostic model that incorporates HIV-related factors, tumor characteristics, HAART, and chemotherapy. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TREATMENT OF LYMPHOMA BY VH4-34 ENCODED ANTIBODIES Principal Investigator & Institution: Teng, Nelson N.; Associate Professor; Gynecology and Obstetrics; Stanford University Stanford, Ca 94305 Timing: Fiscal Year 2000; Project Start 01-JUL-2000; Project End 31-DEC-2004 Summary: (Applicant's Description) Our recent in vitro and preclinical studies have shown that certain human mAbs derived from the V4-34 gene are cytotoxic to normal and malignant B lymphocytes. 216, the most cytotoxic of V4-34 derived Ab from our library, has shown minimum toxicity accompanied by significant protection in a human lymphoma models developed in CB17-scid/scid and NOD/LtSz-scid/scid mice. MAb 216 meets all the criteria for an efficacious treatment. Its ligand does not down regulate and is present on majority of B cell lymphomas. It will be associated with minimal toxicity, side effects and immunogenicity. Toxicity is mediated by two independent mechanisms. The first is effector independent, temperature dependent pathway that cross-links the cytoskeletally associated B cell ligand leading to disruption of the cell membrane integrity. The second is the conventional pathway of complement fixation. Toxicity is B cell specific and will not lead to general immune suppression since stem cells are not affected. Finally this human IgM is easy to prepare and use. In this proposal phase I evaluation of human Ab 216 for treatment of recurrent of B cell lymphoma will be undertaken. Twelve patients with relapsed lymphoma who have failed a least one form of therapy will receive escalating doses of 216, with three patients at each dose level. The initial dose will be 50 mgtm2 with subsequent doses escalated as follows: 100 mg/m2, 250 mg/m2 and 400 mg/m2. The pharmacokinetics, toxicity and efficacy of a single injection will be evaluated. Pharmacokinetics of the 216, serum levels and
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immune response to the injected Ab will be measured. Peripheral blood B cell levels will be monitored. Patients receiving doses of 100 mg/m2 or greater will undergo fine needle lymph node biopsy on day 14 for analysis of Ah penetration. Tumor response will be assessed. Because this therapy may benefit the patient with B cell lymphoma and would have no benefit for other subjects only lymphoma patients will be studied. There will be no control subjects. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: TYROSINE KINASE FUSION IN HEMATOLOGIC MALIGNANCY Principal Investigator & Institution: Gilliland, D Gary.; Associate Professor; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2001; Project Start 10-MAY-2000; Project End 31-MAR-2002 Summary: This project will characterize the role of tyrosine kinase fusions in pathogenesis of hematologic malignancy, through development of murine models of leukemia and lymphoma. Our laboratory has recently cloned several tyrosine kinase fusions which will provide the basis for these studies. We have cloned the TELPDGFRbeta fusion and related variants associated with t(5;12) chronic myelomonocytic leukemia (CMML), and a novel TEL-ABL fusion associated with acute myeloid leukemia. Our collaborator, has cloned athe NPM-ALK tyrosine kinase fusion associated with high grade lymphomas. We will develop murine models of leukemia and lymphoma using the TEL-PDGFRbeta, TEL-ABL and NPM-ALK fusions. As with BCRABL in chronic myelogenous leukemia (CML), TEL-PDGFRbeta, TEL- ABL and NPMALK may confer a malignant phenotype by constitutive activation of the tyrosine kinase domains of PDGFRbeta and ALK. In Specific Aim 1 we will characterize involvement of TEL and PDGFRbeta in patients with (i) CMML and t(5;12) translocation, (ii) CMML with normal karyotype, (iii) other FAB subtypes of myelodysplastic syndrome, (iv) myeloid metaplasia and myelofibrosis, (v), acute monocytic leukemias, and (vi) hematologic malignancy with 12p13 cytogenetic abnormalities. These studies will help to clarify the role of TEL and PDGFRbeta in pathogenesis of hematologic malignancy, and may provide insight into functional domains which are important in transforming activity. In Specific Aim 2, transforming activity of the TEL-PDGFRbeta and TEL-ABL fusion gene will be confirmed in stably transfected mammalian cell lines. Expression of TEL-PDGFRbeta and TEL-ABL fusions will be confirmed by immunoblotting and in vitro kinase assays. Specific Aims 1 and 2 will provide the basis for Specific Aim 3 will assess transforming potential of the TEL-PDGFRbeta, TEL-ABL and NPM- ALK fusions in murine bone marrow transplant models of leukemia and lymphoma. Evaluation of transplanted mice will include detailed histopathologic examination; white blood cell differential and immunophenotype analysis to determine lineage involvement of hematological malignancy; and analysis of leukemic cells and leukemic cell lines from transplanted mice for evidence of proviral integration and expression of the fusion protein. These studies will characterize the role of the TEL- PDGFRbeta, TEL-ABL and NPM-ALK fusion proteins in pathogenesis of leukemia and lymphoma, and may provide insight into more effective therapy of hematologic malignancy mediated by tyrosine kinase fusions. Furthermore, these studies will provide a foundation for immunotherapeutic approaches to leukemia and lymphoma. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: UCLA/JCCC--SOUTHWEST ONCOLOGY GROUP Principal Investigator & Institution: Barstis, John; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, Ca 90024
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Timing: Fiscal Year 2001; Project Start 05-FEB-1993; Project End 31-DEC-2003 Summary: Support is requested to permit the University of California, Los Angeles, Center for the Health Sciences (UCLA/CHS) and its affiliated hospitals and physicians to continue participation as a full member in the scientific efforts of the Southwest Oncology Group (SWOG). UCLA/CHS affiliated hospitals include Olive View Medical Center (OVMC), Wadsworth Veterans Administration Medical Center (WVA), and Harbor General Hospital (HGH), and will be referred to as the University. The University entered SWOG as a probationary member in May 1990 with full membership status established in October 1991. Using the SWOG group mechanism as a multidisciplinary focus for clinical cancer research, the University's objectives include: (1) continue to further strengthen clinical cancer investigations at the University and within the NCI designated Jonsson Comprehensive Cancer Center (JCCC); (2) bridge the expertise in translational research within the University to strengthen SWOG's scientific efforts; (3) become major patient contributors to the group's phase III and multimodality studies with special emphasis on recruiting minority patients to clinical trials; and (4) enhance accrual by expanding the current University CGOP relationships to include the recently established UCLA/JCCC Network sites. Specifically, the University's aim is to continue its clinical research leadership by developing appropriate proposals in its areas of expertise, utilizing the University's translational and clinical strengths as they apply to: (1) the use of biological agents, products of molecular genetics, combination cytokine therapy, gene therapy, and cellular adoptive immunotherapy, in the treatment of solid tumors; (2) integrate the JCCC Clinical Program Areas of (A) leukemia (lymphoma, myeloma), BMT, and (B) solid tumor oncology, into the three specific aims noted above; and (3) enhance the SWOG program by using UCLA/JCCC expertise in cancer control, quality of life issues including minority initiatives in breast cancer and lung cancer, survivorship issues for lymphoma patients, and behavioral modification programs. Lastly, the diverse sociocultural atmosphere of Southern California, particularly at OVMC and HGH, provides the University with a large minority patient population. This, along with the designation of UCLA/CHS as a NCI designated Comprehensive Cancer Center, attracts patients seeking new therapeutic modalities and clinical trials and provides a large pool of patients for these studies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: WUMC-CANCER AND LEUKEMIA GROUP B Principal Investigator & Institution: Bartlett, Nancy L.; Internal Medicine; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2003; Project Start 08-MAY-1998; Project End 31-MAR-2009 Summary: (adapted from the applicant's abstract): Washington University has been a CALGB main member institution since 1986. Over the last five years, the cancer research program at the Washington University Medical Center (WUMC) has experienced tremendous growth. Barnes-Jewish Hospital, the largest hospital in St. Louis, diagnoses more than 5,400 patients a year with cancer and remains the major referral center for southeast Missouri and southern Illinois. The Siteman Cancer Center (SCC) at WUMC received NCI-designated Cancer Center status in August 2001. The infrastructure developed by the SCC to compete successfully for the NCI Cancer Center Support Grant has significantly enhanced our ability to carry out all aspects of clinical cancer research, including cooperative group trials. Our recent efforts to expand institutional research studies will significantly enhance our ability to contribute concepts to CALGB during the next grant cycle, specifically in the areas of Hematologic malignancies, thoracic oncology, and pharmacogenomics. Between 1998 and 2002, 16 Washington University
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physicians and research assistants served on 36 different CALGB scientific and administrative committees. WUMC investigators chaired 12 CALGB studies, including Phase II studies in non-Hodgkin's lymphoma, Hodgkin's lymphoma, prostate cancer, mesothelioma, and several pharmacokinetic and pharmacogenomic correlative science studies. Six additional studies are in the final stages of development. Accrual to CALGB trials has continued to increase during this grant period, with an average of 183 patients per year registered to therapeutic and non-therapeutic trials from 1998 to 2001. Accrual to therapeutic trials increased from 61 patients in 1998 to 105 in 2001. Based on registrations to date, projected accrual to CALGB trials for 2002 is estimated to be 312, with 136 to therapeutic studies. Plans for the next grant cycle include 1) continued involvement by all current WUMC investigators, 2) increased participation by our Phase I investigators to facilitate development of Phase II studies within CALGB, 3) involvement of at least five additional WUMC investigators in CALGB activities including faculty interested in GU oncology, quality of life, stem cell transplant and leukemia, leukemia correlative sciences, and radiation oncology, and 5) continued efforts to increase accruals, particularly minority accruals, to CALGB trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “lymphoma” (or synonyms) into the search box. This search gives you access to full-text articles. The following is a sample of items found for lymphoma in the PubMed Central database: •
A dominant inhibitory mutant of the type II transforming growth factor beta receptor in the malignant progression of a cutaneous T-cell lymphoma. by Knaus PI, Lindemann D, DeCoteau JF, Perlman R, Yankelev H, Hille M, Kadin ME, Lodish HF.; 1996 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231343
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A link between increased transforming activity of lymphoma-derived MYC mutant alleles, their defective regulation by p107, and altered phosphorylation of the c-Myc transactivation domain. by Hoang AT, Lutterbach B, Lewis BC, Yano T, Chou TY, Barrett JF, Raffeld M, Hann SR, Dang CV.; 1995 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230642
3 4
Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
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A model for spontaneous B-lineage lymphomas in IgH[mu]-HOX11 transgenic mice. by Hough MR, Reis MD, Singaraja R, Bryce DM, Kamel-Reid S, Dardick I, Breitman ML, Dube ID.; 1998 Nov 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24927
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A New Primary Effusion Lymphoma-Derived Cell Line Yields a Highly Infectious Kaposi's Sarcoma Herpesvirus-Containing Supernatant. by Cannon JS, Ciufo D, Hawkins AL, Griffin CA, Borowitz MJ, Hayward GS, Ambinder RF.; 2000 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=102057
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A subpopulation of normal B cells latently infected with Epstein-Barr virus resembles Burkitt lymphoma cells in expressing EBNA-1 but not EBNA-2 or LMP1. by Chen F, Zou JZ, di Renzo L, Winberg G, Hu LF, Klein E, Klein G, Ernberg I.; 1995 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189092
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Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-[kappa]B. by Mathas S, Hinz M, Anagnostopoulos I, Krappmann D, Lietz A, Jundt F, Bommert K, Mechta-Grigoriou F, Stein H, Dorken B, Scheidereit C.; 2002 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126136
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Activation of c-myc promoter P1 by immunoglobulin [kappa]gene enhancers in Burkitt lymphoma: functional characterization of the intron enhancer motifs [kappa]B, E box 1 and E box 2, and of the 3[prime prime or minute] enhancer motif PU. by Wittekindt NE, Hortnagel K, Geltinger C, Polack A.; 2000 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=102546
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Activation of Jak/STAT Proteins Involved in Signal Transduction Pathway Mediated by Receptor for Interleukin 2 in Malignant T Lymphocytes Derived from Cutaneous Anaplastic Large T-Cell Lymphoma and Sezary Syndrome. by Zhang Q, Nowak I, Vonderheid EC, Rook AH, Kadin ME, Nowell PC, Shaw LM, Wasik MA.; 1996 Aug 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=38610
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Alpha Interferon Inhibits Human Herpesvirus 8 (HHV-8) Reactivation in Primary Effusion Lymphoma Cells and Reduces HHV-8 Load in Cultured Peripheral Blood Mononuclear Cells. by Monini P, Carlini F, Sturzl M, Rimessi P, Superti F, Franco M, Melucci-Vigo G, Cafaro A, Goletti D, Sgadari C, Butto' S, Leone P, Leone P, Chiozzini C, Barresi C, Tinari A, Bonaccorsi A, Capobianchi MR, Giuliani M, di Carlo A, Andreoni M, Rezza G, Ensoli B.; 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=104182
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An Epstein --Barr-related herpesvirus from marmoset lymphomas. by Cho YG, Ramer J, Rivailler P, Quink C, Garber RL, Beier DR, Wang F.; 2001 Jan 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=14736
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Analysis of gene expression during myc oncogene-induced lymphomagenesis in the bursa of Fabricius. by Neiman PE, Ruddell A, Jasoni C, Loring G, Thomas SJ, Brandvold KA, Lee RM, Burnside J, Delrow J.; 2001 May 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=33476
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Analysis of vacA, cagA, and IS605 Genotypes and Those Determined by PCR Amplification of DNA between Repetitive Sequences of Helicobacter pylori Strains Isolated from Patients with Nonulcer Dyspepsia or Mucosa-Associated Lymphoid Tissue Lymphoma. by van Doorn NE, Namavar F, van Doorn LJ, Durrani Z, Kuipers EJ, Vandenbroucke-Grauls CM.; 1999 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=85157
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Antibody responses of splenectomized patients with non-Hodgkin's lymphoma to immunization with polyvalent pneumococcal vaccines. by Petrasch S, Kuhnemund O, Reinacher A, Uppenkamp M, Reinert R, Schmiegel W, Lutticken R, Brittinger G.; 1997 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=170631
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Anti-CD20 Monoclonal Antibody Treatment of Human Herpesvirus 8-Associated, Body Cavity-Based Lymphoma with an Unusual Phenotype in a Human Immunodeficiency Virus-Negative Patient. by Perez CL, Rudoy S.; 2001 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96184
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Avian bic, a Gene Isolated from a Common Retroviral Site in Avian Leukosis VirusInduced Lymphomas That Encodes a Noncoding RNA, Cooperates with c-myc in Lymphomagenesis and Erythroleukemogenesis. by Tam W, Hughes SH, Hayward WS, Besmer P.; 2002 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=155062
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Bax Loss Impairs Myc-Induced Apoptosis and Circumvents the Selection of p53 Mutations during Myc-Mediated Lymphomagenesis. by Eischen CM, Roussel MF, Korsmeyer SJ, Cleveland JL.; 2001 Nov 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=99936
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B-Cell Lymphoma Induction by Akv Murine Leukemia Viruses Harboring One or Both Copies of the Tandem Repeat in the U3 Enhancer. by Lovmand J, Sorensen AB, Schmidt J, Ostergaard M, Luz A, Pedersen FS.; 1998 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=110375
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BCL8, a novel gene involved in translocations affecting band 15q11 --13 in diffuse large-cell lymphoma. by Dyomin VG, Rao PH, Dalla-Favera R, Chaganti RS.; 1997 May 27; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20847
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bic, a novel gene activated by proviral insertions in avian leukosis virus-induced lymphomas, is likely to function through its noncoding RNA. by Tam W, Ben-Yehuda D, Hayward WS.; 1997 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=231875
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Calorie Restriction Suppresses Subgenomic Mink Cytopathic Focus-Forming Murine Leukemia Virus Transcription and Frequency of Genomic Expression While Impairing Lymphoma Formation. by Shield BA, Engelman RW, Fukaura Y, Good RA, Day NK.; 1991 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53089
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Cancer dormancy and cell signaling: Induction of p21waf1 initiated by membrane IgM engagement increases survival of B lymphoma cells. by Marches R, Hsueh R, Uhr JW.; 1999 Jul 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17581
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Cancer Dormancy: Isolation and Characterization of Dormant Lymphoma Cells. by Yefenof E, Picker LJ, Scheuermann RH, Tucker TF, Vitetta ES, Uhr JW.; 1993 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=45973
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Cellular Tropism and Viral Interleukin-6 Expression Distinguish Human Herpesvirus 8 Involvement in Kaposi's Sarcoma, Primary Effusion Lymphoma, and Multicentric Castleman's Disease. by Staskus KA, Sun R, Miller G, Racz P, Jaslowski A, Metroka C, Brett-Smith H, Haase AT.; 1999 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=104197
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Characterization of a mutant calcineurin A alpha gene expressed by EL4 lymphoma cells. by Fruman DA, Pai SY, Burakoff SJ, Bierer BE.; 1995 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230625
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Characterization of pal-1, a common proviral insertion site in murine leukemia virusinduced lymphomas of c-myc and Pim-1 transgenic mice. by Scheijen B, Jonkers J, Acton D, Berns A.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191018
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Characterization of the Transforming Activity of p80, a Hyperphosphorylated Protein in a Ki-1 Lymphoma Cell Line with Chromosomal Translocation t(2;5). by Fujimoto J, Shiota M, Iwahara T, Seki N, Satoh H, Mori S, Yamamoto T.; 1996 Apr 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39508
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Cholesterol-dependent clustering of IL-2R[alpha] and its colocalization with HLA and CD48 on T lymphoma cells suggest their functional association with lipid rafts. by Vereb G, Matko J, Vamosi G, Ibrahim SM, Magyar E, Varga S, Szollosi J, Jenei A, Gaspar R Jr, Waldmann TA, Damjanovich S.; 2000 May 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18550
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Clonal Evolution of a Follicular Lymphoma: Evidence for Antigen Selection. by Bahler DW, Levy R.; 1992 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=49585
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Cloned Shiga Toxin 2 B Subunit Induces Apoptosis in Ramos Burkitt's Lymphoma B Cells. by Marcato P, Mulvey G, Armstrong GD.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=127801
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CmC(A /T)GG DNA methylation in mature B cell lymphoma gene silencing. by Malone CS, Miner MD, Doerr JR, Jackson JP, Jacobsen SE, Wall R, Teitell M.; 2001 Aug 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=56973
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c-Myc Proteolysis by the Ubiquitin-Proteasome Pathway: Stabilization of c-Myc in Burkitt's Lymphoma Cells. by Gregory MA, Hann SR.; 2000 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=85426
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Constitutive activation of Stat5a by retrovirus integration in early pre-B lymphomas of SL /Kh strain mice. by Tsuruyama T, Nakamura T, Jin G, Ozeki M, Yamada Y, Hiai H.; 2002 Jun 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123054
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Cooperative action of germ-line mutations in decorin and p53 accelerates lymphoma tumorigenesis. by Iozzo RV, Chakrani F, Perrotti D, McQuillan DJ, Skorski T, Calabretta B, Eichstetter I.; 1999 Mar 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15900
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Cutaneous T-Cell Lymphoma in a Cardiac Transplant Recipient. by McMullan DM, Radovancevic B, Jackow CM, Frazier OH, Duvic M.; 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=101179
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Cytochrome P450 CYP1B1 determines susceptibility to 7,12dimethylbenz[a]anthracene-induced lymphomas. by Buters JT, Sakai S, Richter T, Pineau T, Alexander DL, Savas U, Doehmer J, Ward JM, Jefcoate CR, Gonzalez FJ.; 1999 Mar 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26722
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Deregulation of PAX-5 by Translocation of the E[mu] Enhancer of the IgH Locus Adjacent to Two Alternative PAX-5 Promoters in a Diffuse Large-Cell Lymphoma. by Busslinger M, Klix N, Pfeffer P, Graninger PG, Kozmik Z.; 1996 Jun 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39201
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Detection of Epstein-Barr virus DNA in cerebrospinal fluid for diagnosis of AIDSrelated central nervous system lymphoma. by Arribas JR, Clifford DB, Fichtenbaum CJ, Roberts RL, Powderly WG, Storch GA.; 1995 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=228219
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Differential Epstein-Barr virus gene expression in B-cell subsets recovered from lymphomas in SCID mice after transplantation of human peripheral blood lymphocytes. by Rochford R, Mosier DE.; 1995 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=188558
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Differential Expression of Viral Bcl-2 Encoded by Kaposi's Sarcoma-Associated Herpesvirus and Human Bcl-2 in Primary Effusion Lymphoma Cells and Kaposi's Sarcoma Lesions. by Widmer I, Wernli M, Bachmann F, Gudat F, Cathomas G, Erb P.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=135929
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Differential Regulation of Epstein-Barr Virus (EBV) Latent Gene Expression in Burkitt Lymphoma Cells Infected with a Recombinant EBV Strain. by Trivedi P, Spinsanti P, Cuomo L, Volpe M, Takada K, Frati L, Faggioni A.; 2001 May 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114250
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Differential tumorigenicity between Epstein-Barr virus genome-positive and genomenegative cell lines with t(11;14)(q13;q32) derived from mantle cell lymphoma. by Daibata M, Kubonishi I, Miyoshi I.; 1996 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191000
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Disease activity and risk of lymphoma in patients with rheumatoid arthritis: nested case-control study. by Baecklund E, Ekbom A, Sparen P, Feltelius N, Klareskog L.; 1998 Jul 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28610
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Disruption of Myc-Tubulin Interaction by Hyperphosphorylation of c-Myc during Mitosis or by Constitutive Hyperphosphorylation of Mutant c-Myc in Burkitt's
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Disruption of pre-TCR expression accelerates lymphomagenesis in E2A-deficient mice. by Engel I, Murre C.; 2002 Aug 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123255
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Distinct Biology of Kaposi's Sarcoma-Associated Herpesvirus from Primary Lesions and Body Cavity Lymphomas. by Friborg J Jr, Kong WP, Flowers CC, Flowers SL, Sun Y, Foreman KE, Nickoloff BJ, Nabel GJ.; 1998 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=110538
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Distribution of human herpesvirus-8 latently infected cells in Kaposi's sarcoma, multicentric Castleman's disease, and primary effusion lymphoma. by Dupin N, Fisher C, Kellam P, Ariad S, Tulliez M, Franck N, van Marck E, Salmon D, Gorin I, Escande JP, Weiss RA, Alitalo K, Boshoff C.; 1999 Apr 13; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16369
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Dysregulated Synthesis of Intracellular Type 1 and Type 2 Cytokines by T Cells of Patients with Cutaneous T-Cell Lymphoma. by Lee BN, Duvic M, Tang CK, BuesoRamos C, Estrov Z, Reuben JM.; 1999 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=95664
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Dysregulated TCL1 promotes multiple classes of mature B cell lymphoma. by Hoyer KK, French SW, Turner DE, Nguyen MT, Renard M, Malone CS, Knoetig S, Qi CF, Su TT, Cheroutre H, Wall R, Rawlings DJ, Morse HC III, Teitell MA.; 2002 Oct 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=137894
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E2A deficiency leads to abnormalities in alphabeta T-cell development and to rapid development of T-cell lymphomas. by Bain G, Engel I, Robanus Maandag EC, te Riele HP, Voland JR, Sharp LL, Chun J, Huey B, Pinkel D, Murre C.; 1997 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=232330
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EBNA-1 Sequences in Endemic and Sporadic Burkitt's Lymphoma. by Bhatia K, Magrath I.; 1999 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=112804
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Ectopic expression of E47 or E12 promotes the death of E2A-deficient lymphomas. by Engel I, Murre C.; 1999 Feb 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15339
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Episomal amplification or chromosomal integration of the viral genome: alternative pathways in hamster polyomavirus-induced lymphomas. by Mazur S, Feunteun J, de La Roche Saint Andre C.; 1995 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189006
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Epstein --Barr virus RNA confers resistance to interferon-[alpha]-induced apoptosis in Burkitt's lymphoma. by Nanbo A, Inoue K, Adachi-Takasawa K, Takada K.; 2002 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=125896
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Epstein-Barr Virus (EBV) Nuclear Protein 2-Induced Disruption of EBV Latency in the Burkitt's Lymphoma Cell Line Akata: Analysis by Tetracycline-Regulated Expression. by Fujiwara S, Nitadori Y, Nakamura H, Nagaishi T, Ono Y.; 1999 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=112573
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Epstein-Barr Virus and the Somatic Hypermutation of Immunoglobulin Genes in Burkitt's Lymphoma Cells. by Harris RS, Croom-Carter DS, Rickinson AB, Neuberger MS.; 2001 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114624
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Epstein-Barr Virus Contributes to the Malignant Phenotype and to Apoptosis Resistance in Burkitt's Lymphoma Cell Line Akata. by Komano J, Sugiura M, Takada K.; 1998 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=110333
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Epstein-Barr Virus Nuclear Antigen 1 Sequences in Endemic and Sporadic Burkitt's Lymphoma Reflect Virus Strains Prevalent in Different Geographic Areas. by Habeshaw G, Yao QY, Bell AI, Morton D, Rickinson AB.; 1999 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=103916
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Epstein-Barr Virus Regulates c-MYC, Apoptosis, and Tumorigenicity in Burkitt Lymphoma. by Ruf IK, Rhyne PW, Yang H, Borza CM, Hutt-Fletcher LM, Cleveland JL, Sample JT.; 1999 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=83959
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Epstein-Barr Virus Small RNAs Potentiate Tumorigenicity of Burkitt Lymphoma Cells Independently of an Effect on Apoptosis. by Ruf IK, Rhyne PW, Yang C, Cleveland JL, Sample JT.; 2000 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=102063
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Establishment of B-Cell Lymphoma Cell Lines Persistently Infected with Hepatitis C Virus In Vivo and In Vitro: the Apoptotic Effects of Virus Infection. by Sung VM, Shimodaira S, Doughty AL, Picchio GR, Can H, Yen TS, Lindsay KL, Levine AM, Lai MM.; 2003 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=140883
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Evi-5, a common site of retroviral integration in AKXD T-cell lymphomas, maps near Gfi-1 on mouse chromosome 5. by Liao X, Buchberg AM, Jenkins NA, Copeland NG.; 1995 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189633
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Exclusive Expression of Epstein-Barr Virus Nuclear Antigen 1 in Burkitt Lymphoma Arises from a Third Promoter, Distinct from the Promoters Used in Latently Infected Lymphocytes. by Schaefer BC, Woisetschlaeger M, Strominger JL, Speck SH.; 1991 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52124
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Expression of cyclin D2 in Epstein-Barr virus-positive Burkitt's lymphoma cell lines is related to methylation status of the gene. by Sinclair AJ, Palmero I, Holder A, Peters G, Farrell PJ.; 1995 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=188707
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Expression of the Epstein --Barr virus latent membrane protein 1 induces B cell lymphoma in transgenic mice. by Kulwichit W, Edwards RH, Davenport EM, Baskar JF, Godfrey V, Raab-Traub N.; 1998 Sep 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21748
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Fast and high-affinity binding of B-lymphotropic papovavirus to human Blymphoma cell lines. by Herrmann M, Oppenlander M, Pawlita M.; 1995 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189591
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Follicular Lymphomas can be Induced to Present Alloantigen Efficiently: A Conceptual Model to Improve Their Tumor Immunogenicity. by Schultze JL, Cardoso AA, Freeman GJ, Seamon MJ, Daley J, Pinkus GS, Gribben JG, Nadler LN.; 1995 Aug 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41124
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Frequency of vacA Genotypes and Cytotoxin Activity in Helicobacter pylori Associated with Low-Grade Gastric Mucosa-Associated Lymphoid Tissue Lymphoma. by Miehlke S, Meining A, Morgner A, Bayerdorffer E, Lehn N, Stolte M, Graham DY, Go MF.; 1998 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=105053
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Frequent disruption of the Nf1 gene by a novel murine AIDS virus-related provirus in BXH-2 murine myeloid lymphomas. by Cho BC, Shaughnessy JD Jr, Largaespada DA, Bedigian HG, Buchberg AM, Jenkins NA, Copeland NG.; 1995 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189634
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Frequent Somatic Hypermutation of the 5' Noncoding Region of the BCL6 Gene in BCell Lymphoma. by Migliazza A, Martinotti S, Chen W, Fusco C, Ye BH, Knowles DM, Offit K, Chaganti RS, Dalla-Favera R.; 1995 Dec 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40389
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Gastric adenocarcinoma in a patient re-infected with H. pylori after regression of MALT lymphoma with successful anti-H. pylori therapy and gastric resection: a case report. by Ghoshal UC, Guha D, Bandyopadhyay S, Pal C, Chakraborty S, Ghoshal U, Ghosh TK, Pal BB, Banerjee PK.; 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=102757
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Genetic determinant of rapid-onset B-cell lymphoma by avian leukosis virus. by Smith MR, Smith RE, Dunkel I, Hou V, Beemon KL, Hayward WS.; 1997 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191929
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Genome-Based Identification of Cancer Genes by Proviral Tagging in Mouse Retrovirus-Induced T-Cell Lymphomas. by Kim R, Trubetskoy A, Suzuki T, Jenkins NA, Copeland NG, Lenz J.; 2003 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=140962
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Human Herpesvirus 8 (HHV-8)-Encoded Cytokines Induce Expression of and Autocrine Signaling by Vascular Endothelial Growth Factor (VEGF) in HHV-8Infected Primary-Effusion Lymphoma Cell Lines and Mediate VEGF-Independent Antiapoptotic Effects. by Liu C, Okruzhnov Y, Li H, Nicholas J.; 2001 Nov 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114673
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Human Immunodeficiency Virus Replication in a Primary Effusion Lymphoma Cell Line Stimulates Lytic-Phase Replication of Kaposi's Sarcoma-Associated Herpesvirus. by Varthakavi V, Browning PJ, Spearman P.; 1999 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=113088
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Identification of Notch1 as a Frequent Target for Provirus Insertional Mutagenesis in T-Cell Lymphomas Induced by Leukemogenic Mutants of Mouse Mammary Tumor Virus. by Yanagawa SI, Lee JS, Kakimi K, Matsuda Y, Honjo T, Ishimoto A.; 2000 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=112415
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Identification of the Gene Associated with the Recurring Chromosomal Translocations t(3;14)(q27;q32) and t(3;22)(q27;q11) in B-Cell Lymphomas. by Baron BW, Nucifora G, McCabe N, Espinosa R III, Beau MM.; 1993 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46696
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Identification of the Neoplastically Transformed Cells in Marek's Disease Herpesvirus-Induced Lymphomas: Recognition by the Monoclonal Antibody AV37. by Burgess SC, Davison TF.; 2002 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=136297
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Immunoglobulin G1 Antibody Response to Helicobacter pylori Heat Shock Protein 60 Is Closely Associated with Low-Grade Gastric Mucosa-Associated Lymphoid Tissue Lymphoma. by Ishii E, Yokota K, Sugiyama T, Fujinaga Y, Ayada K, Hokari I, Hayashi S, Hirai Y, Asaka M, Oguma K.; 2001 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=96225
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Importance of a c-Myb binding site for lymphomagenesis by the retrovirus SL3-3. by Nieves A, Levy LS, Lenz J.; 1997 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191175
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In vivo growth of a murine lymphoma cell line alters regulation of expression of HSP72. by Davidson S, Hoj P, Gabriele T, Anderson RL.; 1995 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=232009
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Increased Induction of Osteopetrosis, but Unaltered Lymphomagenicity, by Murine Leukemia Virus SL3-3 after Mutation of a Nuclear Factor 1 Site in the Enhancer. by Ethelberg S, Tzschaschel BD, Luz A, Diaz-Cano SJ, Pedersen FS, Schmidt J.; 1999 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=113096
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Increased lymphomagenicity and restored disease specificity of AML1 site (core) mutant SL3-3 murine leukemia virus by a second-site enhancer variant evolved in vivo. by Ethelberg S, Lovmand J, Schmidt J, Luz A, Pedersen FS.; 1997 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=192069
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Induction of an exceptionally high-level, nontranslated, Epstein-Barr virus-encoded polyadenylated transcript in the Burkitt's lymphoma line Daudi. by Gao Y, Smith PR, Karran L, Lu QL, Griffin BE.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191027
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Induction of B-Cell Lymphoma in BALB/c Nude Mice with an Ecotropic, B-Tropic Helper Virus Present in the Murine AIDS Virus Stock. by Tayar L, Higo K, Kubo Y, Wang Y, Lu LM, Zhang F, Iwatani Y, Wang L, Ono T, Maeda M, Sakai H, Ishimoto A.; 1999 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=103991
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Induction of tolerance to immunogenic tumor antigens associated with lymphomagenesis in HOX11 transgenic mice. by Rosic-Kablar S, Chan K, Reis MD, Dube ID, Hough MR.; 2000 Nov 21; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27219
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Infection by Mink Cell Focus-Forming Viruses Confers Interleukin 2 (IL-2) Independence to an IL-2-Dependent Rat T-Cell Lymphoma Line. by Tsichlis PN, Bear SE.; 1991 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51715
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Inhibition of glycolipid shedding rescues recognition of a CD1 + T cell lymphoma by natural killer T (NKT) cells. by Sriram V, Cho S, Li P, O'Donnell PW, Dunn C, Hayakawa K, Blum JS, Brutkiewicz RR.; 2002 Jun 11; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123044
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Interferon [alpha] Induces the Expression of Retinoblastoma Gene Product in Human Burkitt Lymphoma Daudi Cells: Role in Growth Regulation. by Kumar R, Atlas I.; 1992 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=49549
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Interferon-independent and -induced regulation of Epstein-Barr virus EBNA-1 gene transcription in Burkitt lymphoma. by Nonkwelo C, Ruf IK, Sample J.; 1997 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191971
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Intracellular Forms of Human NOTCH1 Functionally Activate Essential Epstein-Barr Virus Major Latent Promoters in the Burkitt's Lymphoma BJAB Cell Line but Repress These Promoters in Jurkat Cells. by Cotter M, Callahan J, Aster J, Robertson E.; 2000 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111484
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Kaposi's sarcoma-associated herpesvirus contains G protein-coupled receptor and cyclin D homologs which are expressed in Kaposi's sarcoma and malignant lymphoma. by Cesarman E, Nador RG, Bai F, Bohenzky RA, Russo JJ, Moore PS, Chang Y, Knowles DM.; 1996 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190906
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Kaposi's Sarcoma-Associated Herpesvirus Open Reading Frame 50/Rta Protein Activates the Entire Viral Lytic Cycle in the HH-B2 Primary Effusion Lymphoma Cell Line. by Gradoville L, Gerlach J, Grogan E, Shedd D, Nikiforow S, Metroka C, Miller G.; 2000 Jul 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=112123
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Large B-Cell Lymphoma of the Atria. by AlZeerah MA, Singh R, Jarrous A.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152843
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Life-Span, T-Cell Responses, and Incidence of Lymphomas in Congenic Mice. by Salazar M, Leong T, Tu N, Gelman RS, Watson AL, Bronson R, Iglesiaas A, Mann M, Good RA, Yunis EJ.; 1995 Apr 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=42088
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Localization of Epstein-Barr Virus-Encoded RNAs EBER-1 and EBER-2 in Interphase and Mitotic Burkitt Lymphoma Cells. by Schwemmle M, Clemens MJ, Hilse K, Pfeifer K, Troster H, Muller WE, Bachmann M.; 1992 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=50324
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Long terminal repeat enhancer core sequences in proviruses adjacent to c-myc in Tcell lymphomas induced by a murine retrovirus. by Morrison HL, Soni B, Lenz J.; 1995 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=188593
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Long-Distance Activation of the Myc Protooncogene by Provirus Insertion in Mlvi-1 or Mlvi-4 in Rat T-Cell Lymphomas. by Lazo PA, Lee JS, Tsichlis PN.; 1990 Jan 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53222
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Loss of p21 increases sensitivity to ionizing radiation and delays the onset of lymphoma in atm-deficient mice. by Wang YA, Elson A, Leder P.; 1997 Dec 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=25064
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Loss of p27Kip1 but not p21Cip1 decreases survival and synergizes with MYC in murine lymphomagenesis. by Martins CP, Berns A.; 2002 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126110
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LR1 Regulates c-Myc Transcription in B-Cell Lymphomas. by Brys A, Maizels N.; 1994 May 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=43900
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Lymphomas and High-Level Expression of Murine Leukemia Viruses in CFW Mice. by Taddesse-Heath L, Chattopadhyay SK, Dillehay DL, Lander MR, Nagashfar Z, Morse HC III, Hartley JW.; 2000 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=112200
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Lyn Tyrosine Kinase Signals Cell Cycle Arrest but not Apoptosis in B- Lineage Lymphoma Cells. by Scheuermann RH, Racila E, Tucker T, Yefenof E, Street NE, Vitetta ES, Picker LJ, Uhr JW.; 1994 Apr 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=43720
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Mantle cell lymphoma is characterized by inactivation of the ATM gene. by Schaffner C, Idler I, Stilgenbauer S, Dohner H, Lichter P.; 2000 Mar 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16005
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Membrane-Associated CD19-LYN Complex is an Endogenous p53-Independent and Bcl-2-Independent Regulator of Apoptosis in Human B-Lineage Lymphoma Cells. by Myers DE, Jun X, Waddick KG, Forsyth C, Chelstrom LM, Gunther RL, Tumer NE, Bolen J, Uckun FM.; 1995 Oct 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40844
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Minimal truncation of the c-myb gene product in rapid-onset B-cell lymphoma. by Jiang W, Kanter MR, Dunkel I, Ramsay RG, Beemon KL, Hayward WS.; 1997 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191928
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Molecular Analysis of a Chromosomal Translocation, t(9:14)(p13;q32), in a Diffuse Large-Cell Lymphoma Cell Line Expressing the Ki-1 Antigen. by Ohno H, Furukawa T, Fukuhara S, Zong SQ, Kamesaki H, Shows TB, Beau MM, McKeithan TW, Kawakami T, Honjo T.; 1990 Jan 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53318
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Molecular and Immunophenotypical Characterization of a Feline Immunodeficiency Virus (FIV)-Associated Lymphoma: a Direct Role for FIV in B-Lymphocyte Transformation? by Beatty JA, Callanan JJ, Terry A, Jarrett O, Neil JC.; 1998 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=109433
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Moloney murine leukemia virus-induced lymphomas in p53-deficient mice: overlapping pathways in tumor development? by Baxter EW, Blyth K, Donehower LA, Cameron ER, Onions DE, Neil JC.; 1996 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190045
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Multiplex PCR for diagnosis of AIDS-related central nervous system lymphoma and toxoplasmosis. by Roberts TC, Storch GA.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=229553
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Murine Interleukin 2 Receptor [beta] Chain: Dysregulated Gene Expression in Lymphoma Line EL-4 caused by a Promoter Insertion. by Kono T, Doi T, Yamada G, Hatakeyama M, Minamoto S, Tsudo M, Miyasaka M, Miyata T, Taniguchi T.; 1990 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=53572
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Murine Leukemia Virus Proviral Insertions between the N-ras and unr Genes in BCell Lymphoma DNA Affect the Expression of N-ras Only. by Martin-Hernandez J, Sorensen AB, Pedersen FS.; 2001 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114780
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Negative autoregulation of BCL-6 is bypassed by genetic alterations in diffuse large B cell lymphomas. by Wang X, Li Z, Naganuma A, Ye BH.; 2002 Nov 12; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=137537
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Nitric Oxide Production in SJL Mice Bearing the RcsX Lymphoma: A Model for in vivo Toxicological Evaluation of NO[center dot]. by Gal A, Tamir S, Tannenbaum SR, Wogan GN.; 1996 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=38086
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Novel Endogenous Type D Retroviral Particles Expressed at High Levels in a SCID Mouse Thymic Lymphoma. by Ristevski S, Purcell DF, Marshall J, Campagna D, Nouri S, Fenton SP, McPhee DA, Kannourakis G.; 1999 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=112507
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Nucleophosmin-Anaplastic Lymphoma Kinase of Large-Cell Anaplastic Lymphoma Is a Constitutively Active Tyrosine Kinase That Utilizes Phospholipase C-[gamma] To Mediate Its Mitogenicity. by Bai RY, Dieter P, Peschel C, Morris SW, Duyster J.; 1998 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=109278
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Occult Cardiac Lymphoma Presenting with Cardiac Tamponade. by Wilhite DB, Quigley RL.; 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152839
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Oligonucleotide microarrays demonstrate the highest frequency of ATM mutations in the mantle cell subtype of lymphoma. by Fang NY, Greiner TC, Weisenburger DD, Chan WC, Vose JM, Smith LM, Armitage JO, Mayer RA, Pike BL, Collins FS, Hacia JG.; 2003 Apr 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=154352
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Oncogenic Role of Epstein-Barr Virus-Encoded RNAs in Burkitt's Lymphoma Cell Line Akata. by Komano J, Maruo S, Kurozumi K, Oda T, Takada K.; 1999 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=113031
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Ongoing immunoglobulin somatic mutation in germinal center B cell-like but not in activated B cell-like diffuse large cell lymphomas. by Lossos IS, Alizadeh AA, Eisen MB, Chan WC, Brown PO, Botstein D, Staudt LM, Levy R.; 2000 Aug 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27813
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Onset of natural killer cell lymphomas in transgenic mice carrying a truncated HMGI-C gene by the chronic stimulation of the IL-2 and IL-15 pathway. by Baldassarre G, Fedele M, Battista S, Vecchione A, Klein-Szanto AJ, Santoro M, Waldmann TA, Azimi N, Croce CM, Fusco A.; 2001 Jul 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=35452
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Open reading frame 26 of human herpesvirus 8 encodes a tetradecanoyl phorbol acetate- and butyrate-inducible 32-kilodalton protein expressed in a body cavitybased lymphoma cell line. by O'Neill E, Douglas JL, Chien ML, Garcia JV.; 1997 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191701
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p38-mediated Regulation of an Fas-associated Death Domain Protein-independent Pathway Leading to Caspase-8 Activation during TGF[beta]-induced Apoptosis in Human Burkitt Lymphoma B Cells BL41. by Schrantz N, Bourgeade MF, Mouhamad S, Leca G, Sharma S, Vazquez A.; 2001 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=60162
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p53 Deficiency Increases Transformation by v-Abl and Rescues the Ability of a CTerminally Truncated v-Abl Mutant To Induce Pre-B Lymphoma In Vivo. by Zou X, Cong F, Coutts M, Cattoretti G, Goff SP, Calame K.; 2000 Jan 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=85151
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p53 Mutations in Human Lymphoid Malignancies: Association with Burkitt Lymphoma and Chronic Lymphocytic Leukemia. by Gaidano G, Ballerini P, Gong JZ, Inghirami G, Neri A, Newcomb EW, Magrath IT, Knowles DM, Dalla-Favera R.; 1991 Jun 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=51883
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Partial T and B lymphocyte immunodeficiency and predisposition to lymphoma in patients with hypomorphic mutations in Artemis. by Moshous D, Pannetier C, Chasseval RD, Deist FL, Cavazzana-Calvo M, Romana S, Macintyre E, Canioni D, Brousse N, Fischer A, Casanova JL, Villartay JP.; 2003 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151863
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PRAD1, a Candidate BLC1 Oncogene: Mapping and Expression in Centrocytic Lymphoma. by Rosenberg CL, Wong E, Petty EM, Bale AE, Tsujimoto Y, Harris NL, Arnold A.; 1991 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52773
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Predominant Role of [alpha]4-Integrins for Distinct Steps of Lymphoma Metastasis. by Gosslar U, Jonas P, Luz A, Lifka A, Naor D, Hamann A, Holzmann B.; 1996 May 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39363
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Preferential Localization of the Epstein-Barr Virus (EBV) Oncoprotein LMP-1 to Nuclei in Human T Cells: Implications for Its Role in the Development of EBV Genome-Positive T-Cell Lymphomas. by Xu J, Ahmad A, Menezes J.; 2002 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=136072
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Pretarget radiotherapy with an anti-CD25 antibody-streptavidin fusion protein was effective in therapy of leukemia /lymphoma xenografts. by Zhang M, Zhang Z, Garmestani K, Schultz J, Axworthy DB, Goldman CK, Brechbiel MW, Carrasquillo JA, Waldmann TA.; 2003 Feb 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=149929
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Propagation of Rat Parvovirus in Thymic Lymphoma Cell Line C58(NT)D and Subsequent Appearance of a Resistant Cell Clone after Lytic Infection. by Ueno Y, Harada T, Iseki H, Ohshima T, Sugiyama F, Yagami KI.; 2001 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114887
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Proviral activation of the c-myb proto-oncogene is detectable in preleukemic mice infected neonatally with Moloney murine leukemia virus but not in resulting end stage T lymphomas. by Belli B, Wolff L, Nazarov V, Fan H.; 1995 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189334
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Rapid production of specific vaccines for lymphoma by expression of the tumorderived single-chain Fv epitopes in tobacco plants. by McCormick AA, Kumagai MH, Hanley K, Turpen TH, Hakim I, Grill LK, Tuse D, Levy S, Levy R.; 1999 Jan 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15200
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Recognition of the Epstein-Barr Virus-Encoded Nuclear Antigens EBNA-4 and EBNA6 by HLA-A11-Restricted Cytotoxic T Lymphocytes: Implications for DownRegulation of HLA-A11 in Burkitt Lymphoma. by Gavioli R, Campos-Lima PO, Kurilla MG, Kieff E, Klein G, Masucci MG.; 1992 Jul 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=49397
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Redefining the Epstein-Barr Virus-Encoded Nuclear Antigen EBNA-1 Gene Promoter and Transcription Initiation Site in Group I Burkitt Lymphoma Cell Lines. by Schaefer BC, Strominger JL, Speck SH.; 1995 Nov 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40652
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Regression of a Murine Gammaherpesvirus 68-Positive B-Cell Lymphoma Mediated by CD4 T Lymphocytes. by Robertson KA, Usherwood EJ, Nash AA.; 2001 Apr 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114142
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Replacement of the Epstein-Barr Virus Plasmid with the EBER Plasmid in Burkitt's Lymphoma Cells. by Maruo S, Nanbo A, Takada K.; 2001 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114569
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Restoration of Surface IgM-Mediated Apoptosis in an Anti-IgM-Resistant Variant of WEHI-231 Lymphoma Cells by HS1, a Protein-Tyrosine Kinase Substrate. by Fukuda T, Kitamura D, Taniuchi I, Maekawa Y, Benhamou LE, Sarthou P, Watanabe T.; 1995 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41327
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Restricted Epstein-Barr Virus Protein Expression in Burkitt Lymphoma is Due to a Different Epstein-Barr Nuclear Antigen 1 Transcriptional Initiation Site. by Sample J, Brooks L, Sample C, Young L, Rowe M, Gregory C, Rickinson A, Kieff E.; 1991 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52079
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Retroviral insertional activation of the c-myb proto-oncogene in a Marek's disease Tlymphoma cell line. by Le Rouzic E, Perbal B.; 1996 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190808
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Risk of HIV related Kaposi's sarcoma and non-Hodgkin's lymphoma with potent antiretroviral therapy: prospective cohort study. by Ledergerber B, Telenti A, Egger M.; 1999 Jul 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28149
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Role of bcl-2 in Epstein-Barr Virus-Induced Malignant Conversion of Burkitt's Lymphoma Cell Line Akata. by Komano J, Takada K.; 2001 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114063
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Role of the F-box protein Skp2 in lymphomagenesis. by Latres E, Chiarle R, Schulman BA, Pavletich NP, Pellicer A, Inghirami G, Pagano M.; 2001 Feb 27; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=30169
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Role of the nucleophosmin (NPM) portion of the non-Hodgkin's lymphomaassociated NPM-anaplastic lymphoma kinase fusion protein in oncogenesis. by Bischof D, Pulford K, Mason DY, Morris SW.; 1997 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=232080
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Second-site proviral enhancer alterations in lymphomas induced by enhancer mutants of SL3-3 murine leukemia virus: negative effect of nuclear factor 1 binding site. by Ethelberg S, Hallberg B, Lovmand J, Schmidt J, Luz A, Grundstrom T, Pedersen FS.; 1997 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191173
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Selection for c-myc Integration Sites in Polyclonal T-Cell Lymphomas. by Broussard DR, Mertz JA, Lozano M, Dudley JP.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153816
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Selection for Loss of p53 Function in T-Cell Lymphomagenesis Is Alleviated by Moloney Murine Leukemia Virus Infection in myc Transgenic Mice. by Baxter EW, Blyth K, Cameron ER, Neil JC.; 2001 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114551
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Selection of Reversions and Suppressors of a Mutation in the CBF Binding Site of a Lymphomagenic Retrovirus. by Martiney MJ, Rulli K, Beaty R, Levy LS, Lenz J.; 1999 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=104287
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Selective switch between latency and lytic replication of Kaposi's sarcoma herpesvirus and Epstein-Barr virus in dually infected body cavity lymphoma cells. by Miller G, Heston L, Grogan E, Gradoville L, Rigsby M, Sun R, Shedd D, Kushnaryov VM, Grossberg S, Chang Y.; 1997 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191053
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Serological detection of cutaneous T-cell lymphoma-associated antigens. by Eichmuller S, Usener D, Dummer R, Stein A, Thiel D, Schadendorf D.; 2001 Jan 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=14639
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Serum Antibody Responses to Helicobacter pylori and the cagA Marker in Patients with Mucosa-Associated Lymphoid Tissue Lymphoma. by Taupin A, Occhialini A, Ruskone-Fourmestraux A, Delchier JC, Rambaud JC, Megraud F.; 1999 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=95744
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Sint1, a Common Integration Site in SL3-3-Induced T-Cell Lymphomas, Harbors a Putative Proto-Oncogene with Homology to the Septin Gene Family. by Sorensen AB, Lund AH, Ethelberg S, Copeland NG, Jenkins NA, Pedersen FS.; 2000 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111696
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Stability of AML1 (core) site enhancer mutations in T lymphomas induced by attenuated SL3-3 murine leukemia virus mutants. by Amtoft HW, Sorensen AB, Bareil C, Schmidt J, Luz A, Pedersen FS.; 1997 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=191741
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Sunlight exposure and non-Hodgkin's lymphoma. by Weir E.; 2001 Aug 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=81350
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Suppressor Mutations within the Core Binding Factor (CBF/AML1) Binding Site of a T-Cell Lymphomagenic Retrovirus. by Martiney MJ, Levy LS, Lenz J.; 1999 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=104459
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Synthetic Peptide Ligands of the Antigen Binding Receptor Induce Programmed Cell Death in a Human B-Cell Lymphoma. by Renschler MF, Bhatt RR, Dower WJ, Levy R.; 1994 Apr 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=43633
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T cell leukemia I oncogene expression depends on the presence of Epstein --Barr virus in the virus- carrying Burkitt lymphoma lines. by Kiss C, Nishikawa J, Takada K, Trivedi P, Klein G, Szekely L.; 2003 Apr 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=153638
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T-Cell Lymphoma Caused by Herpesvirus Saimiri C488 Independently of ie14/vsag, a Viral Gene with Superantigen Homology. by Knappe A, Thurau M, Niphuis H, Hiller C, Wittmann S, Kuhn EM, Rosenwirth B, Fleckenstein B, Heeney J, Fickenscher H.; 1998 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=109857
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TCL1 oncogene expression in AIDS-related lymphomas and lymphoid tissues. by Teitell M, Damore MA, Sulur GG, Turner DE, Stern MH, Said JW, Denny CT, Wall R.; 1999 Aug 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22292
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The bfl-1 Gene Is Transcriptionally Upregulated by the Epstein-Barr Virus LMP1, and Its Expression Promotes the Survival of a Burkitt's Lymphoma Cell Line. by D'Souza B, Rowe M, Walls D.; 2000 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=112177
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The c-myc Locus Is a Common Integration Site in Type B Retrovirus-Induced T-Cell Lymphomas. by Rajan L, Broussard D, Lozano M, Lee CG, Kozak CA, Dudley JP.; 2000 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111733
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The Epstein-Barr virus BamHI F promoter is an early lytic promoter: lack of correlation with EBNA 1 gene transcription in group 1 Burkitt's lymphoma cell lines. by Schaefer BC, Strominger JL, Speck SH.; 1995 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=189321
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The feline leukemia virus long terminal repeat contains a potent genetic determinant of T-cell lymphomagenicity. by Pantginis J, Beaty RM, Levy LS, Lenz J.; 1997 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230290
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The IgG Fc receptor, Fc[gamma]RIIB, is a target for deregulation by chromosomal translocation in malignant lymphoma. by Callanan MB, Le Baccon P, Mossuz P, Duley S, Bastard C, Hamoudi R, Dyer MJ, Klobeck G, Rimokh R, Sotto JJ, Leroux D.; 2000 Jan 4; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26659
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The Kaposi's Sarcoma-Associated Herpesvirus G Protein-Coupled Receptor Has Broad Signaling Effects in Primary Effusion Lymphoma Cells. by Cannon M, Philpott NJ, Cesarman E.; 2003 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=140579
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The Kaposi's Sarcoma-Associated Herpesvirus K12 Transcript from a Primary Effusion Lymphoma Contains Complex Repeat Elements, Is Spliced, and Initiates from a Novel Promoter. by Li H, Komatsu T, Dezube BJ, Kaye KM.; 2002 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=136876
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The Type B Leukemogenic Virus Truncated Superantigen Is Dispensable for T-Cell Lymphomagenesis. by Mustafa F, Bhadra S, Johnston D, Lozano M, Dudley JP.; 2003 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=149533
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Transcription Mapping of the Kaposi's Sarcoma-Associated Herpesvirus (Human Herpesvirus 8) Genome in a Body Cavity-Based Lymphoma Cell Line (BC-1). by Sarid R, Flore O, Bohenzky RA, Chang Y, Moore PS.; 1998 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=124571
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Transcription Pattern of Human Herpesvirus 8 Open Reading Frame K3 in Primary Effusion Lymphoma and Kaposi's Sarcoma. by Rimessi P, Bonaccorsi A, Sturzl M, Fabris M, Brocca-Cofano E, Caputo A, Melucci-Vigo G, Falchi M, Cafaro A, Cassai E, Ensoli B, Monini P.; 2001 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=114445
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Transduction of Notch2 in feline leukemia virus-induced thymic lymphoma. by Rohn JL, Lauring AS, Linenberger ML, Overbaugh J.; 1996 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=190881
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Transformation of follicular lymphoma to diffuse large-cell lymphoma: Alternative patterns with increased or decreased expression of c-myc and its regulated genes. by Lossos IS, Alizadeh AA, Diehn M, Warnke R, Thorstenson Y, Oefner PJ, Brown PO, Botstein D, Levy R.; 2002 Jun 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=124393
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Treatment of Premalignancy: Prevention of Lymphoma in Radiation Leukemia VirusInoculated Mice by Cyclosporin A and Immunotoxin. by Yefenof E, Abboud G, Epszteyn S, Vitetta ES.; 1992 Jan 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=48312
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Tumor Control in a Model of Bone Marrow Transplantation and Acute LiverInfiltrating B-Cell Lymphoma: an Unpredicted Novel Function of Cytomegalovirus. by Erlach KC, Podlech J, Rojan A, Reddehase MJ.; 2002 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=135996
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Tumor Progression Locus 2 (Tpl-2) Encodes a Protein Kinase Involved in the Progression of Rodent T-Cell Lymphomas and in T-Cell Activation. by Patriotis C, Makris A, Bear SE, Tsichlis PN.; 1993 Mar 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46064
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Vaccination with Syngeneic, Lymphoma-Derived Immunoglobulin Idiotype Combined with Granulocyte/Macrophage Colony-Stimulating Factor Primes Mice for a Protective T-Cell Response. by Kwak LW, Young HA, Pennington RW, Weeks SD.; 1996 Oct 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=38268
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Variation in gene expression patterns in follicular lymphoma and the response to rituximab. by Bohen SP, Troyanskaya OG, Alter O, Warnke R, Botstein D, Brown PO, Levy R.; 2003 Feb 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=149935
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v-rel Induces ectopic expression of an adhesion molecule, DM-GRASP, during Blymphoma development. by Zhang G, Slaughter C, Humphries EH.; 1995 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=230405
The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 6
PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with lymphoma, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “lymphoma” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for lymphoma (hyperlinks lead to article summaries): •
A case of a diffuse large B-cell lymphoma of plasmablastic type associated with the t(2;5)(p23;q35) chromosome translocation. Author(s): Adam P, Katzenberger T, Seeberger H, Gattenlohner S, Wolf J, Steinlein C, Schmid M, Muller-Hermelink HK, Ott G. Source: The American Journal of Surgical Pathology. 2003 November; 27(11): 1473-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14576483&dopt=Abstract
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A case of malignant lymphoma of the ovary manifesting like an advanced ovarian cancer. Author(s): Yamada T, Iwao N, Kasamatsu H, Mori H. Source: Gynecologic Oncology. 2003 July; 90(1): 215-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821369&dopt=Abstract
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A practical approach to the diagnosis of Hodgkin lymphoma. Author(s): Listinsky CM. Source: American Journal of Clinical Pathology. 2002 June; 117 Suppl: S76-94. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14569804&dopt=Abstract
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A preparatory regimen of total body irradiation, busulphan and melphalan for allogeneic bone marrow transplantation in childhood high-risk leukemia and lymphoma. Author(s): Yoshihara T, Naya M, Tsunamoto K, Hojo M, Hibi S, Morimoto A, Todo S, Imashuku S. Source: Anticancer Res. 2003 March-April; 23(2C): 1739-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820450&dopt=Abstract
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A Salmonella typhi OmpC fusion protein expressing the CD154 Trp140-Ser149 amino acid strand binds CD40 and activates a lymphoma B-cell line. Author(s): Vega MI, Santos-Argumedo L, Huerta-Yepez S, Luria-Perez R, OrtizNavarrete V, Isibasi A, Gonzalez-Bonilla CR. Source: Immunology. 2003 October; 110(2): 206-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14511234&dopt=Abstract
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A systematic overview of radiation therapy effects in Hodgkin's lymphoma. Author(s): Gustavsson A, Osterman B, Cavallin-Stahl E. Source: Acta Oncologica (Stockholm, Sweden). 2003; 42(5-6): 589-604. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14596517&dopt=Abstract
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A systematic overview of radiation therapy effects in non-Hodgkin's lymphoma. Author(s): Gustavsson A, Osterman B, Cavallin-Stahl E. Source: Acta Oncologica (Stockholm, Sweden). 2003; 42(5-6): 605-19. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14596518&dopt=Abstract
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Aberrant promoter CpG methylation as a molecular marker for disease monitoring in natural killer cell lymphomas. Author(s): Siu LL, Chan JK, Wong KF, Choy C, Kwong YL. Source: British Journal of Haematology. 2003 July; 122(1): 70-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823347&dopt=Abstract
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Abnormalities on 1q and 7q are associated with poor outcome in sporadic Burkitt's lymphoma. A cytogenetic and comparative genomic hybridization study. Author(s): Garcia JL, Hernandez JM, Gutierrez NC, Flores T, Gonzalez D, Calasanz MJ, Martinez-Climent JA, Piris MA, Lopez-Capitan C, Gonzalez MB, Odero MD, San Miguel JF. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 2016-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513052&dopt=Abstract
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Acute pancreatitis induced by diffuse pancreatic invasion of adult T-cell leukemia/lymphoma cells. Author(s): Mori A, Kikuchi Y, Motoori S, Watanabe J, Shinozaki M, Eguchi M. Source: Digestive Diseases and Sciences. 2003 October; 48(10): 1979-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14627344&dopt=Abstract
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ALK-positive anaplastic large cell lymphoma with leukemic peripheral blood involvement is a clinicopathologic entity with an unfavorable prognosis. Report of three cases and review of the literature. Author(s): Onciu M, Behm FG, Raimondi SC, Moore S, Harwood EL, Pui CH, Sandlund JT. Source: American Journal of Clinical Pathology. 2003 October; 120(4): 617-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14560573&dopt=Abstract
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ALK-positive anaplastic large-cell lymphoma: strong T and B anti-tumour responses may cause hypocellular aspects of lymph nodes mimicking inflammatory lesions. Author(s): Borisch B, Yerly S, Cerato Ch, Schwaller J, Wacker P, Ozsahin AH, Brousse N, Hoessli DC. Source: European Journal of Haematology. 2003 October; 71(4): 243-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950232&dopt=Abstract
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ALK-positive plasmablastic B-cell lymphoma with expression of the NPM-ALK fusion transcript: report of 2 cases. Author(s): Onciu M, Behm FG, Downing JR, Shurtleff SA, Raimondi SC, Ma Z, Morris SW, Kennedy W, Jones SC, Sandlund JT. Source: Blood. 2003 October 1; 102(7): 2642-4. Epub 2003 June 19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816858&dopt=Abstract
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An indolent B-cell lymphoma with t(2;8)(p12;q24) abnormality and absence of C-MYC amplification and TP53 deletion. A new variant? Author(s): Potti A, Panwalkar A, Ingebretson MC, Tharapel SA, Goodell M, Dayton MV, Mehdi SA. Source: Cancer Genetics and Cytogenetics. 2003 July 1; 144(1): 76-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12810261&dopt=Abstract
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An unusual cause of new-onset atrial flutter: primary cardiac lymphoma. Author(s): Hayes D Jr, Liles DK, Sorrell VL. Source: Southern Medical Journal. 2003 August; 96(8): 799-802. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14515922&dopt=Abstract
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Analysis of a clonally related mantle cell and Hodgkin lymphoma indicates EpsteinBarr virus infection of a Hodgkin/Reed-Sternberg cell precursor in a germinal center. Author(s): Tinguely M, Rosenquist R, Sundstrom C, Amini RM, Kuppers R, Hansmann ML, Brauninger A. Source: The American Journal of Surgical Pathology. 2003 November; 27(11): 1483-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14576485&dopt=Abstract
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Anaplastic large cell lymphoma presenting as a pleural effusion and mimicking primary effusion lymphoma. A report of 2 cases. Author(s): Chan AC, Chan JK, Yan KW, Kwong YL. Source: Acta Cytol. 2003 September-October; 47(5): 809-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14526684&dopt=Abstract
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Angioimmunoblastic T-cell lymphoma associated with an antibody to human immunodeficiency virus protein. Author(s): Muta T, Yamano Y. Source: International Journal of Hematology. 2003 August; 78(2): 160-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953812&dopt=Abstract
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Anti-HCV and HCV-RNA prevalence and clinical correlations in cases with nonHodgkin's lymphoma. Author(s): Paydas S, Kilic B, Yavuz S, Disel U, Tanriverdi K, Sahin B, Burgut R. Source: American Journal of Hematology. 2003 October; 74(2): 89-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508793&dopt=Abstract
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Autologous hematopoietic stem cell transplant in first remission in non-Hodgkin's lymphoma. Author(s): Tomblyn M, Winter JN. Source: Expert Rev Anticancer Ther. 2003 June; 3(3): 281-94. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820773&dopt=Abstract
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B cell clonality in multiple localizations of primary central nervous system lymphomas in AIDS patients. Author(s): Pilozzi E, Talerico C, Uccini S, Addesso M, Rossi R, Vago L, Antinori A, Ruco LP. Source: Leukemia & Lymphoma. 2003 June; 44(6): 963-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854894&dopt=Abstract
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Baseline and treatment-induced chromosomal abnormalities in peripheral blood lymphocytes of Hodgkin's lymphoma patients. Author(s): M'kacher R, Girinsky T, Koscielny S, Dossou J, Violot D, Beron-Gaillard N, Ribrag V, Bourhis J, Bernheim A, Parmentier C, Carde P. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 October 1; 57(2): 321-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12957241&dopt=Abstract
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BCL-2 family proteins in peripheral T-cell lymphomas: correlation with tumour apoptosis and proliferation. Author(s): Rassidakis GZ, Jones D, Lai R, Ramalingam P, Sarris AH, McDonnell TJ, Medeiros LJ. Source: The Journal of Pathology. 2003 June; 200(2): 240-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12754745&dopt=Abstract
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BCL-3 overexpression in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma. Author(s): Rassidakis GZ, Oyarzo MP, Medeiros LJ. Source: Blood. 2003 August 1; 102(3): 1146-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12869493&dopt=Abstract
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BCL6 gene translocation in follicular lymphoma: a harbinger of eventual transformation to diffuse aggressive lymphoma. Author(s): Akasaka T, Lossos IS, Levy R. Source: Blood. 2003 August 15; 102(4): 1443-8. Epub 2003 May 08. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738680&dopt=Abstract
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BCL6 overexpression prevents increase in reactive oxygen species and inhibits apoptosis induced by chemotherapeutic reagents in B-cell lymphoma cells. Author(s): Kurosu T, Fukuda T, Miki T, Miura O. Source: Oncogene. 2003 July 17; 22(29): 4459-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12881702&dopt=Abstract
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Bexarotene gel: a new skin-directed treatment option for cutaneous T-cell lymphomas. Author(s): Martin AG. Source: J Drugs Dermatol. 2003 April; 2(2): 155-67. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12852367&dopt=Abstract
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Bexarotene reverses alopecia in cutaneous T-cell lymphoma. Author(s): Hanson M, Hill A, Duvic M. Source: The British Journal of Dermatology. 2003 July; 149(1): 193-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890219&dopt=Abstract
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Beyond “bad news”: the diagnosis, prognosis and classification of lymphomas and lymphoma patients in the age of biomedicine (1945-1995). Author(s): Keating P, Cambrosio A. Source: Medical History. 2003 July; 47(3): 291-313. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905916&dopt=Abstract
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Bilateral primary renal lymphoma. Author(s): O'Sullivan AW, Lee G, Fitzgerald E, O'Sullivan GC. Source: Ir J Med Sci. 2003 January-March; 172(1): 44-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760465&dopt=Abstract
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Bilateral upper and lower lid fatty herniation: an unusual presentation of nonHodgkin's lymphoma. Author(s): Bracaglia R, Fortunato R, Gentileschi S, La Rocca LM, Bruno I. Source: British Journal of Plastic Surgery. 2003 January; 56(1): 53-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12706154&dopt=Abstract
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Blastoid mantle cell lymphoma: evidence for nonrandom cytogenetic abnormalities additional to t(11;14) and generation of a mouse model. Author(s): M'kacher R, Farace F, Bennaceur-Griscelli A, Violot D, Clausse B, Dossou J, Valent A, Parmentier C, Ribrag V, Bosq J, Carde P, Turhan AG, Bernheim A. Source: Cancer Genetics and Cytogenetics. 2003 May; 143(1): 32-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742154&dopt=Abstract
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Blockade of Hsp27 overcomes Bortezomib/proteasome inhibitor PS-341 resistance in lymphoma cells. Author(s): Chauhan D, Li G, Shringarpure R, Podar K, Ohtake Y, Hideshima T, Anderson KC. Source: Cancer Research. 2003 October 1; 63(19): 6174-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14559800&dopt=Abstract
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Blood transfusions and non-Hodgkin's lymphoma. Author(s): Chow EJ, Holly EA. Source: Epidemiologic Reviews. 2002; 24(2): 269-79. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12762097&dopt=Abstract
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Bone involvement and abcess formation by neutrophil-rich CD30+ anaplastic largecell lymphoma mimicking skeletal infection in an AIDS patient. Author(s): Mira JA, Fernandez-Alonso J, Macias J, Saez C, Japon MA, Pereda T, Pineda JA. Source: The Journal of Infection. 2003 July; 47(1): 73-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12850166&dopt=Abstract
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Borrelia-associated primary cutaneous MALT lymphoma in a nonendemic region. Author(s): de la Fouchardiere A, Vandenesch F, Berger F. Source: The American Journal of Surgical Pathology. 2003 May; 27(5): 702-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12717258&dopt=Abstract
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Burkitt lymphoma arising in organ transplant recipients: a clinicopathologic study of five cases. Author(s): Gong JZ, Stenzel TT, Bennett ER, Lagoo AS, Dunphy CH, Moore JO, Rizzieri DA, Tepperberg JH, Papenhausen P, Buckley PJ. Source: The American Journal of Surgical Pathology. 2003 June; 27(6): 818-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12766587&dopt=Abstract
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Burkitt-like lymphoma in an infant: a case report. Author(s): Klumb CE, de Resende LM, Stefanoff CG, Vicuna CH, Renault IZ, Maia RC. Source: Revista Do Hospital Das Clinicas. 2003 January-February; 58(1): 33-6. Epub 2003 April 30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12754588&dopt=Abstract
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Calcification in splenic lymphoma before chemotherapy. Author(s): Dai MS, Chao TY, Yu CY. Source: Southern Medical Journal. 2003 August; 96(8): 836-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14515933&dopt=Abstract
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CD23 expression in mantle cell lymphoma: clinicopathologic features of 18 cases. Author(s): Schlette E, Fu K, Medeiros LJ. Source: American Journal of Clinical Pathology. 2003 November; 120(5): 760-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14608904&dopt=Abstract
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Characteristics of Hodgkin's lymphoma after infectious mononucleosis. Author(s): Hjalgrim H, Askling J, Rostgaard K, Hamilton-Dutoit S, Frisch M, Zhang JS, Madsen M, Rosdahl N, Konradsen HB, Storm HH, Melbye M. Source: The New England Journal of Medicine. 2003 October 2; 349(14): 1324-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14523140&dopt=Abstract
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Characterization of variant patterns of nodular lymphocyte predominant hodgkin lymphoma with immunohistologic and clinical correlation. Author(s): Fan Z, Natkunam Y, Bair E, Tibshirani R, Warnke RA. Source: The American Journal of Surgical Pathology. 2003 October; 27(10): 1346-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508396&dopt=Abstract
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Chlorambucil in combination with induction and maintenance rituximab is feasible and active in indolent non-Hodgkin's lymphoma. Author(s): Martinelli G, Laszlo D, Bertolini F, Pastano R, Mancuso P, Calleri A, Vanazzi A, Santoro P, Cavalli F, Zucca E. Source: British Journal of Haematology. 2003 October; 123(2): 271-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14531908&dopt=Abstract
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Cholesterol-dependent infection of Burkitt's lymphoma cell lines by Epstein-Barr virus. Author(s): Katzman RB, Longnecker R. Source: The Journal of General Virology. 2003 November; 84(Pt 11): 2987-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14573803&dopt=Abstract
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Chromosome aberrations in canine multicentric lymphomas detected with comparative genomic hybridisation and a panel of single locus probes. Author(s): Thomas R, Smith KC, Ostrander EA, Galibert F, Breen M. Source: British Journal of Cancer. 2003 October 20; 89(8): 1530-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14562028&dopt=Abstract
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Clinical features and outcome of primary effusion lymphoma in HIV-infected patients: a single-institution study. Author(s): Simonelli C, Spina M, Cinelli R, Talamini R, Tedeschi R, Gloghini A, Vaccher E, Carbone A, Tirelli U. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 November 1; 21(21): 3948-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14581418&dopt=Abstract
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Clinical perspectives of primary cardiac lymphoma. Author(s): Gowda RM, Khan IA. Source: Angiology. 2003 September-October; 54(5): 599-604. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14565636&dopt=Abstract
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Comparable outcomes of radiation therapy without high-dose methotrexate for patients with primary central nervous system lymphoma. Author(s): Ishikawa H, Hasegawa M, Tamaki Y, Hayakawa K, Akimoto T, Sakurai H, Mitsuhashi N, Niibe H, Tamura M, Nakano T. Source: Japanese Journal of Clinical Oncology. 2003 September; 33(9): 443-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14594937&dopt=Abstract
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Comparative studies of somatic and ongoing mutations in immunoglobulin heavychain variable region genes in diffuse large B-cell lymphomas of the stomach and the small intestine. Author(s): Go JH, Kim DS, Kim TJ, Ko YH, Ra HK, Rhee JC, Kim SW, Ree HJ. Source: Archives of Pathology & Laboratory Medicine. 2003 November; 127(11): 1443-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14567725&dopt=Abstract
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Comparison of Epstein-Barr virus presence in Hodgkin lymphoma in pediatric versus adult Argentine patients. Author(s): De Matteo E, Baron AV, Chabay P, Porta J, Dragosky M, Preciado MV. Source: Archives of Pathology & Laboratory Medicine. 2003 October; 127(10): 1325-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14521462&dopt=Abstract
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Current trends in large cell lymphoma. Author(s): Fisher RI, Shah P. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 October; 17(10): 1948-60. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14513044&dopt=Abstract
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Cutaneous T-cell lymphoma with adrenal insufficiency. Author(s): Blaikley JF, Atkinson P, Almond MK. Source: Journal of the Royal Society of Medicine. 2003 October; 96(10): 503-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14519731&dopt=Abstract
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Cutaneous type of adult T cell leukemia/lymphoma: a new entity among cutaneous lymphomas. Author(s): Yagi H, Takigawa M, Hashizume H. Source: The Journal of Dermatology. 2003 September; 30(9): 641-3. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14578552&dopt=Abstract
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Cytogenetic evidence for the origin of neoplastic cells in CD5-positive marginal zone B-cell lymphoma. Author(s): Batstone P, Forsyth L, Goodlad JR. Source: Human Pathology. 2003 October; 34(10): 1065-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14608544&dopt=Abstract
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Cytogenetic findings in blastoid mantle cell lymphoma. Author(s): Khoury JD, Sen F, Abruzzo LV, Hayes K, Glassman A, Medeiros LJ. Source: Human Pathology. 2003 October; 34(10): 1022-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14608536&dopt=Abstract
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Cytologic findings of marginal zone lymphoma. Author(s): Crapanzano JP, Lin O. Source: Cancer. 2003 October 25; 99(5): 301-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14579297&dopt=Abstract
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Cytomorphologic differentiation of Hodgkin's lymphoma and Ki-1+ anaplastic large cell lymphoma in fine needle aspirates. Author(s): Mourad WA, al Nazer M, Tulbah A. Source: Acta Cytol. 2003 September-October; 47(5): 744-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14526672&dopt=Abstract
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Cytomorphologic spectrum of small lymphocytic lymphoma in patients with an accelerated clinical course. Author(s): Shin HJ, Caraway NP, Katz RL. Source: Cancer. 2003 October 25; 99(5): 293-300. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14579296&dopt=Abstract
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Definition of TCR epitopes for CTL-mediated attack of cutaneous T cell lymphoma. Author(s): Winter D, Fiebiger E, Meraner P, Auer H, Brna C, Strohal R, Trautinger F, Knobler R, Fischer GF, Stingl G, Maurer D. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 September 1; 171(5): 271424. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928425&dopt=Abstract
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Definitive intraoperative radiotherapy for musculoskeletal sarcomas and malignant lymphoma in combination with surgical excision. Author(s): Sakayama K, Kidani T, Fujibuchi T, Yamamoto H, Shibata T, Fujii T, Ochi T, Kawamura M. Source: International Journal of Clinical Oncology / Japan Society of Clinical Oncology. 2003 June; 8(3): 174-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851842&dopt=Abstract
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Delayed expression of apoptosis in human lymphoma cells undergoing low-dose taxol-induced mitotic stress. Author(s): Allman R, Errington RJ, Smith PJ. Source: British Journal of Cancer. 2003 May 19; 88(10): 1649-58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771935&dopt=Abstract
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Detection of germinal center B-cell lymphoma in archival specimens: critical evaluation of Bcl-6 protein expression in diffuse large B-cell lymphoma of the tonsil. Author(s): Ree HJ, Ohsima K, Aozasa K, Takeuchi K, Kim CW, Yang WI, Huh JY, Lee SS, Ko YH, Kwon MS, Cho EY, Choi YL, Rhee JC, Kikuchi M, Mori S. Source: Human Pathology. 2003 June; 34(6): 610-6. Erratum In: Hum Pathol. 2003 July; 34(7): 730. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12827616&dopt=Abstract
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Diagnosis of conjunctival B-cell lymphoma by polymerase chain reaction heteroduplex analysis. Author(s): Strauss EC, Warren JF, Margolis TP, Holsclaw DS. Source: American Journal of Ophthalmology. 2003 July; 136(1): 207-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12834702&dopt=Abstract
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Diagnosis of primary cutaneous B-cell lymphoma by immunohistochemical and in situ hybridization methods. Author(s): Mendes S, Dreno B. Source: Acta Dermato-Venereologica. 2003; 83(3): 167-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816148&dopt=Abstract
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Dietary ginger constituents, galanals A and B, are potent apoptosis inducers in Human T lymphoma Jurkat cells. Author(s): Miyoshi N, Nakamura Y, Ueda Y, Abe M, Ozawa Y, Uchida K, Osawa T. Source: Cancer Letters. 2003 September 25; 199(2): 113-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12969783&dopt=Abstract
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Differential expression and function of A20 and TRAF1 in Hodgkin lymphoma and anaplastic large cell lymphoma and their induction by CD30 stimulation. Author(s): Durkop H, Hirsch B, Hahn C, Foss HD, Stein H. Source: The Journal of Pathology. 2003 June; 200(2): 229-39. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12754742&dopt=Abstract
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Differential patterns of human cytomegalovirus gene expression in various T-cell lines carrying human T-cell leukemia-lymphoma virus type I: role of Tax-activated cellular transcription factors. Author(s): Beck Z, Bacsi A, Liu X, Ebbesen P, Andirko I, Csoma E, Konya J, Nagy E, Toth FD. Source: Journal of Medical Virology. 2003 September; 71(1): 94-104. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12858414&dopt=Abstract
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Differential recruitment of caspase 8 to cFlip confers sensitivity or resistance to Fasmediated apoptosis in a subset of familial lymphoma patients. Author(s): Baumler C, Duan F, Onel K, Rapaport B, Jhanwar S, Offit K, Elkon KB. Source: Leukemia Research. 2003 September; 27(9): 841-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804643&dopt=Abstract
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Differentiating primary central nervous system lymphoma from glioma in humans using localised proton magnetic resonance spectroscopy. Author(s): Harting I, Hartmann M, Jost G, Sommer C, Ahmadi R, Heiland S, Sartor K. Source: Neuroscience Letters. 2003 May 22; 342(3): 163-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12757890&dopt=Abstract
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Diffuse large B-cell lymphoma occurring in patients with lymphoplasmacytic lymphoma/Waldenstrom macroglobulinemia. Clinicopathologic features of 12 cases. Author(s): Lin P, Mansoor A, Bueso-Ramos C, Hao S, Lai R, Medeiros LJ. Source: American Journal of Clinical Pathology. 2003 August; 120(2): 246-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12931555&dopt=Abstract
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Diffuse large B-cell lymphoma of bone: an analysis of differentiation-associated antigens with clinical correlation. Author(s): de Leval L, Braaten KM, Ancukiewicz M, Kiggundu E, Delaney T, Mankin HJ, Harris NL. Source: The American Journal of Surgical Pathology. 2003 September; 27(9): 1269-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12960812&dopt=Abstract
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Diffuse large B-cell lymphoma with occult marrow involvement and a novel t(9;10)(q32;q22). Author(s): Wong KF, So CC. Source: Cancer Genetics and Cytogenetics. 2003 November; 147(1): 68-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14580773&dopt=Abstract
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Diffuse large B-cell lymphoma: insights gained from gene expression profiling. Author(s): Lossos IS, Levy R. Source: International Journal of Hematology. 2003 May; 77(4): 321-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774918&dopt=Abstract
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Dioxin emissions from a solid waste incinerator and risk of non-Hodgkin lymphoma. Author(s): Floret N, Mauny F, Challier B, Arveux P, Cahn JY, Viel JF. Source: Epidemiology (Cambridge, Mass.). 2003 July; 14(4): 392-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12843761&dopt=Abstract
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DNA damage responses and chemosensitivity in the E mu-myc mouse lymphoma model. Author(s): Schmitt CA, Wallace-Brodeur RR, Rosenthal CT, McCurrach ME, Lowe SW. Source: Cold Spring Harb Symp Quant Biol. 2000; 65: 499-510. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760067&dopt=Abstract
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DNA sequence profile of TP53 gene mutations in childhood B-cell non-Hodgkin's lymphomas: prognostic implications. Author(s): Klumb CE, Furtado DR, de Resende LM, Carrico MK, Coelho AM, de Meis E, Maia RC, Rumjanek FD. Source: European Journal of Haematology. 2003 August; 71(2): 81-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890146&dopt=Abstract
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Dose-intense chemotherapy every 2 weeks with dose-intense cyclophosphamide, doxorubicin, vincristine, and prednisone may improve survival in intermediate- and high-grade lymphoma: a phase II study of the Southwest Oncology Group (SWOG 9349). Author(s): Blayney DW, LeBlanc ML, Grogan T, Gaynor ER, Chapman RA, Spiridonidis CH, Taylor SA, Bearman SI, Miller TP, Fisher RI; Southwest Oncology Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 1; 21(13): 2466-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829664&dopt=Abstract
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Double-phase Tc-99m MIBI scintigraphy as a therapeutic predictor in patients with non-Hodgkin's lymphoma. Author(s): Song HC, Lee JJ, Bom HS, Chung IJ, Kim HJ, Park YK, Kim EE. Source: Clinical Nuclear Medicine. 2003 June; 28(6): 457-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12911092&dopt=Abstract
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EBER-1 positive diffuse large cell lymphoma presenting as lupus nephritis. Author(s): Lin MH, Huang JJ, Chen TY, Chen FF, Chang KC, Liu MF, Huang WT, Su WC, Tsao CJ. Source: Lupus. 2003; 12(6): 486-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12873053&dopt=Abstract
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Emperipolesis in a case of B-cell lymphoma: a rare phenomenon outside of RosaiDorfman disease. Author(s): Lopes LF, Bacchi MM, Coelho KI, Filho AA, Bacchi CE. Source: Annals of Diagnostic Pathology. 2003 October; 7(5): 310-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14571435&dopt=Abstract
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Endobronchial presentation of Hodgkin lymphoma: a review of the literature. Author(s): Kiani B, Magro CM, Ross P. Source: The Annals of Thoracic Surgery. 2003 September; 76(3): 967-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963248&dopt=Abstract
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Enteropathy-associated T-cell lymphoma involving the colon and extraintestinal Bcell lymphoma in celiac disease. Author(s): Varadarajulu S, Lewin D. Source: Digestive Diseases and Sciences. 2003 July; 48(7): 1298-302. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870786&dopt=Abstract
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Epigenetic changes in the DAP-kinase CpG island in pediatric lymphoma. Author(s): Shiramizu B, Mick P. Source: Medical and Pediatric Oncology. 2003 December; 41(6): 527-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14595709&dopt=Abstract
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Epstein-Barr virus in biopsies from patients with Hodgkin and non-Hodgkin lymphoma at the University of Puerto Rico immunohistochemistry laboratory. Author(s): Cordova Perez FJ, Gonzalez-Keelan CI, Velez R. Source: P R Health Sci J. 2003 June; 22(2): 125-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12866135&dopt=Abstract
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Epstein-Barr virus infection in colorectal neoplasms associated with inflammatory bowel disease: detection of the virus in lymphomas but not in adenocarcinomas. Author(s): Wong NA, Herbst H, Herrmann K, Kirchner T, Krajewski AS, Moorghen M, Niedobitek F, Rooney N, Shepherd NA, Niedobitek G. Source: The Journal of Pathology. 2003 October; 201(2): 312-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14517849&dopt=Abstract
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Epstein-Barr virus-associated intravascular large T-cell lymphoma presenting as acute renal failure in a patient with acquired immune deficiency syndrome. Author(s): Merchant SH, Viswanatha DS, Zumwalt RE, Foucar K. Source: Human Pathology. 2003 September; 34(9): 950-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14562294&dopt=Abstract
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Epstein-Barr virus-related plasmablastic lymphomas arising from long-standing sacrococcygeal cysts in immunosuppressed patients. Author(s): Ojanguren J, Collazos J, Martinez C, Alvarez J, Mayo J. Source: Aids (London, England). 2003 July 4; 17(10): 1582-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12824797&dopt=Abstract
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ESMO Minimum Clinical Recommendations for diagnosis, treatment and follow-up of newly diagnosed follicular lymphoma. Author(s): Hiddemann W; European Society for Medical Oncology. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 August; 14(8): 1163-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12881368&dopt=Abstract
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Ethanol fixation of lymphoma samples as an alternative approach for preservation of the nucleic acids. Author(s): Soukup J, Krskova L, Hilska I, Kodet R. Source: Neoplasma. 2003; 50(4): 300-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937845&dopt=Abstract
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Evaluation for the development of 11q23 rearrangements in lymphoma patients treated with a high dose VP-16 and cyclophosphamide salvage regimen. Author(s): Mangel J, Duncan A, Lachance S. Source: Leukemia & Lymphoma. 2003 June; 44(6): 1001-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854902&dopt=Abstract
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Evaluation of immunologic crossreaction of antiasparaginase antibodies in acute lymphoblastic leukemia (ALL) and lymphoma patients. Author(s): Wang B, Relling MV, Storm MC, Woo MH, Ribeiro R, Pui CH, Hak LJ. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 August; 17(8): 1583-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886246&dopt=Abstract
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Expression of activation-induced cytidine deaminase is confined to B-cell nonHodgkin's lymphomas of germinal-center phenotype. Author(s): Smit LA, Bende RJ, Aten J, Guikema JE, Aarts WM, van Noesel CJ. Source: Cancer Research. 2003 July 15; 63(14): 3894-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12873980&dopt=Abstract
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Expression of anaplastic lymphoma kinase in non-Hodgkin's lymphomas and other malignant neoplasms. Biological, diagnostic, and clinical implications. Author(s): Wasik MA. Source: American Journal of Clinical Pathology. 2002 December; 118 Suppl: S81-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14569815&dopt=Abstract
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Expression of CCL5/RANTES by Hodgkin and Reed-Sternberg cells and its possible role in the recruitment of mast cells into lymphomatous tissue. Author(s): Fischer M, Juremalm M, Olsson N, Backlin C, Sundstrom C, Nilsson K, Enblad G, Nilsson G. Source: International Journal of Cancer. Journal International Du Cancer. 2003 November 1; 107(2): 197-201. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949794&dopt=Abstract
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Extension of nasopharyngeal lymphoma to the middle and external ear. Author(s): Gordin A, Ben-Arieh Y, Goldenberg D, Netzer A, Golz A. Source: The Annals of Otology, Rhinology, and Laryngology. 2003 July; 112(7): 644-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12903686&dopt=Abstract
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Extranodal imaging manifestations of non-Hodgkin's lymphoma. Author(s): Zhang J, Wang R, Li Y, Zhang F. Source: J Huazhong Univ Sci Technolog Med Sci. 2003; 23(3): 324-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14526448&dopt=Abstract
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Extraoular muscle palsies in subcutaneous panniculitis-like T-cell lymphoma. Author(s): Leonard GD, Hegde U, Butman J, Jaffe ES, Wilson WH. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 1; 21(15): 2993-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885820&dopt=Abstract
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Extrasalivary lymphoma development in Sjogren's syndrome: clonal evolution from parotid gland lymphoproliferation and role of local triggering. Author(s): Gasparotto D, De Vita S, De Re V, Marzotto A, De Marchi G, Scott CA, Gloghini A, Ferraccioli G, Boiocchi M. Source: Arthritis and Rheumatism. 2003 November; 48(11): 3181-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14613281&dopt=Abstract
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Factors predicting long-term survival in low-risk diffuse large B-cell lymphoma. Author(s): Moller MB, Pedersen NT, Christensen BE. Source: American Journal of Hematology. 2003 October; 74(2): 94-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508794&dopt=Abstract
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Factors predicting the response to rituximab in indolent lymphoma. Author(s): Lee D. Source: Clin Lymphoma. 2003 June; 4(1): 19-21. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837149&dopt=Abstract
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Favorable response to treatment of a child with T-cell-rich large B-cell lymphoma presenting with liver failure. Author(s): Sathiapalan RK, Hainau B, Al-Mane K, Belgaumi AF. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 October; 25(10): 809-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14528106&dopt=Abstract
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FDG PET in the follow-up management of patients with newly diagnosed Hodgkin and non-Hodgkin lymphoma after first-line chemotherapy. Author(s): Lavely WC, Delbeke D, Greer JP, Morgan DS, Byrne DW, Price RR, Hallahan DE. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 October 1; 57(2): 307-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12957239&dopt=Abstract
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Feasibility and toxicity of high-dose therapy (HDT) supported by peripheral blood stem cells in elderly patients with multiple myeloma and non-Hodgkin's lymphoma: survey from a single institution. Author(s): Magagnoli M, Castagna L, Balzarotti M, Sarina B, Timofeeva I, Bertuzzi A, Compasso S, Nozza A, Siracusano L, Santoro A. Source: American Journal of Hematology. 2003 August; 73(4): 267-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12879431&dopt=Abstract
100 Lymphoma
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Feline epitheliotropic intestinal malignant lymphoma: 10 cases (1997-2000). Author(s): Carreras JK, Goldschmidt M, Lamb M, McLear RC, Drobatz KJ, Sorenmo KU. Source: J Vet Intern Med. 2003 May-June; 17(3): 326-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774974&dopt=Abstract
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Fertility in young women after chemotherapy with alkylating agents for Hodgkin and non-Hodgkin lymphomas. Author(s): Franchi-Rezgui P, Rousselot P, Espie M, Briere J, Pierre Marolleau J, Gisselbrecht C, Brice P. Source: The Hematology Journal : the Official Journal of the European Haematology Association / Eha. 2003; 4(2): 116-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750730&dopt=Abstract
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First-line treatment with brief-duration chemotherapy plus rituximab in elderly patients with intermediate-grade non-Hodgkin's lymphoma: phase II trial. Author(s): Hainsworth JD, Litchy S, Lamb MR, Rodriguez GI, Scroggin C Jr, Greco FA. Source: Clin Lymphoma. 2003 June; 4(1): 36-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837153&dopt=Abstract
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Flavopiridol in untreated or relapsed mantle-cell lymphoma: results of a phase II study of the National Cancer Institute of Canada Clinical Trials Group. Author(s): Kouroukis CT, Belch A, Crump M, Eisenhauer E, Gascoyne RD, Meyer R, Lohmann R, Lopez P, Powers J, Turner R, Connors JM; National Cancer Institute of Canada Clinical Trials Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 May 1; 21(9): 1740-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735303&dopt=Abstract
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Fludarabine versus cyclophosphamide, vincristine, and prednisone in recurrent lowgrade lymphomas. Author(s): Alliot C. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 1; 21(13): 2626; Author Reply 2626-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829689&dopt=Abstract
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Fluorescence in situ hybridization detection of chromosome IGH/BCL2 translocations from paraffin-embedded tissue: evaluation in follicular lymphoma. Author(s): Hirose Y, Masaki Y, Ozaki M. Source: International Journal of Hematology. 2003 August; 78(2): 154-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953811&dopt=Abstract
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Fluorescence in situ hybridization: method of choice for a definitive diagnosis of mantle cell lymphoma. Author(s): Sun T, Nordberg ML, Cotelingam JD, Veillon DM, Ryder J. Source: American Journal of Hematology. 2003 September; 74(1): 78-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949897&dopt=Abstract
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Follicular lymphoma cell lines, an in vitro model for antigenic selection and cytokinemediated growth regulation of germinal centre B cells. Author(s): Eray M, Postila V, Eeva J, Ripatti A, Karjalainen-Lindsberg ML, Knuutila S, Andersson LC, Pelkonen J. Source: Scandinavian Journal of Immunology. 2003 June; 57(6): 545-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791092&dopt=Abstract
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Follicular lymphoma of the stomach: immunohistochemical and molecular genetic studies. Author(s): Kanda M, Ohshima K, Suzumiya J, Haraoka S, Kawasaki C, Sakisaka S, Kikuchi M. Source: Journal of Gastroenterology. 2003; 38(6): 584-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856675&dopt=Abstract
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Four cases of central nervous system involvement of breast malignant lymphoma. Author(s): Yamazaki H, Hanada M, Kitada M, Kuyama J, Sato T, Nishikubo M, Ishida T, Inoue T, Inoue T. Source: Japanese Journal of Clinical Oncology. 2003 August; 33(8): 399-403. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14523060&dopt=Abstract
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Functional domains of chicken mitochondrial transcription factor A for the maintenance of mitochondrial DNA copy number in lymphoma cell line DT40. Author(s): Matsushima Y, Matsumura K, Ishii S, Inagaki H, Suzuki T, Matsuda Y, Beck K, Kitagawa Y. Source: The Journal of Biological Chemistry. 2003 August 15; 278(33): 31149-58. Epub 2003 May 20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12759347&dopt=Abstract
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Gallium nitrate in the treatment of lymphoma. Author(s): Straus DJ. Source: Seminars in Oncology. 2003 April; 30(2 Suppl 5): 25-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776257&dopt=Abstract
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Gastric mucosa-associated lymphoid tissue lymphoma. Author(s): Ahmad A, Govil Y, Frank BB. Source: The American Journal of Gastroenterology. 2003 May; 98(5): 975-86. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12809817&dopt=Abstract
102 Lymphoma
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Gastrointestinal lymphoma. Author(s): Bierman PJ. Source: Curr Treat Options Oncol. 2003 October; 4(5): 421-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941202&dopt=Abstract
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Gelatinases (MMP-2 and MMP-9), TIMP-1 expression and the extent of neovascularization in aggressive non-Hodgkin's lymphomas. Author(s): Kuittinen O, Apaja-Sarkkinen M, Turpeenniemi-Hujanen T. Source: European Journal of Haematology. 2003 August; 71(2): 91-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890147&dopt=Abstract
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Gene expression patterns in AIDS versus non-AIDS-related diffuse large B-cell lymphoma. Author(s): Patrone L, Henson SE, Teodorovic J, Malone CS, French SW, Wall R, Teitell MA. Source: Experimental and Molecular Pathology. 2003 April; 74(2): 129-39. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12710944&dopt=Abstract
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Gene expression profiles of cutaneous B cell lymphoma. Author(s): Storz MN, van de Rijn M, Kim YH, Mraz-Gernhard S, Hoppe RT, Kohler S. Source: The Journal of Investigative Dermatology. 2003 May; 120(5): 865-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713594&dopt=Abstract
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Genetic and molecular genetic studies in the diagnosis of atypical lymphoid hyperplasias versus lymphoma. Author(s): Swerdlow SH. Source: Human Pathology. 2003 April; 34(4): 346-51. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733114&dopt=Abstract
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Genetic and molecular genetic studies in the diagnosis of B-cell lymphomas I: mantle cell lymphoma, follicular lymphoma, and Burkitt's lymphoma. Author(s): Campo E. Source: Human Pathology. 2003 April; 34(4): 330-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733111&dopt=Abstract
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Genetic and molecular genetic studies in the diagnosis of B-cell lymphomas: marginal zone lymphomas. Author(s): Muller-Hermelink HK. Source: Human Pathology. 2003 April; 34(4): 336-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733112&dopt=Abstract
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Genistein reduces NF-kappa B in T lymphoma cells via a caspase-mediated cleavage of I kappa B alpha. Author(s): Baxa DM, Yoshimura FK. Source: Biochemical Pharmacology. 2003 September 15; 66(6): 1009-18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963487&dopt=Abstract
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Genomic alterations in blastic natural killer/extranodal natural killer-like T cell lymphoma with cutaneous involvement. Author(s): Mao X, Onadim Z, Price EA, Child F, Lillington DM, Russell-Jones R, Young BD, Whittaker S. Source: The Journal of Investigative Dermatology. 2003 September; 121(3): 618-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925224&dopt=Abstract
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Geographical and ecological analyses of childhood acute leukaemias and lymphomas in north-west England. Author(s): McNally RJ, Alston RD, Cairns DP, Eden OB, Birch JM. Source: British Journal of Haematology. 2003 October; 123(1): 60-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14510943&dopt=Abstract
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Granulomatous eccrinotropic lymphomatoid papulosis. Author(s): Crowson AN, Baschinsky DY, Kovatich A, Magro C. Source: American Journal of Clinical Pathology. 2003 May; 119(5): 731-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760293&dopt=Abstract
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Growth regulation by p27Kip1 is abrogated by multiple mechanisms in aggressive malignant lymphomas. Author(s): Lin Z, Lim S, Lim MS. Source: British Journal of Haematology. 2003 June; 121(5): 739-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780788&dopt=Abstract
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Guttate morphoea in human T-cell lymphoma/lymphotrophic virus type-1 (HTLV-1) infection. Author(s): Oiso N, Fukai K, Hosomi N, Ishii M. Source: Clinical and Experimental Dermatology. 2003 July; 28(4): 380-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823298&dopt=Abstract
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Helicobacter pylori antigen-specific T-cell responses at gastric level in chronic gastritis, peptic ulcer, gastric cancer and low-grade mucosa-associated lymphoid tissue (MALT) lymphoma. Author(s): D'Elios MM, Amedei A, Del Prete G. Source: Microbes and Infection / Institut Pasteur. 2003 July; 5(8): 723-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12814773&dopt=Abstract
104 Lymphoma
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Helicobacter-independent, chemotherapy-resistant, radiosensitive gastric MALT lymphoma with massive deposits of amyloidlike substance. Author(s): Matsumoto H, Koga H, Iida M, Suekane H, Tarumi K, Hoshika K, Mikami Y, Haruma K. Source: Digestive Diseases and Sciences. 2003 October; 48(10): 2018-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14627350&dopt=Abstract
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Hematopoietic stem cell transplantation for non-Hodgkin's lymphoma. Author(s): Holmberg LA, Stewart FM. Source: Oncology (Huntingt). 2003 May; 17(5): 627-32, 635, 640; Discussion 640-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12800792&dopt=Abstract
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Hepatosplenic gamma delta T-cell lymphoma with leukemic phase successfully treated with 2-chlorodeoxyadenosine. Author(s): Gopcsa L, Banyai A, Tamaska J, Karadi A, Matolcsy A, Paloczi K. Source: Haematologia. 2002; 32(4): 519-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803128&dopt=Abstract
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Hepatosplenic T cell lymphoma with no expression of cytotoxic molecules. Author(s): Sadahira Y, Notohara K, Manabe T. Source: Journal of Clinical Pathology. 2003 August; 56(8): 631-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890821&dopt=Abstract
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High frequency of genetic aberrations in enteropathy-type T-cell lymphoma. Author(s): Baumgartner AK, Zettl A, Chott A, Ott G, Muller-Hermelink HK, Starostik P. Source: Laboratory Investigation; a Journal of Technical Methods and Pathology. 2003 October; 83(10): 1509-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14563952&dopt=Abstract
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High incidence of thromboembolism in patients with central nervous system lymphoma. Author(s): Goldschmidt N, Linetsky E, Shalom E, Varon D, Siegal T. Source: Cancer. 2003 September 15; 98(6): 1239-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12973848&dopt=Abstract
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High level of cannabinoid receptor 1, absence of regulator of G protein signalling 13 and differential expression of Cyclin D1 in mantle cell lymphoma. Author(s): Islam TC, Asplund AC, Lindvall JM, Nygren L, Liden J, Kimby E, Christensson B, Smith CI, Sander B. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1880-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970790&dopt=Abstract
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High pretreatment interleukin-10 is an independent predictor of poor failure-free survival in patients with Hodgkin's lymphoma. Author(s): Salgami EV, Efstathiou SP, Vlachakis V, Sekara EV, Syrigos KN, Roussou PP. Source: Haematologia. 2002; 32(4): 377-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12803112&dopt=Abstract
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High response rates and lasting remissions after low-dose involved field radiotherapy in indolent lymphomas. Author(s): Haas RL, Poortmans P, de Jong D, Aleman BM, Dewit LG, Verheij M, Hart AA, van Oers MH, van der Hulst M, Baars JW, Bartelink H. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 1; 21(13): 2474-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829665&dopt=Abstract
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High-dose therapy and autologous stem-cell transplantation versus conventional therapy for patients with advanced Hodgkin's lymphoma responding to front-line therapy. Author(s): Federico M, Bellei M, Brice P, Brugiatelli M, Nagler A, Gisselbrecht C, Moretti L, Colombat P, Luminari S, Fabbiano F, Di Renzo N, Goldstone A, Carella AM; EBMT/GISL/ANZLG/SFGM/GELA Intergroup HD01 Trial. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 15; 21(12): 2320-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12805333&dopt=Abstract
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High-dose therapy for follicular lymphoma revisited: not if, but when? Author(s): Lister TA. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 November 1; 21(21): 3894-6. Epub 2003 September 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14517186&dopt=Abstract
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High-dose therapy improves progression-free survival and survival in relapsed follicular non-Hodgkin's lymphoma: results from the randomized European CUP trial. Author(s): Schouten HC, Qian W, Kvaloy S, Porcellini A, Hagberg H, Johnson HE, Doorduijn JK, Sydes MR, Kvalheim G. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 November 1; 21(21): 3918-27. Epub 2003 September 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14517188&dopt=Abstract
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Histopathologic features of splenic small B-cell lymphomas. A study of 42 cases with a definitive diagnosis by the World Health Organization classification. Author(s): Kansal R, Ross CW, Singleton TP, Finn WG, Schnitzer B. Source: American Journal of Clinical Pathology. 2003 September; 120(3): 335-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14502797&dopt=Abstract
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History of antibiotic use and risk of non-Hodgkin's lymphoma (NHL). Author(s): Kato I, Koenig KL, Baptiste MS, Lillquist PP, Frizzera G, Burke JS, Watanabe H, Shore RE. Source: International Journal of Cancer. Journal International Du Cancer. 2003 October 20; 107(1): 99-105. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925963&dopt=Abstract
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HIV-associated primary cervical non-Hodgkin's lymphoma and two other cases of primary pelvic non-Hodgkin's lymphoma. Author(s): Pham DC, Guthrie TH, Ndubisi B. Source: Gynecologic Oncology. 2003 July; 90(1): 204-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821366&dopt=Abstract
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Hodgkin's lymphoma cell lines express a fusion protein encoded by intergenically spliced mRNA for the multilectin receptor DEC-205 (CD205) and a novel C-type lectin receptor DCL-1. Author(s): Kato M, Khan S, Gonzalez N, O'Neill BP, McDonald KJ, Cooper BJ, Angel NZ, Hart DN. Source: The Journal of Biological Chemistry. 2003 September 5; 278(36): 34035-41. Epub 2003 June 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12824192&dopt=Abstract
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Hodgkin's lymphoma manifesting with hypoglycemia. Author(s): Soares-Welch CV, Zeldenrust SR, Conover CA, Grant CS, Service FJ. Source: Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2003 January-February; 9(1): 96-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917097&dopt=Abstract
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Hodgkin's lymphoma presenting as Tietze's syndrome. Author(s): Uthman I, El-Hajj I, Traboulsi R, Taher A. Source: Arthritis and Rheumatism. 2003 October 15; 49(5): 737. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14558067&dopt=Abstract
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Hodgkin's lymphoma: the hazards of success. Author(s): Connors JM. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 September 15; 21(18): 3388-90. Epub 2003 August 04. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12900526&dopt=Abstract
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Identification of chromosomal copy number changes associated with transformation of follicular lymphoma to diffuse large B-cell lymphoma. Author(s): Boonstra R, Bosga-Bouwer A, Mastik M, Haralambieva E, Conradie J, van den Berg E, van den Berg A, Poppema S. Source: Human Pathology. 2003 September; 34(9): 915-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14562288&dopt=Abstract
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Imaging characteristics of diffuse primary cutaneous B-cell lymphoma of the cranial vault with orbital and brain invasion. Author(s): Kantarci M, Erdem T, Alper F, Gundogdu C, Okur A, Aktas A. Source: Ajnr. American Journal of Neuroradiology. 2003 August; 24(7): 1324-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917120&dopt=Abstract
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Imaging-guided percutaneous splenic biopsy using a 20- or 22-gauge cutting-edge core biopsy needle for the diagnosis of malignant lymphoma. Author(s): Lieberman S, Libson E, Maly B, Lebensart P, Ben-Yehuda D, Bloom AI. Source: Ajr. American Journal of Roentgenology. 2003 October; 181(4): 1025-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14500223&dopt=Abstract
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Impact of concomitant antiblastic chemotherapy and highly active antiretroviral therapy on human immunodeficiency virus (HIV) viremia and genotyping in HIVinfected patients with non-Hodgkin lymphoma. Author(s): Simonelli C, Zanussi S, Cinelli R, Dal Maso L, Di Gennaro G, D'Andrea M, Nasti G, Spina M, Vaccher E, De Paoli P, Tirelli U. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2003 September 15; 37(6): 820-7. Epub 2003 August 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12955644&dopt=Abstract
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Improvement of systemic human immunodeficiency virus-related non-Hodgkin lymphoma outcome in the era of highly active antiretroviral therapy. Author(s): Vaccher E, Spina M, Talamini R, Zanetti M, di Gennaro G, Nasti G, Tavio M, Bernardi D, Simonelli C, Tirelli U. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2003 December 1; 37(11): 1556-64. Epub 2003 November 06. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14614680&dopt=Abstract
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Individual quality of life in long-term survivors of Hodgkin's lymphoma--a comparative study. Author(s): Wettergren L, Bjorkholm M, Axdorph U, Bowling A, Langius-Eklof A. Source: Quality of Life Research : an International Journal of Quality of Life Aspects of Treatment, Care and Rehabilitation. 2003 August; 12(5): 545-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13677499&dopt=Abstract
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Indolent mantle cell lymphoma with nodal involvement and mutated immunoglobulin heavy chain genes. Author(s): Nodit L, Bahler DW, Jacobs SA, Locker J, Swerdlow SH. Source: Human Pathology. 2003 October; 34(10): 1030-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14608537&dopt=Abstract
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Infection and lymphoma. Author(s): Ambinder R. Source: The New England Journal of Medicine. 2003 October 2; 349(14): 1309-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14523136&dopt=Abstract
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Infrequent somatic Fas mutations but no evidence of Bcl10 mutations or t(11;18) in primary cutaneous MALT-type lymphoma. Author(s): Gronbaek K, Ralfkiaer E, Kalla J, Skovgaard GL, Guldberg P. Source: The Journal of Pathology. 2003 September; 201(1): 134-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12950026&dopt=Abstract
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Inhibition of constitutive NF-kappa B activation in mantle cell lymphoma B cells leads to induction of cell cycle arrest and apoptosis. Author(s): Pham LV, Tamayo AT, Yoshimura LC, Lo P, Ford RJ. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 July 1; 171(1): 88-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816986&dopt=Abstract
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Inhibition of JAK3 induces apoptosis and decreases anaplastic lymphoma kinase activity in anaplastic large cell lymphoma. Author(s): Amin HM, Medeiros LJ, Ma Y, Feretzaki M, Das P, Leventaki V, Rassidakis GZ, O'Connor SL, McDonnell TJ, Lai R. Source: Oncogene. 2003 August 21; 22(35): 5399-407. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12934099&dopt=Abstract
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Inhibition of the translocated c-myc in Burkitt's lymphoma by a PNA complementary to the E mu enhancer. Author(s): Cutrona G, Carpaneto EM, Ponzanelli A, Ulivi M, Millo E, Scarfi S, Roncella S, Benatti U, Boffa LC, Ferrarini M. Source: Cancer Research. 2003 October 1; 63(19): 6144-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14559793&dopt=Abstract
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Insertion of the CCND1 gene into the IgH locus in a case of leukaemic small cell mantle lymphoma with normal chromosomes 11 and 14. Author(s): Aventin A, Nomdedeu J, Briones J, Espinosa I, Bordes R, Sierra J. Source: Journal of Clinical Pathology. 2003 October; 56(10): 798-800. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14514791&dopt=Abstract
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Integrative assessment of multiple pesticides as risk factors for non-Hodgkin's lymphoma among men. Author(s): De Roos AJ, Zahm SH, Cantor KP, Weisenburger DD, Holmes FF, Burmeister LF, Blair A. Source: Occupational and Environmental Medicine. 2003 September; 60(9): E11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937207&dopt=Abstract
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Intensive chemotherapy with cyclophosphamide, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, and high-dose cytarabine (CODOX-M/IVAC) for human immunodeficiency virus-associated Burkitt lymphoma. Author(s): Wang ES, Straus DJ, Teruya-Feldstein J, Qin J, Portlock C, Moskowitz C, Goy A, Hedrick E, Zelenetz AD, Noy A. Source: Cancer. 2003 September 15; 98(6): 1196-205. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12973843&dopt=Abstract
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Intensive chemotherapy with rituximab is safe and effective in AIDS non-Hodgkin's lymphoma. Author(s): Rey J, Charbonnier A, Schiano de Colella JM, Stoppa AM, Poizot-Martin I, Gastaut JA, Costello RT. Source: Aids (London, England). 2003 September 5; 17(13): 2006-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12960844&dopt=Abstract
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Interferon treatment of childhood conjunctival lymphoma. Author(s): Lucas RS, Mortimore R, Sullivan TJ, Waldie M. Source: The British Journal of Ophthalmology. 2003 September; 87(9): 1191. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928301&dopt=Abstract
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Interleukin 15: a key to disrupted intraepithelial lymphocyte homeostasis and lymphomagenesis in celiac disease. Author(s): Mention JJ, Ben Ahmed M, Begue B, Barbe U, Verkarre V, Asnafi V, Colombel JF, Cugnenc PH, Ruemmele FM, McIntyre E, Brousse N, Cellier C, Cerf-Bensussan N. Source: Gastroenterology. 2003 September; 125(3): 730-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949719&dopt=Abstract
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Involved-field radiotherapy is equally effective and less toxic compared with extended-field radiotherapy after four cycles of chemotherapy in patients with earlystage unfavorable Hodgkin's lymphoma: results of the HD8 trial of the German Hodgkin's Lymphoma Study Group. Author(s): Engert A, Schiller P, Josting A, Herrmann R, Koch P, Sieber M, Boissevain F, De Wit M, Mezger J, Duhmke E, Willich N, Muller RP, Schmidt BF, Renner H, MullerHermelink HK, Pfistner B, Wolf J, Hasenclever D, Loffler M, Diehl V; German Hodgkin's Lymphoma Study Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 October 1; 21(19): 3601-8. Epub 2003 August 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12913100&dopt=Abstract
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Is B-lineage acute lymphoblastic leukemia with a mature phenotype and l1 morphology a precursor B-lymphoblastic leukemia/lymphoma or Burkitt leukemia/lymphoma? Author(s): Li S, Lew G. Source: Archives of Pathology & Laboratory Medicine. 2003 October; 127(10): 1340-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14521459&dopt=Abstract
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Kaposi's sarcoma-associated herpesvirus-infected primary effusion lymphoma has a plasma cell gene expression profile. Author(s): Jenner RG, Maillard K, Cattini N, Weiss RA, Boshoff C, Wooster R, Kellam P. Source: Proceedings of the National Academy of Sciences of the United States of America. 2003 September 2; 100(18): 10399-404. Epub 2003 August 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925741&dopt=Abstract
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Lack of evidence for the presence of Simian virus 40 DNA in cutaneous lymphomas. Author(s): Yazdi AS, Puchta U, Flaig MJ, Sander CA. Source: The Journal of Investigative Dermatology. 2003 July; 121(1): 212-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839586&dopt=Abstract
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Lacrimal sac lymphoma in a child. Author(s): Schefler AC, Shields CL, Shields JA, Demirci H, Maus M, Eagle RC Jr. Source: Archives of Ophthalmology. 2003 September; 121(9): 1330-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963620&dopt=Abstract
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Laparoscopy-assisted colon resection for mucosa-associated lymphoid tissue (MALT) lymphoma in the cecum. Author(s): Takada M, Ichihara T, Fukumoto S, Nomura H, Kuroda Y. Source: Hepatogastroenterology. 2003 July-August; 50(52): 1003-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12845967&dopt=Abstract
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Large B-cell lymphoma presenting in the spleen: identification of different clinicopathologic conditions. Author(s): Mollejo M, Algara P, Mateo MS, Menarguez J, Pascual E, Fresno MF, Camacho FI, Piris MA. Source: The American Journal of Surgical Pathology. 2003 July; 27(7): 895-902. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826881&dopt=Abstract
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L-asparaginase-based regimen in the treatment of refractory midline nasal/nasal-type T/NK-cell lymphoma. Author(s): Yong W, Zheng W, Zhang Y, Zhu J, Wei Y, Zhu D, Li J. Source: International Journal of Hematology. 2003 August; 78(2): 163-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953813&dopt=Abstract
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Late-effects among survivors of leukaemia and lymphoma during childhood and adolescence. Author(s): Robison LL, Bhatia S. Source: British Journal of Haematology. 2003 August; 122(3): 345-59. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12877662&dopt=Abstract
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Leukemia and lymphoma of natural killer lineage cells. Author(s): Oshimi K. Source: International Journal of Hematology. 2003 July; 78(1): 18-23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894846&dopt=Abstract
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Local cryoglobulin deposition in primary central nervous system lymphoma. Author(s): Paueksakon P, Shaya M, Harper R, Hicks J, Truong L, Goodman JC, Powell SZ. Source: Human Pathology. 2003 July; 34(7): 720-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12874771&dopt=Abstract
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Long term follow up of Helicobacter pylori induced gastric diffuse large B cell MALT lymphoma following eradication treatment alone. Author(s): Sinharay R. Source: Gut. 2003 September; 52(9): 1385. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912879&dopt=Abstract
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Long-term effect of a watch and wait policy versus immediate systemic treatment for asymptomatic advanced-stage non-Hodgkin lymphoma: a randomised controlled trial. Author(s): Ardeshna KM, Smith P, Norton A, Hancock BW, Hoskin PJ, MacLennan KA, Marcus RE, Jelliffe A, Vaughan G, Hudson, Linch DC; British National Lymphoma Investigation. Source: Lancet. 2003 August 16; 362(9383): 516-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932382&dopt=Abstract
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Long-term remission of primary central nervous system lymphoma by intensified methotrexate chemotherapy. Author(s): Watanabe T, Katayama Y, Yoshino A, Komine C, Yokoyama T, Fukushima T. Source: Journal of Neuro-Oncology. 2003 May; 63(1): 87-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12814260&dopt=Abstract
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Long-term survival in patients with human immunodeficiency virus-associated small non-cleaved cell lymphoma: the role for short course intensive chemotherapy. Author(s): Astrow AB, Tarabay G, Salerno VE, Cook WA, Lin R, Lascher S, Li Z, Mazumder A, Halperin I, Cho J, Jaffar Z, McLaughlin M, Blum RH, Kempin SJ. Source: Hematological Oncology. 2003 September; 21(3): 131-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14579241&dopt=Abstract
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Low frequency of bcl-2 rearrangement in HCV-associated non-Hodgkin's lymphoma tissue. Author(s): Libra M, De Re V, De Vita S, Gasparotto D, Gloghini A, Rupolo M, Degan M, Marzotto A, Stivala F, Carbone A, Boiocchi M. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 July; 17(7): 1433-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835744&dopt=Abstract
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Low-dose gemcitabine plus cisplatin in previously treated, relapsed non-Hodgkin's lymphoma. Author(s): Wong SF, Lindgren T, Hsu D, Tran G. Source: American Journal of Hematology. 2003 August; 73(4): 298. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12879441&dopt=Abstract
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Lymphoblastic lymphoma of childhood and the LSA2-L2 protocol: the 30-year experience at Memorial-Sloan-Kettering Cancer Center. Author(s): Mora J, Filippa DA, Qin J, Wollner N. Source: Cancer. 2003 September 15; 98(6): 1283-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12973853&dopt=Abstract
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Lymphocyte-predominant Hodgkin's lymphoma in children: therapeutic abstention after initial lymph node resection--a Study of the French Society of Pediatric Oncology. Author(s): Pellegrino B, Terrier-Lacombe MJ, Oberlin O, Leblanc T, Perel Y, Bertrand Y, Beard C, Edan C, Schmitt C, Plantaz D, Pacquement H, Vannier JP, Lambilliote C, Couillault G, Babin-Boilletot A, Thuret I, Demeocq F, Leverger G, Delsol G, LandmanParker J; Study of the French Society of Pediatric Oncology. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 1; 21(15): 2948-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885814&dopt=Abstract
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Lymphoma development in a patient receiving anti-TNF therapy. Author(s): Ziakas PD, Giannouli S, Tzioufas AG, Voulgarelis M. Source: Haematologica. 2003 July; 88(7): Ecr25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12857572&dopt=Abstract
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Lymphomas after tumor necrosis factor antagonist therapy: comment on the article by Brown et al. Author(s): Yazici H. Source: Arthritis and Rheumatism. 2003 August; 48(8): 2389. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905496&dopt=Abstract
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Lymphomas. Author(s): Nayak LM, Deschler DG. Source: Otolaryngologic Clinics of North America. 2003 August; 36(4): 625-46. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14567057&dopt=Abstract
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Lymphomatoid papulosis associated with mycosis fungoides: a study of 21 patients including analyses for clonality. Author(s): Zackheim HS, Jones C, Leboit PE, Kashani-Sabet M, McCalmont TH, Zehnder J. Source: Journal of the American Academy of Dermatology. 2003 October; 49(4): 620-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14512906&dopt=Abstract
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Malawi pilot study of Burkitt lymphoma treatment. Author(s): Hesseling PB, Broadhead R, Molyneux E, Borgstein E, Schneider JW, Louw M, Mansvelt EP, Wessels G. Source: Medical and Pediatric Oncology. 2003 December; 41(6): 532-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14595710&dopt=Abstract
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Mantle cell lymphoma of the hard palate: a case report and review of the differential diagnosis based on the histomorphology and immunophenotyping pattern. Author(s): Chang CC, Rowe JJ, Hawkins P, Sadeghi EM. Source: Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 2003 September; 96(3): 316-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12973287&dopt=Abstract
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Matrix-metalloproteinases in Hodgkin lymphoma. Author(s): Thorns C, Bernd HW, Hatton D, Merz H, Feller AC, Lange K. Source: Anticancer Res. 2003 March-April; 23(2B): 1555-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820423&dopt=Abstract
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Mediastinal T-cell lymphoma in a boy 7 years after treatment of supratentorial primitive neuroectodermal tumor. Author(s): Lehrnbecher T, Deinlein F, Marx A, Kuhl J. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 August; 25(8): 657-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902924&dopt=Abstract
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Mesenteric malignant lymphoma detected with routine color Doppler ultrasonography. Author(s): Hosaka S, Watanabe M, Matsuzawa K, Maruyama K, Ikeuchi Y, Kawasaki S, Miwa S. Source: Intern Med. 2003 June; 42(6): 500-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12857048&dopt=Abstract
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Metachronous lymphomas of the breast. Author(s): Cimsit G, Aribal E. Source: Jbr-Btr. 2003 May-June; 86(3): 150-1. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12880159&dopt=Abstract
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Micronodular T-cell/histiocyte-rich large B-cell lymphoma of the spleen: histology, immunophenotype, and differential diagnosis. Author(s): Dogan A, Burke JS, Goteri G, Stitson RN, Wotherspoon AC, Isaacson PG. Source: The American Journal of Surgical Pathology. 2003 July; 27(7): 903-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826882&dopt=Abstract
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MLL-AF4 gene rearrangement in a child with Epstein-Barr virus-related posttransplant B-cell lymphoma. Author(s): Corapcioglu F, Olgun N, Sarialioglu F, Uysal KM, Oren H, Sercan O. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 September; 25(9): 740-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12972812&dopt=Abstract
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Molecular diagnosis of primary mediastinal B cell lymphoma identifies a clinically favorable subgroup of diffuse large B cell lymphoma related to Hodgkin lymphoma. Author(s): Rosenwald A, Wright G, Leroy K, Yu X, Gaulard P, Gascoyne RD, Chan WC, Zhao T, Haioun C, Greiner TC, Weisenburger DD, Lynch JC, Vose J, Armitage JO, Smeland EB, Kvaloy S, Holte H, Delabie J, Campo E, Montserrat E, Lopez-Guillermo A, Ott G, Muller-Hermelink HK, Connors JM, Braziel R, Grogan TM, Fisher RI, Miller TP, LeBlanc M, Chiorazzi M, Zhao H, Yang L, Powell J, Wilson WH, Jaffe ES, Simon R, Klausner RD, Staudt LM. Source: The Journal of Experimental Medicine. 2003 September 15; 198(6): 851-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975453&dopt=Abstract
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Monoclonal antibodies in the management of newly diagnosed, aggressive B-cell lymphoma. Author(s): Coiffier B. Source: Curr Hematol Rep. 2003 January; 2(1): 23-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901151&dopt=Abstract
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Monoclonal antibody therapy of non-Hodgkin's lymphoma: the Rituximab story. Author(s): Saleh M. Source: J Med Assoc Ga. 2003 Winter-Spring; 92(1): 39-46. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12743905&dopt=Abstract
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MR imaging of primary urethral lymphoma in a man. Author(s): Ryu JA, Kim B. Source: Ajr. American Journal of Roentgenology. 2003 August; 181(2): 600-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12876063&dopt=Abstract
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Multicenter study of pegylated liposomal doxorubicin in patients with cutaneous Tcell lymphoma. Author(s): Wollina U, Dummer R, Brockmeyer NH, Konrad H, Busch JO, Kaatz M, Knopf B, Koch HJ, Hauschild A. Source: Cancer. 2003 September 1; 98(5): 993-1001. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12942567&dopt=Abstract
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Multicolour fluorescence in situ hybridization analysis of t(14;18)-positive follicular lymphoma and correlation with gene expression data and clinical outcome. Author(s): Lestou VS, Gascoyne RD, Sehn L, Ludkovski O, Chhanabhai M, Klasa RJ, Husson H, Freedman AS, Connors JM, Horsman DE. Source: British Journal of Haematology. 2003 September; 122(5): 745-59. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930384&dopt=Abstract
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Multiple BCL6 translocation partners in individual cases of gastric lymphoma. Author(s): Chen YW, Liang AC, Au WY, Chu KM, Wong KY, Hu X, Lu L, Tang JC, Chan KW, Beh SL, Kwong YL, Liang RH, Srivastava G. Source: Blood. 2003 September 1; 102(5): 1931-2; Author Reply 1932. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930733&dopt=Abstract
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Multiple extranodal sites at presentation in non-Hodgkin's lymphoma. Author(s): Singh D, Sharma A, Mohanti BK, Thulkar S, Bahadur S, Sharma SC, Gupta SD. Source: American Journal of Hematology. 2003 September; 74(1): 75-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949896&dopt=Abstract
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Multiple molecular mechanisms contribute to radiation sensitivity in mantle cell lymphoma. Author(s): M'kacher R, Bennaceur A, Farace F, Lauge A, Plassa LF, Wittmer E, Dossou J, Violot D, Deutsch E, Bourhis J, Stoppa-Lyonnet D, Ribrag V, Carde P, Parmentier C, Bernheim A, Turhan AG. Source: Oncogene. 2003 September 11; 22(39): 7905-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970738&dopt=Abstract
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Multiple renal cystic lesions and acute renal failure in non-Hodgkin's testicular lymphoma--a case report. Author(s): Gupta D, Sandhu JS, Singh HP, Sandhu P. Source: Renal Failure. 2003 March; 25(2): 307-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12739837&dopt=Abstract
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Multipoint methylation analysis indicates a distinctive epigenetic phenotype among testicular germ cell tumors and testicular malignant lymphomas. Author(s): Kawakami T, Okamoto K, Kataoka A, Koizumi S, Iwaki H, Sugihara H, Reeve AE, Ogawa O, Okada Y. Source: Genes, Chromosomes & Cancer. 2003 September; 38(1): 97-101. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12874790&dopt=Abstract
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Mutations of the BIK gene in human peripheral B-cell lymphomas. Author(s): Arena V, Martini M, Luongo M, Capelli A, Larocca LM. Source: Genes, Chromosomes & Cancer. 2003 September; 38(1): 91-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12874789&dopt=Abstract
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Nasal and nasal-type natural killer (NK)/T-cell lymphoma: immunophenotype and Epstein-Barr virus (EBV) association. Author(s): Peh SC, Quen QW. Source: Med J Malaysia. 2003 June; 58(2): 196-204. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14569739&dopt=Abstract
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Nasopharyngeal/nasal type T/NK lymphomas: analysis of 14 cases and review of the literature. Author(s): Garcia-Cosio M, Santon A, Mendez MC, Rivas C, Martin C, Bellas C. Source: Tumori. 2003 May-June; 89(3): 278-84. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12908783&dopt=Abstract
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Natural killer cells in human peripheral blood and primary cutaneous natural killer cell lymphomas may express cutaneous lymphocyte antigen. Author(s): Chang SE, Kim MJ, Lee WS, Kang YK, Moon KC, Koh JK, Choi JH. Source: Acta Dermato-Venereologica. 2003; 83(3): 162-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816147&dopt=Abstract
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Natural killer cell-type body cavity lymphoma following chronic active Epstein-Barr virus infection. Author(s): Ogata M, Imamura T, Mizunoe S, Ohtsuka E, Kikuchi H, Nasu M. Source: American Journal of Hematology. 2003 June; 73(2): 126-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749015&dopt=Abstract
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Nitrate in community water supplies and incidence of non-Hodgkin's lymphoma in Sardinia, Italy. Author(s): Cocco P, Broccia G, Aru G, Casula P, Muntoni S, Cantor KP, Ward MH. Source: Journal of Epidemiology and Community Health. 2003 July; 57(7): 510-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821696&dopt=Abstract
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No evidence of skin infection with Chlamydia pneumoniae in patients with cutaneous T cell lymphoma. Author(s): Rossler MJ, Rappl G, Muche M, Hasselmann DO, Sterry W, Tilgen W, Reinhold U. Source: Clinical Microbiology and Infection : the Official Publication of the European Society of Clinical Microbiology and Infectious Diseases. 2003 July; 9(7): 721-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925116&dopt=Abstract
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Nodal marginal zone B-cell lymphoma with a novel t(X;5)(q28;q22): conventional and molecular cytogenetic analysis. Author(s): Cook JR, Sherer ME, Shekhter-Levin S, Swerdlow SH. Source: Cancer Genetics and Cytogenetics. 2003 June; 143(2): 154-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12781450&dopt=Abstract
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Nodal marginal zone lymphoma: a heterogeneous tumor: a comprehensive analysis of a series of 27 cases. Author(s): Camacho FI, Algara P, Mollejo M, Garcia JF, Montalban C, Martinez N, Sanchez-Beato M, Piris MA. Source: The American Journal of Surgical Pathology. 2003 June; 27(6): 762-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12766579&dopt=Abstract
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Non-Hodgkin lymphoma in elderly patients: experience at Taipei Veterans General Hospital. Author(s): Bai LY, Yang MH, Chiou TJ, Liu JH, Yen CC, Wang WS, Hsiao LT, Chao TC, Chen PM. Source: Cancer. 2003 September 15; 98(6): 1188-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12973842&dopt=Abstract
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Non-Hodgkin lymphoma presenting with obstructive jaundice. Author(s): Ravindra KV, Stringer MD, Prasad KR, Kinsey SE, Lodge JP. Source: The British Journal of Surgery. 2003 July; 90(7): 845-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854111&dopt=Abstract
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Non-Hodgkin lymphoma. Author(s): Evans LS, Hancock BW. Source: Lancet. 2003 July 12; 362(9378): 139-46. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12867117&dopt=Abstract
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Non-Hodgkin's lymphoma developing in a pacemaker pocket. Author(s): Hojo N, Yakushijin Y, Narumi H, Minamoto Y, Sakai I, Takada K, Hato T, Yasukawa M, Fujita S. Source: International Journal of Hematology. 2003 May; 77(4): 387-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774929&dopt=Abstract
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Non-Hodgkin's lymphoma of the brainstem with atrial septal mass. Author(s): Prakash B, Nayak SD, Mathew V, Bhaskar N, Natarajan M, Pranesh MB. Source: J Assoc Physicians India. 2003 March; 51: 311-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12839362&dopt=Abstract
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Non-Hodgkin's lymphoma of the nasopharynx: CT and MR imaging. Author(s): King AD, Lei KI, Richards PS, Ahuja AT. Source: Clinical Radiology. 2003 August; 58(8): 621-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12887955&dopt=Abstract
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Non-muscle myosin heavy chain (MYH9): a new partner fused to ALK in anaplastic large cell lymphoma. Author(s): Lamant L, Gascoyne RD, Duplantier MM, Armstrong F, Raghab A, Chhanabhai M, Rajcan-Separovic E, Raghab J, Delsol G, Espinos E. Source: Genes, Chromosomes & Cancer. 2003 August; 37(4): 427-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12800156&dopt=Abstract
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Not just another fall in the elderly. Bilateral adrenal lymphoma presenting with adrenal insufficiency causing weakness. Author(s): Gillett M, Haak S. Source: Aust Fam Physician. 2003 April; 32(4): 248-50. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735264&dopt=Abstract
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Obstructive jaundice as the presenting manifestation of Burkitt's lymphoma in a 4year-old boy. Author(s): Hsu CF, Ko SF, Hsiao CC, Shieh CS, Huang CC, Huang FC. Source: J Formos Med Assoc. 2003 February; 102(2): 105-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709739&dopt=Abstract
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Orbital lymphoma and subacute or chronic inflammatory pseudotumor: differentiation with two-phase helical computed tomography. Author(s): Moon WJ, Na DG, Ryoo JW, Kim MJ, Kim YD, Lim do H, Byun HS. Source: Journal of Computer Assisted Tomography. 2003 July-August; 27(4): 510-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12886134&dopt=Abstract
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Outcome of follicular lymphoma grade 3: is anthracycline necessary as front-line therapy? Author(s): Chau I, Jones R, Cunningham D, Wotherspoon A, Maisey N, Norman AR, Jain P, Bishop L, Horwich A, Catovsky D. Source: British Journal of Cancer. 2003 July 7; 89(1): 36-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12838297&dopt=Abstract
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Outpatient regimen rituximab plus ifosfamide, carboplatin and etoposide (R-ICE) for relapsed non-Hodgkin's lymphoma. Author(s): Vose J, Sneller V. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003; 14 Suppl 1: I17-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736226&dopt=Abstract
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Outpatient-based ifosfamide, carboplatin and etoposide (ICE) chemotherapy in transplant-eligible patients with non-Hodgkin's lymphoma and Hodgkin's disease. Author(s): Hertzberg MS, Crombie C, Benson W, Taper J, Gottlieb D, Bradstock KF. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003; 14 Suppl 1: I11-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736225&dopt=Abstract
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Overview of non-Hodgkin's lymphoma: biology, staging, and treatment. Author(s): Fisher RI. Source: Seminars in Oncology. 2003 April; 30(2 Suppl 4): 3-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12728402&dopt=Abstract
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Pathologic quiz case: a 72-year-old man with fatigue and proteinuria. Angiotropic (intravascular) large B-cell lymphoma. Author(s): Ozolek J, Nodit L, Bastacky S, Craig F, Nalesnik M. Source: Archives of Pathology & Laboratory Medicine. 2003 October; 127(10): 1380-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14521449&dopt=Abstract
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Pathologic quiz case: a pelvic mass in a 20-year-old man. Diffuse large B-cell lymphoma with Homer-Wright-type rosette formation. Author(s): Jun SY, Huh J, Park SH, Ro JY. Source: Archives of Pathology & Laboratory Medicine. 2003 October; 127(10): E411-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14521440&dopt=Abstract
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Pathology quiz case. Nasal T/NK-cell lymphoma. Author(s): Chen HL, Cheng PW, Tsai CC. Source: Archives of Otolaryngology--Head & Neck Surgery. 2003 October; 129(10): 11356. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14568802&dopt=Abstract
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Patients presenting with CNS lesions. Case 1. Primary low-grade mucosa-associated B-cell lymphoma of the dura. Author(s): Lima VS, Leite EB, Fonseca RP, Fernandes AS Jr. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 November 1; 21(21): 4058-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14581428&dopt=Abstract
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Polymorphism in the hMSH2 gene (gIVS 12-6T-->C) and risk of non-Hodgkin lymphoma in a Japanese population. Author(s): Hishida A, Matsuo K, Hamajima N, Ito H, Ogura M, Kagami Y, Taji H, Morishima Y, Emi N, Tajima K. Source: Cancer Genetics and Cytogenetics. 2003 November; 147(1): 71-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14580774&dopt=Abstract
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Polyomavirus SV40 infection and lymphomas in Spain. Author(s): Vilchez RA, Butel JS. Source: International Journal of Cancer. Journal International Du Cancer. 2003 November 10; 107(3): 505-6; Author Reply 507-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14506754&dopt=Abstract
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Predictive value of early 18F-fluoro-deoxyglucose positron emission tomography in chemosensitive relapsed lymphoma. Author(s): Schot B, van Imhoff G, Pruim J, Sluiter W, Vaalburg W, Vellenga E. Source: British Journal of Haematology. 2003 October; 123(2): 282-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14531910&dopt=Abstract
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Prevalence and pattern of antinuclear autoantibodies in 347 patients with nonHodgkin's lymphoma. Author(s): Guyomard S, Salles G, Coudurier M, Rousset H, Coiffier B, Bienvenu J, Fabien N. Source: British Journal of Haematology. 2003 October; 123(1): 90-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14510947&dopt=Abstract
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Primary brain lymphomas after kidney transplantation: presentation and outcome. Author(s): Snanoudj R, Durrbach A, Leblond V, Caillard S, Hurault De Ligny B, Noel C, Rondeau E, Moulin B, Mamzer-Bruneel MF, Lacroix C, Charpentier B. Source: Transplantation. 2003 September 27; 76(6): 930-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14508356&dopt=Abstract
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Primary central nervous system lymphoma in Korea: comparison of B- and T-cell lymphomas. Author(s): Choi JS, Nam DH, Ko YH, Seo JW, Choi YL, Suh YL, Ree HJ. Source: The American Journal of Surgical Pathology. 2003 July; 27(7): 919-28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12826884&dopt=Abstract
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Primary cutaneous follicle center cell lymphoma of the scalp successfully treated with anti CD20 monoclonal antibody and CHOP combination therapy with no subsequent permanent loss of hair. Author(s): Imai Y, Isoda K, Ito E, Hakamada A, Yamanishi K, Mizutani H. Source: The Journal of Dermatology. 2003 September; 30(9): 683-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14578559&dopt=Abstract
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Primary gastric Burkitt lymphoma in childhood: associated with Helicobacter pylori? Author(s): Moschovi M, Menegas D, Stefanaki K, Constantinidou CV, TzortzatouStathopoulou F. Source: Medical and Pediatric Oncology. 2003 November; 41(5): 444-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14515383&dopt=Abstract
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Primary malignant lymphoma of the trigeminal region treated with rapid infusion of high-dose MTX and radiation: case report and review of the literature. Author(s): Kinoshita M, Izumoto S, Oshino S, Nonaka M, Moriuchi S, Maruno M, Yoshimine T. Source: Surgical Neurology. 2003 October; 60(4): 343-8; Discussion 348. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14505860&dopt=Abstract
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Primary non-Hodgkin lymphoma of the humerus following traumatic injury: case report. Author(s): Stemberga V, Dobi-Babic R, Bosnar A, Cuculic D, Fuckar D, Stifter S, Kusec R, Marusic-Vrsalovic M, Jonjic N. Source: Hematological Oncology. 2003 September; 21(3): 109-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14579239&dopt=Abstract
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Primary non-Hodgkin's lymphoma of the bile ducts mimicking cholangiocarcinoma. Author(s): Das K, Fisher A, Wilson DJ, dela Torre AN, Seguel J, Koneru B. Source: Surgery. 2003 September; 134(3): 496-500. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14555939&dopt=Abstract
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Primary pleural lymphomas. Author(s): Ahmad H, Pawade J, Falk S, Morgan JA, Balacumaraswami L. Source: Thorax. 2003 October; 58(10): 908-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14514950&dopt=Abstract
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Primary pulmonary Hodgkin's lymphoma with Epstein-Barr and cytomegaly virus infections. A case report and differential diagnosis. Author(s): Stachura T, Malinowski E. Source: Pol J Pathol. 2003; 54(1): 79-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12817885&dopt=Abstract
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Prognostic features of splenic lymphoma with villous lymphocytes. Author(s): Iannitto E, Ammatuna E, Florena AM, Franco V. Source: British Journal of Haematology. 2003 October; 123(2): 370-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14531926&dopt=Abstract
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Prognostic significance of CD44 expression in diffuse large B cell lymphoma of activated and germinal centre B cell-like types: a tissue microarray analysis of 90 cases. Author(s): Tzankov A, Pehrs AC, Zimpfer A, Ascani S, Lugli A, Pileri S, Dirnhofer S. Source: Journal of Clinical Pathology. 2003 October; 56(10): 747-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14514777&dopt=Abstract
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Prominent intrasinusoidal infiltration of the bone marrow by mantle cell lymphoma. Author(s): Schenka AA, Gascoyne RD, Duchayne E, Delsol G, Brousset P. Source: Human Pathology. 2003 August; 34(8): 789-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14506640&dopt=Abstract
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Quantitative assessment of contaminating tumor cells in autologous peripheral blood stem cells of B-cell non-Hodgkin lymphomas using immunoglobulin heavy chain gene allele-specific oligonucleotide real-time quantitative-polymerase chain reaction. Author(s): Yashima A, Maesawa C, Uchiyama M, Tarusawa M, Satoh T, Satoh M, Enomoto S, Sugawara K, Numaoka H, Murai K, Utsugisawa T, Ishida Y, Masuda T. Source: Leukemia Research. 2003 October; 27(10): 925-34. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860013&dopt=Abstract
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Radioimmunotherapy for non-Hodgkin's lymphoma. Author(s): Emmanouilides C. Source: Seminars in Oncology. 2003 August; 30(4): 531-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939722&dopt=Abstract
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Radioimmunotherapy of relapsed or refractory low-grade, follicular, or transformed B-cell non-Hodgkin's lymphoma. Author(s): Dillman RO. Source: Curr Hematol Rep. 2003 January; 2(1): 30-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901152&dopt=Abstract
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Radiotherapy for extranodal, marginal zone, B-cell lymphoma of mucosa-associated lymphoid tissue originating in the ocular adnexa: a multiinstitutional, retrospective review of 50 patients. Author(s): Uno T, Isobe K, Shikama N, Nishikawa A, Oguchi M, Ueno N, Itami J, Ohnishi H, Mikata A, Ito H. Source: Cancer. 2003 August 15; 98(4): 865-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12910532&dopt=Abstract
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Radiotherapy for stage I-III nodal low-grade non-Hodgkin's lymphoma. Author(s): Ott OJ, Rodel C, Gramatzki M, Niedobitek G, Sauer R, Grabenbauer GG. Source: Strahlentherapie Und Onkologie : Organ Der Deutschen Rontgengesellschaft. [et Al]. 2003 October; 179(10): 694-701. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14566478&dopt=Abstract
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Rapamycin inhibits the interleukin 10 signal transduction pathway and the growth of Epstein Barr virus B-cell lymphomas. Author(s): Nepomuceno RR, Balatoni CE, Natkunam Y, Snow AL, Krams SM, Martinez OM. Source: Cancer Research. 2003 August 1; 63(15): 4472-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907620&dopt=Abstract
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Rate of death due to leukemia/lymphoma in patients with rheumatoid arthritis. Author(s): Wolfe F, Fries JF. Source: Arthritis and Rheumatism. 2003 September; 48(9): 2694-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=13130492&dopt=Abstract
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Real-time PCR assay compared to nested PCR and antigenemia assays for detecting cytomegalovirus reactivation in adult T-cell leukemia-lymphoma patients. Author(s): Ikewaki J, Ohtsuka E, Kawano R, Ogata M, Kikuchi H, Nasu M. Source: Journal of Clinical Microbiology. 2003 September; 41(9): 4382-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12958273&dopt=Abstract
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Recombinant human erythropoietin, epoetin beta, in patients with relapsed lymphoma treated with aggressive sequential salvage chemotherapy--results of a randomized trial. Author(s): Glossmann JP, Engert A, Wassmer G, Flechtner H, Ko Y, Rudolph C, Metzner B, Dorken B, Wiedenmann S, Diehl V, Josting A. Source: Annals of Hematology. 2003 August; 82(8): 469-75. Epub 2003 June 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12910374&dopt=Abstract
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Recurrence of Bcl-2/IgH polymerase chain reaction positivity following a prolonged molecular remission can be unrelated to the original follicular lymphoma clone. Author(s): Ladetto M, Mantoan B, Ricca I, Astolfi M, Drandi D, Compagno M, Vallet S, dell'Aquila M, Alfarano A, Rossatto P, Rocci A, Vitolo U, Corradini P, Boccadoro M, Tarella C. Source: Experimental Hematology. 2003 September; 31(9): 784-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12962724&dopt=Abstract
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Regulation of tumour necrosis factor-related apoptosis-inducing ligand (TRAIL)induced apoptosis in Burkitt's lymphoma cell lines. Author(s): Mouzakiti A, Packham G. Source: British Journal of Haematology. 2003 July; 122(1): 61-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823346&dopt=Abstract
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Response to highly active antiretroviral therapy strongly predicts outcome in patients with AIDS-related lymphoma. Author(s): Hoffmann C, Wolf E, Fatkenheuer G, Buhk T, Stoehr A, Plettenberg A, Stellbrink HJ, Jaeger H, Siebert U, Horst HA. Source: Aids (London, England). 2003 July 4; 17(10): 1521-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12824790&dopt=Abstract
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Reversible choreoathetosis in primary cerebral lymphoma: clinicoradiologic correlation. Author(s): Tan EK, Chan LL, Auchus AP, Wong MC. Source: European Neurology. 2003; 50(1): 53-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12824713&dopt=Abstract
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Reversible non-thrombotic occlusion of the superior sagittal sinus caused by metastatic malignant lymphoma--case report. Author(s): Matsumoto K, Ohta M, Takeshita I. Source: Neurol Med Chir (Tokyo). 2003 July; 43(7): 349-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12924595&dopt=Abstract
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Risk of breast cancer and breast cancer characteristics in women treated with supradiaphragmatic radiation for Hodgkin lymphoma: Mayo Clinic experience. Author(s): Wahner-Roedler DL, Nelson DF, Croghan IT, Achenbach SJ, Crowson CS, Hartmann LC, O'Fallon WM. Source: Mayo Clinic Proceedings. 2003 June; 78(6): 708-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12934780&dopt=Abstract
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Rituximab in combination with vinorelbine/gemcitabine chemotherapy in patients with primary refractory or early relapsed T cell rich B cell lymphoma. A pilot study. Author(s): Xiros N, Economopoulos T, Valsami S, Rontogianni D, Fountzilas G, Raptis S. Source: Leukemia Research. 2003 December; 27(12): 1097-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921946&dopt=Abstract
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Seasonal differences in the onset of the EBV-positive and -negative forms of paediatric Hodgkin's lymphoma. Author(s): Reiman A, Powell JE, Flavell KJ, Grundy RG, Mann JR, Parkes S, Redfern D, Young LS, Murray PG. Source: British Journal of Cancer. 2003 October 6; 89(7): 1200-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14520445&dopt=Abstract
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Sensitization of ara-C-resistant lymphoma cells by a pronucleotide analogue. Author(s): Galmarini CM, Clarke ML, Santos CL, Jordheim L, Perigaud C, Gosselin G, Cros E, Mackey JR, Dumontet C. Source: International Journal of Cancer. Journal International Du Cancer. 2003 October 20; 107(1): 149-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12925971&dopt=Abstract
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Severe recalcitrant necrotizing leucocytoclastic vasculitis in non-Hodgkin's lymphoma associated with hepatitis C: successful treatment with the combination of antiviral and immunosuppressive therapy. Author(s): Zou W, Kreuter A, Schlottmann R, Bartke U, Altmeyer P, Wu NP, Brockmeyer NH. Source: Acta Dermato-Venereologica. 2003; 83(3): 224-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816162&dopt=Abstract
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Situs inversus totalis with malignant lymphoma of the stomach: report of a case. Author(s): Murakami S, Terakado M, Misumi M, Tsuji Y, Okubo K, Hirayama R, Inoue K, Arai E. Source: Surgery Today. 2003; 33(7): 533-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14507000&dopt=Abstract
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Spatial proximity of translocation-prone gene loci in human lymphomas. Author(s): Roix JJ, McQueen PG, Munson PJ, Parada LA, Misteli T. Source: Nature Genetics. 2003 July; 34(3): 287-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12808455&dopt=Abstract
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Spinal Burkitt's lymphoma manifesting as nocturnal abdominal pain and constipation: a case report. Author(s): Fang SB, Hsiao CH, Tseng CL. Source: Annals of Tropical Paediatrics. 2003 September; 23(3): 215-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14567838&dopt=Abstract
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Spontaneous membrane transfer through homotypic synapses between lymphoma cells. Author(s): Poupot M, Fournie JJ. Source: Journal of Immunology (Baltimore, Md. : 1950). 2003 September 1; 171(5): 251723. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12928401&dopt=Abstract
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Stage III follicular lymphoma: long-term follow-up and patterns of failure. Author(s): Ha CS, Kong JS, McLaughlin P, Tucker SL, Fayad LE, Hess MA, Wilder RB, Cabanillas F, Cox JD. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 November 1; 57(3): 748-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14529780&dopt=Abstract
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Stereotactic radiosurgery in the treatment of primary central nervous system lymphoma. Author(s): Dong Y, Pan L, Wang B, Wang E, Zhang N, Cai P, Dai J. Source: Chinese Medical Journal. 2003 August; 116(8): 1166-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12935403&dopt=Abstract
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Synergistic effects of chemotherapeutic drugs in lymphoma cells are associated with down-regulation of inhibitor of apoptosis proteins (IAPs), prostate-apoptosisresponse-gene 4 (Par-4), death-associated protein (Daxx) and with enforced caspase activation. Author(s): Chow KU, Nowak D, Boehrer S, Ruthardt M, Knau A, Hoelzer D, Mitrou PS, Weidmann E. Source: Biochemical Pharmacology. 2003 September 1; 66(5): 711-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12948851&dopt=Abstract
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Targeting oncogenic fusion genes in leukemias and lymphomas by RNA interference. Author(s): Damm-Welk C, Fuchs U, Wossmann W, Borkhardt A. Source: Seminars in Cancer Biology. 2003 August; 13(4): 283-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14563123&dopt=Abstract
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Thalidomide therapy induces response in relapsed mantle cell lymphoma. Author(s): Damaj G, Lefrere F, Delarue R, Varet B, Furman R, Hermine O. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2003 September; 17(9): 1914-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970798&dopt=Abstract
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The B-cell transcription factors BSAP, Oct-2, and BOB.1 and the pan-B-cell markers CD20, CD22, and CD79a are useful in the differential diagnosis of classic Hodgkin lymphoma. Author(s): Browne P, Petrosyan K, Hernandez A, Chan JA. Source: American Journal of Clinical Pathology. 2003 November; 120(5): 767-77. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14608905&dopt=Abstract
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The homeobox gene Hex induces T-cell-derived lymphomas when overexpressed in hematopoietic precursor cells. Author(s): George A, Morse HC 3rd, Justice MJ. Source: Oncogene. 2003 October 2; 22(43): 6764-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14555989&dopt=Abstract
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The interaction and functional properties of leukocyte molecules of human leukemia/lymphoma cells. Author(s): Koubek K, Babusikova O. Source: Sb Lek. 2003; 104(2): 183-97. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14577128&dopt=Abstract
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The molecular mechanism of arsenic trioxide-induced apoptosis and oncosis in leukemia/lymphoma cell lines. Author(s): Zhu J, Okumura H, Ohtake S, Nakamura S, Nakao S. Source: Acta Haematologica. 2003; 110(1): 1-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975549&dopt=Abstract
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Treatment of HCV-related mantle-cell lymphoma with ribavirin and pegylated interferon Alfa. Author(s): Levine AM, Shimodaira S, Lai MM. Source: The New England Journal of Medicine. 2003 November 20; 349(21): 2078-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14627800&dopt=Abstract
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Treatment of low-grade B-cell lymphoma with the monoclonal antibody rituximab. Author(s): Dillman RO. Source: Seminars in Oncology. 2003 August; 30(4): 434-47. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939712&dopt=Abstract
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Treatment of lymphoma relapses after allogeneic hematopoietic stem cell transplantation with intensive chemotherapy followed by infusion of hematopoietic stem cell from the original donor. Author(s): Au WY, Lie AK, Siu LL, Chan EC, Ooi GC, Leung AY, Liang R, Kwong YL. Source: Annals of Hematology. 2003 September; 82(9): 548-51. Epub 2003 July 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14504811&dopt=Abstract
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Two immunoglobulin G fragment C receptor polymorphisms independently predict response to rituximab in patients with follicular lymphoma. Author(s): Weng WK, Levy R. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 November 1; 21(21): 3940-7. Epub 2003 September 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975461&dopt=Abstract
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Ultraviolet B treatment for pruritus in Hodgkin's lymphoma. Author(s): Kaptanoglu AF, Oskay T. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 July; 17(4): 489-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12834480&dopt=Abstract
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Unusual locations of involvement by malignancies: Case 4. Bilateral hypopyon heralding CNS relapse of cutaneous natural killer cell lymphoma. Author(s): Hon C, Kwok AK, Shek TW, Au WY. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 September 1; 21(17): 3373-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12947077&dopt=Abstract
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Unusual manifestation of Sweet's syndrome in B-cell lymphoma. Author(s): Kuner N, Hartschuh W, Jappe U. Source: Acta Dermato-Venereologica. 2003; 83(4): 308-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12926812&dopt=Abstract
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Unusual sequence of VDJ rearrangement revealed by molecular analysis in a patient with indolent lymphoma. Author(s): Cerny J, Slavickova A, Krepelova A, Trneny M, Karban J, Klener P. Source: Haematologica. 2003 May; 88(5): Ecr15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12745284&dopt=Abstract
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Use of ibritumomab tiuxetan anti-CD20 radioimmunotherapy in a non-Hodgkin's lymphoma patient previously treated with a yttrium-90-labeled anti-CD22 monoclonal antibody. Author(s): Tsai DE, Maillard I, Schuster SJ, Nasta SD, Porter DL, Klumpp TR, Goldenberg DM, Luger SM, Alavi A, Sharkey RM, Hartzell KB, Stadtmauer EA. Source: Clin Lymphoma. 2003 June; 4(1): 56-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837157&dopt=Abstract
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Utility of surgical resection with or without radiation therapy in patients with lowgrade gastric mucosa-associated lymphoid tissue lymphoma. Author(s): Zinzani PL, Tani M, Barbieri E, Stefoni V, Alinari L, Baccarani M. Source: Haematologica. 2003 July; 88(7): 830-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12857565&dopt=Abstract
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Vaccination of patients with cutaneous T-cell lymphoma using intranodal injection of autologous tumor-lysate-pulsed dendritic cells. Author(s): Maier T, Tun-Kyi A, Tassis A, Jungius KP, Burg G, Dummer R, Nestle FO. Source: Blood. 2003 October 1; 102(7): 2338-44. Epub 2003 April 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714511&dopt=Abstract
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Value of F-18 fluorodeoxyglucose positron emission tomography for predicting the clinical outcome of patients with aggressive lymphoma prior to and after autologous stem-cell transplantation. Author(s): Filmont JE, Czernin J, Yap C, Silverman DH, Quon A, Phelps ME, Emmanouilides C. Source: Chest. 2003 August; 124(2): 608-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907550&dopt=Abstract
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Vav-promoter regulated oncogenic fusion protein NPM-ALK in transgenic mice causes B-cell lymphomas with hyperactive Jun kinase. Author(s): Turner SD, Tooze R, Maclennan K, Alexander DR. Source: Oncogene. 2003 October 30; 22(49): 7750-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14586401&dopt=Abstract
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VH mutation status and VDJ rearrangement structure in mantle cell lymphoma: correlation with genomic aberrations, clinical characteristics, and outcome. Author(s): Kienle D, Krober A, Katzenberger T, Ott G, Leupolt E, Barth TF, Moller P, Benner A, Habermann A, Muller-Hermelink HK, Bentz M, Lichter P, Dohner H, Stilgenbauer S. Source: Blood. 2003 October 15; 102(8): 3003-9. Epub 2003 July 03. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12842981&dopt=Abstract
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Viral latent proteins as targets for Kaposi's sarcoma and Kaposi's sarcoma-associated herpesvirus (KSHV/HHV-8) induced lymphoma. Author(s): Staudt MR, Dittmer DP. Source: Current Drug Targets. Infectious Disorders. 2003 June; 3(2): 129-35. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769790&dopt=Abstract
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XIAP-mediated caspase inhibition in Hodgkin's lymphoma-derived B cells. Author(s): Kashkar H, Haefs C, Shin H, Hamilton-Dutoit SJ, Salvesen GS, Kronke M, Jurgensmeier JM. Source: The Journal of Experimental Medicine. 2003 July 21; 198(2): 341-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12874265&dopt=Abstract
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CHAPTER 2. NUTRITION AND LYMPHOMA Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and lymphoma.
Finding Nutrition Studies on Lymphoma The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “lymphoma” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7
Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
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The following information is typical of that found when using the “Full IBIDS Database” to search for “lymphoma” (or a synonym): •
A new weapon in the treatment of non-Hodgkin's lymphoma. Author(s): Department of Radiology, Jennie Edmundson Memorial Hospital, Council Bluffs, Iowa, USA.
[email protected] Source: Lipcamon, J D Sahl, B Radiol-Manage. 2002 Sep-October; 24(5): 13-5 0198-7097
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A Phase I study with an anti-CD30 ricin A-chain immunotoxin (Ki-4.dgA) in patients with refractory CD30+ Hodgkin's and non-Hodgkin's lymphoma. Author(s): Department of Internal Medicine I, University of Koeln, Joseph-StelzmannStrasse 9, D-50924 Koeln, Germany. Source: Schnell, R Staak, O Borchmann, P Schwartz, C Matthey, B Hansen, H Schindler, J Ghetie, V Vitetta, E S Diehl, V Engert, A Clin-Cancer-Res. 2002 June; 8(6): 1779-86 10780432
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Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B. Author(s): Max-Delbruck-Center for Molecular Medicine and Universitatsklinikum Charite, Robert-Rossle-Klinik, Humboldt University, Lindenberger Weg 80, D-13125 Berlin. Source: Mathas, S Hinz, M Anagnostopoulos, I Krappmann, D Lietz, A Jundt, F Bommert, K Mechta Grigoriou, F Stein, H Dorken, B Scheidereit, C EMBO-J. 2002 August 1; 21(15): 4104-13 0261-4189
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AIDS-related primary central nervous system lymphoma: prolonged remission associated with highly active antiretroviral therapy. Author(s): Department of Medicine, Faculty of Medicine, Khon Kaen University, Thailand. Source: Chotmongkol, V Pesee, M J-Med-Assoc-Thai. 2002 May; 85(5): 634-7 0125-2208
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Alpha-tocopheryl succinate sensitises a T lymphoma cell line to TRAIL-induced apoptosis by suppressing NF-kappaB activation. Author(s): Department of Pathology, The Gade Institute, University of Bergen, Norway. Source: Dalen, H Neuzil, J Br-J-Cancer. 2003 January 13; 88(1): 153-8 0007-0920
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Anticancer activities of curcumin on human Burkitt's lymphoma. Author(s): Fujian Institute of Hematology, Union Hospital, Fujian Medical University, Fuzhou 350001, China. Source: Wu, Y Chen, Y Xu, J Lu, L Zhonghua-Zhong-Liu-Za-Zhi. 2002 July; 24(4): 348-52 0253-3766
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Arginine butyrate increases the cytotoxicity of DAB(389)IL-2 in leukemia and lymphoma cells by upregulation of IL-2Rbeta gene. Author(s): Hematology-Oncology Department, New England Medical Center, Tufts University, Boston, MA, USA. Source: Shao, R H Tian, X Gorgun, G Urbano, A G Foss, F M Leuk-Res. 2002 December; 26(12): 1077-83 0145-2126
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Autologous stem cell transplantation in patients with mantle cell lymphoma. Author(s): Department of Medicine, Helsinki University Central Hospital, Finland. Source: Oinonen, R Jantunen, E Itala, M Lehtinen, T Kuittinen, O Franssila, K Wiklund, T Elonen, E Leuk-Lymphoma. 2002 June; 43(6): 1229-37 1042-8194
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Bendamustine in the treatment of non-Hodgkin's lymphoma: results and future perspectives. Author(s): Department of Hamatologie/Onkologie, Medizinische Universitatsklinik, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany. Source: Rummel, Mathias J Mitrou, Paris S Hoelzer, Dieter Semin-Oncol. 2002 August; 29(4 Suppl 13): 27-32 0093-7754
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Bilateral central serous chorioretinopathy in a patient treated with systemic corticosteroids for non-Hodgkin lymphoma. Author(s): Department of Ophthalmology, University of Ferrara, Italy.
[email protected] Source: Bandello, F Incorvaia, C Rosa, N Parmeggiani, F Costagliola, C Sebastiani, A Eur-J-Ophthalmol. 2002 Mar-April; 12(2): 123-6 1120-6721
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Bilateral peripheral facial palsy secondary to lymphoma in a patient with HIV/AIDS: a case report and literature review. Author(s): Federal University of Parana, Clinical Hospital of Curitiba, PR, Brazil. Source: Sasaki, Maria das Gracas Leite, Patricia G B Leite, Andrea G B de Almeida, Sergio Monteiro Braz-J-Infect-Dis. 2002 February; 6(1): 50-4 1413-8670
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Bilateral, primary, low-grade, diffuse B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) of the breast. Author(s): Department of Surgery, 251 Hellenic Air Force Hospital, Athens, Greece. Source: Zobolas, B Sakorafas, G H Kourakli, I Tsiotou, A G Breast-J. 2002 NovDecember; 8(6): 382 1075-122X
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Burkitt's lymphoma: single-centre experience with modified BFM protocol. Author(s): Department of Haematology, Queen Elizabeth Hospital, Edgbaston, Birmingham, UK. Source: Harris, E Paneesha, S Jackson, N Jones, L Mahendra, P Clin-Lab-Haematol. 2002 April; 24(2): 111-4 0141-9854
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CD5+ T-cell/histiocyte-rich large B-cell lymphoma. Author(s): Department of Pathology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
[email protected] Source: Chang, C C Bunyi Teopengco, E Eshoa, C Chitambar, C R Kampalath, B ModPathol. 2002 October; 15(10): 1051-7 0893-3952
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Chemotherapy with irinotecan (CPT-11), a topoisomerase-I inhibitor, for refractory and relapsed non-Hodgkin's lymphoma. Author(s): Division of Laboratory Medicine, Chiba Cancer Center Hospital, Japan.
[email protected] Source: Takagi, T Saotome, T Leuk-Lymphoma. 2001 August; 42(4): 577-86 1042-8194
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Chimeric anti-CD20 monoclonal antibody (Mabthera) in remission induction and maintenance treatment of relapsed follicular non-Hodgkin's lymphoma: a phase III randomized clinical trial--Intergroup Collaborative Study. Author(s): Department of Hematology, Academic Medical Centre Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
[email protected] Source: Van Oers, M H Hagenbeek, A Van Glabbeke, M Teodorovic, I Ann-Hematol. 2002 October; 81(10): 553-7 0939-5555
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CNOP for diffuse aggressive non-Hodgkin's lymphoma: the Nebraska lymphoma study group experience. Author(s): Section of Hematology/Oncology, University of Nebraska Medical Center, Nebraska Medical Center, Omaha 68198-7680, USA.
[email protected]
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Source: Vose, J M Weisenburger, D D Lynch, J C Bierman, P J Chan, J C Bast, M Aoun, P Bociek, G Greiner, T Armitage, J O Leuk-Lymphoma. 2002 April; 43(4): 799-804 10428194 •
Combination chemotherapy and radiotherapy for primary central nervous system lymphoma: Radiation Therapy Oncology Group Study 93-10. Author(s): Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.
[email protected] Source: DeAngelis, L M Seiferheld, W Schold, S C Fisher, B Schultz, C J J-Clin-Oncol. 2002 December 15; 20(24): 4643-8 0732-183X
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Combined therapy in the treatment of primary mediastinal B-cell lymphoma: conventional versus escalated chemotherapy. Author(s): Research Unit in Oncology Diseases, Oncology Hospital, National Medical Center, Instituto Mexicano del Seguro Social, Apartado Postal 7-1220, 06700, Mexico D.F., Mexico.
[email protected] Source: Aviles, A Garcia, E L Fernandez, R Gonzalez, J L Neri, N Diaz Maqueo, J C AnnHematol. 2002 July; 81(7): 368-73 0939-5555
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Comparative study of low-dose oral granisetron plus dexamethasone and high-dose metoclopramide plus dexamethasone in prevention of nausea and vomiting induced by CHOP-therapy in young patients with non-Hodgkin's lymphoma. Author(s): Department of Medicine, Phramongkutklao Hospital, Bangkok 10400, Thailand. Source: Numbenjapon, T Sriswasdi, C Mongkonsritragoon, W Leelasiri, A Prayoonwiwat, W J-Med-Assoc-Thai. 2002 November; 85(11): 1156-63 0125-2208
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Cure in a case of primary hepatic lymphoma. Author(s): Dept. of Medicine, Sir Ganga Ram Hospital, Old Rajinder Nagar, New Delhi, India. Source: Murthy, S A Singh, B Bhalla, S Arora, A Vohra, R Aggarwal, S Indian-J-Cancer. 2000 December; 37(4): 165-72 0019-509X
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Diagnostic fine-needle aspiration cytology and immunocytochemistry analysis of a primary thyroid lymphoma presenting as an anatomic emergency. Author(s): Laboratory and Clinic of Experimental Medicine and Endocrinology, Universitaire Ziekenhuizen, Leuven, Belgium. Source: Van, D Drijkoningen, M Oyen, R Vanfleteren, E Bouillon, R Thyroid. 2002 February; 12(2): 169-73 1050-7256
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Diffuse large B-cell lymphoma with fibrillary matrix. Author(s): Laboratoire d'Anatomie Pathologique, CHU Saint-Pierre/Institut Jules Bordet, Universite Libre de Bruxelles, Brussels, Belgium.
[email protected] Source: Dargent, J L Meiers, I Lespagnard, L Ma, Y Dehou, M F Verhest, A DiagnCytopathol. 2002 October; 27(4): 223-6 8755-1039
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Early decline in left ventricular ejection fraction predicts doxorubicin cardiotoxicity in lymphoma patients. Author(s): Department of Medicine, Kuopio University Hospital and University of Kuopio, FIN 70211 Kuopio, Finland.
[email protected] Source: Nousiainen, T Jantunen, E Vanninen, E Hartikainen, J Br-J-Cancer. 2002 June 5; 86(11): 1697-700 0007-0920
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Efficacy of an early intensification treatment integrating chemotherapy, autologous stem cell transplantation and radiotherapy for poor risk primary mediastinal large B cell lymphoma with sclerosis. Author(s): Department of Hematology, Niguarda Ca' Granda Hospital, Piazza Ospedale Maggiore, 20162 Milan, Italy. Source: Cairoli, R Grillo, G Tedeschi, A Gargantini, L Marenco, P Tresoldi, E Barbarano, L Nosari, A M Morra, E Bone-Marrow-Transplant. 2002 Mar; 29(6): 473-7 0268-3369
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Exposure to pesticides as risk factor for non-Hodgkin's lymphoma and hairy cell leukemia: pooled analysis of two Swedish case-control studies. Author(s): Department of Oncology, Orebro University Hospital, Sweden.
[email protected] Source: Hardell, L Eriksson, M Nordstrom, M Leuk-Lymphoma. 2002 May; 43(5): 1043-9 1042-8194
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Functional interaction of protein kinase CK2 and c-Myc in lymphomagenesis. Author(s): Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts, MA 02118, USA. Source: Channavajhala, Padmalatha Seldin, David C Oncogene. 2002 August 8; 21(34): 5280-8 0950-9232
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Gallium-67 scintigraphy in lymphoma: is there a benefit of image fusion with computed tomography? Author(s): Service de Medecine Nucleaire, Centre Francois Baclesse, Caen, France. Source: Chajari, M Lacroix, J Peny, A M Chesnay, E Batalla, A Henry AMarch, M Delcambre, C Genot, J Y Fruchard, C Bardet, S Eur-J-Nucl-Med-Mol-Imaging. 2002 Mar; 29(3): 380-7 1619-7070
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HA1004, an inhibitor of serine/threonine protein kinases, restores the sensitivity of thymic lymphomas to Ca2+-mediated apoptosis through a protein kinase Aindependent mechanism. Author(s): Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw.
[email protected] Source: Matuszyk, J Cebrat, M Kalas, W Strzadala, L Int-Immunopharmacol. 2002 March; 2(4): 435-42 1567-5769
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Human B-cell lymphoma cell lines are highly sensitive to apoptosis induced by alltrans retinoic acid and interferon-gamma. Author(s): Department of Hematology and Internal Medicine IV, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara-shi, Kanagawa 228-8555, Japan.
[email protected] Source: Niitsu, N Higashihara, M Honma, Y Leuk-Res. 2002 August; 26(8): 745-55 01452126
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IgH PCR of zinc formalin-fixed, paraffin-embedded non-lymphomatous gastric samples produces artifactual “clonal” bands not observed in paired tissues unexposed to zinc formalin. Author(s): Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, Florida 32610-0275, USA.
[email protected] Source: Ahrens, K Braylan, R Almasri, N Foss, R Rimsza, L J-Mol-Diagn. 2002 August; 4(3): 159-63 1525-1578
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In vitro and in vivo effect of HPMA copolymer-bound doxorubicin targeted to transferrin receptor of B-cell lymphoma 38C13. Author(s): Department of Immunology, Institute of Microbiology, Academy of Sciences of the Czech Republic, Prague.
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Source: Kovar, M Strohalm, J Ulbrich, K Rihova, B J-Drug-Target. 2002 February; 10(1): 23-30 1061-186X •
Incomplete inactivation of voltage-dependent K+ channels in human B lymphoma cells. Author(s): Department of Medicine, Division of Nephrology, University of Alabama at Birmingham, 1530 Third Avenue South, Birmingham, Alabama 35294, USA. Source: Zhou, Z H Unlap, T Li, L Ma, H P J-Membr-Biol. 2002 July 15; 188(2): 97-105 0022-2631
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Induction of apoptosis by bexarotene in cutaneous T-cell lymphoma cells: relevance to mechanism of therapeutic action. Author(s): Department of Dermatology, The University of Texas M.D. Anderson Cancer Center, Houston 77030, USA. Source: Zhang, C Hazarika, P Ni, X Weidner, D A Duvic, M Clin-Cancer-Res. 2002 May; 8(5): 1234-40 1078-0432
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Inhibition of oxidative phosphorylation underlies the antiproliferative and proapoptotic effects of mofarotene (Ro 40-8757) in Burkitt's lymphoma cells. Author(s): Immunovirology and Biotherapy Unit, Italy. Source: Cariati, R Zancai, P Righetti, E Rizzo, S De Rossi, A Boiocchi, M Dolcetti, R Oncogene. 2003 February 13; 22(6): 906-18 0950-9232
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Intravascular lymphoma involving the central and peripheral nervous systems in a dog. Author(s): Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, 3900 Delancey Street, Philadelphia, Pennsylvania 19104, USA. Source: Bush, W W Throop, J L McManus, P M Kapatkin, A S Vite, C H Van Winkle, T J J-Am-Anim-Hosp-Assoc. 2003 Jan-February; 39(1): 90-6 0587-2871
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Irinotecan in relapsed or refractory non-Hodgkin's lymphomas. Indications of activity in a phase II trial. Author(s): Department of Lymphoma and Myeloma, The University of Texas M. D. Anderson Cancer Center, Houston, USA.
[email protected] Source: Sarris, A H Phan, A Goy, A Romaguera, J Hagemeister, F B Rodriguez, M A McLaughlin, P Pro, B Medeiros, L J Samuels, B Mesina, O Bleyer, A W Cabanillas, F Oncology-(Huntingt). 2002 Aug; 16(8 Suppl 7): 27-31 0890-9091
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Iron-oxide-enhanced MR imaging of bone marrow in patients with non-Hodgkin's lymphoma: differentiation between tumor infiltration and hypercellular bone marrow. Author(s): Department of Radiology, Technical University of Munich, Ismaninger Strasse 22, 81675 Munich, Germany.
[email protected] Source: Daldrup Link, Heike E Rummeny, Ernst J Ihssen, Bettina Kienast, Joachim Link, Thomas M Eur-Radiol. 2002 June; 12(6): 1557-66 0938-7994
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Leptomeningeal involvement in a patient with splenic lymphoma with villous lymphocytes. Author(s): Division of Hematology/Oncology, The Brooklyn Hospital Center, New York 11201, USA.
[email protected] Source: Gotlib, V Singareddy, S Gergis, U Vakios, J Guevara, E Chadburn, A Yavorkovsky, L L Patel, A Butt, A Nayak, A Leuk-Lymphoma. 2002 June; 43(6): 1337-40 1042-8194
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Lymphoma or pseudolymphoma? Source: Kruspe, R Broussard, A Santanilla, J Gupta, S Espinoza, C Lopez, F A Kantrow, S J-La-State-Med-Soc. 2002 Jul-August; 154(4): 178-81; quiz 181-2 0024-6921
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Malignant lymphoma of the heart. Featured echocardiogram and case report. Author(s): University of Arizona, Sarver Heart Center, Tucson, USA. Source: Memon, A Q Xavier, L Cardiol-Revolume 2002 Nov-December; 10(6): 323-5 1061-5377
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Mobilizing potential of ifosfamide/vinorelbine-based chemotherapy in pretreated malignant lymphoma. Author(s): Department of Medical Oncology and Hematology, Istituto Clinico Humanitas, Rozzano, Milan, Italy. Source: Magagnoli, M Sarina, B Balzarotti, M Castagna, L Timofeeva, I Nozza, A Bertuzzi, A Siracusano, L Sinnone, M Santoro, A Bone-Marrow-Transplant. 2001 November; 28(10): 923-7 0268-3369
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Outcome of B-cell non-Hodgkin lymphoma protocol CCCG-B NHL97: a report from Chinese multi-center cooperative group. Author(s): Department of Hematology/Oncology, Shanghai Children's Medical Center, Shanghai Second Medical University, Shanghai, China.
[email protected] Source: Tang, J Y Pan, C Chen, J Chen, H Wu, Y Xue, H Zhao, H Gu, L J Fu, R Y Wang, Y P Med-Pediatr-Oncol. 2002 September; 39(3): 212-4 0098-1532
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Phase I evaluation of prolonged-infusion gemcitabine with irinotecan for relapsed or refractory leukemia or lymphoma. Author(s): Division of Medical Oncology and Transplantation, Duke University Medical Center, and the Duke Oncology Consortium, Durham, NC 27710, USA. Source: Bass, Adam J Gockerman, Jon P Hammett, Eve DeCastro, Carlos M Adams, David J Rosner, Gary L Payne, Nancy Davis, Patti Foster, Traci Moore, Joseph O Rizzieri, David A J-Clin-Oncol. 2002 July 1; 20(13): 2995-3000 0732-183X
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Phase II study of sequential topotecan and etoposide in patients with intermediate grade non-Hodgkin's lymphoma: a National Cancer Institute of Canada Clinical Trials Group study. Author(s): Department of Medical Oncology and Hematology, Princess Margaret Hospital, Toronto, Canada.
[email protected] Source: Crump, M Couban, S Meyer, R Rudinskas, L Zanke, B Gluck, S Maksymiuk, A Hoskins, P Matthews, S Eisenhauer, E Leuk-Lymphoma. 2002 August; 43(8): 1581-7 1042-8194
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Primary breast lymphoma successfully treated with combination therapy including local radiation therapy: a report of two cases. Author(s): Department of Radiology, Maebashi Red Cross Hospital, Japan. Source: Suzuki, Y Ito, J Hasegawa, M Katano, S Saito, J Ito, H Radiat-Med. 2002 JanFebruary; 20(1): 37-9 0288-2043
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Primary central nervous system lymphomas. Author(s): Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021-6700, USA.
[email protected] Source: DeAngelis, L M Curr-Treat-Options-Oncol. 2001 August; 2(4): 309-18 1527-2729
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Primary cutaneous CD30 (Ki-1)-positive non-anaplastic B-cell lymphoma. Author(s): Department of Dermatology, University Hospital, School of Medicine, Malaga, Spain.
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Source: Herrera, E Gallardo, M Bosch, R Cabra, B Aneri, V Sanchez, P J-Cutan-Pathol. 2002 March; 29(3): 181-4 0303-6987 •
Primary cutaneous lymphoblastic lymphoma presenting in an 8-week old infant. Author(s): Department of Pathology, Cleveland Clinic Foundation, OH 44195, USA. Source: Trupiano, J K Bringelsen, K Hsi, E D J-Cutan-Pathol. 2002 February; 29(2): 107-12 0303-6987
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Primary hepatic lymphoma in a patient with Sjogren's syndrome. Author(s): Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. Source: Tsuruta, S Enjoji, M Nakamuta, M Makihata, T Kotoh, K Sakai, H Ando, B E Nawata, H J-Gastroenterol. 2002; 37(2): 129-32 0944-1174
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Primary lymphoma of the bladder: a report of three cases. Author(s): Department of Urology, Beaumont Hospital, Dublin, Ireland.
[email protected] Source: Power, R E Kay, E W O'Connell, F Jaber, A A Donovan, M G Hickey, D P Creagh, T A Ir-J-Med-Sci. 2001 Jul-September; 170(3): 196-7 0021-1265
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Primary malignant lymphoma of the prostate--a report of three cases. Author(s): Department of Oncology, Soroka University Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
[email protected] Source: Mermershtain, W Benharroch, D Lavrenkov, K Geffen, D B German, I Cohen, Y Leuk-Lymphoma. 2001 August; 42(4): 809-11 1042-8194
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Primary non-Hodgkin lymphoma of the right colon: a retrospective clinicalpathological study. Author(s): Department of Digestive Surgery, Hospital do Servidor Publico Estadual, Sao Paulo, Brazil. jaqueswaisberguol.com.br Source: Waisberg, J Bromberg, S H Franco, M I Matheus, C O Zanotto, A Petrolino, L F Beltrami, A M Godoy, A C Int-Surg. 2001 Jan-March; 86(1): 20-5 0020-8868
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Progressive external ophthalmoplegia: a paraneoplastic manifestation of lymphoma. Author(s):
[email protected] Source: Ascaso, F J Torres, M Bergua, J M Alvarez, R Cristobal, J A Eur-J-Ophthalmol. 2002 Jul-August; 12(4): 315-8 1120-6721
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Prolonged single-agent versus combination chemotherapy in indolent follicular lymphomas: a study of the cancer and leukemia group B. Author(s): University of Minnesota Medical School, Division of Hematology, Oncology and Transplantation, Minneapolis, MN 55455, USA.
[email protected] Source: Peterson, B A Petroni, G R Frizzera, G Barcos, M Bloomfield, C D Nissen, N I Hurd, D D Henderson, E S Sartiano, G P Johnson, J L Holland, J F Gottlieb, A J J-ClinOncol. 2003 January 1; 21(1): 5-15 0732-183X
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Randomized phase III study of fludarabine phosphate versus cyclophosphamide, vincristine, and prednisone in patients with recurrent low-grade non-Hodgkin's lymphoma previously treated with an alkylating agent or alkylator-containing regimen. Author(s): Division of Medical Oncology, British Columbia Cancer Agency, Vancouver, Canada.
[email protected] Source: Klasa, R J Meyer, R M Shustik, C Sawka, C A Smith, A Guevin, R Maksymiuk, A Rubinger, M Samosh, M Laplante, S Grenier, J F J-Clin-Oncol. 2002 December 15; 20(24): 4649-54 0732-183X
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Randomized study to evaluate the use of high-dose therapy as part of primary treatment for “aggressive” lymphoma. Author(s): Department of Hematology, Universitatsklinikum Marburg, Germany.
[email protected] Source: Kaiser, U Uebelacker, I Abel, U Birkmann, J Trumper, L Schmalenberg, H Karakas, T Metzner, B Hossfeld, D K Bischoff, H G Franke, A Reiser, M Muller, P Mantovani, L Grundeis, M Rothmann, F von Seydewitz, C U Mesters, R M Steinhauer, E U Krahl, D Schumacher, K Kneba, M Baudis, M Schmitz, N Pfab, R Koppler, H Parwaresch, R Pfreundschuh, M Havemann, K J-Clin-Oncol. 2002 November 15; 20(22): 4413-9 0732-183X
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Real-time polymerase chain reaction estimation of bone marrow tumor burden using clonal immunoglobulin heavy chain gene and bcl-1/JH rearrangements in mantle cell lymphoma. Author(s): Department of Hematology, Rigshospitalet, Copenhagen, Denmark.
[email protected] Source: Andersen, Niels S Donovan, John W Zuckerman, Amy Pedersen, Lone Geisler, Christian Gribben, John G Exp-Hematol. 2002 July; 30(7): 703-10 0301-472X
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Regression of HTLV1 associated intracardiac lymphoma following chemotherapy. Source: Hamaad, A Davis, R C Connolly, D L Heart. 2002 December; 88(6): 621 1468201X
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Role of glutathione depletion and reactive oxygen species generation in apoptotic signaling in a human B lymphoma cell line. Author(s): Department of Radiation Oncology, Stanford University, Stanford, California, CA 94305-5105, USA. Source: Armstrong, J S Steinauer, K K Hornung, B Irish, J M Lecane, P Birrell, G W Peehl, D M Knox, S J Cell-Death-Differ. 2002 March; 9(3): 252-63 1350-9047
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Secondary pancreatic involvement by diffuse large B-cell lymphoma presenting as acute pancreatitis: treatment and outcome. Author(s): Department of Gastroenterology and Hepatology, Henry Mondor University Hospital, Creteil, France. Source: Bernardeau, M Auroux, J Cavicchi, M Haioun, C Tsakiris, L Delchier, J C Pancreatology. 2002; 2(4): 427-30 1424-3903
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Seventy-two hour continuous infusion flavopiridol in relapsed and refractory mantle cell lymphoma. Author(s): Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA. Source: Lin, T S Howard, O M Neuberg, D S Kim, H H Shipp, M A Leuk-Lymphoma. 2002 April; 43(4): 793-7 1042-8194
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Stage IV CD30+ anaplastic large cell lymphoma: response to acitretin and interferonalpha. Author(s): Department of Dermatology, Westmead Hospital, Westmead, New South Wales, Australia.
[email protected] Source: Ong, C Sullivan, J Hertzberg, M Stapleton, K Australas-J-Dermatol. 2002 August; 43(3): 207-10 0004-8380
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Successful autologous peripheral blood stem cell transplantation in transformed follicular lymphoma previously treated with radioimmunotherapy (iodine (131)I tositumomab). Author(s): University of Loyola Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA.
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Source: Cooney, J Stiff, P Kaminski, M Bone-Marrow-Transplant. 2002 Mar; 29(6): 523-5 0268-3369 •
Th1/Th2 cytokine expression and its relationship with tumor growth in B cell nonHodgkin's lymphoma (NHL). Author(s): Institute for Cancer Studies, University of Sheffield Medical School, UK.
[email protected] Source: Jones, E A Pringle, J H Angel, C A Rees, R C Leuk-Lymphoma. 2002 June; 43(6): 1313-21 1042-8194
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The incidence of thyroid abnormalities in adults irradiated for lymphoma. Author(s): The University of Sheffield, Medical School, Sheffield, UK. Source: Ding, S H Pledge, S D Harrison, B J Peck, R J Bull, M J Holland, P Weetman, A Hancock, B W Int-J-Oncol. 2002 May; 20(5): 1065-9 1019-6439
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The response of L5178Y lymphoma sublines to oxidative stress: antioxidant defence, iron content and nuclear translocation of the p65 subunit of NF-kappaB. Author(s): Department of Radiobiology and Health Protection, Institute of Nuclear Chemistry and Technology, Warszawa, Poland. Source: Bouzyk, E Gradzka, I Iwanenko, T Kruszewski, M Sochanowicz, B Szumiel, I Acta-Biochim-Pol. 2000; 47(4): 881-8 0001-527X
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The role of mitoxantrone in non-Hodgkin's lymphoma. Author(s): College of Medicine, University of Nebraska Medical Center, Omaha 681986545, USA. Source: Armitage, J O Oncology-(Huntingt). 2002 April; 16(4): 490-502, 507-8; discussion 511-2, 514 0890-9091
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The role of molecular monitoring in autotransplantation for non-Hodgkin's lymphoma. Author(s): Department of Oncology, Transplant and Advances in Medicine - Section of Hematology, University of Pisa, Italy. Source: Galimberti, S Marasca, R Caracciolo, F Fazzi, R Papineschi, F Benedetti, E Guerrini, F Morabito, F Oliva, E Di Renzo, N Federico, M Petrini, M Torelli, G BoneMarrow-Transplant. 2002 April; 29(7): 581-7 0268-3369
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Treatment of canine lymphoma by veterinarians in first opinion practice in England. Author(s): Queen's Veterinary School Hospital, University of Cambridge. Source: Mellanby, R J Herrtage, M E Dobson, J M J-Small-Anim-Pract. 2002 May; 43(5): 198-202 0022-4510
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Two cases of therapy-related acute promyelocytic leukemia (t-APL) after mantle cell lymphoma and gestational trophoblastic disease. Author(s): University Department of Medicine, Professorial Block, Queen Mary Hospital, Pokfulam Road, Hong Kong.
[email protected] Source: Au, W Y Ma, S K Chung, L P Chim, C S Kwong, Y L Ann-Hematol. 2002 November; 81(11): 659-61 0939-5555
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Unusual sites of involvement in non-Hodgkin's lymphoma: Case 2. Isolated meningeal anaplastic large-cell lymphoma. Author(s): Institut Gustave-Roussy, Villejuif, France. Source: Aloulou, S Bosq, J Vanel, D Ribrag, V J-Clin-Oncol. 2002 November 1; 20(21): 4395-7 0732-183X
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Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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The following is a specific Web list relating to lymphoma; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
Vitamins Folic Acid Source: Integrative Medicine Communications; www.drkoop.com Vitamin B9 (Folic Acid) Alternative names: Folate, Folic Acid Source: Integrative Medicine Communications; www.drkoop.com
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Minerals Folate Source: Integrative Medicine Communications; www.drkoop.com Vanadium Source: Healthnotes, Inc.; www.healthnotes.com
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Food and Diet High-fiber Diet Source: Healthnotes, Inc.; www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND LYMPHOMA Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to lymphoma. At the conclusion of this chapter, we will provide additional sources.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to lymphoma and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “lymphoma” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to lymphoma: •
14-day variant of the bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone regimen in advanced-stage Hodgkin's lymphoma: results of a pilot study of the German Hodgkin's Lymphoma Study Group. Author(s): Sieber M, Bredenfeld H, Josting A, Reineke T, Rueffer U, Koch T, Naumann R, Boissevain F, Koch P, Worst P, Soekler M, Eich H, Muller-Hermelink HK, Franklin J, Paulus U, Wolf J, Engert A, Diehl V; German Hodgkin's Lymphoma Study Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 May 1; 21(9): 1734-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12721249&dopt=Abstract
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18FDG positron emission tomography versus 67Ga scintigraphy as prognostic test during chemotherapy for non-Hodgkin's lymphoma. Author(s): Zijlstra JM, Hoekstra OS, Raijmakers PG, Comans EF, van der Hoeven JJ, Teule GJ, Jonkhoff AR, v Tinteren H, Lammertsma AA, Huijgens PC.
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Source: British Journal of Haematology. 2003 November; 123(3): 454-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14617005&dopt=Abstract •
18F-FDG PET evaluation of the response to therapy for lymphoma and for breast, lung, and colorectal carcinoma. Author(s): Kostakoglu L, Goldsmith SJ. Source: Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine. 2003 February; 44(2): 224-39. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571214&dopt=Abstract
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18F-fluoro-deoxy-glucose positron emission tomography (18F-FDG-PET) for assessment of enteropathy-type T cell lymphoma. Author(s): Hoffmann M, Vogelsang H, Kletter K, Zettinig G, Chott A, Raderer M. Source: Gut. 2003 March; 52(3): 347-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12584214&dopt=Abstract
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2-deoxy-2-[F-18]fluoro-D-glucose imaging with positron emission tomography for initial staging of Hodgkin's disease and lymphoma. Author(s): Delbeke D, Martin WH, Morgan DS, Kinney MC, Feurer I, Kovalsky E, Arrowsmith T, Greer JP. Source: Molecular Imaging and Biology : Mib : the Official Publication of the Academy of Molecular Imaging. 2002 January; 4(1): 105-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14538054&dopt=Abstract
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A case of extra-nodal lymphoma presenting as post-menopausal bleeding. Author(s): Macnab JL, Beattie GJ, Court SJ, Davie RM, Cook MK. Source: Journal of Obstetrics and Gynaecology : the Journal of the Institute of Obstetrics and Gynaecology. 2003 May; 23(3): 321-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12918486&dopt=Abstract
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A case of treatment-related myelodysplastic syndrome and acute myelogenous leukemia following high-dose chemotherapy with autologous stem cell transplantation for non-Hodgkin's lymphoma. Author(s): Jang GD, Kim SW, Suh CW, Kim EK, Bahng HS, Jeong YH, Park IG, Kim WK, Kim SH, Suh EJ, Park CJ, Ji HS, Lee JS. Source: Journal of Korean Medical Science. 2002 August; 17(4): 555-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12172056&dopt=Abstract
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A dexamethasone, vinblastine, cyclophosphamide, etoposide, methotrexate and bleomycin (D-VICEMB) protocol as first-line treatment of patients aged 70 years or older affected by intermediate/high grade non-Hodgkin's lymphoma. Author(s): Angrilli F, Pennese E, Di Marzio A, Liberatore E, Di Lorenzo R, Fioritoni G.
Alternative Medicine 145
Source: Haematologica. 2002 November; 87(11): 1227-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12414356&dopt=Abstract •
A dose-finding study of glycosylated G-CSF (Lenograstim) combined with CHOP therapy for stem cell mobilization in patients with non-Hodgkin's lymphoma. Author(s): Takeyama K, Ogura M, Morishima Y, Kasai M, Kiyama Y, Ohnishi K, Mitsuya H, Kawano F, Masaki Y, Sasaki T, Chou T, Yokozawa T, Tobinai K; Lenograstim/Lymphoma Study Group. Source: Japanese Journal of Clinical Oncology. 2003 February; 33(2): 78-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629058&dopt=Abstract
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A new approach to the diagnosis and treatment of intravascular lymphoma. Author(s): Baehring JM, Longtine J, Hochberg FH. Source: Journal of Neuro-Oncology. 2003 February; 61(3): 237-48. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12675317&dopt=Abstract
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A novel trypsin inhibitor from Peltophorum dubium seeds, with lectin-like properties, triggers rat lymphoma cell apoptosis. Author(s): Fernanda Troncoso M, Cerda Zolezzi P, Hellman U, Wolfenstein-Todel C. Source: Archives of Biochemistry and Biophysics. 2003 March 1; 411(1): 93-104. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12590927&dopt=Abstract
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A phase 2 trial of CHOP chemotherapy followed by tositumomab/iodine I 131 tositumomab for previously untreated follicular non-Hodgkin lymphoma: Southwest Oncology Group Protocol S9911. Author(s): Press OW, Unger JM, Braziel RM, Maloney DG, Miller TP, LeBlanc M, Gaynor ER, Rivkin SE, Fisher RI. Source: Blood. 2003 September 1; 102(5): 1606-12. Epub 2003 May 08. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12738671&dopt=Abstract
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A phase I-II study of rituximab, ifosfamide, mitoxantrone and etoposide (R-IME) for B cell non-Hodgkin's lymphoma prior to and after high-dose chemotherapy and autologous stem cell transplantation (HDC-ASCT). Author(s): Joyce RM, Regan M, Ottaway J, Umiel T, Tetreault JC, Levine J, McDermott D, Hurley D, Giallombardo N, Smith T, Lamontagne D, Uhl L, Avigan D. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003; 14 Suppl 1: I21-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736227&dopt=Abstract
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A preliminary study of the effect of external qigong on lymphoma growth in mice. Author(s): Chen KW, Shiflett SC, Ponzio NM, He B, Elliott DK, Keller SE.
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Source: Journal of Alternative and Complementary Medicine (New York, N.Y.). 2002 October; 8(5): 615-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12470443&dopt=Abstract •
A prospective study of P-IMVP-16/CBDCA: a novel salvage chemotherapy for patients with aggressive non-Hodgkin's lymphoma who had previously received CHOP therapy as first-line chemotherapy. Author(s): Sawada M, Tsurumi H, Yamada T, Hara T, Fukuno K, Goto H, Shimizu M, Kasahara S, Yoshikawa T, Kanemura N, Oyama M, Takami T, Moriwaki H. Source: European Journal of Haematology. 2002 June; 68(6): 354-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12225393&dopt=Abstract
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A randomised multicentre trial of modified CHOP versus MCOP in patients aged 65 years and over with aggressive non-Hodgkin's lymphoma. Author(s): Bessell EM, Burton A, Haynes AP, Glaholm J, Child JA, Cullen MH, Davies JM, Smith GM, Ellis IO, Jack A, Jones EL; Central Lymphoma Group UK. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 February; 14(2): 258-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562653&dopt=Abstract
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A relapsed non-Hodgkin lymphoma presenting as panhypopituitarism successfully treated by chemotherapy. Author(s): Buchler T, Ferra C, Virgili N, Montanya E, Granena A. Source: Journal of Neuro-Oncology. 2002 August; 59(1): 35-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12222836&dopt=Abstract
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A significant diffuse component predicts for inferior survival in grade 3 follicular lymphoma, but cytologic subtypes do not predict survival. Author(s): Hans CP, Weisenburger DD, Vose JM, Hock LM, Lynch JC, Aoun P, Greiner TC, Chan WC, Bociek RG, Bierman PJ, Armitage JO. Source: Blood. 2003 March 15; 101(6): 2363-7. Epub 2002 November 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12424193&dopt=Abstract
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Abdominal irradiation after chemotherapy in non-Hodgkin's lymphoma: review of 32 patients. Author(s): Brihi E, Akoum R, Saade M, Chahine G. Source: Molecular Immunology. 2003 July; 39(17-18): 1121-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835089&dopt=Abstract
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Accuracy of whole-body 18F-FDP-PET for restaging malignant lymphoma. Author(s): Mikosch P, Gallowitsch HJ, Zinke-Cerwenka W, Heinisch M, Pipam W, Eibl M, Kresnik E, Unterweger O, Linkesch W, Lind P.
Alternative Medicine 147
Source: Acta Medica Austriaca. 2003; 30(2): 41-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752087&dopt=Abstract •
ACOD, a modified CHOP regimen for elderly patients with aggressive nonHodgkin's lymphoma. Author(s): Santoro P, Martinelli G, Ferrucci PF, Mingrone W, Cocorocchio E, Conconi A, Peccatori FA, De Luzio K, Mazzetta C, Zucca E, Cavalli F. Source: Leukemia & Lymphoma. 2003 May; 44(5): 801-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802917&dopt=Abstract
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Adoptive transfer of costimulated T cells induces lymphocytosis in patients with relapsed/refractory non-Hodgkin lymphoma following CD34+-selected hematopoietic cell transplantation. Author(s): Laport GG, Levine BL, Stadtmauer EA, Schuster SJ, Luger SM, Grupp S, Bunin N, Strobl FJ, Cotte J, Zheng Z, Gregson B, Rivers P, Vonderheide RH, Liebowitz DN, Porter DL, June CH. Source: Blood. 2003 September 15; 102(6): 2004-13. Epub 2003 May 22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763934&dopt=Abstract
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Age-adjusted International Prognostic Index predicts autologous stem cell transplantation outcome for patients with relapsed or primary refractory diffuse large B-cell lymphoma. Author(s): Hamlin PA, Zelenetz AD, Kewalramani T, Qin J, Satagopan JM, Verbel D, Noy A, Portlock CS, Straus DJ, Yahalom J, Nimer SD, Moskowitz CH. Source: Blood. 2003 September 15; 102(6): 1989-96. Epub 2003 April 03. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12676776&dopt=Abstract
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Aggressive lymphoma: improving treatment outcome with rituximab. Author(s): Coiffier B, Pfreundschuh M, Stahel R, Vose J, Zinzani PL. Source: Anti-Cancer Drugs. 2002 November; 13 Suppl 2: S43-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12710590&dopt=Abstract
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An extremely rare case of synchronous occurrence in the larynx of intravascular lymphoma and in situ squamous cell carcinoma. Author(s): Hadjileontis CG, Kostopoulos IS, Kaloutsi VD, Nikolaou AC, Kotoula VA, Papadimitriou CS. Source: Leukemia & Lymphoma. 2003 June; 44(6): 1053-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854909&dopt=Abstract
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An international evaluation of CODOX-M and CODOX-M alternating with IVAC in adult Burkitt's lymphoma: results of United Kingdom Lymphoma Group LY06 study. Author(s): Mead GM, Sydes MR, Walewski J, Grigg A, Hatton CS, Pescosta N, Guarnaccia C, Lewis MS, McKendrick J, Stenning SP, Wright D, Norbert P; UKLG LY06 collaborators.
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Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 August; 13(8): 1264-74. Erratum In: Ann Oncol. 2002 December; 13(12): 1961. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12181251&dopt=Abstract •
An unusual cause of new-onset atrial flutter: primary cardiac lymphoma. Author(s): Hayes D Jr, Liles DK, Sorrell VL. Source: Southern Medical Journal. 2003 August; 96(8): 799-802. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14515922&dopt=Abstract
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Anemia of cancer in intermediate-grade non-Hodgkin's lymphoma. Author(s): Morrow TJ, Volpe S, Gupta S, Tannous RE, Fridman M. Source: Southern Medical Journal. 2002 August; 95(8): 889-96. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12190227&dopt=Abstract
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Angiocentric T-cell lymphoma presenting as midface destructive lesion: case report and literature review. Author(s): Yih WY, Stewart JC, Kratochvil FJ, Zieper MB. Source: Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 2002 September; 94(3): 353-60. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12324793&dopt=Abstract
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Anorectal lymphoma without effusion associated with human herpesvirus-8 and type 1 Epstein-Barr virus in an HIV-infected patient. Author(s): Navarro JT, Ribera JM, Junca J, Milla F. Source: Human Pathology. 2003 June; 34(6): 630. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12827623&dopt=Abstract
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Anti-oxidant activity of Centella asiatica on lymphoma-bearing mice. Author(s): Jayashree G, Kurup Muraleedhara G, Sudarslal S, Jacob VB. Source: Fitoterapia. 2003 July; 74(5): 431-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837356&dopt=Abstract
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Antitumour activity of Bauhinia variegata on Dalton's ascitic lymphoma. Author(s): Rajkapoor B, Jayakar B, Murugesh N. Source: Journal of Ethnopharmacology. 2003 November; 89(1): 107-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14522440&dopt=Abstract
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Assessment of tumor burden and treatment response by 18F-fluorodeoxyglucose injection and positron emission tomography in patients with cutaneous T- and B-cell lymphomas. Author(s): Shapiro M, Yun M, Junkins-Hopkins JM, Vittorio CC, Schulman N, Saidman BH, Fried RG, Rook AH, Alavi A.
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Source: Journal of the American Academy of Dermatology. 2002 October; 47(4): 623-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12271315&dopt=Abstract •
Autologous stem cell transplant for relapsed and refractory peripheral T-cell lymphoma: variable outcome according to pathological subtype. Author(s): Song KW, Mollee P, Keating A, Crump M. Source: British Journal of Haematology. 2003 March; 120(6): 978-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12648067&dopt=Abstract
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Autologous stem-cell transplantation as a component of initial treatment for poor-risk patients with aggressive non-Hodgkin's lymphoma: resolved issues versus remaining opportunity. Author(s): Fisher RI. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 November 15; 20(22): 4411-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431961&dopt=Abstract
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BCL6 overexpression prevents increase in reactive oxygen species and inhibits apoptosis induced by chemotherapeutic reagents in B-cell lymphoma cells. Author(s): Kurosu T, Fukuda T, Miki T, Miura O. Source: Oncogene. 2003 July 17; 22(29): 4459-68. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12881702&dopt=Abstract
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Bendamustine in the treatment of non-Hodgkin's lymphoma: results and future perspectives. Author(s): Rummel MJ, Mitrou PS, Hoelzer D. Source: Seminars in Oncology. 2002 August; 29(4 Suppl 13): 27-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12170430&dopt=Abstract
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Bilateral, primary, low-grade, diffuse B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) of the breast. Author(s): Zobolas B, Sakorafas GH, Kourakli I, Tsiotou AG. Source: The Breast Journal. 2002 November-December; 8(6): 382. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390362&dopt=Abstract
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Calcification in splenic lymphoma before chemotherapy. Author(s): Dai MS, Chao TY, Yu CY. Source: Southern Medical Journal. 2003 August; 96(8): 836-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14515933&dopt=Abstract
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Camptothecin induces urokinase-type plasminogen activator gene-expression in human RC-K8 malignant lymphoma and H69 small cell lung cancer cells. Author(s): Shibakura M, Niiya K, Kiguchi T, Nakata Y, Tanimoto M.
150 Lymphoma
Source: Acta Medica Okayama. 2002 October; 56(5): 223-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12530505&dopt=Abstract •
Caspase 3-mediated inactivation of rac GTPases promotes drug-induced apoptosis in human lymphoma cells. Author(s): Zhang B, Zhang Y, Shacter E. Source: Molecular and Cellular Biology. 2003 August; 23(16): 5716-25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12897143&dopt=Abstract
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CD5+ T-cell/histiocyte-rich large B-cell lymphoma. Author(s): Chang CC, Bunyi-Teopengco E, Eshoa C, Chitambar CR, Kampalath B. Source: Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc. 2002 October; 15(10): 1051-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12379751&dopt=Abstract
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Challenges in the management of Burkitt's lymphoma. Author(s): Levine AM. Source: Clin Lymphoma. 2002 December; 3 Suppl 1: S19-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12521385&dopt=Abstract
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Chemoresistant or aggressive lymphoma predicts for a poor outcome following reduced-intensity allogeneic progenitor cell transplantation: an analysis from the Lymphoma Working Party of the European Group for Blood and Bone Marrow Transplantation. Author(s): Robinson SP, Goldstone AH, Mackinnon S, Carella A, Russell N, de Elvira CR, Taghipour G, Schmitz N; Lymphoma Working Party of the European Group for Blood and Bone Marrow Transplantation. Source: Blood. 2002 December 15; 100(13): 4310-6. Epub 2002 August 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393626&dopt=Abstract
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Chemotherapy for management of localised high-grade gastric B-cell lymphoma: how much is necessary? Author(s): Raderer M, Chott A, Drach J, Montalban C, Dragosics B, Jager U, Puspok A, Osterreicher C, Zielinski CC. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 July; 13(7): 1094-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12176789&dopt=Abstract
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Chimeric anti-CD20 monoclonal antibody (Mabthera) in remission induction and maintenance treatment of relapsed follicular non-Hodgkin's lymphoma: a phase III randomized clinical trial--Intergroup Collaborative Study. Author(s): Van Oers MH, Hagenbeek A, Van Glabbeke M, Teodorovic I.
Alternative Medicine 151
Source: Annals of Hematology. 2002 October; 81(10): 553-7. Epub 2002 October 17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12424535&dopt=Abstract •
CHOP compared with CHOP plus granulocyte colony-stimulating factor in elderly patients with aggressive non-Hodgkin's lymphoma. Author(s): Doorduijn JK, van der Holt B, van Imhoff GW, van der Hem KG, Kramer MH, van Oers MH, Ossenkoppele GJ, Schaafsma MR, Verdonck LF, Verhoef GE, Steijaert MM, Buijt I, Uyl-de Groot CA, van Agthoven M, Mulder AH, Sonneveld P. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 August 15; 21(16): 3041-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915593&dopt=Abstract
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CHOP is superior to CNOP in elderly patients with aggressive lymphoma while outcome is unaffected by filgrastim treatment: results of a Nordic Lymphoma Group randomized trial. Author(s): Osby E, Hagberg H, Kvaloy S, Teerenhovi L, Anderson H, Cavallin-Stahl E, Holte H, Myhre J, Pertovaara H, Bjorkholm M; Nordic Lymphoma Group. Source: Blood. 2003 May 15; 101(10): 3840-8. Epub 2003 January 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12531794&dopt=Abstract
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CHOP with high dose cyclophosphamide consolidation versus CHOP alone as initial therapy for advanced stage, indolent non-Hodgkin's lymphomas. Author(s): Pan D, Qin J, Farber C, O'Brien J, Filippa D, Portlock CS. Source: Leukemia & Lymphoma. 2003 June; 44(6): 967-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854895&dopt=Abstract
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Clinical features and outcome of primary effusion lymphoma in HIV-infected patients: a single-institution study. Author(s): Simonelli C, Spina M, Cinelli R, Talamini R, Tedeschi R, Gloghini A, Vaccher E, Carbone A, Tirelli U. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 November 1; 21(21): 3948-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14581418&dopt=Abstract
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Clinical impact of whole body FDG-PET on the staging and therapeutic decision making for malignant lymphoma. Author(s): Sasaki M, Kuwabara Y, Koga H, Nakagawa M, Chen T, Kaneko K, Hayashi K, Nakamura K, Masuda K. Source: Ann Nucl Med. 2002 July; 16(5): 337-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12230093&dopt=Abstract
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Clinical profiles of human immunodeficiency virus-associated lymphoma in Hong Kong. Author(s): Mak YK, Chan CH, Li CK, Lee MP, Tsang YW.
152 Lymphoma
Source: Hong Kong Medical Journal = Xianggang Yi Xue Za Zhi / Hong Kong Academy of Medicine. 2003 April; 9(2): 91-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12668818&dopt=Abstract •
Clinical significance of positron emission tomography for lymphoma patients. Author(s): Chen Q, Wu HB, Gao L, Zou YT. Source: Di Yi June Yi Da Xue Xue Bao. 2003 January; 23(1): 71-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527523&dopt=Abstract
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Combination chemotherapy and radiotherapy for primary central nervous system lymphoma: Radiation Therapy Oncology Group Study 93-10. Author(s): DeAngelis LM, Seiferheld W, Schold SC, Fisher B, Schultz CJ; Radiation Therapy Oncology Group Study 93-10. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 December 15; 20(24): 4643-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488408&dopt=Abstract
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Combination of ifosfamide, methotrexate, and etoposide (IMVP) as a salvage therapy for relapsed and refractory aggressive non-Hodgkin lymphoma: retrospective study. Author(s): Aurer I, Durakovic N, Radman I, Nemet D, Zupancic-Salek S, KovacevicMetelko J, Bogdanic V, Sertic D, Mrsic M, Mikulic M, Labar B. Source: Croatian Medical Journal. 2002 October; 43(5): 550-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12402394&dopt=Abstract
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Combined therapy in the treatment of primary mediastinal B-cell lymphoma: conventional versus escalated chemotherapy. Author(s): Aviles A, Garcia EL, Fernandez R, Gonzalez JL, Neri N, Diaz-Maqueo JC. Source: Annals of Hematology. 2002 July; 81(7): 368-73. Epub 2002 June 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12185505&dopt=Abstract
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Combined treatment with anti-CD20 (rituximab) and CHOP in relapsed advancedstage follicular lymphomas. Author(s): Domingo-Domenech E, Gonzalez-Barca E, Estany C, Sureda A, Besalduch J, Fernandez de Sevilla A. Source: Haematologica. 2002 November; 87(11): 1229-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12414357&dopt=Abstract
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Comparative study of low-dose oral granisetron plus dexamethasone and high-dose metoclopramide plus dexamethasone in prevention of nausea and vomiting induced by CHOP-therapy in young patients with non-Hodgkin's lymphoma. Author(s): Numbenjapon T, Sriswasdi C, Mongkonsritragoon W, Leelasiri A, Prayoonwiwat W.
Alternative Medicine 153
Source: J Med Assoc Thai. 2002 November; 85(11): 1156-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12546311&dopt=Abstract •
Complete remission in advanced blastic NK-cell lymphoma/leukemia in elderly patients using the hyper-CVAD regimen. Author(s): Shapiro M, Wasik MA, Junkins-Hopkins JM, Rook AH, Vittorio CC, Itakura H, Frankel MC, Georgala S, Schuster SJ. Source: American Journal of Hematology. 2003 September; 74(1): 46-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12949889&dopt=Abstract
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Concurrent mediastinal B cell lymphoma and chronic myeloid leukemia with an unusually favorable response to chemotherapy. Author(s): Au WY, Ma SK, Wan TS, Wang EP, Lau TC, Kwong YL. Source: Leukemia & Lymphoma. 2003 March; 44(3): 535-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688328&dopt=Abstract
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Cost analysis of CHOP (-like) chemotherapy regimens for patients with newly diagnosed aggressive non-Hodgkin's lymphoma. Author(s): van Agthoven M, Faber LM, Uyl-de Groot CA, Sonneveld P, Verdonck LF, Willemze R, Kluin-Nelemans JC, Lowenberg B, Huijgens PC. Source: European Journal of Haematology. 2002 October; 69(4): 213-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431240&dopt=Abstract
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Cyclophosphamide, etoposide and G-CSF to mobilize peripheral blood stem cells for autologous stem cell transplantation in patients with lymphoma. Author(s): Mollee P, Pereira D, Nagy T, Song K, Saragosa R, Keating A, Crump M. Source: Bone Marrow Transplantation. 2002 September; 30(5): 273-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12209348&dopt=Abstract
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Cytometric evaluation of peripheral blood lymphocytes in dogs with lymphoma during chemotherapy. Author(s): Winnicka A, Jagielski D, Hoffmann-Jagielska M, Lechowski R. Source: Journal of Veterinary Medicine. A, Physiology, Pathology, Clinical Medicine. 2002 August; 49(6): 303-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12227473&dopt=Abstract
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Cytotoxic gamma/delta subcutaneous panniculitis-like T-cell lymphoma: report of a case with pulmonary involvement unresponsive to therapy. Author(s): Guizzardi M, Hendrickx IA, Mancini LL, Monti M. Source: Journal of the European Academy of Dermatology and Venereology : Jeadv. 2003 March; 17(2): 219-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12705758&dopt=Abstract
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Cytotoxicity of inorganic mercury in murine T and B lymphoma cell lines: involvement of reactive oxygen species, Ca(2+) homeostasis, and cytokine gene expression. Author(s): Kim SH, Sharma RP. Source: Toxicology in Vitro : an International Journal Published in Association with Bibra. 2003 August; 17(4): 385-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12849721&dopt=Abstract
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Delayed expression of apoptosis in human lymphoma cells undergoing low-dose taxol-induced mitotic stress. Author(s): Allman R, Errington RJ, Smith PJ. Source: British Journal of Cancer. 2003 May 19; 88(10): 1649-58. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12771935&dopt=Abstract
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Deoxycoformycin-containing combination chemotherapy for adult T-cell leukemialymphoma: Japan Clinical Oncology Group Study (JCOG9109). Author(s): Tsukasaki K, Tobinai K, Shimoyama M, Kozuru M, Uike N, Yamada Y, Tomonaga M, Araki K, Kasai M, Takatsuki K, Tara M, Mikuni C, Hotta T; Lymphoma Study Group of the Japan Clinical Oncology Group. Source: International Journal of Hematology. 2003 February; 77(2): 164-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12627852&dopt=Abstract
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Dietary ginger constituents, galanals A and B, are potent apoptosis inducers in Human T lymphoma Jurkat cells. Author(s): Miyoshi N, Nakamura Y, Ueda Y, Abe M, Ozawa Y, Uchida K, Osawa T. Source: Cancer Letters. 2003 September 25; 199(2): 113-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12969783&dopt=Abstract
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Diffuse large B-cell lymphoma with fibrillary matrix. Author(s): Dargent JL, Meiers I, Lespagnard L, Ma Y, Dehou MF, Verhest A. Source: Diagnostic Cytopathology. 2002 October; 27(4): 223-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12357500&dopt=Abstract
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Dose-intense chemotherapy every 2 weeks with dose-intense cyclophosphamide, doxorubicin, vincristine, and prednisone may improve survival in intermediate- and high-grade lymphoma: a phase II study of the Southwest Oncology Group (SWOG 9349). Author(s): Blayney DW, LeBlanc ML, Grogan T, Gaynor ER, Chapman RA, Spiridonidis CH, Taylor SA, Bearman SI, Miller TP, Fisher RI; Southwest Oncology Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 1; 21(13): 2466-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829664&dopt=Abstract
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Dose-intensified CHOP (double-CHOP) followed by consolidation with high-dose chemotherapy for high and high-intermediate risk aggressive non-Hodgkin's lymphomas. Author(s): Yamazaki T, Sawada U, Kura Y, Ito T, Kaneita Y, Yasukawa K, Horie T. Source: Leukemia & Lymphoma. 2002 November; 43(11): 2117-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12533036&dopt=Abstract
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Early autologous stem-cell transplantation versus conventional chemotherapy as front-line therapy in high-risk, aggressive non-Hodgkin's lymphoma: an Italian multicenter randomized trial. Author(s): Martelli M, Gherlinzoni F, De Renzo A, Zinzani PL, De Vivo A, Cantonetti M, Falini B, Storti S, Meloni G, Rizzo M, Molinari AL, Lauria F, Moretti L, Lauta VM, Mazza P, Guardigni L, Pescarmona E, Pileri SA, Mandelli F, Tura S. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 April 1; 21(7): 1255-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663712&dopt=Abstract
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Early cardiotoxicity of the CHOP regimen in aggressive non-Hodgkin's lymphoma. Author(s): Limat S, Demesmay K, Voillat L, Bernard Y, Deconinck E, Brion A, Sabbah A, Woronoff-Lemsi MC, Cahn JY. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 February; 14(2): 277-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12562656&dopt=Abstract
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Early restaging positron emission tomography with ( 18)F-fluorodeoxyglucose predicts outcome in patients with aggressive non-Hodgkin's lymphoma. Author(s): Spaepen K, Stroobants S, Dupont P, Vandenberghe P, Thomas J, de Groot T, Balzarini J, De Wolf-Peeters C, Mortelmans L, Verhoef G. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 September; 13(9): 1356-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12196360&dopt=Abstract
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Early restaging positron emission tomography with 18F-fluorodeoxyglucose in aggressive non-Hodgkin's lymphomas: is it too easy to be true? Author(s): Balzarotti M, Magagnoli M, Santoro A. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 July; 14(7): 1155-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12853364&dopt=Abstract
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Early therapy monitoring with FDG-PET in aggressive non-Hodgkin's lymphoma and Hodgkin's lymphoma. Author(s): Torizuka T, Nakamura F, Kanno T, Futatsubashi M, Yoshikawa E, Okada H, Kobayashi M, Ouchi Y.
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Source: European Journal of Nuclear Medicine and Molecular Imaging. 2003 October 22 [epub Ahead of Print] http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14574514&dopt=Abstract •
Effect of Indigofera aspalathoides against Dalton's ascitic lymphoma. Author(s): Christina AJ, Alwin Jose M, Heison Robert SJ, Kothai R, Chidambaranathan N, Muthumani P. Source: Fitoterapia. 2003 April; 74(3): 280-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727494&dopt=Abstract
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Enteropathy-type T-cell lymphoma showing repeated small bowel rupture and refractoriness to chemotherapy: a case report. Author(s): Kataoka I, Arima F, Nishimoto J, Watanabe T, Kobayashi Y, Tamura R, Yamamoto S, Matsuno Y, Shimoda T, Tobinai K. Source: Japanese Journal of Clinical Oncology. 2002 December; 32(12): 546-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12578905&dopt=Abstract
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Epidemiology of Burkitt's lymphoma in Enugu, Nigeria. Author(s): Oguonu T, Emodi I, Kaine W. Source: Annals of Tropical Paediatrics. 2002 December; 22(4): 369-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12530287&dopt=Abstract
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ESHAP salvage therapy for relapsed or refractory non-Hodgkin's lymphoma. Author(s): Choi CW, Paek CW, Seo JH, Kim BS, Shin SW, Kim YH, Kim JS. Source: Journal of Korean Medical Science. 2002 October; 17(5): 621-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12378012&dopt=Abstract
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Ethanol-eluted extract of Rhus verniciflua stokes inhibits cell growth and induces apoptosis in human lymphoma cells. Author(s): Lee JC, Kim J, Jang YS. Source: J Biochem Mol Biol. 2003 July 31; 36(4): 337-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12895289&dopt=Abstract
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Evaluation for the development of 11q23 rearrangements in lymphoma patients treated with a high dose VP-16 and cyclophosphamide salvage regimen. Author(s): Mangel J, Duncan A, Lachance S. Source: Leukemia & Lymphoma. 2003 June; 44(6): 1001-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854902&dopt=Abstract
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Evaluation of a 6-month chemotherapy protocol with no maintenance therapy for dogs with lymphoma. Author(s): Garrett LD, Thamm DH, Chun R, Dudley R, Vail DM.
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Source: J Vet Intern Med. 2002 November-December; 16(6): 704-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12465768&dopt=Abstract •
Excellent long-term survival in patients with early-stage primary bone lymphoma treated with doxorubicin-based chemotherapy and local radiotherapy. Author(s): Stein ME, Epelbaum R, Zaidan J, Kuten A, Ben-Schachar M, Haim N. Source: American Journal of Clinical Oncology : the Official Publication of the American Radium Society. 2002 December; 25(6): 603-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12478009&dopt=Abstract
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F-18-FDG-PET in a patient with Hashimoto's thyroiditis and MALT lymphoma recurrence of the thyroid. Author(s): Mikosch P, Wurtz FG, Gallowitsch HJ, Kresnik E, Lind P. Source: Wiener Medizinische Wochenschrift (1946). 2003; 153(3-4): 89-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12658970&dopt=Abstract
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Favorable response to treatment of a child with T-cell-rich large B-cell lymphoma presenting with liver failure. Author(s): Sathiapalan RK, Hainau B, Al-Mane K, Belgaumi AF. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2003 October; 25(10): 809-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14528106&dopt=Abstract
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FDG PET in the follow-up management of patients with newly diagnosed Hodgkin and non-Hodgkin lymphoma after first-line chemotherapy. Author(s): Lavely WC, Delbeke D, Greer JP, Morgan DS, Byrne DW, Price RR, Hallahan DE. Source: International Journal of Radiation Oncology, Biology, Physics. 2003 October 1; 57(2): 307-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12957239&dopt=Abstract
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First-line treatment with brief-duration chemotherapy plus rituximab in elderly patients with intermediate-grade non-Hodgkin's lymphoma: phase II trial. Author(s): Hainsworth JD, Litchy S, Lamb MR, Rodriguez GI, Scroggin C Jr, Greco FA. Source: Clin Lymphoma. 2003 June; 4(1): 36-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837153&dopt=Abstract
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FK506 restores sensitivity of thymic lymphomas to calcium-mediated apoptosis and the inducible expression of Fas ligand. Author(s): Kalas W, Matuszyk J, Ziolo E, Strzadala L. Source: Anticancer Res. 2003 March-April; 23(2B): 1613-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12820430&dopt=Abstract
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Flavopiridol in untreated or relapsed mantle-cell lymphoma: results of a phase II study of the National Cancer Institute of Canada Clinical Trials Group. Author(s): Kouroukis CT, Belch A, Crump M, Eisenhauer E, Gascoyne RD, Meyer R, Lohmann R, Lopez P, Powers J, Turner R, Connors JM; National Cancer Institute of Canada Clinical Trials Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 May 1; 21(9): 1740-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735303&dopt=Abstract
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Fludarabine versus cyclophosphamide, vincristine, and prednisone in recurrent lowgrade lymphomas. Author(s): Alliot C. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 1; 21(13): 2626; Author Reply 2626-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829689&dopt=Abstract
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Fludarabine, mitoxantrone, dexamethasone (FND) compared with an alternating triple therapy (ATT) regimen in patients with stage IV indolent lymphoma. Author(s): Tsimberidou AM, McLaughlin P, Younes A, Rodriguez MA, Hagemeister FB, Sarris A, Romaguera J, Hess M, Smith TL, Yang Y, Ayala A, Preti A, Lee MS, Cabanillas F. Source: Blood. 2002 December 15; 100(13): 4351-7. Epub 2002 August 08. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393618&dopt=Abstract
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Fluorine-18-fluorodeoxyglucose positron emission tomography metabolic imaging in patients with lymphoma. Author(s): Huic D, Dodig D. Source: Croatian Medical Journal. 2002 October; 43(5): 541-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12402392&dopt=Abstract
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Focus on lymphomas. Author(s): Staudt LM, Wilson WH. Source: Cancer Cell. 2002 November; 2(5): 363-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12450791&dopt=Abstract
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Genistein reduces NF-kappa B in T lymphoma cells via a caspase-mediated cleavage of I kappa B alpha. Author(s): Baxa DM, Yoshimura FK. Source: Biochemical Pharmacology. 2003 September 15; 66(6): 1009-18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963487&dopt=Abstract
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Hepatosplenic T-gammadelta lymphoma in a patient with Crohn's disease treated with azathioprine. Author(s): Navarro JT, Ribera JM, Mate JL, Granada I, Junca J, Batlle M, Milla F, Feliu E.
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Source: Leukemia & Lymphoma. 2003 March; 44(3): 531-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688327&dopt=Abstract •
HHV8-related non-Hodgkin's lymphoma of the spermatic cord in a patient with HIVassociated multicentric Castleman disease. Author(s): Boulanger E, Briere J, Gaulard P, Droz D, Oksenhendler E. Source: American Journal of Hematology. 2003 January; 72(1): 70-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508272&dopt=Abstract
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High survival rate in childhood non-Hodgkin lymphoma without CNS involvement: results of BFM 95 study in Kuwait. Author(s): Mottl H, Bajciova V, Nemec J, Al Shemmari S, Al Awadi S. Source: Pediatric Hematology and Oncology. 2003 March; 20(2): 103-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12554521&dopt=Abstract
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High-dose cyclophosphamide, BCNU, and VP-16 (CBV) conditioning before allogeneic stem cell transplantation for patients with non-Hodgkin's lymphoma. Author(s): Rossi HA, Becker PS, Emmons RV, Westervelt P, Levy W, Liu Q, Clark Y, Ballen K. Source: Bone Marrow Transplantation. 2003 March; 31(6): 441-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665838&dopt=Abstract
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High-dose infusional ifosfamide, etoposide plus methylprednisolone followed by dexamethasone, high-dose ara-C and cisplatinum and autologous stem cell transplantation for refractory or relapsed aggressive non-Hodgkin's lymphoma. Author(s): Salar A, Martino R, Perea G, Ribera JM, Lopez-Guillermo A, Guardia R, Escoda L, Altes A, Sierra J, Montserrat E. Source: Haematologica. 2002 October; 87(10): 1028-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12368156&dopt=Abstract
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High-dose radioimmunotherapy versus conventional high-dose therapy and autologous hematopoietic stem cell transplantation for relapsed follicular nonHodgkin lymphoma: a multivariable cohort analysis. Author(s): Gopal AK, Gooley TA, Maloney DG, Petersdorf SH, Eary JF, Rajendran JG, Bush SA, Durack LD, Golden J, Martin PJ, Matthews DC, Appelbaum FR, Bernstein ID, Press OW. Source: Blood. 2003 October 1; 102(7): 2351-7. Epub 2003 May 15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750161&dopt=Abstract
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High-dose sequential chemotherapy and peripheral blood progenitor cell autografting in patients with refractory and/or recurrent Hodgkin lymphoma: a multicenter study of the intergruppo Italiano Linfomi showing prolonged disease free survival in patients treated at first recurrence. Author(s): Tarella C, Cuttica A, Vitolo U, Liberati M, Di Nicola M, Cortelazzo S, Rosato
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R, Rosanelli C, Di Renzo N, Musso M, Pavone E, Santini G, Pescarollo A, De Crescenzo A, Federico M, Gallamini A, Pregno P, Romano R, Coser P, Gallo E, Boccadoro M, Barbui T, Pileri A, Gianni AM, Levis A. Source: Cancer. 2003 June 1; 97(11): 2748-59. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767087&dopt=Abstract •
High-dose therapy and autologous stem-cell transplantation versus conventional therapy for patients with advanced Hodgkin's lymphoma responding to front-line therapy. Author(s): Federico M, Bellei M, Brice P, Brugiatelli M, Nagler A, Gisselbrecht C, Moretti L, Colombat P, Luminari S, Fabbiano F, Di Renzo N, Goldstone A, Carella AM; EBMT/GISL/ANZLG/SFGM/GELA Intergroup HD01 Trial. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 15; 21(12): 2320-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12805333&dopt=Abstract
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High-dose therapy for follicular lymphoma revisited: not if, but when? Author(s): Lister TA. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 November 1; 21(21): 3894-6. Epub 2003 September 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14517186&dopt=Abstract
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High-dose therapy improves progression-free survival and survival in relapsed follicular non-Hodgkin's lymphoma: results from the randomized European CUP trial. Author(s): Schouten HC, Qian W, Kvaloy S, Porcellini A, Hagberg H, Johnson HE, Doorduijn JK, Sydes MR, Kvalheim G. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 November 1; 21(21): 3918-27. Epub 2003 September 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14517188&dopt=Abstract
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High-dose therapy in diffuse large cell lymphoma: results and prognostic factors in 452 patients from the GEL-TAMO Spanish Cooperative Group. Author(s): Caballero MD, Perez-Simon JA, Iriondo A, Lahuerta JJ, Sierra J, Marin J, Gandarillas M, Arranz R, Zuazu J, Rubio V, Fernandez de Sevilla A, Carreras E, GarciaConde J, Garcia-Larana J, Grande C, Sureda A, Vidal MJ, Rifon J, Perez-Equiza C, Varela R, Moraleda JM, Garcia Ruiz JC, Albo C, Cabrera R, San Miguel JF, Conde E. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003 January; 14(1): 140-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488306&dopt=Abstract
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Hydroa vacciniforme-like primary cutaneous CD8-positive T-cell lymphoma. Author(s): Chen HH, Hsiao CH, Chiu HC.
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Source: The British Journal of Dermatology. 2002 September; 147(3): 587-91. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12207607&dopt=Abstract •
Ifosfamide, carboplatin, etoposide (ICE)-based second-line chemotherapy for the management of relapsed and refractory aggressive non-Hodgkin's lymphoma. Author(s): Zelenetz AD, Hamlin P, Kewalramani T, Yahalom J, Nimer S, Moskowitz CH. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003; 14 Suppl 1: I5-10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736224&dopt=Abstract
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Ifosfamide, epirubicin and etoposide (IEV) in non-Hodgkin's lymphoma and Hodgkin's disease: the Italian experience. Author(s): Zinzani PL. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003; 14 Suppl 1: I43-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736231&dopt=Abstract
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Immune reconstitution during intensive chemotherapy in patients with human immunodeficiency virus related non-Hodgkin lymphoma. Author(s): Costello RT, Brunet C, Dignat-George F, Sampol J, Olive D, Gastaut JA. Source: The Hematology Journal : the Official Journal of the European Haematology Association / Eha. 2002; 3(4): 216-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12189569&dopt=Abstract
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Immunochemotherapy: the new standard in aggressive non-Hodgkin's lymphoma in the elderly. Author(s): Coiffier B. Source: Seminars in Oncology. 2003 February; 30(1 Suppl 2): 21-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12652461&dopt=Abstract
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Immunogenicity of a plasmid DNA vaccine encoding chimeric idiotype in patients with B-cell lymphoma. Author(s): Timmerman JM, Singh G, Hermanson G, Hobart P, Czerwinski DK, Taidi B, Rajapaksa R, Caspar CB, Van Beckhoven A, Levy R. Source: Cancer Research. 2002 October 15; 62(20): 5845-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12384547&dopt=Abstract
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Immunophenotypic characterization of normal peripheral blood B lymphocyte by flow cytometry: reference for diagnosis of chronic B cell leukemia/lymphoma. Author(s): Zheng ZJ, Xu RL.
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Source: Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2003 August; 11(4): 398-404. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12962571&dopt=Abstract •
Immunopotentiation in mice bearing a spontaneous transplantable T-cell lymphoma: role of thymic extract. Author(s): Shanker A, Singh SM. Source: Neoplasma. 2003; 50(4): 272-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937840&dopt=Abstract
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Impact of concomitant antiblastic chemotherapy and highly active antiretroviral therapy on human immunodeficiency virus (HIV) viremia and genotyping in HIVinfected patients with non-Hodgkin lymphoma. Author(s): Simonelli C, Zanussi S, Cinelli R, Dal Maso L, Di Gennaro G, D'Andrea M, Nasti G, Spina M, Vaccher E, De Paoli P, Tirelli U. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2003 September 15; 37(6): 820-7. Epub 2003 August 28. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12955644&dopt=Abstract
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Importance of F18-fluorodeoxy-D-2-glucose positron emission tomography (FDGPET) for staging and therapy control of Hodgkin's lymphoma in childhood and adolescence - consequences for the GPOH-HD 2003 protocol. Author(s): Korholz D, Kluge R, Wickmann L, Hirsch W, Luders H, Lotz I, Dannenberg C, Hasenclever D, Dorffel W, Sabri O. Source: Onkologie. 2003 October; 26(5): 489-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14605468&dopt=Abstract
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Improvement in Sjogren's syndrome following therapy with rituximab for marginal zone lymphoma. Author(s): Somer BG, Tsai DE, Downs L, Weinstein B, Schuster SJ; American College of Rheumatology ad hoc Committee on Immunologic Testing Guidelines. Source: Arthritis and Rheumatism. 2003 June 15; 49(3): 394-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794796&dopt=Abstract
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Increasing chemotherapy intensity in aggressive lymphomas: a renewal? Author(s): Coiffier B. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 1; 21(13): 2457-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829662&dopt=Abstract
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Inhibition of constitutive STAT3 activity sensitizes resistant non-Hodgkin's lymphoma and multiple myeloma to chemotherapeutic drug-mediated apoptosis. Author(s): Alas S, Bonavida B.
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Source: Clinical Cancer Research : an Official Journal of the American Association for Cancer Research. 2003 January; 9(1): 316-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12538484&dopt=Abstract •
Inhibition of MEK induces fas expression and apoptosis in lymphomas overexpressing Ras. Author(s): Kalas W, Kisielow P, Strzadala L. Source: Leukemia & Lymphoma. 2002 July; 43(7): 1469-74. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12389631&dopt=Abstract
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Intensified CHOP regimen in aggressive lymphomas: maximal dose intensity and dose density of doxorubicin and cyclophosphamide. Author(s): Balzarotti M, Spina M, Sarina B, Magagnoli M, Castagna L, Milan I, Ripa C, Latteri F, Bernardi D, Bertuzzi A, Nozza A, Roncalli M, Morenghi E, Tirelli U, Santoro A. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 September; 13(9): 1341-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12196358&dopt=Abstract
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Intensive chemotherapy with cyclophosphamide, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, and high-dose cytarabine (CODOX-M/IVAC) for human immunodeficiency virus-associated Burkitt lymphoma. Author(s): Wang ES, Straus DJ, Teruya-Feldstein J, Qin J, Portlock C, Moskowitz C, Goy A, Hedrick E, Zelenetz AD, Noy A. Source: Cancer. 2003 September 15; 98(6): 1196-205. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12973843&dopt=Abstract
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Intensive chemotherapy with rituximab is safe and effective in AIDS non-Hodgkin's lymphoma. Author(s): Rey J, Charbonnier A, Schiano de Colella JM, Stoppa AM, Poizot-Martin I, Gastaut JA, Costello RT. Source: Aids (London, England). 2003 September 5; 17(13): 2006-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12960844&dopt=Abstract
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Intestinal non-Hodgkin's lymphoma: a multicenter prospective clinical study from the German Study Group on Intestinal non-Hodgkin's Lymphoma. Author(s): Daum S, Ullrich R, Heise W, Dederke B, Foss HD, Stein H, Thiel E, Zeitz M, Riecken EO. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 July 15; 21(14): 2740-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12860953&dopt=Abstract
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Intravascular lymphoma involving the central and peripheral nervous systems in a dog. Author(s): Bush WW, Throop JL, McManus PM, Kapatkin AS, Vite CH, Van Winkle TJ.
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Source: Journal of the American Animal Hospital Association. 2003 January-February; 39(1): 90-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12549621&dopt=Abstract •
Intravascular lymphoma presenting with bone marrow involvement and leukemic phase. Author(s): Khoury H, Dalal BI, Nantel SH. Source: Leukemia & Lymphoma. 2003 June; 44(6): 1043-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12854907&dopt=Abstract
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Intravascular lymphoma presenting with cauda equina syndrome: treated with CHOP and rituxan. Author(s): Davis TS. Source: Leukemia & Lymphoma. 2003 May; 44(5): 887-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802932&dopt=Abstract
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Involved-field radiotherapy for advanced Hodgkin's lymphoma. Author(s): Aleman BM, Raemaekers JM, Tirelli U, Bortolus R, van 't Veer MB, Lybeert ML, Keuning JJ, Carde P, Girinsky T, van der Maazen RW, Tomsic R, Vovk M, van Hoof A, Demeestere G, Lugtenburg PJ, Thomas J, Schroyens W, De Boeck K, Baars JW, KluinNelemans JC, Carrie C, Aoudjhane M, Bron D, Eghbali H, Smit WG, Meerwaldt JH, Hagenbeek A, Pinna A, Henry-Amar M; European Organization for Research and Treatment of Cancer Lymphoma Group. Source: The New England Journal of Medicine. 2003 June 12; 348(24): 2396-406. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12802025&dopt=Abstract
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Involved-field radiotherapy is equally effective and less toxic compared with extended-field radiotherapy after four cycles of chemotherapy in patients with earlystage unfavorable Hodgkin's lymphoma: results of the HD8 trial of the German Hodgkin's Lymphoma Study Group. Author(s): Engert A, Schiller P, Josting A, Herrmann R, Koch P, Sieber M, Boissevain F, De Wit M, Mezger J, Duhmke E, Willich N, Muller RP, Schmidt BF, Renner H, MullerHermelink HK, Pfistner B, Wolf J, Hasenclever D, Loffler M, Diehl V; German Hodgkin's Lymphoma Study Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 October 1; 21(19): 3601-8. Epub 2003 August 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12913100&dopt=Abstract
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Irinotecan in relapsed or refractory non-Hodgkin's lymphomas. Indications of activity in a phase II trial. Author(s): Sarris AH, Phan A, Goy A, Romaguera J, Hagemeister FB, Rodriguez MA, McLaughlin P, Pro B, Medeiros LJ, Samuels B, Mesina O, Bleyer AW, Cabanillas F. Source: Oncology (Huntingt). 2002 August; 16(8 Suppl 7): 27-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12199630&dopt=Abstract
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Lacrimal sac lymphoma in a child. Author(s): Schefler AC, Shields CL, Shields JA, Demirci H, Maus M, Eagle RC Jr. Source: Archives of Ophthalmology. 2003 September; 121(9): 1330-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963620&dopt=Abstract
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Large bowel lymphoma: an analysis of prognostic factors and therapy in 53 patients. Author(s): Aviles A, Neri N, Huerta-Guzman J. Source: Journal of Surgical Oncology. 2002 June; 80(2): 111-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12173380&dopt=Abstract
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L-asparaginase-based regimen in the treatment of refractory midline nasal/nasal-type T/NK-cell lymphoma. Author(s): Yong W, Zheng W, Zhang Y, Zhu J, Wei Y, Zhu D, Li J. Source: International Journal of Hematology. 2003 August; 78(2): 163-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12953813&dopt=Abstract
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Long-term follow-up of a prospective study of combined modality therapy for stage III indolent non-Hodgkin's lymphoma. Author(s): Seymour JF, Pro B, Fuller LM, Manning JT, Hagemeister FB, Romaguera J, Rodriguez MA, Ha CS, Smith TL, Ayala A, Hess M, Cox JD, Cabanillas F, McLaughlin P. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 1; 21(11): 2115-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775737&dopt=Abstract
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Low-dose epirubicin in combination with cyclophosphamide, vinblastine and prednisone (mini-CEOP) for the treatment of aggressive non-Hodgkin's lymphoma in elderly patients. Author(s): Veneri D, Zanetti F, Franchini M, Krampera M, Pizzolo G. Source: Haematologica. 2002 November; 87(11): Elt43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12414364&dopt=Abstract
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Lymphoblastic lymphoma of childhood and the LSA2-L2 protocol: the 30-year experience at Memorial-Sloan-Kettering Cancer Center. Author(s): Mora J, Filippa DA, Qin J, Wollner N. Source: Cancer. 2003 September 15; 98(6): 1283-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12973853&dopt=Abstract
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Malignant lymphoma of the heart. Featured echocardiogram and case report. Author(s): Memon AQ, Xavier L. Source: Cardiology in Review. 2002 November-December; 10(6): 323-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12390686&dopt=Abstract
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Massive metastatic intracardiac lymphoma presenting with complete heart block with resolution following chemotherapy. Author(s): Clifford SM, Guerra SM, Mangion JR. Source: Echocardiography (Mount Kisco, N.Y.). 2003 February; 20(2): 201-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848690&dopt=Abstract
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Mitoxantrone/ifosfamide/etoposide salvage regimen with rituximab for in vivo purging in patients with relapsed lymphoma. Author(s): Emmanouilides C, Lill M, Telatar M, Rosenfelt F, Grody W, Territo M, Rosen P. Source: Clin Lymphoma. 2002 September; 3(2): 111-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12435284&dopt=Abstract
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Modified chop-chemotherapy plus rituximab for diffuse large b-cell lymphoma complicating ataxia-telangiectasia. Author(s): Rossi G, Zecca M, Marchi A, de Stefano P, Sammarchi L, Locatelli F. Source: British Journal of Haematology. 2003 January; 120(2): 369-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12542504&dopt=Abstract
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Modified ESHAP as salvage chemotherapy for recurrent or refractory non-Hodgkin's lymphoma: results of a single-center study of 32 patients. Modified etoposide, methylprednisolone, cytarabine and cisplatin. Author(s): Ozturk MA, Barista I, Altundag MK, Turker A, Yalcin S, Celik I, Gullu I, Guler N, Ozisik Y, Kars A, Kansu E, Baltali E, Tekuzman G. Source: Chemotherapy. 2002 December; 48(5): 252-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12476042&dopt=Abstract
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Modulation of Immune Response of BALB/Mice Bearing Lymphoma L5178Y Treated with Bitter Yellow Juice of Aloe vera (L) in vivo. Author(s): Oronzo-Barocio A, Zaitseva G, Chavez-Anaya A, Arceta-Gonzalez VI, Puebla-Perez AM, Alfaro-Bustamante F, Zimina IV, Arion VY. Source: Russ J Immunol. 1999 April; 4(1): 43-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687115&dopt=Abstract
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MOPP chemotherapy for treatment of resistant lymphoma in dogs: a retrospective study of 117 cases (1989-2000). Author(s): Rassnick KM, Mauldin GE, Al-Sarraf R, Mauldin GN, Moore AS, Mooney SC. Source: J Vet Intern Med. 2002 September-October; 16(5): 576-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12322709&dopt=Abstract
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Myelodysplastic syndrome and acute myeloid leukemia after autotransplantation for lymphoma: a multicenter case-control study. Author(s): Metayer C, Curtis RE, Vose J, Sobocinski KA, Horowitz MM, Bhatia S, Fay
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JW, Freytes CO, Goldstein SC, Herzig RH, Keating A, Miller CB, Nevill TJ, Pecora AL, Rizzo JD, Williams SF, Li CY, Travis LB, Weisdorf DJ. Source: Blood. 2003 March 1; 101(5): 2015-23. Epub 2002 October 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393427&dopt=Abstract •
Nasal NK/T-cell lymphoma with disseminated disease treated with aggressive combined therapy. Author(s): Aviles A, Neri N, Fernandez R, Calva A, Huerta-Guzman J, Nambo MJ. Source: Medical Oncology (Northwood, London, England). 2003; 20(1): 13-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665679&dopt=Abstract
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Neutropenia associated with vincristine and L-asparaginase induction chemotherapy for canine lymphoma. Author(s): Northrup NC, Rassnick KM, Snyder LA, Stone MS, Kristal O, Cotter SM, Moore AS. Source: J Vet Intern Med. 2002 September-October; 16(5): 570-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12322708&dopt=Abstract
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Non-Hodgkin's lymphomas. Author(s): Theodossiou C, Schwarzenberger P. Source: Clinical Obstetrics and Gynecology. 2002 September; 45(3): 820-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12370624&dopt=Abstract
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Not just another fall in the elderly. Bilateral adrenal lymphoma presenting with adrenal insufficiency causing weakness. Author(s): Gillett M, Haak S. Source: Aust Fam Physician. 2003 April; 32(4): 248-50. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12735264&dopt=Abstract
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Obstructive sleep apnea syndrome as first manifestation of pharyngeal nonHodgkin's lymphoma. Author(s): Gomez-Merino E, Arriero JM, Chiner E, Signes-Costa J, Marco J. Source: Respiration; International Review of Thoracic Diseases. 2003 January-February; 70(1): 107-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12584402&dopt=Abstract
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One-year follow-up of a patient with reversible tricuspid valve stenosis due to lymphomatic mass into the right atrioventricular wall. Author(s): Chrissos D, Kalmantis T, Belegrati M, Katsaros A, Tapanlis E, Katsimichas A, Triantafillou G, Kallikazaros I. Source: Echocardiography (Mount Kisco, N.Y.). 2002 October; 19(7 Pt 1): 565-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12376008&dopt=Abstract
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Optimal therapy of primary ocular lymphoma. Author(s): Plowman PN, Taylor A, Jackson AS, Lightman S, Pavesio C. Source: Clin Oncol (R Coll Radiol). 2002 December; 14(6): 521. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12512978&dopt=Abstract
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Outcome of B-cell non-Hodgkin lymphoma protocol CCCG-B NHL97: a report from Chinese multi-center cooperative group. Author(s): Tang JY, Pan C, Chen J, Chen H, Wu Y, Xue H, Zhao H, Gu LJ, Fu RY, Wang YP. Source: Medical and Pediatric Oncology. 2002 September; 39(3): 212-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12210455&dopt=Abstract
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Outpatient regimen rituximab plus ifosfamide, carboplatin and etoposide (R-ICE) for relapsed non-Hodgkin's lymphoma. Author(s): Vose J, Sneller V. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003; 14 Suppl 1: I17-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736226&dopt=Abstract
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Outpatient-based ifosfamide, carboplatin and etoposide (ICE) chemotherapy in transplant-eligible patients with non-Hodgkin's lymphoma and Hodgkin's disease. Author(s): Hertzberg MS, Crombie C, Benson W, Taper J, Gottlieb D, Bradstock KF. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003; 14 Suppl 1: I11-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736225&dopt=Abstract
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Overview of rational and individualized therapeutic strategies for non-Hodgkin's lymphomas. Author(s): Armitage JO. Source: Clin Lymphoma. 2002 December; 3 Suppl 1: S5-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12521383&dopt=Abstract
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Patients with high-risk aggressive lymphoma treated with frontline intensive chemotherapy and autografting: evidence of marked differences in outcome between patients with age-adjusted International Prognostic Index scores 2 and 3. Author(s): Cuttica A, Zallio F, Ladetto M, Di Nicola M, Caracciolo D, Magni M, Marinone C, Dell'Aquila M, Rosace M, Pileri A, Boccadoro M, Gianni AM, Tarella C. Source: Cancer. 2003 September 1; 98(5): 983-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12942566&dopt=Abstract
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Patient-specific, 3-dimensional dosimetry in non-Hodgkin's lymphoma patients treated with 131I-anti-B1 antibody: assessment of tumor dose-response. Author(s): Sgouros G, Squeri S, Ballangrud AM, Kolbert KS, Teitcher JB, Panageas KS, Finn RD, Divgi CR, Larson SM, Zelenetz AD.
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Source: Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine. 2003 February; 44(2): 260-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571219&dopt=Abstract •
Pegylated liposomal doxorubicin in the CHOP regimen for older patients with aggressive (stages III/IV) non-Hodgkin's lymphoma. Author(s): Tsavaris N, Kosmas C, Vadiaka M, Giannouli S, Siakantaris MP, Vassilakopoulos T, Pangalis GA. Source: Anticancer Res. 2002 May-June; 22(3): 1845-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12168880&dopt=Abstract
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PET for staging of Hodgkin's disease and non-Hodgkin's lymphoma. Author(s): Schiepers C, Filmont JE, Czernin J. Source: European Journal of Nuclear Medicine and Molecular Imaging. 2003 June; 30 Suppl 1: S82-8. Epub 2003 April 26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12719922&dopt=Abstract
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PET scans in the staging of lymphoma: current status. Author(s): Friedberg JW, Chengazi V. Source: The Oncologist. 2003; 8(5): 438-47. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14530496&dopt=Abstract
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Phase 2 trial of infusional cyclophosphamide, doxorubicin, and etoposide in patients with poor-prognosis, intermediate-grade non-Hodgkin lymphoma: an Eastern Cooperative Oncology Group trial (E3493). Author(s): Sparano JA, Weller E, Nazeer T, Habermann T, Traynor AE, Manalo J, Cassileth P. Source: Blood. 2002 September 1; 100(5): 1634-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12176882&dopt=Abstract
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Phase I trial of fludarabine and paclitaxel in non-Hodgkin's lymphoma. Author(s): Abbasi MR, Sparano JA, Sarta C, Wiernik PH. Source: Medical Oncology (Northwood, London, England). 2003; 20(1): 53-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12665685&dopt=Abstract
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Phase II study of docetaxel in patients with relapsed or refractory malignant lymphoma. Author(s): Zekri JM, Hough RE, Davies JM, Molife R, Hancock BW, Lorigan PC. Source: British Journal of Cancer. 2003 May 6; 88(9): 1335-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12778057&dopt=Abstract
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Phase II study of sequential topotecan and etoposide in patients with intermediate grade non-Hodgkin's lymphoma: a National Cancer Institute of Canada Clinical
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Trials Group study. Author(s): Crump M, Couban S, Meyer R, Rudinskas L, Zanke B, Gluck S, Maksymiuk A, Hoskins P, Matthews S, Eisenhauer E. Source: Leukemia & Lymphoma. 2002 August; 43(8): 1581-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400600&dopt=Abstract •
Pilot phase I/II study of new salvage therapy (CHASE) for refractory or relapsed malignant lymphoma. Author(s): Ogura M, Kagami Y, Taji H, Suzuki R, Miura K, Takeuchi T, Morishima Y. Source: International Journal of Hematology. 2003 June; 77(5): 503-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841390&dopt=Abstract
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Porphyria cutanea tarda, dermatomyositis and non-Hodgkin lymphoma in virus C infection. Author(s): Bauza A, Espana A, Lloret P. Source: Eur J Dermatol. 2003 May-June; 13(3): 302-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804996&dopt=Abstract
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Position paper on the therapeutic use of rituximab in CD20-positive diffuse large Bcell non-Hodgkin's lymphoma. Author(s): Pettengell R, Linch D; Haemato-Oncology Task Force of the British Committee for Standards in Haematology. Source: British Journal of Haematology. 2003 April; 121(1): 44-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12670330&dopt=Abstract
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Positron emission tomography for the staging of Hodgkin's lymphoma--increasing the body of evidence in favor of the method. Author(s): Menzel C, Dobert N, Mitrou P, Mose S, Diehl M, Berner U, Grunwald F. Source: Acta Oncologica (Stockholm, Sweden). 2002; 41(5): 430-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12442918&dopt=Abstract
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Positron Emission Tomography in Diagnosis and Therapy Monitoring of Patients with Lymphoma. Author(s): Romer W, Schwaiger M. Source: Clinical Positron Imaging : Official Journal of the Institute for Clinical P.E.T. 1998 March; 1(2): 101-110. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14516598&dopt=Abstract
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Positron emission tomography in the management of lymphomas. Author(s): O'Doherty MJ, Macdonald EA, Barrington SF, Mikhaeel NG, Schey S. Source: Clin Oncol (R Coll Radiol). 2002 October; 14(5): 415-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12555882&dopt=Abstract
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Positron emission tomography with [(18)F]FDG for therapy response monitoring in lymphoma patients. Author(s): Spaepen K, Stroobants S, Verhoef G, Mortelmans L. Source: European Journal of Nuclear Medicine and Molecular Imaging. 2003 June; 30 Suppl 1: S97-105. Epub 2003 April 23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12709831&dopt=Abstract
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Postpneumonectomy-like syndrome after chemoradiation therapy for lymphoma. Author(s): Veronesi G, Spaggiari L, Solli PG, Leo F, Villa G, Pastorino U. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 December; 13(12): 1945-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12453864&dopt=Abstract
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Pre- and post-treatment evaluation of non-Hodgkin's lymphoma. Author(s): Mavromatis BH, Cheson BD. Source: Best Practice & Research. Clinical Haematology. 2002 September; 15(3): 429-47. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12468398&dopt=Abstract
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Predictive value of early 18F-fluoro-deoxyglucose positron emission tomography in chemosensitive relapsed lymphoma. Author(s): Schot B, van Imhoff G, Pruim J, Sluiter W, Vaalburg W, Vellenga E. Source: British Journal of Haematology. 2003 October; 123(2): 282-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14531910&dopt=Abstract
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Presentation serum selenium predicts for overall survival, dose delivery, and first treatment response in aggressive non-Hodgkin's lymphoma. Author(s): Last KW, Cornelius V, Delves T, Sieniawska C, Fitzgibbon J, Norton A, Amess J, Wilson A, Rohatiner AZ, Lister TA. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 June 15; 21(12): 2335-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12805335&dopt=Abstract
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Primary B-cell lymphoma of the clivus: case report. Author(s): Tsai VW, Rybak L, Espinosa J, Kuhn MJ, Kamel OW, Mathews F, Glatz FR. Source: Surgical Neurology. 2002 September-October; 58(3-4): 246-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12480233&dopt=Abstract
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Primary cardiac lymphoma diagnosed by transvenous biopsy under transesophageal echocardiographic guidance and treated with systemic chemotherapy. Author(s): Kang SM, Rim SJ, Chang HJ, Choi D, Cho SY, Cho SH, Chung N.
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Source: Echocardiography (Mount Kisco, N.Y.). 2003 January; 20(1): 101-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12848708&dopt=Abstract •
Primary cutaneous follicle center cell lymphoma of the scalp successfully treated with anti CD20 monoclonal antibody and CHOP combination therapy with no subsequent permanent loss of hair. Author(s): Imai Y, Isoda K, Ito E, Hakamada A, Yamanishi K, Mizutani H. Source: The Journal of Dermatology. 2003 September; 30(9): 683-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14578559&dopt=Abstract
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Primary mediastinal large B-cell lymphoma with sclerosis in pediatric and adolescent patients: treatment and results from three therapeutic studies of the Berlin-FrankfurtMunster Group. Author(s): Seidemann K, Tiemann M, Lauterbach I, Mann G, Simonitsch I, Stankewitz K, Schrappe M, Zimmermann M, Niemeyer C, Parwaresch R, Riehm H, Reiter A; NHL Berlin-Frankfurt-Munster Group. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 May 1; 21(9): 1782-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12721255&dopt=Abstract
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Primary mediastinal large B-cell lymphoma. Author(s): Ergul SM, Lal A, Afri L, Frei-Lahr D. Source: Southern Medical Journal. 2002 September; 95(9): 1005-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12356098&dopt=Abstract
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Primary neutrophil-rich, CD30-positive anaplastic large cell lymphoma of the stomach: case report and review of the literature. Author(s): Kahaleh M, Hermans P, Buset M, Dargent JL. Source: Acta Gastroenterol Belg. 2002 October-December; 65(4): 237-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12619433&dopt=Abstract
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Primary NK/T cell lymphoma of the testis. A case report and review of the literature. Author(s): Kim YB, Chang SK, Yang WI, Hahn JS, Koom WS, Shim SJ, Park W, Lee KK, Suh CO, Kim GE. Source: Acta Haematologica. 2003; 109(2): 95-100. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12624494&dopt=Abstract
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Primary non-Hodgkin's lymphoma of the bladder with bone marrow involvement. Author(s): Oh KC, Zang DY. Source: Korean J Intern Med. 2003 March; 18(1): 40-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760267&dopt=Abstract
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Primary non-Hodgkin's lymphoma of the uterine cervix successfully treated by neoadjuvant chemotherapy: case report. Author(s): Szantho A, Balega J J, Csapo Z, Sreter L L, Matolcsy A, Papp Z. Source: Gynecologic Oncology. 2003 April; 89(1): 171-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12694673&dopt=Abstract
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Primary treatment with autologous stem cell transplantation in mantle cell lymphoma: outcome related to remission pretransplant. Author(s): Andersen NS, Pedersen L, Elonen E, Johnson A, Kolstad A, Franssila K, Langholm R, Ralfkiaer E, Akerman M, Eriksson M, Kuittinen O, Geisler CH; Nordic Lymphoma Group. Source: European Journal of Haematology. 2003 August; 71(2): 73-80. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890145&dopt=Abstract
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Prognostic significance of 18F-fluorodeoxyglucose positron emission tomography in lymphoma. Author(s): Weihrauch MR, Dietlein M, Schicha H, Diehl V, Tesch H. Source: Leukemia & Lymphoma. 2003 January; 44(1): 15-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12691138&dopt=Abstract
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Prognostic value of FDG-PET in malignant lymphoma. Author(s): Becherer A, Jaeger U, Szabo M, Kletter K. Source: Q J Nucl Med. 2003 March; 47(1): 14-21. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714950&dopt=Abstract
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Prognostic value of pretransplantation positron emission tomography using fluorine 18-fluorodeoxyglucose in patients with aggressive lymphoma treated with high-dose chemotherapy and stem cell transplantation. Author(s): Spaepen K, Stroobants S, Dupont P, Vandenberghe P, Maertens J, Bormans G, Thomas J, Balzarini J, De Wolf-Peeters C, Mortelmans L, Verhoef G. Source: Blood. 2003 July 1; 102(1): 53-9. Epub 2003 February 27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12609836&dopt=Abstract
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Progressive external ophthalmoplegia: a paraneoplastic manifestation of lymphoma. Author(s): Ascaso FJ, Torres M, Bergua JM, Alvarez R, Cristobal JA. Source: Eur J Ophthalmol. 2002 July-August; 12(4): 315-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12220003&dopt=Abstract
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Prolonged single-agent versus combination chemotherapy in indolent follicular lymphomas: a study of the cancer and leukemia group B. Author(s): Peterson BA, Petroni GR, Frizzera G, Barcos M, Bloomfield CD, Nissen NI, Hurd DD, Henderson ES, Sartiano GP, Johnson JL, Holland JF, Gottlieb AJ.
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Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 January 1; 21(1): 5-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12506163&dopt=Abstract •
Pulmonary low-grade MALT-lymphoma associated with localized pulmonary amyloidosis. A case report. Author(s): Wieker K, Rocken C, Koenigsmann M, Roessner A, Franke A. Source: Amyloid : the International Journal of Experimental and Clinical Investigation : the Official Journal of the International Society of Amyloidosis. 2002 September; 9(3): 190-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12408682&dopt=Abstract
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Pure red cell aplasia due to parvovirus following treatment with CHOP and rituximab for B-cell lymphoma. Author(s): Song KW, Mollee P, Patterson B, Brien W, Crump M. Source: British Journal of Haematology. 2002 October; 119(1): 125-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12358915&dopt=Abstract
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Radiotherapy versus combined therapy in early stages with bulky disease aggressive malignant lymphoma. Author(s): Aviles A, Fernandez R, Calva A, Neri N, Huerta-Guzman J, Nambo MJ. Source: Hematology (Amsterdam, Netherlands). 2003 February; 8(1): 7-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623421&dopt=Abstract
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Randomized phase II study of biweekly CHOP and dose-escalated CHOP with prophylactic use of lenograstim (glycosylated G-CSF) in aggressive non-Hodgkin's lymphoma: Japan Clinical Oncology Group Study 9505. Author(s): Itoh K, Ohtsu T, Fukuda H, Sasaki Y, Ogura M, Morishima Y, Chou T, Aikawa K, Uike N, Mizorogi F, Ohno T, Ikeda S, Sai T, Taniwaki M, Kawano F, Niimi M, Hotta T, Shimoyama M, Tobinai K; Members of the lymphoma study group of the Japan Clinical Oncology Group (JCOG). Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 September; 13(9): 1347-55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12196359&dopt=Abstract
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Randomized phase III study of fludarabine phosphate versus cyclophosphamide, vincristine, and prednisone in patients with recurrent low-grade non-Hodgkin's lymphoma previously treated with an alkylating agent or alkylator-containing regimen. Author(s): Klasa RJ, Meyer RM, Shustik C, Sawka CA, Smith A, Guevin R, Maksymiuk A, Rubinger M, Samosh M, Laplante S, Grenier JF. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 December 15; 20(24): 4649-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12488409&dopt=Abstract
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Randomized study to evaluate the use of high-dose therapy as part of primary treatment for “aggressive” lymphoma. Author(s): Kaiser U, Uebelacker I, Abel U, Birkmann J, Trumper L, Schmalenberg H, Karakas T, Metzner B, Hossfeld DK, Bischoff HG, Franke A, Reiser M, Muller P, Mantovani L, Grundeis M, Rothmann F, von Seydewitz CU, Mesters RM, Steinhauer EU, Krahl D, Schumacher K, Kneba M, Baudis M, Schmitz N, Pfab R, Koppler H, Parwaresch R, Pfreundschuh M, Havemann K. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 November 15; 20(22): 4413-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12431962&dopt=Abstract
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Randomized trial of 8-week versus 12-week VNCOP-B plus G-CSF regimens as frontline treatment in elderly aggressive non-Hodgkin's lymphoma patients. Author(s): Zinzani PL, Gherlinzoni F, Storti S, Zaccaria A, Pavone E, Moretti L, Gentilini P, Guardigni L, De Renzo A, Fattori PP, Falini B, Lauta VM, Mannina D, Zaja F, Mazza P, Volpe E, Lauria F, Aitini E, Ciccone F, Tani M, Stefoni V, Alinari L, Baccarani M, Tura S. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 September; 13(9): 1364-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12196361&dopt=Abstract
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Randomized, multicenter, open-label study of pegfilgrastim compared with daily filgrastim after chemotherapy for lymphoma. Author(s): Vose JM, Crump M, Lazarus H, Emmanouilides C, Schenkein D, Moore J, Frankel S, Flinn I, Lovelace W, Hackett J, Liang BC. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2003 February 1; 21(3): 514-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12560443&dopt=Abstract
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Regression of HTLV1 associated intracardiac lymphoma following chemotherapy. Author(s): Hamaad A, Davis RC, Connolly DL. Source: Heart (British Cardiac Society). 2002 December; 88(6): 621. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12433893&dopt=Abstract
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Remarkable remission of a follicular lymphoma treated with rituximab and polychemotherapy (CHOP). Author(s): Schmook T, Stockfleth E, Lischner S, Gahn B, Christophers E, Hauschild A. Source: Clinical and Experimental Dermatology. 2003 January; 28(1): 31-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12558625&dopt=Abstract
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Retrospective comparison between CHOP-PVP and CHOP protocols for nonHodgkin's lymphoma. Author(s): Gan H, Zhang F, Lin Y.
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Source: Zhonghua Zhong Liu Za Zhi. 2002 July; 24(4): 397-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12408775&dopt=Abstract •
Rituximab (anti-CD20 monoclonal antibody) as consolidation of first-line CHOP chemotherapy in patients with follicular lymphoma: a phase II study. Author(s): Jaeger G, Neumeister P, Brezinschek R, Hofler G, Quehenberger F, Linkesch W, Sill H. Source: European Journal of Haematology. 2002 July; 69(1): 21-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12270058&dopt=Abstract
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Rituximab in combination with CNOP chemotherapy in patients with previously untreated indolent non-Hodgkin's lymphoma. Author(s): Economopoulos T, Fountzilas G, Pavlidis N, Kalantzis D, Papageorgiou E, Christodoulou C, Hamilos G, Nicolaides C, Dimopoulos M. Source: The Hematology Journal : the Official Journal of the European Haematology Association / Eha. 2003; 4(2): 110-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750729&dopt=Abstract
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Rituximab in combination with vinorelbine/gemcitabine chemotherapy in patients with primary refractory or early relapsed T cell rich B cell lymphoma. A pilot study. Author(s): Xiros N, Economopoulos T, Valsami S, Rontogianni D, Fountzilas G, Raptis S. Source: Leukemia Research. 2003 December; 27(12): 1097-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12921946&dopt=Abstract
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Rituximab plus CHOP (R-CHOP) overcomes bcl-2--associated resistance to chemotherapy in elderly patients with diffuse large B-cell lymphoma (DLBCL). Author(s): Mounier N, Briere J, Gisselbrecht C, Emile JF, Lederlin P, Sebban C, Berger F, Bosly A, Morel P, Tilly H, Bouabdallah R, Reyes F, Gaulard P, Coiffier B. Source: Blood. 2003 June 1; 101(11): 4279-84. Epub 2003 February 06. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12576316&dopt=Abstract
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Rituximab-mediated sensitization of B-non-Hodgkin's lymphoma (NHL) to cytotoxicity induced by paclitaxel, gemcitabine, and vinorelbine. Author(s): Emmanouilides C, Jazirehi AR, Bonavida B. Source: Cancer Biotherapy & Radiopharmaceuticals. 2002 December; 17(6): 621-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12537665&dopt=Abstract
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Salvage surgery for primary non-Hodgkin's lymphoma of the thyroid gland with histopathological complete response to radio-chemotherapy: report of a case. Author(s): Shimizu J, Ishida Y, Takehara A, Kinoshita T, Tatsuzawa Y, Kawaura Y, Matsumoto I, Imai M.
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Source: Surgery Today. 2003; 33(1): 45-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12560906&dopt=Abstract •
Salvage treatment with etoposide (VP-16), ifosfamide and cytarabine (Ara-C) for patients with recurrent primary central nervous system lymphoma. Author(s): Arellano-Rodrigo E, Lopez-Guillermo A, Bessell EM, Nomdedeu B, Montserrat E, Graus F. Source: European Journal of Haematology. 2003 April; 70(4): 219-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12656744&dopt=Abstract
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Serum levels of soluble CD30 improve International Prognostic Score in predicting the outcome of advanced Hodgkin's lymphoma. Author(s): Zanotti R, Trolese A, Ambrosetti A, Nadali G, Visco C, Ricetti MM, Benedetti F, Pizzolo G. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2002 December; 13(12): 1908-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12453859&dopt=Abstract
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Splenic marginal zone lymphoma: clinical characteristics and prognostic factors in a series of 60 patients. Author(s): Chacon JI, Mollejo M, Munoz E, Algara P, Mateo M, Lopez L, Andrade J, Carbonero IG, Martinez B, Piris MA, Cruz MA. Source: Blood. 2002 September 1; 100(5): 1648-54. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12176884&dopt=Abstract
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Spontaneous (pathological) splenic rupture in a blastic variant of mantle cell lymphoma: a case report and literature review. Author(s): Lunning MA, Stetler-Stevenson M, Silberstein PT, Zenger V, Marti GE. Source: Clin Lymphoma. 2002 September; 3(2): 117-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12435285&dopt=Abstract
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Stage I-IIE primary non-Hodgkin's lymphoma of the testis: results of a prospective trial by the GOELAMS Study Group. Author(s): Linassier C, Desablens B, Lefrancq T, Le Prise PY, Harousseau JL, Jacob C, Gandhour C, Haillot O, Lucas V, Leloup R, Escoffre M, Colombat P, Tabuteau S; GOELAMS Study Group. Source: Clin Lymphoma. 2002 December; 3(3): 167-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12521394&dopt=Abstract
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Steroid-free chemotherapy decreases risk of hepatitis B virus (HBV) reactivation in HBV-carriers with lymphoma. Author(s): Cheng AL, Hsiung CA, Su IJ, Chen PJ, Chang MC, Tsao CJ, Kao WY, Uen WC, Hsu CH, Tien HF, Chao TY, Chen LT, Whang-Peng J; Lymphoma Committee of Taiwan Cooperative Oncology Group.
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Source: Hepatology (Baltimore, Md.). 2003 June; 37(6): 1320-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774010&dopt=Abstract •
Strategic approach to the management of Hodgkin's disease incorporating salvage therapy with high-dose ifosfamide, etoposide and epirubicin: a Northern Region Lymphoma Group study (UK). Author(s): Proctor SJ, Jackson GH, Lennard A, Angus B, Wood K, Lucraft HL, White J, Windebank K, Taylor PR; Northern Region Lymphoma Group. Source: Annals of Oncology : Official Journal of the European Society for Medical Oncology / Esmo. 2003; 14 Suppl 1: I47-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736232&dopt=Abstract
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Subcutaneous panniculitis-like T-cell lymphoma during pregnancy with successful autologous stem cell transplantation. Author(s): Reimer P, Rudiger T, Muller J, Rose C, Wilhelm M, Weissinger F. Source: Annals of Hematology. 2003 May; 82(5): 305-9. Epub 2003 April 18. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12707721&dopt=Abstract
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Successful chemotherapy in a male patient with malignant lymphoma and Leber's hereditary optic neuropathy (LHON). Author(s): Zanssen S, Buse G. Source: American Journal of Hematology. 2003 April; 72(4): 263-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12666138&dopt=Abstract
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Successful salvage therapy of irinotecan for relapsed Hodgkin's lymphoma. Author(s): Urushihata K, Koizumi T, Kaneki T, Yamaguchi S, Fujimoto K, Kubo K. Source: Intern Med. 2002 August; 41(8): 648-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12211535&dopt=Abstract
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Successful treatment of advanced peripheral T-cell lymphoma with an angiocentric growth pattern complicated with hemophagocytic syndrome by high-dose chemotherapy and autologous peripheral blood stem cell transplantation. Author(s): Sato T, Kogawa K, Iyama S, Kobayashi D, Sato Y, Kuribayashi K, Takada K, Hagiwara S, Oku T, Takahashi S, Matsunaga T, Takahashi M, Terui T, Kato J, Niitsu Y. Source: Annals of Hematology. 2002 December; 81(12): 739-43. Epub 2002 November 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12483373&dopt=Abstract
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Successful treatment of BALT lymphoma with combined chemotherapy. Author(s): Ali R, Ozkalemkas F, Ozcelik T, Ozkocaman V, Ozan U, Tunali A, Filiz G, Gozu O. Source: Thorax. 2003 April; 58(4): 368-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12668812&dopt=Abstract
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Tailored chemotherapy for malignant lymphoma arising in the setting of posttransplant lymphoproliferative disorder after solid organ transplantation. Author(s): Watts RG, Hilliard LM, Berkow RL. Source: Journal of Pediatric Hematology/Oncology : Official Journal of the American Society of Pediatric Hematology/Oncology. 2002 November; 24(8): 622-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12439033&dopt=Abstract
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Technetium-99m tetrofosmin imaging in malignant lymphomas. Author(s): Schillaci O, Filippis AM, Anselmo AP, Monteleone F, Capoccetti F, Massa R, Maurizi Enrici R, Scopinaro F. Source: Tumori. 2002 May-June; 88(3): S24-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12365376&dopt=Abstract
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Telomere length shortening in non-Hodgkin's lymphoma patients undergoing chemotherapy. Author(s): Lee JJ, Nam CE, Cho SH, Park KS, Chung IJ, Kim HJ. Source: Annals of Hematology. 2003 August; 82(8): 492-5. Epub 2003 June 21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12910376&dopt=Abstract
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The rapidly expanding role of rituximab in the treatment of aggressive B-cell lymphoma. Author(s): Cooper D. Source: Cancer Journal (Sudbury, Mass.). 2002 September-October; 8(5): 364-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12416891&dopt=Abstract
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The role of local radiation therapy for mediastinal disease in adults with T-cell lymphoblastic lymphoma. Author(s): Dabaja BS, Ha CS, Thomas DA, Wilder RB, Gopal R, Cortes J, Bueso-Ramos C, Hess MA, Cox JD, Kantarjian HM. Source: Cancer. 2002 May 15; 94(10): 2738-44. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12173345&dopt=Abstract
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Treatment of adult T-cell leukemia-lymphoma by CHOP followed by therapy with antinucleosides, alpha interferon and oral etoposide. Author(s): Besson C, Panelatti G, Delaunay C, Gonin C, Brebion A, Hermine O, Plumelle Y. Source: Leukemia & Lymphoma. 2002 December; 43(12): 2275-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12613513&dopt=Abstract
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Treatment of elderly Hodgkin's lymphoma patients with a novel 5-drug regimen (ODBEP): a phase II study. Author(s): Macpherson N, Klasa RJ, Gascoyne R, O'Reilly SE, Voss N, Connors JM.
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Source: Leukemia & Lymphoma. 2002 July; 43(7): 1395-402. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12389619&dopt=Abstract •
Treatment of HBV-carrying lymphoma patients with Rituximab and CHOP: a diagnostic and therapeutic challenge. Author(s): Skrabs C, Muller C, Agis H, Mannhalter C, Jager U. Source: Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2002 September; 16(9): 1884-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12200717&dopt=Abstract
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Treatment of large cell lymphoma in elderly patients with a mitoxantrone, cyclophosphamide, etoposide, and prednisone regimen: long-term follow-up results. Author(s): Rigacci L, Carpaneto A, Alterini R, Carrai V, Bernardi F, Bellesi G, Longo G, Bosi A, Rossi Ferrini P. Source: Cancer. 2003 January 1; 97(1): 97-104. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12491510&dopt=Abstract
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Treatment of lymphoma relapses after allogeneic hematopoietic stem cell transplantation with intensive chemotherapy followed by infusion of hematopoietic stem cell from the original donor. Author(s): Au WY, Lie AK, Siu LL, Chan EC, Ooi GC, Leung AY, Liang R, Kwong YL. Source: Annals of Hematology. 2003 September; 82(9): 548-51. Epub 2003 July 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14504811&dopt=Abstract
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Treatment paradigms in aggressive non-Hodgkin's lymphoma in elderly patients. Author(s): Coiffer B. Source: Clin Lymphoma. 2002 December; 3 Suppl 1: S12-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12521384&dopt=Abstract
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Treatment results of aggressive B non-Hodgkin's lymphoma in advanced age considering comorbidity. Author(s): Sonnen R, Schmidt WP, Kuse R, Schmitz N. Source: British Journal of Haematology. 2002 December; 119(3): 634-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12437637&dopt=Abstract
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Two cases of therapy-related acute promyelocytic leukemia (t-APL) after mantle cell lymphoma and gestational trophoblastic disease. Author(s): Au WY, Ma SK, Chung LP, Chim CS, Kwong YL. Source: Annals of Hematology. 2002 November; 81(11): 659-61. Epub 2002 November 06. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12454706&dopt=Abstract
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Unrelated bone marrow transplantation for non-Hodgkin's lymphoma: a study from the Japan Marrow Donor Program.
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Author(s): Izutsu K, Kanda Y, Ohno H, Sao H, Ogawa H, Miyazaki Y, Kawa K, Kodera Y, Kato S, Morishima Y, Hirai H. Source: Blood. 2003 November 6 [epub Ahead of Print] http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14604976&dopt=Abstract •
Unusual sites of involvement in non-Hodgkin's lymphoma: Case 2. Isolated meningeal anaplastic large-cell lymphoma. Author(s): Aloulou S, Bosq J, Vanel D, Ribrag V. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 November 1; 20(21): 4395-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12409340&dopt=Abstract
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Unusual sites of involvement in non-Hodgkin's lymphoma: Case 3. Intussusception as a rare complication of mantle-cell lymphoma. Author(s): Sucker C, Klima KM, Doelken G, Heidecke CD, Lorenz G, Stockschlaeder M. Source: Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 2002 November 1; 20(21): 4397-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12409341&dopt=Abstract
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Update on hybrid conjugate-view SPECT tumor dosimetry and response in 131Itositumomab therapy of previously untreated lymphoma patients. Author(s): Koral KF, Dewaraja Y, Li J, Lin Q, Regan DD, Zasadny KR, Rommelfanger SG, Francis IR, Kaminski MS, Wahl RL. Source: Journal of Nuclear Medicine : Official Publication, Society of Nuclear Medicine. 2003 March; 44(3): 457-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12621015&dopt=Abstract
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Use of FISH in an aggressive diffuse large B cell lymphoma. Author(s): Smith A, Kirkpatrick P, St Heaps L, Sharma P, Roman M, Harvey T, Crombie C. Source: Pathology. 2003 February; 35(1): 90-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12701697&dopt=Abstract
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Use of random skin biopsy to diagnose intravascular lymphoma presenting as fever of unknown origin. Author(s): Gill S, Melosky B, Haley L, ChanYan C. Source: The American Journal of Medicine. 2003 January; 114(1): 56-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12543290&dopt=Abstract
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Value of F-18 fluorodeoxyglucose positron emission tomography for predicting the clinical outcome of patients with aggressive lymphoma prior to and after autologous stem-cell transplantation. Author(s): Filmont JE, Czernin J, Yap C, Silverman DH, Quon A, Phelps ME, Emmanouilides C.
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Source: Chest. 2003 August; 124(2): 608-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12907550&dopt=Abstract •
VIII International Conference on malignant lymphoma. June 12-15, 2002 Lugano, Switzerland. Author(s): Gibson AD, D'Orazio A. Source: Clin Lymphoma. 2002 September; 3(2): 75-81. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12435279&dopt=Abstract
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When lymphoma and heart failure cross paths. Author(s): Nomiyama K, Shibuya T, Kataoka C, Aoki Y. Source: Journal of Hematotherapy & Stem Cell Research. 2003 February; 12(1): 7-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12662430&dopt=Abstract
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You're the flight surgeon. Non-Hodgkins lymphoma. Author(s): O'Donnell KR, Kane PD. Source: Aviation, Space, and Environmental Medicine. 2003 July; 74(7): 785-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12862336&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
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The following is a specific Web list relating to lymphoma; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •
General Overview Aids and Hiv Source: Integrative Medicine Communications; www.drkoop.com Amyloidosis Source: Integrative Medicine Communications; www.drkoop.com Cancer Prevention and Diet Source: Healthnotes, Inc.; www.healthnotes.com Celiac Disease Source: Healthnotes, Inc.; www.healthnotes.com Dermatitis Herpetiformis Source: Healthnotes, Inc.; www.healthnotes.com High Cholesterol Source: Integrative Medicine Communications; www.drkoop.com Hiv and Aids Source: Integrative Medicine Communications; www.drkoop.com Hypercholesterolemia Source: Integrative Medicine Communications; www.drkoop.com Lymphoma Source: Integrative Medicine Communications; www.drkoop.com Uveitis Source: Integrative Medicine Communications; www.drkoop.com
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Herbs and Supplements Aloe Alternative names: Aloe vera L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Aristolochia Alternative names: Snakeroot, Guaco; Aristolochia sp Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Bryonia Bryony Alternative names: Bryony; Bryonia sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
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Coenzyme Q10 Source: Integrative Medicine Communications; www.drkoop.com Coq10 Source: Integrative Medicine Communications; www.drkoop.com Curcuma Alternative names: Turmeric; Curcuma longa L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Melatonin Source: Integrative Medicine Communications; www.drkoop.com Phytolacca Alternative names: Poke root, Endod; Phytolacca dodecandra L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Thuja Occid Alternative names: Arbor Vitae; Thuja occidentalis Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Turmeric Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10062,00.html Uncaria Catclaw Alternative names: Cat's Claw, Uno de Gato; Uncaria tomentosa (Willd.) D.C. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Zingiber Alternative names: Ginger; Zingiber officinale Roscoe Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON LYMPHOMA Overview In this chapter, we will give you a bibliography on recent dissertations relating to lymphoma. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “lymphoma” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on lymphoma, we have not necessarily excluded nonmedical dissertations in this bibliography.
Dissertations on Lymphoma ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to lymphoma. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
A Case-control Study of Hepatitis C Virus Infection and Non-hodgkin's Lymphoma in Egypt by Cowgill, Karen Deirdre; PhD from The Johns Hopkins University, 2002, 209 pages http://wwwlib.umi.com/dissertations/fullcit/3046437
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Antidepressant Medication Use and the Risk of Non-hodgkin's Lymphoma: a Population-based Case-control Study by Bahl, Saira; MSC from University of Toronto (canada), 2002, 105 pages http://wwwlib.umi.com/dissertations/fullcit/MQ73827
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Bystander Cells and Prognosis in Hodgkin Lymphoma by Molin, Daniel; PhD from Uppsala Universitet (Sweden), 2002, 86 pages http://wwwlib.umi.com/dissertations/fullcit/f824721
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Cell Surface Proteins in Canine Malignant Lymphoma Identification of the T200 Glycoprotein Family by Sarmiento, Ulla Maija Kumpunen; PhD from University of Guelph (Canada), 1986 http://wwwlib.umi.com/dissertations/fullcit/NL28985
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Cell Types in Canine Lymphoma Morphology, Morphometry, Phenotypes, and Prognostic Correlations by Carter, Ronald Frederick; PhD from University of Guelph (Canada), 1988 http://wwwlib.umi.com/dissertations/fullcit/NL40522
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Cellular Antigens in Bovine Lymphoma by Jacobs, R. M; PhD from University of Guelph (Canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK43809
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Characterization of Genetic Events Involving Igh Switch Regions in Gastric Lowgrade Malt Lymphomas and B-cll by Nardini, Elena; PhD from Open University (United Kingdom), 2002 http://wwwlib.umi.com/dissertations/fullcit/f428545
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Characterization of Kaposi's Sarcoma Associated Herpesvirus (kshv) Infection of Primary Effusion Lymphoma Cell Lines and Dermal Microvascular Endothelial Cells by Poole, Lynn Janet; PhD from The Johns Hopkins University, 2002, 232 pages http://wwwlib.umi.com/dissertations/fullcit/3028317
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Circulating Tumor Markers in Extranodal Lymphomas by Lei, Ieng Kit Kenny; Md from Chinese University of Hong Kong (People's Republic of China), 2003, 118 pages http://wwwlib.umi.com/dissertations/fullcit/3077691
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Cloning of Pma-induced Cdna Sequences from El4 Mouse Lymphoma Cells by Elliott, John Francis; PhD from University of Alberta (Canada), 1987 http://wwwlib.umi.com/dissertations/fullcit/NL37614
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Constitutive Activation of Nf-kappab Virally-associated Lymphomas: Analysis of Pro-survival Pathways and Therapeutic Potential by Pharmacological Inhibition by Keller, Shannon A.; PhD from Cornell University Medical College, 2002, 144 pages http://wwwlib.umi.com/dissertations/fullcit/3057636
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Dysregulated Lymphocyte Homeostasis in Diabetes and Lymphoma Development by Chiu, Priscilla Pui Lam; PhD from University of Toronto (canada), 2002, 223 pages http://wwwlib.umi.com/dissertations/fullcit/NQ74727
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Effect of Highly Active Antiretroviral Therapy on Survival among Hiv-infected Men with Kaposi's Sarcoma or Non-hodgkin's Lymphoma by Tam, Henry Ky; PhD from University of California, Los Angeles, 2002, 113 pages http://wwwlib.umi.com/dissertations/fullcit/3066460
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Genetic Analysis of Murine Leukemia Virus-induced Leukemia and Lymphoma Indicates a Role for Rho Family Guanosine Triphosphatase Signaling in Oncogenesis by Himmel, Karen Lynn; PhD from University of Minnesota, 2002, 119 pages http://wwwlib.umi.com/dissertations/fullcit/3058643
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Hodgkin Lymphoma: Studies of Advanced Stages, Relapses and the Relation to Nonhodgkin Lymphomas by Amini, Rose-Marie; PhD from Uppsala Universitet (Sweden), 2002, 64 pages http://wwwlib.umi.com/dissertations/fullcit/f824657
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Living Beyond the Sword of Damocles: the Quality of Life of Long-term Survivors of Leukemia and Lymphoma by Zebrack, Bradley Jay; PhD from University of Michigan, 1999, 255 pages http://wwwlib.umi.com/dissertations/fullcit/9959895
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Mechanism of Dna Damage, Cell Cycle Arrest and Apoptosis in Indolent B-cell Lymphomas by Mensah-Osman, Edith Josephine; PhD from Wayne State University, 2003, 124 pages http://wwwlib.umi.com/dissertations/fullcit/3086452
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Pathogenesis of Chemically Induced Malignant Lymphoma in Mice by Joshi, Vijay V; Advdeg from The University of Western Ontario (Canada), 1970 http://wwwlib.umi.com/dissertations/fullcit/NK06974
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Pathways Leading to Apoptosis Resistance in a Murine B-cell Lymphoma Cell System by Kurland, John Ford; PhD from The Univ. of Texas H.S.C. at Houston Grad. Sch. of Biomed. Sci., 2003, 124 pages http://wwwlib.umi.com/dissertations/fullcit/3083497
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Regulation of the Epstein-Barr Virus Ebna-1 Promoter in Burkitt Lymphoma by Crum, Michelle Mary; PhD from The University of Tennessee Center for the Health Sciences, 2002, 156 pages http://wwwlib.umi.com/dissertations/fullcit/3067790
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Role of Mitochondrial Sensitivity and Preferential Activation of Map Kinase Pathways in Regulating Drug Sensitivity and Resistance of Selected B-lymphoma Cell Lines by O'Brien, Kerry Ann; PhD from Cornell University, 2002, 225 pages http://wwwlib.umi.com/dissertations/fullcit/3050391
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The Effects of Hypoferremia on a Murine Lymphoma and a Comparison with Neisseria Meningitidis by Caldwell, Margaret; PhD from McGill University (Canada), 1987 http://wwwlib.umi.com/dissertations/fullcit/NL44329
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The Reduction of Nfkappab by Genistein in T Lymphoma Cell Lines Generated by Mink Cell Focus-forming Virus by Baxa, Dwayne Milton; PhD from Wayne State University, 2002, 89 pages http://wwwlib.umi.com/dissertations/fullcit/3071755
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The Role of Insulin Receptor Substrate-1 in Anaplastic Lymphoma Kinase Signaling by Kuo, Angera H.; PhD from Georgetown University Medical Center, 2003, 171 pages http://wwwlib.umi.com/dissertations/fullcit/3085392
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The Role of Ski/sno Oncoproteins As Negative Regulators of the Tgf-beta/smad Signaling Pathway in B-cell Non-hodgkin's Lymphoma (nhl-b) by Lo, Piao; PhD from The Univ. of Texas H.S.C. at Houston Grad. Sch. of Biomed. Sci., 2002, 72 pages http://wwwlib.umi.com/dissertations/fullcit/3046060
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The Role of Thec-myc Oncogene and Protein Kinase Ck2 in B Lymphoma Cells by Shen, Jian; PhD from Boston University, 2002, 203 pages http://wwwlib.umi.com/dissertations/fullcit/3031589
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Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. CLINICAL TRIALS AND LYMPHOMA Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning lymphoma.
Recent Trials on Lymphoma The following is a list of recent trials dedicated to lymphoma.8 Further information on a trial is available at the Web site indicated. •
10-Propargyl-10-Deazaaminopterin in Treating Patients With Recurrent or Refractory Non-Hodgkin's Lymphoma or Hodgkin's Lymphoma Condition(s): adult Hodgkin's lymphoma; adult non-Hodgkin's lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Memorial Sloan-Kettering Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of 10-propargyl-10-deazaaminopterin in treating patients who have recurrent or refractory non-Hodgkin's lymphoma or Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00052442
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Antineoplaston Therapy in Treating Patients With Low-Grade Non-Hodgkin's Lymphoma Condition(s): adult non-Hodgkin's lymphoma; Follicular Mixed Cell Lymphoma; follicular small cleaved cell lymphoma Study Status: This study is currently recruiting patients.
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These are listed at www.ClinicalTrials.gov.
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Sponsor(s): Burzynski Research Institute Purpose - Excerpt: RATIONALE: Antineoplastons are naturally occurring substances found in urine. Antineoplastons may inhibit the growth of cancer cells. PURPOSE: Phase II trial to study the effectiveness of antineoplaston therapy in treating patients who have low-grade non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003499 •
Antineoplaston Therapy in Treating Patients With Recurrent or Refractory HighGrade Stage II, Stage III, or Stage IV Non-Hodgkin's Lymphoma Condition(s): adult diffuse small noncleaved cell and Burkitt's lymphoma; adult immunoblastic large cell lymphoma; adult lymphoblastic lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Burzynski Research Institute Purpose - Excerpt: RATIONALE: Antineoplastons are naturally-occurring substances found in urine. Antineoplastons may inhibit the growth of cancer cells. PURPOSE: Phase II trial to study the effectiveness of antineoplaston therapy in treating patients with recurrent or refractory high-grade stage II, stage III, or stage IV non-Hodgkin's lymphoma following previous chemotherapy. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003501
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Antineoplaston Therapy in Treating Patients With Refractory or Recurrent Intermediate-Grade Stage II, Stage III, or Stage IV Non-Hodgkin's Lymphoma Condition(s): adult diffuse large cell lymphoma; adult diffuse mixed cell lymphoma; adult diffuse small cleaved cell lymphoma; Follicular Large Cell Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Burzynski Research Institute Purpose - Excerpt: RATIONALE: Antineoplastons are naturally-occurring substances found in urine. Antineoplastons may inhibit the growth of cancer cells. PURPOSE: Phase II trial to study the effectiveness of antineoplaston therapy in treating patients with refractory or recurrent intermediate-grade stage II, stage III, or stage IV nonHodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003500
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Autologous Cytotoxic T-Lymphocytes in Treating Patients With Relapsed EpsteinBarr Virus-Associated Hodgkin's Lymphoma or Non-Hodgkin's Lymphoma Condition(s): Hodgkin's lymphoma; childhood small noncleaved cell lymphoma; NonHodgkin's Lymphoma; post-transplant lymphoproliferative disorder; recurrent and refractory childhood Hodgkin's lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Baylor College of Medicine; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Biological therapies use different ways to stimulate the immune system and stop cancer cells from growing. Treating a person's cytotoxic T lymphocytes in the laboratory and reinfusing them may cause a stronger immune response to kill Epstein-Barr virus-associated cancer cells. PURPOSE: Phase I trial to study the effectiveness of autologous cytotoxic T-lymphocytes in treating patients who have relapsed Epstein-Barr virus-associated Hodgkin's lymphoma or non-Hodgkin's lymphoma. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00070226
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Biological Therapy in Treating Patients With Lymphoma or Lymphoproliferative Disease Condition(s): childhood Hodgkin's lymphoma; childhood non-Hodgkin's lymphoma; Leukemia; Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Memorial Sloan-Kettering Cancer Center Purpose - Excerpt: RATIONALE: Some types of lymphoma or lymphoproliferative disease are associated with Epstein-Barr virus. White blood cells from donors who are immune to Epstein-Barr virus may be an effective treatment for those cancers. PURPOSE: Phase I/II trial to study the effectiveness of biological therapy in treating patients with Epstein-Barr virus-associated lymphoma or lymphoproliferative disease. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002663
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Chemoradiotherapy and Peripheral Stem Cell Transplantation Compared With Combination Chemotherapy in Treating Patients With Non-Hodgkin's Lymphoma Condition(s): adult diffuse large cell lymphoma; adult diffuse mixed cell lymphoma; adult diffuse small cleaved cell lymphoma; adult diffuse small noncleaved cell and Burkitt's lymphoma; adult immunoblastic large cell lymphoma; Follicular Large Cell Lymphoma Study Status: This study is currently recruiting patients.
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Sponsor(s): Southwest Oncology Group; National Cancer Institute (NCI); Cancer and Leukemia Group B; Eastern Cooperative Oncology Group; National Cancer Institute of Canada Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage cancer cells. Peripheral stem cell transplantation may allow the doctor to give higher doses of chemotherapy and radiation and kill more cancer cells. It is not yet known whether chemoradiotherapy plus peripheral stem cell transplantation is more effective than combination chemotherapy alone in treating nonHodgkin's lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of chemoradiotherapy plus peripheral stem cell transplantation with combination chemotherapy in treating patients who have stage II, stage III, or stage IV non-Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004031 •
Chemotherapy and Radiation Therapy Plus Bone Marrow or Peripheral Stem Cell Transplantation in Treating Patients With Relapsed or Refractory T-cell Lymphoma, Hodgkin's Lymphoma, or Non-Hodgkin's Lymphoma Condition(s): adult Hodgkin's lymphoma; adult non-Hodgkin's lymphoma; Cutaneous T-Cell Lymphoma; mycosis fungoides and Sezary syndrome Study Status: This study is currently recruiting patients. Sponsor(s): Robert H. Lurie Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage cancer cells. Bone marrow or peripheral stem cell transplantation may allow the doctor to give higher doses of chemotherapy drugs and radiation therapy and kill more cancer cells. PURPOSE: Phase I/II trial to study the effectiveness of chemotherapy and radiation therapy plus bone marrow or peripheral stem cell transplantation in treating patients who have refractory or relapsed T-cell lymphoma, Hodgkin's lymphoma, or non-Hodgkin's lymphoma. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004907
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Combination Chemotherapy and Bone Marrow and/or Peripheral Stem Cell Transplantation in Treating Patients With Non-Hodgkin's Lymphoma Condition(s): adult diffuse large cell lymphoma; adult diffuse mixed cell lymphoma; adult diffuse small cleaved cell lymphoma; adult diffuse small noncleaved cell and Burkitt's lymphoma; adult immunoblastic large cell lymphoma; adult lymphoblastic lymphoma Study Status: This study is currently recruiting patients.
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Sponsor(s): Fox Chase Cancer Center Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Bone marrow and peripheral stem cell transplantation may allow doctors to give high doses of chemotherapy and kill more tumor cells. PURPOSE: Phase II trial to study the effectiveness of combination chemotherapy with cyclophosphamide, etoposide and cisplatin followed by bone marrow and/or peripheral stem cell transplantation in patients with relapsed or refractory intermediate- or high-grade non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002521 •
Combination Chemotherapy Followed By Radiation Therapy in Treating Patients With Aggressive Non-Hodgkin's Lymphoma Condition(s): adult non-Hodgkin's lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): German High-Grade Non-Hodgkin's Lymphoma Study Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug and giving the drugs in different ways may kill more cancer cells. Radiation therapy uses high-energy x-rays to damage cancer cells. It is not yet known which combination chemotherapy regimen followed by radiation therapy is more effective in treating aggressive non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of two combination chemotherapy regimens followed by radiation therapy in treating patients who have aggressive non-Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00053768
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Combination Chemotherapy in Treating Patients With Aggressive Non-Hodgkin's Lymphoma Condition(s): adult diffuse large cell lymphoma; adult diffuse mixed cell lymphoma; adult immunoblastic large cell lymphoma; Follicular Large Cell Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): British National Lymphoma Investigation Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. It is not yet known which regimen of combination chemotherapy is most effective for non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of two regimens of combination chemotherapy in treating patients who have aggressive non-Hodgkin's lymphoma. Phase(s): Phase III
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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005867 •
Combination Chemotherapy in Treating Patients With Previously Untreated Advanced Hodgkin's Lymphoma Condition(s): adult Hodgkin's lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): British National Lymphoma Investigation Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. It is not yet known which combination chemotherapy regimen is more effective in treating patients who have advanced Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of two different combination chemotherapy regimens in treating patients who have advanced Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00041210
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Combination Chemotherapy in Treating Patients With Recurrent or Refractory Leukemia or Lymphoma Condition(s): childhood Hodgkin's lymphoma; childhood non-Hodgkin's lymphoma; Leukemia; Lymphoma; myelodysplastic and myeloproliferative diseases Study Status: This study is currently recruiting patients. Sponsor(s): Ireland Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of combining cytarabine and mitoxantrone in treating patients who have recurrent or refractory leukemia or lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00047021
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Combination Chemotherapy Plus Filgrastim in Treating Patients With HIV-Related Non-Hodgkin's Lymphoma Condition(s): AIDS-Related Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): British National Lymphoma Investigation
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Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. Colony-stimulating factors such as filgrastim may increase the number of immune cells found in bone marrow or peripheral blood and may help a person's immune system recover from the side effects of chemotherapy. PURPOSE: Phase I/II trial to study the effectiveness of combining filgrastim with combination chemotherapy in treating patients who have HIV-related non-Hodgkin's lymphoma. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00032149 •
Combination Chemotherapy Plus Filgrastim With or Without Rituximab in Treating Older Patients With Non-Hodgkin's Lymphoma Condition(s): adult diffuse large cell lymphoma; adult low grade non-Hodgkin's lymphoma; adult non-Hodgkin's lymphoma; Follicular Large Cell Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Commissie Voor Klinisch Toegepast Onderzoek Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Monoclonal antibodies such as rituximab can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal cells. Combining monoclonal antibody therapy with chemotherapy may kill more tumor cells. It is not yet known if combination chemotherapy plus filgrastim is more effective with or without rituximab in treating non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to determine the effectiveness of combination chemotherapy plus filgrastim with or without rituximab in treating older patients who have non-Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00028717
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Combination Chemotherapy Plus Peripheral Stem Cell Transplantation in Treating Patients With Newly Diagnosed Aggressive Non-Hodgkin's Lymphoma Condition(s): adult diffuse large cell lymphoma; adult diffuse mixed cell lymphoma; adult immunoblastic large cell lymphoma; anaplastic large cell lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Swiss Institute for Applied Cancer Research Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining peripheral stem cell transplantation with more than one drug regimen may kill more tumor cells. It is not known whether receiving standard combination chemotherapy alone is more effective than receiving multiple combination chemotherapy plus peripheral stem cell transplantation for aggressive non-Hodgkin's lymphoma. PURPOSE: Randomized
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phase III trial to compare the effectiveness of standard combination chemotherapy alone with that of multiple combination chemotherapy regimens plus peripheral stem cell transplantation in treating patients who have newly diagnosed aggressive nonHodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003215 •
Combination Chemotherapy With or Without Etoposide in Treating Older Patients With Non-Hodgkin's Lymphoma Condition(s): adult T-cell leukemia and lymphoma; Cutaneous T-Cell Lymphoma; NonHodgkin's Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): EORTC Lymphoma Cooperative Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. It is not yet known which combination chemotherapy regimen is more effective in treating non-Hodgkin's lymphoma. PURPOSE: Randomized phase II/III trial to compare the effectiveness of combination chemotherapy with or without etoposide in treating older patients who have nonHodgkin's lymphoma that has not been previously treated. Phase(s): Phase II; Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00060385
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Combination Chemotherapy With or Without Monoclonal Antibody Therapy in Treating Patients With Newly Diagnosed Non-Hodgkin's Lymphoma Condition(s): Follicular Large Cell Lymphoma; Follicular Mixed Cell Lymphoma; follicular small cleaved cell lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Southwest Oncology Group; National Cancer Institute (NCI); Cancer and Leukemia Group B Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Monoclonal antibodies can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal cells. It is not yet known whether combination chemotherapy is more effective with or without monoclonal antibody therapy for non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of combination chemotherapy with or without monoclonal antibody therapy in treating patients who have newly diagnosed non-Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006721 •
Combination Chemotherapy With or Without Rituximab in Treating Older Patients With Non-Hodgkin's Lymphoma Condition(s): adult T-cell leukemia and lymphoma; anaplastic large cell lymphoma; angioimmunoblastic T-cell lymphoma; childhood small noncleaved cell lymphoma; Non-Hodgkin's Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): German High-Grade Non-Hodgkin's Lymphoma Study Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Monoclonal antibodies such as rituximab can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal cells. It is not yet known whether combination chemotherapy is more effective with or without rituximab in treating aggressive non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of cyclophosphamide, doxorubicin, vincristine, and prednisone with or without rituximab in treating older patients who have aggressive non-Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00052936
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Combination Chemotherapy With or Without Rituximab in Treating Patients With Relapsed Non-Hodgkin's Lymphoma Condition(s): Follicular Large Cell Lymphoma; Follicular Mixed Cell Lymphoma; follicular small cleaved cell lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): EORTC Lymphoma Cooperative Group; British National Lymphoma Investigation; Stichting Hemato-Oncologie voor Volwassenen Nederland; Australian New Zealand Lymphoma Group; National Cancer Institute of Canada; Nordic Lymphoma Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Monoclonal antibodies such as rituximab can locate cancer cells and either kill them or deliver cancer-killing substances to them without harming normal cells. It is not yet known whether chemotherapy is more effective with or without rituximab for relapsed non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of combination chemotherapy with or without rituximab in treating patients who have relapsed non-Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004179
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Combination Chemotherapy, Peripheral Stem Cell Transplantation, and Biological Therapy in Treating Patients With Solid Tumors or Lymphoma Condition(s): adult solid tumor; childhood Hodgkin's lymphoma; childhood nonHodgkin's lymphoma; childhood solid tumor; Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Fred Hutchinson Cancer Research Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining chemotherapy with peripheral stem cell transplantation may allow the doctor to give higher doses of chemotherapy drugs and kill more tumor cells. Biological therapies such as interleukin-2 use different ways to stimulate the immune system and stop cancer cells from growing. PURPOSE: Phase II trial to study the effectiveness of combination chemotherapy, peripheral stem cell transplantation, and interleukin-2 in treating patients who have solid tumors or lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00027937
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Depsipeptide to Treat T-Cell Lymphomas Condition(s): Cutaneous T Cell Lymphoma; Peripheral T Cell Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: This study will test the safety and effectiveness of a new anticancer drug called depsipeptide in treating T-cell lymphomas. Depsipeptide has been shown to kill cancer cells in laboratory studies and to shrink various kinds of tumors in animal models. This study will evaluate the response of T-cell lymphomas to depsipeptide and determine how well patients tolerate the drug over a period of several months. Patients with peripheral T-cell lymphoma and cutaneous T-cell lymphoma (Sezary syndrome and mycosis fungoides) 18 years of age or older may be eligible for this study. Candidates will be screened with a medical history and physical examination, computerized tomography (CT) scans of the chest, abdomen and pelvis, electrocardiogram, blood tests, and possibly a bone marrow biopsy. For the biopsy, the hip area is anesthetized and bone marrow is drawn from the hipbone using a special needle. Participants will receive an intravenous (through a vein) infusion of depsipeptide on days 1 and 5 of each 21-day treatment cycle. The drug will be infused over 4 hours through an arm vein or through a central line (a catheter placed under the skin of the chest or neck and passed into a major vein). This catheter is used to deliver the chemotherapy and to draw blood samples for tests to measure the effects of the drug on the body and on the cancer cells. Patients will be admitted to the hospital for the first treatment cycle. If medically feasible, subsequent cycles will be administered on an outpatient basis. Patients may also be asked to undergo additional tumor biopsies before and after treatment and to have a procedure called apheresis, in which immune cells of the blood are collected. For this procedure, whole blood is collected through a needle placed in an arm vein. The blood circulates through a machine that separates it into its components. The white cells are removed, and the red cells, platelets and plasma are
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returned to the body, either through the same needle used to draw the blood or through a second needle placed in the other arm. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00007345 •
Filgrastim and Chemotherapy Followed by Peripheral Stem Cell Transplantation in Treating Patients With Hodgkin's Lymphoma or Non-Hodgkin's Lymphoma Condition(s): Hodgkin's lymphoma; adult T-cell leukemia and lymphoma; NonHodgkin's Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): University of Minnesota Cancer Center Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining chemotherapy with peripheral stem cell transplantation may allow the doctor to give higher doses of chemotherapy drugs and kill more tumor cells. Colony-stimulating factors such as filgrastim may increase the number of immune cells found in bone marrow or peripheral blood and may help a person's immune system recover from the side effects of chemotherapy. PURPOSE: Phase II trial to study the effectiveness of filgrastim and chemotherapy followed by peripheral stem transplantation in treating patients who have Hodgkin's lymphoma or non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005985
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Fludarabine and Cyclophosphamide Followed by Peripheral Transplantation in Treating Patients With Leukemia or Lymphoma
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Condition(s): adult non-Hodgkin's lymphoma; Chronic Lymphocytic Leukemia; Prolymphocytic Leukemia Study Status: This study is currently recruiting patients. Sponsor(s): Cancer and Leukemia Group B; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Peripheral stem cell transplantation may be able to replace immune cells that were destroyed by chemotherapy. PURPOSE: Phase II trial to study the effectiveness of fludarabine and cyclophosphamide followed by peripheral stem cell transplantation in treating patients who have leukemia or lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006252
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FR901228 in Treating Patients With T-Cell Lymphoma Condition(s): adult non-Hodgkin's lymphoma; anaplastic large cell lymphoma; Cutaneous T-Cell Lymphoma; mycosis fungoides and Sezary syndrome Study Status: This study is currently recruiting patients. Sponsor(s): National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of FR901228 in treating patients who have T-cell lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00020436
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Molecular Risk Assessment in Planning Treatment for Patients With Non-Hodgkin's Lymphoma Condition(s): adult diffuse large cell lymphoma; childhood diffuse large cell lymphoma; childhood large cell lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Ireland Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Analyzing genes that are present in cancer cells may be useful as a method for predicting the response of non-Hodgkin's lymphoma to cancer treatment. Imaging procedures such as positron emission tomography (PET) scans may improve the ability to measure how well cancer has responded to treatment. PURPOSE: Phase II trial to study the effectiveness of molecular risk assessment in predicting response to therapy in patients who are receiving treatment for non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00055640
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Oblimersen and Gemcitabine in Treating Patients With Advanced Solid Tumor or Lymphoma Condition(s): adult Hodgkin's lymphoma; adult T-cell leukemia and lymphoma; adult non-Hodgkin's lymphoma; adult solid tumor; Cutaneous T-Cell Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Stanford University; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy such as gemcitabine use different ways to stop cancer cells from dividing so they stop growing or die. Oblimersen may increase the effectiveness of gemcitabine by making cancer cells more sensitive to the drug. PURPOSE: Phase I trial to study the effectiveness of combining oblimersen with gemcitabine in treating patients who have metastatic or unresectable solid tumors or lymphoma. Phase(s): Phase I
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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00060112 •
Oxaliplatin in Treating Patients With Relapsed or Refractory Non-Hodgkin's Lymphoma Condition(s): Waldenstrom's Macroglobulinemia; adult T-cell leukemia and lymphoma; adult non-Hodgkin's lymphoma; angioimmunoblastic T-cell lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): M.D. Anderson Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of oxaliplatin in treating patients who have relapsed or refractory non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006473
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Pegfilgrastim Compared With Filgrastim To Increase Peripheral Stem Cells Before Autologous Stem Cell Transplantation in Treating Patients With Lymphoma Condition(s): adult Hodgkin's lymphoma; adult non-Hodgkin's lymphoma; Cutaneous T-Cell Lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Jonsson Comprehensive Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Colony-stimulating factors such as filgrastim and pegfilgrastim may increase the number of peripheral stem cells that can be collected during leukapheresis. Autologous stem cell transplantation may allow the doctor to give higher doses of chemotherapy drugs and kill more cancer cells. PURPOSE: Randomized phase II trial to compare the effectiveness of pegfilgrastim with that of filgrastim in increasing the number of peripheral stem cells in patients who are undergoing autologous stem cell transplantation for Hodgkin's lymphoma or non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00060229
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Pegfilgrastim in Treating Neutropenia After Chemotherapy in Patients With Mantle Cell or Diffuse Large B-Cell Non-Hodgkin's Lymphoma Condition(s): adult diffuse large cell lymphoma; adult low grade non-Hodgkin's lymphoma; adult non-Hodgkin's lymphoma; Neutropenia Study Status: This study is currently recruiting patients.
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Sponsor(s): Jonsson Comprehensive Cancer Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Colony-stimulating factors such as pegfilgrastim may increase the number of immune system cells found in bone marrow or peripheral blood and may be effective in preventing or controlling neutropenia caused by chemotherapy. PURPOSE: Randomized phase II trial to compare the effectiveness of two pegfilgrastim regimens in treating neutropenia after chemotherapy in patients who have mantle cell or diffuse large B-cell non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00066833 •
Peripheral Stem Transplantation in Treating Patients With Refractory or Relapsed Non-Hodgkin's Lymphoma Condition(s): adult non-Hodgkin's lymphoma; childhood large cell lymphoma; childhood lymphoblastic lymphoma; childhood small noncleaved cell lymphoma; Graft Versus Host Disease Study Status: This study is currently recruiting patients. Sponsor(s): Fred Hutchinson Cancer Research Center; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining chemotherapy with autologous and allogeneic peripheral stem cell transplantation may allow the doctor to give higher doses of chemotherapy drugs to kill more tumor cells. PURPOSE: Phase I/II trial to study the effectiveness of autologous peripheral stem cell transplantation followed by allogeneic peripheral stem cell transplantation in treating patients who have refractory or relapsed non-Hodgkin's lymphoma. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005803
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Radiation Therapy in Treating Patients With Stage I or Stage II Non-Hodgkin's Lymphoma Condition(s): adult non-Hodgkin's lymphoma; Follicular Large Cell Lymphoma; Follicular Mixed Cell Lymphoma; follicular small cleaved cell lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): EORTC Lymphoma Cooperative Group; EORTC Radiotherapy Cooperative Group Purpose - Excerpt: RATIONALE: Radiation therapy uses high-energy x-rays to damage tumor cells. Giving radiation therapy in different ways may kill more tumor cells. It is not yet known which regimen of radiation therapy is more effective for non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of radiation therapy to the involved area with or without total-body irradiation in treating patients who have stage I or stage II non-Hodgkin's lymphoma that has not previously been treated.
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Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00014326 •
Vaccine Therapy and Sargramostim After Rituximab in Treating Patients With Refractory or Progressive Non-Hodgkin's Lymphoma Condition(s): Follicular Large Cell Lymphoma; Follicular Mixed Cell Lymphoma; follicular small cleaved cell lymphoma Study Status: This study is currently recruiting patients. Sponsor(s): Genitope Purpose - Excerpt: RATIONALE: Monoclonal antibodies such as rituximab can locate cancer cells and either kill them or deliver cancer-killing substances to them without harming normal cells. Vaccines made from a person's cancer cells may make the body build an immune response to kill cancer cells. Colony-stimulating factors such as sargramostim may increase the number of immune cells found in bone marrow or peripheral blood. PURPOSE: Phase II trial to study the effectiveness of rituximab followed by vaccine therapy and sargramostim in treating patients who have refractory or progressive non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00071955
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Bryostatin 1 and Interleukin-2 in Treating Patients With Refractory Solid Tumors or Lymphoma Condition(s): Hodgkin's Disease; Non-Hodgkin's Lymphoma; Lymphoid Leukemia; Central Nervous System Lymphoma; Eye Lymphoma; Skin Cancer; Solid Tumor Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute on Aging (NIA); National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Interleukin-2 may stimulate a person's white blood cells to kill cancer cells. Combining chemotherapy and interleukin-2 may kill more cancer cells. PURPOSE: Phase I trial to study the effectiveness of bryostatin 1 and interleukin-2 in treating patients who have refractory solid tumors or lymphoma. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003993
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Chemotherapy and Radiation Therapy Plus Bone Marrow Transplantation in Treating Patients With Aggressive Non-Hodgkin's Lymphoma Condition(s): adult non-Hodgkin's lymphoma
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Study Status: This study is no longer recruiting patients. Sponsor(s): Scotland and Newcastle Lymphoma Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Radiation therapy uses high-energy x-rays to damage cancer cells. Bone marrow transplantation may allow doctors to give higher doses of chemotherapy drugs and kill more cancer cells. PURPOSE: Randomized phase III trial to study the effectiveness of chemotherapy and radiation therapy plus bone marrow transplantation in treating patients who have aggressive non-Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003815 •
Combination Chemotherapy in Treating Patients With AIDS-Related Lymphoma Condition(s): AIDS-related diffuse small cleaved cell lymphoma; AIDS-related small noncleaved cell lymphoma; AIDS-related lymphoblastic lymphoma; AIDS-related diffuse mixed cell lymphoma; AIDS-related immunoblastic large cell lymphoma; AIDSrelated peripheral/systemic lymphoma; AIDS-related diffuse large cell lymphoma; anaplastic large cell lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Eastern Cooperative Oncology Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of combination chemotherapy consisting of liposomal doxorubicin, cyclophosphamide, vincristine, and prednisone in treating patients with AIDS -related lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003388
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Combination Chemotherapy in Treating Patients With Hodgkin's Disease or NonHodgkin's Lymphoma That Has Not Responded to Previous Treatment Condition(s): recurrent grade III follicular large cell lymphoma; recurrent adult immunoblastic large cell lymphoma; recurrent adult diffuse small noncleaved cell/Burkitt's lymphoma; recurrent adult diffuse mixed cell lymphoma; recurrent mantle cell lymphoma; recurrent adult diffuse large cell lymphoma; recurrent adult Hodgkin's disease Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute of Canada Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one drug may kill more tumor cells. PURPOSE: Phase II trial to study the effectiveness of
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combination chemotherapy in treating patients who have Hodgkin's disease or nonHodgkin's lymphoma that has not responded to previous treatment. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00014209 •
Combination Chemotherapy in Treating Patients With Newly Diagnosed Mantle Cell Lymphoma Condition(s): noncontiguous stage II mantle cell lymphoma; stage III mantle cell lymphoma; stage IV mantle cell lymphoma; contiguous stage II mantle cell lymphoma; stage I mantle cell lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); M.D. Anderson Cancer Center Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of different regimens of combination chemotherapy in treating patients with newly diagnosed mantle cell lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003311
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Combination Chemotherapy in Treating Patients With Non-Hodgkin's Lymphoma or Acute Lymphocytic Leukemia Condition(s): L3 adult acute lymphoblastic leukemia; stage IV adult diffuse small noncleaved cell/Burkitt's lymphoma; Burkitt's Lymphoma; stage IV childhood small noncleaved cell lymphoma; B-cell childhood acute lymphoblastic leukemia; stage III adult diffuse small noncleaved cell/Burkitt's lymphoma; B-cell adult acute lymphoblastic leukemia; L3 childhood acute lymphoblastic leukemia; stage III childhood small noncleaved cell lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Pediatric Oncology Group Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of combination chemotherapy in treating patients who have non-Hodgkin's lymphoma or acute lymphocytic leukemia. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005977
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Combination Chemotherapy With or Without Monoclonal Antibody Therapy in Treating Patients With Previously Untreated HIV-Associated Non-Hodgkin's Lymphoma Condition(s): AIDS-related small noncleaved cell lymphoma; Burkitt's Lymphoma; AIDS-related immunoblastic large cell lymphoma; AIDS-related peripheral/systemic lymphoma; AIDS-related diffuse large cell lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); AIDS Associated Malignancies Clinical Trials Consortium Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Monoclonal antibodies such as rituximab can locate cancer cells and either kill them or deliver cancer-killing substances to them without harming normal cells. It is not yet known whether combination chemotherapy plus monoclonal antibody therapy is more effective than combination chemotherapy alone in treating HIV -associated non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of combination chemotherapy with or without monoclonal antibody therapy in treating patients who have previously untreated HIV-associated non-Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003595
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Ifosfamide, Teniposide, and Paclitaxel in Treating Patients With Relapsed NonHodgkin's Lymphoma Condition(s): recurrent grade III follicular large cell lymphoma; recurrent adult immunoblastic large cell lymphoma; recurrent adult diffuse small noncleaved cell/Burkitt's lymphoma; recurrent adult diffuse mixed cell lymphoma; recurrent adult diffuse large cell lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute (NCI); Robert H. Lurie Cancer Center Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining more than one drug may kill more cancer cells. PURPOSE: Phase I/II trial to study the effectiveness of ifosfamide, teniposide, and paclitaxel in treating patients who have relapsed nonHodgkin's lymphoma. Phase(s): Phase I; Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00004916
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Liposomal Vincristine in Treating Patients With Refractory or Relapsed NonHodgkin's Lymphoma Condition(s): recurrent adult immunoblastic large cell lymphoma; recurrent adult T-cell leukemia/lymphoma; recurrent adult diffuse large cell lymphoma; anaplastic large cell lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): Inex Pharmaceuticals Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. PURPOSE: Phase II trial to study the effectiveness of liposomal vincristine in treating patients who have refractory or relapsed non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006383
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Monoclonal Antibody Therapy in Treating Patients With Follicular or Mantle Cell Lymphoma Condition(s): noncontiguous stage II mantle cell lymphoma; stage IV mantle cell lymphoma; recurrent mantle cell lymphoma; contiguous stage II mantle cell lymphoma; stage I mantle cell lymphoma; stage III mantle cell lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): Swiss Institute for Applied Cancer Research Purpose - Excerpt: RATIONALE: Monoclonal antibodies such as rituximab can locate cancer cells and either kill them or deliver cancer-killing substances to them without harming normal cells. It is not yet known which treatment regimen is more effective for lymphoma. PURPOSE: Randomized phase III trial to compare the effectiveness of different regimens of rituximab in treating patients who have follicular or mantle cell lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00003280
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Monoclonal Antibody Therapy in Treating Patients With Relapsed or Refractory Non-Hodgkin's Lymphoma Condition(s): recurrent diffuse small lymphocytic/marginal zone lymphoma; recurrent grade III follicular large cell lymphoma; recurrent grade I follicular small cleaved cell lymphoma; recurrent grade II follicular mixed cell lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): Protein Design Labs Purpose - Excerpt: RATIONALE: Monoclonal antibodies can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal cells. PURPOSE: Randomized phase II trial to compare the effectiveness of two different
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monoclonal antibody regimens in treating patients who have relapsed or refractory nonHodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00014664 •
Monoclonal Antibody Therapy, Paclitaxel, and Cyclosporine in Treating Patients With Recurrent or Refractory Non-Hodgkin's Lymphoma Condition(s): Burkitt's Lymphoma; Lymphocytic Lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): University of California Davis Cancer Center Purpose - Excerpt: RATIONALE: Monoclonal antibodies can locate tumor cells and either kill them or deliver tumor-killing substances to them without harming normal cells. Combining monoclonal antibody therapy with cyclosporine and paclitaxel may be an effective treatment for non-Hodgkin's lymphoma. PURPOSE: Phase I trial to study the effectiveness of radiolabeled monoclonal antibody therapy combined with paclitaxel and cyclosporine in treating patients who have recurrent or refractory non-Hodgkin's lymphoma. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00009776
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Radiation Therapy in Treating Patients With Relapsed or Refractory Non-Hodgkin's Lymphoma Who Have Undergone Stem Cell Transplantation Condition(s): recurrent adult diffuse small noncleaved cell/Burkitt's lymphoma; recurrent adult T-cell leukemia/lymphoma; recurrent adult diffuse large cell lymphoma; anaplastic large cell lymphoma; Waldenstrom's Macroglobulinemia Study Status: This study is no longer recruiting patients. Sponsor(s): National Cancer Institute of Canada Purpose - Excerpt: RATIONALE: Radiation therapy uses high-energy x-rays to damage tumor cells. It is not yet known if giving radiation therapy after stem cell transplantation is more effective than stem cell transplantation alone in treating relapsed or refractory non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to determine the effectiveness of radiation therapy in treating patients who have relapsed or refractory non-Hodgkin's lymphoma and have undergone autologous stem cell transplantation. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00031668
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TITLE:Less Intensive Therapy for Children With Non-Hodgkin's Lymphoma Condition(s): Burkitt's Lymphoma; Lymphoblastic Leukemia; Lymphocytic Lymphoma Study Status: This study is no longer recruiting patients. Sponsor(s): Children's Oncology Group; National Cancer Institute (NCI); Societe Francaise Oncologie Pediatrique; United Kingdom Children's Cancer Study Group Purpose - Excerpt: RATIONALE: Less intensive therapy may attain in the same results as intensive therapy in children with non-Hodgkin's lymphoma. PURPOSE: Randomized phase III trial to study the effectiveness of less intensive therapy for children who have non-Hodgkin's lymphoma. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00002757
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Combination Chemotherapy Followed by Bone Marrow or Peripheral Stem Cell Transplantation in Treating Patients With Non-Hodgkin's Lymphoma or Hodgkin's Lymphoma Condition(s): adult Hodgkin's lymphoma; adult non-Hodgkin's lymphoma Study Status: This study is completed. Sponsor(s): H. Lee Moffitt Cancer Center and Research Institute; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining chemotherapy with peripheral stem cell or bone marrow transplantation may allow the doctor to give higher doses of chemotherapy drugs and kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of combination chemotherapy followed by autologous bone marrow transplantation or peripheral stem cell transplantation in treating patients who have non-Hodgkin's lymphoma or Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006373
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Comparison of Two Combination Chemotherapy Regimens in Treating Patients With Previously Untreated Aggressive Stage II, Stage III, or Stage IV Non-Hodgkin's Lymphoma Condition(s): Lymphocytic Lymphoma; Non-Hodgkin's Lymphoma Study Status: This study is completed. Sponsor(s): National Cancer Institute (NCI); Cancer and Leukemia Group B Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Combining more than one chemotherapy drug may kill more tumor cells. It is not yet known which combination chemotherapy regimen is most effective in treating aggressive non-Hodgkin's lymphoma. PURPOSE: Randomized phase II trial to compare the effectiveness of two
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combination chemotherapy regimens in treating patients who have previously untreated aggressive stage II, stage III, or stage IV non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005964 •
Cyclophosphamide, Doxorubicin, Vincristine, Prednisone, and Radiation Therapy Followed By Rituximab and Yttrium Y 90 Ibritumomab Tiuxetan in Treating Patients With Stage I or Stage II Non-Hodgkin's Lymphoma Condition(s): adult diffuse large cell lymphoma; adult diffuse small noncleaved cell and Burkitt's lymphoma; adult low grade non-Hodgkin's lymphoma; adult non-Hodgkin's lymphoma; anaplastic large cell lymphoma Study Status: This study is not yet open for patient recruitment. Sponsor(s): Southwest Oncology Group; National Cancer Institute (NCI) Purpose - Excerpt: RATIONALE: Drugs used in chemotherapy, such as cyclophosphamide, doxorubicin, vincristine, and prednisone, use different ways to stop cancer cells from dividing so they stop growing or die. Radiation therapy uses highenergy x-rays to damage cancer cells. Monoclonal antibodies, such as rituximab and yttrium Y 90 ibritumomab tiuxetan, can locate cancer cells and either kill them or deliver radioactive cancer-killing substances to them without harming normal cells. Combining chemotherapy with radiation therapy and monoclonal antibody therapy may kill more cancer cells. PURPOSE: Phase II trial to study the effectiveness of combining combination chemotherapy with radiation therapy and monoclonal antibody therapy in treating patients who have stage I or stage II non-Hodgkin's lymphoma. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00070018
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “lymphoma” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials:
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For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON LYMPHOMA Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “lymphoma” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on lymphoma, we have not necessarily excluded nonmedical patents in this bibliography.
Patents on Lymphoma By performing a patent search focusing on lymphoma, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We will tell you how to obtain this information later in the chapter. The following is an 9Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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example of the type of information that you can expect to obtain from a patent search on lymphoma: •
Antigenic epitopes with LYM-1 reactivity and uses thereof Inventor(s): Meares; Claude F. (Davis, CA), O'Donnell; Robert T. (Sacramento, CA), Rose; Larry M. (Carmichael, CA) Assignee(s): The Regents of the University of California (Oakland, CA) Patent Number: 6,217,871 Date filed: October 28, 1998 Abstract: This invention provides novel peptide epitopes recognized by the nonHodgkin's B cell lymphoma reactive Lym-1 antibody. These novel peptide epitopes are capable of generating antibodies directed against Lym-1 peptide epitope expressing BNHL cells. This invention is also directed to the treatment of B-NHL. Excerpt(s): This invention has identified novel peptide epitopes recognized by the B cell lymphoma-reactive Lym-1 antibody. Because Lym-1 specifically reacts with nonHodgkin's B cell lymphoma cells, the invention provides an improved, accurate means to identify cancer patients potentially responsive to Lym-1 antibody used as a cytotoxic therapeutic reagent. The invention also provides methods of generating antibodies directed against non-Hodgkin's B cell lymphoma cells which can be used in the treatment of non-Hodgkin's B cell lymphoma. Low grade B-cell non-Hodgkin's lymphomas (B-NHL) represent a markedly heterogeneous group of lymphoproliferative disorders (Gaidano (1997) Leuk. Lymphoma 26 Suppl. 1:107-113; Gandini (1996) Cancer Genet Cytogenet. 86:120-123). A widely used treatment for these lymphomas involves administration of a B-NHL-specific antibody, called Lym-1. Lym-1 is a murine IgG.sub.2a monoclonal antibody. When conjugated to cytotoxic agents, Lym-1 targets and kills B-NHL lymphoma cells (see, e.g., Rose (1996) Cancer Immunol. Immunother. 43:26-30; Epstein (1987) Cancer Res. 47:830-840). Lym-1 has been radiolabeled with.sup.131 I (see, e.g., DeNardo (1997) Cancer 80:2706-2711) and conjugated to the ribosome inactivating protein gelonin (see, e.g., O'Boyle (1995) J. Immunother. Emphasis Tumor Immunol. 18:221-230). However, these reagents are inherently toxic, and not all B-NHL patients have Lym-1 reactive cancer cells. Thus, there is a need for a means to identify which patients will be responsive to such immunotherapy. While Lym-1 binding is associated with the expression of HLA DR10 by a patient, unfortunately, the absence of DR10, does not consistently correlate with the presence or absence of the Lym-1 reactive epitope. In another words, Lym-1 can react with HLA DR molecules other than DR10. Thus, there is a great need for a means to quickly, efficiently, and accurately determine the presence of a Lym-1 reactive epitope in a B-NHL cancer patient. The present invention, which for the first time identifies Lym-1 reactive peptide epitopes, fulfills these and other needs. Typically, no immune response is generated by the cancer patient against B-NHL cells. However, based on studies with other tumor specific antigens (e.g., PSA antigen in prostate cancer), identification of an immunogenic peptide, followed by its administration with adjuvant, can elicit a tumorspecific immune response (see, e.g., Correale (1998) J. Immunol. 161:3186-3194). See also, Gjertsen (1998) Vox Sang. 74 Suppl 2:489-495, who uses an immunogenic peptide from a carcinogenic, mutant ras polypeptide to generate an immune response to pancreaticand colorectal adenocarcinomas. The present invention, by identifying Lym-1 reactive epitopes on B-NHL cells, provides such a therapeutic immunogenic peptide. Web site: http://www.delphion.com/details?pn=US06217871__
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CD30 ligand oligomers and polypeptides Inventor(s): Armitage; Richard J. (Bainbridge Island, WA), Goodwin; Raymond G. (Seattle, WA), Gruss; Hans-Juergen (Bainbridge Island, WA), Smith; Craig A. (Seattle, WA) Assignee(s): Immunex Corporation (Seattle, WA) Patent Number: 6,143,869 Date filed: May 15, 1998 Abstract: There is disclosed a polypeptide (CD30-L) and DNA sequences, vectors and transformed host cells useful in providing CD30-L polypeptides. The CD30-L polypeptide binds to the receptor known as CD30, which is expressed on a number of cell types, among which are Hodgkin's Disease tumor cells, large cell anaplastic lymphoma cells, adult T-cell leukemia (T-ALL) cells, and a number of other malignant cell types. CD30-L polypeptides find use as carriers for delivering diagnostic and cytotoxic agents to cells expressing the CD30 receptor. Excerpt(s): Hodgkin's Disease is a human lymphoma, the etiology of which is still not well understood. The neoplastic cells of Hodgkin's Disease are known as Hodgkin and Reed-Sternberg (H-RS) cells. CD30 is a 120 kd surface antigen widely used as a clinical marker for Hodgkin's lymphoma and related hematologic malignancies (Froese et al., J. Immunol. 139:2081 (1987); Pfreundschuh et al., Onkologie 12:30 (1989); Carde et al., Eur. J. Cancer 26:474 (1990)). Originally identified by the monoclonal antibody Ki-1, which is reactive with H-RS cells (Schwab et al., Nature (London) 299:65 (1982)), CD30 was subsequently shown to be expressed on a subset of non-Hodgkin's lymphomas (NHL), including Burkitt's lymphoma, as well as several virally-transformed lines (human TCell Lymphotrophic Virus I or II transformed T-cells, and Epstein-Barr Virus transformed B-cells (Stein et al., Blood 66:848 (1985); Andreesen et al., Blood 63:1299 (1984)). That CD30 plays a role in normal lymphoid interactions is suggested by its histological detection on a small population of lymphoid cells in reactive lymph nodes, and by induced expression on purified T- and B-cells following lectin activation (Stein et al., Int. J. Cancer 30:445 (1982) and Stein et al., 1985, supra). Cloning and expression of a gene encoding CD30 has been reported and CD30 has been characterized as a transmembrane protein that possesses substantial homology to the nerve growth factor receptor superfamily (Durkop et al., Cell 68:421, 1992). Durkop et al. suggest that CD30 is the receptor for one or more as yet unidentified growth factors, and recognize the importance of investigating the existence and nature of such growth factors in order to achieve insight into the etiology of Hodgkin's Disease. Prior to the present invention, however, no such growth factors or other molecules that bind to the CD30 receptor were known. A need thus remained for identification and characterization of a ligand for CD30. Web site: http://www.delphion.com/details?pn=US06143869__
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Cell surface protein expressed on human cortical thymocyte and their use Inventor(s): Bae; Young Mee (Seoul, KR), Park; Seong Hoe (7-301, Sang-Ah Apt., No.22, Samsung-dong, Kangnam-ku, 135-090, KR) Assignee(s): Park; Seong Hoe (Kangnam-ku, KR) Patent Number: 6,225,286 Date filed: April 1, 1999 Abstract: A novel protein which is glycoprotein with 120,000 molecular weight and is expressed T lymphoblastic lymphoma and leukemia cells, is useful in the diagnosis of T lymphoblastic lymphoma and leukemia. Excerpt(s): The present invention relates to a cell surface protein expressed on human cortical thymocytes and its use. More particulary, the present invention relates to a novel protein (called "JL1" hereinafter) having molecular weight of about 120,000 dalton expressed exclusively on cortical thymocytes and on malignant cells of T lymphoblastic leukemia, T lymphoblastic lymphoma originated from cortical thymocytes and about 50% of all kinds of leukemia, which are identified by immunohistochemical and flow cytometric analysis, and to its diagnostic an clinical application on leukemia and T lymphoblastic lymphoma. Human body shows the specific responses to foreign substances exposed after birth, and T. and B. lymphocytes and antigen presenting cells are involved in immune responses to protect human body, Lymphocytes are the major components of lymphoid organ cells and have an important role in the specific immune response during circulation through blood and lymph. The major role of B-lymphocytes is to produce antibodies against foreign substances. T lymphocytes are classified into two types, one of which has the function to help the specific immune response and the other has the function of killing cells infected by pathogens. And the role of antigen presenting cells is to engulf infecting antigens non-specifically, and to process them by cleaving into small peptides and provide their information to T lymphocytes. Intrathymic T cell development entails complex series of proliferation, differentiation, and selection stages. T cells are originated from hematopoietic stem cells produced in embryonic liver and postnatal bone marrow. They move into thymus, differentiates, become mature, and after this, move out through blood vessel and become mature T cells. After rearrangement of T cell receptor germline gene in the thymus, thymocytes express T cell receptor complexes on their cell surfaces. The gene rearrangement process requires enzymatic system including RAG-1RAG-2. As a result, extreme T cell receptor diversity can be produced in the course of this complicated process. However, all the T cell receptors produced cannot carry out their appropriated functions in the periphery. The cells which cannot recognize the antigens provided by major histocompatibilty complex (MHC) class I and class II, and cells which show strong response to self antigen are removed. These processes are called positive and negative selection, respectively. T cell receptors can accomplish their appropriate function when they recognize foreign antigen bound to their won MHC molecule on the cell surface. This educational process takes place in the thymus. Web site: http://www.delphion.com/details?pn=US06225286__
Patents 217
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Clinical parameters radioimmunotheraphy
for
determining
hematologic
toxicity
prior
to
Inventor(s): Raestetter; William (Rancho Santa Fe, CA), White; Christine A. (Rancho Santa Fe, CA) Assignee(s): IDEC Pharmaceuticals Corporation (San Diego, CA) Patent Number: 6,451,284 Date filed: July 26, 2000 Abstract: New clinical parameters are reported which may serve as predictors of the hematological toxicity associated with therapeutic radiolabeled antibodies, particularly those antibodies which target lymphoma cells which have a tendency to localize to the bone marrow. Excerpt(s): The present invention reports new clinical parameters for predicting the hematological toxicity which can be expected upon administering a therapeutic radiolabeled anti-CD20 antibody, as well as other therapeutic antibodies which have the potential to target immune cells. The clinical parameters of the present invention are useful alternatives to performing dosimetry trials with gamma-emitting radiolabeled antibodies prior to therapy. The immune system of vertebrates (for example, primates, which include humans, apes, monkeys, etc.) consists of a number of organs and cell types which have evolved to: accurately and specifically recognize foreign microorganisms ("antigen") which invade the vertebrate-host; specifically bind to such foreign microorganisms; and, eliminate/destroy such foreign microorganisms. Lymphocytes, as well as other types of cells, are critical to the immune system. Lymphocytes are produced in the thymus, spleen and bone marrow (adult) and represent about 30% of the total white blood cells present in the circulatory system of humans (adult). There are two major sub-populations of lymphocytes: T cells and B cells. T cells are responsible for cell mediated immunity, while B cells are responsible for antibody production (humoral immunity). However, T cells and B cells can be considered interdependent--in a typical immune response, T cells are activated when the T cell receptor binds to fragments of an antigen that are bound to major histocompatability complex ("MHC") glycoproteins on the surface of an antigen presenting cell; such activation causes release of biological mediators ("interleukins") which, in essence, stimulate B cells to differentiate and produce antibody ("immunoglobulins") against the antigen. Web site: http://www.delphion.com/details?pn=US06451284__ •
Cloning and uses of the genetic locus BCL-6 Inventor(s): Chaganti; Raju S. K. (New York, NY), Dalla-Favera; Riccardo (New York, NY) Assignee(s): Sloan-Kettering Institute for Cancer Research (New York, NY), The Trustees of Columbia University in the City of New York (New York, NY) Patent Number: 6,174,997 Date filed: March 15, 1999 Abstract: This invention provides an isolated vertebrate nucleic acid molecule the bcl-6 locus. This invention also provides an isolated human nucleic acid molecule of bcl-6 locus. This invention further provides a nucleic acid molecule comprising a nucleic acid
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molecule of at least 15 nucleotides capable of specifically hybridizing with a sequence included within the sequence of the nucleic acid molecule of bcl-6 locus. This invention provides an isolated vertebrate nucleic acid molecule of bcl-6 operatively linked to a promoter of RNA transcription. This invention provides a vector which comprises the nucleic acid molecule of bcl-6 locus. This invention provides a host vector system for the production of a polypeptide encoded by bcl-6 locus, which comprises the vector of bcl-6 locus in a suitable host. This invention provides a polypeptide encoded by the isolated vertebrate nucleic acid molecule of bcl-6 locus. This invention provides an antibody capable of binding to polypeptide encoded by bcl-6 locus. This invention provides an antagonist capable of blocking the expression of the polypeptide encoded by bcl-6. This invention provides an antisense molecule capable of hybridizing to the nucleic acid molecule of bcl-6. This invention provides an assay for non-Hodgkin's lymphoma, a method for screening putative therapeutic agents for treatment of non-Hodgkin's lymphoma and a method for diagnosing B-cell lymphoma in a subject. Finally, this invention provides a method of treating a subject with non-Hodgkin's lymphoma. Excerpt(s): Throughout this application various references are referred to within parenthesis. Disclosures of these publications in their entireties are hereby incorporated by reference into this application to more fully describe the state of the art to which this invention pertains. Full bibliographic citation for these references may be found at the end of each Experimental Detail Section. Non-random chromosomal abnormalities are found in up to 90% of patients with non-Hodgkin's lymphoma (NHL) and have been shown to play an important role in lymphomagenesis by activating proto-oncogenes (1). Some of these translocations, which are associated with specific histologic subsets of NHL, have been characterized at the molecular level. In the t(8;14), t(8;22), and t(2;8) translocations associated with Burkitt Lymphoma, L.sub.3 -type acute lymphoblastic leukemia and AIDS-associated non-Hodgkin lymphoma (NHL), a known protooncogene, c-myc, was found juxtaposed to the immunoglobulin (Ig) loci (2,3). In the t(14;18) translocation, which is implicated in follicular-type NHL, molecular analysis of the sequences linked to the Ig locus led to the identification of a novel proto-oncogene, bcl-2 (4-6). The t(11;14) (q13;q32), mainly associated with "mantle zone" lymphoma, appears to involve the juxtaposition of the Ig heavy-chain locus with the bcl-1 locus, the site of the candidate proto-oncogene PRAD-1/cyclin D1 (7,8). These well characterized chromosome translocations are associated, however, with only a fraction of NHL cases, while a number of other recurrent translocations remain to be characterized for their genetic components. One important example of such cytogenetic abnormalities is represented by various alterations affecting band 3q27. This region is involved in translocations with various chromosomal sites including, but not limited, to those carrying the Ig heavy-(14q32) or light-(2p12, 22q11) chain loci (9,10). Overall, 3q27 breakpoints are detectable in 7-12% of B-cell NHL cases by cytogenetic analysis, with t(3;22) (q27;q11) being the most frequent type detectable in 4-5% of NHL (9). The clinicopathologic relevance of 3q27 breakpoints is underscored by its consistent association with diffuse-type NHL, a frequent and clinical aggressive subtype for which no specific molecular lesion has yet been identified (9). Web site: http://www.delphion.com/details?pn=US06174997__
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Conjugates targeted to the interleukin-2 receptor Inventor(s): Clemens; Christopher M. (Salt Lake City, UT), Prakash; Ramesh K. (Salt Lake City, UT) Assignee(s): Watson Laboratories, Inc. (Salt Lake City, UT) Patent Number: 6,251,866 Date filed: August 4, 1998 Abstract: A composition for intracellular delivery of a chemical agent into an interleukin-2-receptor-bearing cell, e.g. an activated T cell, includes a chemical agent and at least one copy of an interleukin-2-receptor-binding and endocytosis-inducing ligand coupled to a water soluble polymer. The ligand binds to a receptor on the interleukin-2-receptor-bearing cell and elicits endocytosis of the composition. The composition also preferably includes a spacer for coupling the chemical agent and the ligand to the polymer. Chemical agents can include cytotoxins, transforming nucleic acids, gene regulators, labels, antigens, drugs, and the like. A preferred water soluble polymer is a polyalkylene oxide, such as polyethlene glycol and polyethylene oxide, and activated derivatives thereof. The composition can further comprise a carrier such as another water soluble polymer, liposome, or particulate. Methods of using these compositions for delivering a chemical agent in vivo or in vitro are also disclosed. A method of detecting a disease, such as T-cell lymphocytic leukemia, T-cell acute lymphoblastic leukemia, peripheral T-cell lymphoma, Hodgkin's disease, or nonHodgkin's lymphoma, associated with elevated levels of soluble IL-2 receptor is also disclosed. Excerpt(s): This invention relates to delivery of chemical agents to cells. More particularly, this invention relates to compositions and methods for intracellular delivery of chemical agents to a specific cell type, i.e. cells bearing the interleukin-2 (IL2) receptor. Toxins that target cell surface receptors or antigens on tumor cells have attracted considerable attention for treatment of cancer. E.g., I. Pastan & D. FitzGerald, Recombinant Toxins for Cancer Treatment, 254 Science 1173 (1991); Anderson et al., U.S. Pat. Nos. 5,169,933 and 5,135,736; Thorpe et al., U.S. Pat. No. 5,165,923; Jansen et al., U.S. Pat. No. 4,906,469; Frankel, U.S. Pat. No. 4,962,188; Uhr et al., U.S. Pat. No. 4,792,447; Masuho et al., U.S. Pat. Nos. 4,450,154 and 4,350,626. These agents include a celltargeting moiety, such as a growth factor or an antigen-binding protein, linked to a plant or bacterial toxin. They kill cells by mechanisms different from conventional chemotherapy, thus potentially reducing or eliminating cross resistance to conventional chemotherapeutic agents. Copending U.S. patent application Ser. No. 08/305,770, filed Sep. 13, 1994, describes compositions and methods for specific intracellular delivery of a chemical agent into a CR2-receptor-bearing cell, e.g. B lymphocytes. The compositions comprise a CR2-receptor-binding and endocytosis-inducing ligand (CBEL) coupled to the chemical agent. The CBEL binds to the CR2 receptor on the surface of B lymphocytes and elicits endocytosis of the composition such that the composition is transported to lysosomes. In the lysosomes, the chemical agent is preferably separated from the remainder of the composition such that the chemical agent can be transported or diffuse into the cytoplasm or nucleus. Optionally, the composition can include a spacer, which can be either biodegradable (in the lysosome) or non- biodegradable, for coupling the CBEL to the chemical agent. Chemical agents can include cytotoxins, transforming nucleic acids, gene regulators, labels, antigens, drugs, and the like. The composition can further comprise a carrier such as another water soluble polymer, liposome, or particulate.
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Web site: http://www.delphion.com/details?pn=US06251866__ •
Establishment of HHV-8.sup.+ lymphoma cell line, virus produced, antibody, diagnostic method and kit for detecting HHV-8 infection Inventor(s): Koeffler; H. Phillip (Los Angeles, CA), Said; Jonathan W. (Sherman Oaks, CA) Assignee(s): Cedars-Sinai Medical Center (Los Angeles, CA) Patent Number: 6,156,498 Date filed: May 14, 1998 Abstract: A method establishes for the first time a HHV-8 producing immortalized lymphoma cell line, which is free of EBV, CMV, and HIV. Large quantities of uncontaminated HHV-8 are produced by the cells, and the virus or immunogenic fragments thereof are used to obtain specific polyclonal and monoclonal antibody. Assays and kits are useful for detecting viral infection in mammalian samples. Excerpt(s): The present invention relates to a lymphoma cell line capable of producing large quantities of Kaposi's sarcoma-associated herpes virus (KSHV or HHV-8), which are substantially free from human immunodeficiency virus (HIV), Cytomegalovirus (CMV) and Epstein-Barr Virus (EBV). This invention also relates to the purified virus produced thereby, and to methods for establishing HHV-8 producing cell lines, and for producing large quantities of the virus, as well as a method and kit for detecting HHV-8 infection. Kaposi's sarcoma (KS) is a rare neoplasm of multi focal origin characterized by red-purple to blue-brown lesions of the skin. Cell proliferation occurs initially in the skin, eventually spreading to other body sites, in particular to the lower extremities. Lymphatic involvement is not unusual in KS patents, and may be present as a lymphadenopathy. Kaposi's sarcoma is the most frequent neoplastic manifestation of HIV infection, and is used as one of the criteria to decide whether an HIV-infected individual is defined as having Acquired Immunodeficiency Syndrome (AIDS). Four different epidemiologic forms of KS have been described: sporadic or classic KS, endemic KS, KS encountered among transplant recipients receiving immunosuppresive therapies, and KS prevalent among patients with human immunodeficiency virus (HIV) infection. The "classic" form of KS was described over a century ago in predominantly elderly men of Mediterranean and Jewish descent. Men are affected by this form of KS 10 to 15 times more often than women, and those affected are typically in their 60s or older, and have an average survival time of approximately 10 years. The "endemic" form of KS has been recognized in certain geographic regions of Central Africa. This is a neoplasm which also affects men more frequently than women, is generally more aggressive than classic KS, and involves the lymph nodes and viscera, as well. A marked increase in the form of KS encountered in patients receiving immunosuppressive therapy, was mostly found in hepatic and renal transplant patients. AIDS patients have a probability of about 40% of developing cancer, especially Kaposi's sarcoma and/or non-Hodgkin's lymphoma. Kaposi's sarcoma has, additionally, been associated with lymphoid cancer in patients both with and without AIDS. Web site: http://www.delphion.com/details?pn=US06156498__
Patents 221
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FldA gene and methods for detecting predisposition to mucosa-associated lymphoid tissue lymphoma of the stomach Inventor(s): Chang; Chih-Shen (Taipei, TW), Chang; Kai-Chih (Taipei, TW), Chen; LiTzong (Taipei, TW), Lin; Jaw-Tow (Taipei, TW), Wang; Jin-Town (Taipei, TW), Yang; Jyh-Chin (Taipei, TW) Assignee(s): National Science Council (Taipei, TW) Patent Number: 6,451,533 Date filed: March 9, 2000 Abstract: The present invention relates to a Helicobacter pylori gene, fldA, a putative flavodoxin gene and whose expression is associated with mucosa-associated lymphoid tissue lymphoma of the stomach (MALToma). A G insertion at position 481 of the fldA gene was more frequently observed in strains associated with MALToma than other strains. Therefore, the present invention provides a new method to identify H. pylori patient with higher risk of developing gastric MALToma. Excerpt(s): The present invention relates to a Helicobacter pylori gene whose expression is associated with mucosa-associated lymphoid tissue lymphoma of the stomach (MALToma), and the use of the DNA composing the gene and the protein encoded by the DNA for detecting predisposition to MALToma. Helicobacter pylori, a spiral gramnegative bacterium, was first isolated in 1982 from the gastric mucosa of a patient with gastritis and peptic ulceration (Marshall B. J. and Warren J. R., Lancet, 1984, 1:13111315). Since then, there is strong evidence showing that H. pylori is the causative agent of chronic active gastritis and has an important role in duodenal ulcerogenesis (Blaser M. J., Sci. Am., 1996, 274:104-107). It has been documented that the relapse rate of both duodenal and gastric ulcers decreases dramatically after eradication of H. pylori, and cure of this chronic relapsing disease (Graham D. Y. et. al., Ann. Intern. Med., 1992, 116:705-708; Hentschel E. et. al., N. Engl. J. Med., 1993, 328:308-312). The infection by H. pylori has also been shown to be associated with adenocarcinoma and mucosaassociated lymphoid tissue lymphoma of the stomach (Nomura A. et. al., N. Engl. J. Med., 1991, 325:1132-1136; Parsonnet J. et. al., N. Engl. J. Med., 1991, 325:1127-1131; Bayerdorffer E. et. al., Lancet, 1995, 345:1591-1594). Although the prevalence of this infection and MALToma is high, only a few infected subjects develop clinically significant diseases. Most patients remain asymptomatic (Blaser M. J., Sci. Am., 1996, 274:104-107). To eradicate the infection in all patients is not feasible in terms of cost, compliance, and possible drug resistance. In addition, variation in host genetic background, environmental factors, and virulence of the bacterial strains may contribute to different clinical outcomes (Blaser M. J., Sci. Am., 1996, 274:104-107). Therefore, it would be useful to find a candidate marker to differentiate the strains that are more harmful to the host. Hence, the inventors of the present application have tried to find a specific antigen of H. pylori associated with gastric MALToma using an immunoscreening strategy. Web site: http://www.delphion.com/details?pn=US06451533__
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Gene therapy for solid tumors, papillomas and warts Inventor(s): Chen; Shu-Hsia (Houston, TX), Woo; Savio L. C. (Houston, TX) Assignee(s): Baylor College of Medicine (Houston, TX) Patent Number: 6,217,860 Date filed: September 24, 1999 Abstract: The present invention provides a novel method of treating localized solid tumors (metastatic carcinomas, papilloma and warts) in an individual. The method comprises delivering a suicide gene, by way of a recombinant adenoviral vector or other DNA transport system, into the solid tumor. Subsequently, a prodrug, such as the drug ganciclovir, is administered to the individual. The methods of the present invention may used to treat several different types of solid tumors including papillomas, warts, colon carcinoma, prostate cancer, breast cancer, lung cancer, melanoma, hepatoma, brain lymphoma and head and neck cancer. Excerpt(s): The present invention relates generally to the field of gene therapy. More particularly, the present invention relates to a novel gene therapy method of treating solid tumors, papillomas and warts using an adenoviral vector, a combination of adenoviral vectors, other viral vectors, and non-viral DNA transporter systems. Direct introduction of therapeutic genes into malignant cells in vivo can provide an effective treatment of localized tumors. Several novel treatment modalities have recently been attempted. For example, one treatment involves the delivery of normal tumor suppressor genes and/or inhibitors of activated oncogenes into tumor cells. A second treatment involves the enhancement of immunogeneity of tumor cells in vivo by the introduction of cytokine genes. A third treatment involves the introduction of genes that encode enzymes capable of conferring to the tumor cells sensitivity to chemotherapeutic agents. The herpes simplex virus-thymidine kinase (HSV-TK) gene can specifically convert a nucleoside analog (ganciclovir) into a toxic intermediate and cause death in dividing cells. It has recently been reported by Culver et al. (Science 256:1550-1552, 1992) that after delivery of the HSV-TK gene by retroviral transduction, subsequent ganciclovir treatment effectively caused brain tumor regression in laboratory animals. An attractive feature of this treatment modality for localized tumors is the so called "bystander" effect. In the "by-stander" effect, the HSV-TK expressing tumor cells prevent the growth of adjacent non-transduced tumor cells in the presence of ganciclovir. Thus, not every tumor cell has to express HSV-TK for effective cancer treatment. The HSV-TK retrovirus used by Culver et al., however, was limited by low viral titer. Thus, effective treatment of brain tumors necessitated the inoculation into animals of virus-producing cells rather than the viral isolate itself. Additionally, in previous experiments with synergeneic rats treated with a retrovirus and ganciclovir, the tumors were necrotic and were invaded by macrophages and lymphocytes. In Example 1, below, athymic mice were used and the tumor cells were destroyed without apparent involvement of the cellular immune response. The prior art remains deficient in the lack of an efficient gene therapy technique for the treatment of solid tumors. Web site: http://www.delphion.com/details?pn=US06217860__
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Human herpesvirus type 8 isolated from human lymphoma cell line Inventor(s): Ganem; Donald E. (San Francisco, CA), Herndier; Brian (Burlingame, CA), McGrath; Michael S. (Burlingame, CA), Ng; Valerie L. (Piedmont, CA) Assignee(s): The Regents of the University of California (Oakland, CA) Patent Number: 6,149,918 Date filed: September 18, 1995 Abstract: A human lymphoma cell line containing a human herpesvirus type 8 (HHV-8) capable of in vitro growth and which produces HHV-8 virus particles upon induction of lytic viral growth is provided. Virus produced by the cell line of the invention is useful for the production of antibodies to an HHV-8 virus particle, viral protein, or viral peptide. Methods of screening a biological sample for the presence of HHV-8 virus particles, viral protein, or viral peptide from a human suspected of being infected with HHV-8 are provided as are methods of screening a biological sample of the human for antibodies to HHV-8. Excerpt(s): The present invention relates to a human lymphoma cell line containing a human herpesvirus, and in particular, to a novel type of human herpesvirus associated with human body cavity-based lymphoma. Individuals infected with the human immunodeficiency virus, type 1 (HIV-1) are at a 60-100 fold increased risk of developing lymphoma as compared to the general population. This risk is likely to increase as a result of improvements in supportive care for opportunistic infections and use of antiretroviral therapy (Gill, P. S. et al. (1987) J. Clin Oncol. 5:1322; Gail, M. H., et al. (1991) J. Natl. Cancer Inst. 83695). The majority of HIV-associated lymphomas are of Bcell origin and constitute a heterogeneous group of lymphomas (Shiramizu, B. T. et al. (1992) J. Clin. Oncol. 10:383; Levine A. M. et al. (1991) Cancer 68:2466). Primary lymphomas arising in the central nervous system (CNS) typically occur in HIV-1 infected individuals with advanced disease who have had multiple opportunistic infections and have few peripheral CD4+ lymphocytes; the majority of these lymphomas are monoclonal and infected with Epstein-Barr virus (EBV). In contrast, lymphomas arising outside of the CNS often occur in HIV-1 infected individuals who are relatively more immunocompetent and who often have had no prior opportunistic infections. Of these peripheral lymphomas, 30% are polyclonal and lack evidence of EBV infection. Web site: http://www.delphion.com/details?pn=US06149918__
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Levitating exercise wand Inventor(s): Ortloff; Angel (392 Abbey Rd., Mt. Tremper, NY 12457) Assignee(s): none reported Patent Number: 6,432,028 Date filed: February 22, 2000 Abstract: A levitating exercise wand and a method for use in therapy, exercise, and recreation is described. The method of use of a levitating exercise wand is to provide a therapeutic exercise subsequent to treatments of diseases such as lymphoma or during exercise therapy during treatment of concentration conditions such as attention deficit disorder. The levitating exercise wand has a rod having an attachment point such as a hole placed toward the upper end of the rod from the center of mass so as to maintain a
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vertical orientation when in motion. A string is attached to the rod and forms a closed loop. A first weight is placed at a lower end of the rod to transfer a center of gravity location. The first weight will allow the wand to have a more controlled motion rather than oscillating or vibrating in an uncontrolled fashion. The method of exercise employing a levitating exercise wand begins with holding an arm with elbow bent at waist level and hand faced such that an index finger is placed topmost with all other fingers extended parallel and a thumb vertical. The string is placed at a midpoint of said index finger. The arm is moved forward and backward in a U-shaped motion around an upper end of said levitating exercise wand. The hand is held level and maintains the levitating wand in a vertical position. The method of exercise may also employ dancing, and movements that will pass the levitating exercise wand around the body. Excerpt(s): This invention relates to amusement and exercise devices, and more particularly to a levitating exercise wand and to the methods of use thereof to provide therapeutic and recreational exercise. The use of wands and sticks in conjunction with recreational exercise is well known. U.S. Pat. No. 5,681,246 (Dougherty) describes a pivoting jump stick for use in areas with restricted overhead space. The pivoting jump stick will allow the user to create the types of exercise similar to those of the classical jump rope. Variations of the wand and stick are shown in U.S. Pat. No. 5,244,445 (Amesquita) and U.S. Pat. No. 5,022,648 (Travis). In Amesquita, the wand is hollowed and filled with weighted spheres. The spheres move within the wand during exercise causing shifting of the mass and increased momentum of the end of the wand. This will cause fuller and more complete twisting of the torso during vigorous exercise. Web site: http://www.delphion.com/details?pn=US06432028__ •
Lymphoma-susceptible transgenic mice and methods for studying drug sensitivity of lymphomas Inventor(s): Lowe; Scott W. (Cold Spring Harbor, NY), Wallace-Brodeur; Rachel R. (Huntington Station, NY) Assignee(s): Cold Spring Harbor Laboratory (Cold Spring Harbor, NY) Patent Number: 6,583,333 Date filed: May 12, 1998 Abstract: A mouse expressing myc in B cells, because of defective function of one or more tumor suppressor genes, is useful for the testing of anti-lymphoma agents and for the testing of genes which may have an effect on the apoptotic pathway. Preferred embodiments include mice of genotypes E.mu.-myc/p53.sup.+/-, E.mu.myc/Rb.sup.+/- and E.mu.-myc/p16.sup.+/-, and cells derived from lymphomas arising in these mice, wherein the cells may have undergone further genetic alteration. Mouse strains, lymphoma cells and cell lines of the invention can be used in methods to discover new anti-lymphoma agents, methods to characterize tumors, and to characterize genes which may affect the development of resistance to anti-tumor agents. Such methods are also part of the invention. Excerpt(s): Tumor suppressors are generally identified as genes in which loss of function causes tumor formation, either as seen by transformation of cells in culture, or by association of mutations with tumors in animals. The usual normal function of these genes is to impose some constraint on the cell cycle or cell growth. In certain cancers, patients develop tumors which have mutations in both alleles of the tumor suppressor gene. p53, Rb and p16 are among the best characterized of the tumor suppressor genes.
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In vitro analysis of human tumor cell lines from some tumor types show a correlation between p53 mutations and resistance to treatment. Burkitt's lymphoma cell lines with mutant p53 are more resistant to a variety of treatments when compared to those with wild type p53 (Fan S., et al., Cancer Res. 54,5824-30, 1994). Consistent with in vitro studies, p53 status is linked to drug resistance in several tumor types. Perhaps the most striking examples occur in lymphoid malignancies, including non-Hodgkin's lymphoma, acute myeloid leukemia, myelodysplastic syndrome, and chronic lymphocytic leukemia (Wattel, E., et al., Blood 84, 3148-57 1994; Wilson, W. H., et al., Blood 89, 601-9 1997). In these tumor types, p53 mutations are rare but generally associated with disease progression and poor prognosis. When patients are classified by p53 status, tumor response (i.e. remission vs. nonresponsive), and survival, patients with p53 mutations are remarkably resistant to therapy and display very short survival times. In this regard, a particularly informative tumor type is acute lymphoblastic leukemia. Here, p53 mutations in primary tumors are exceedingly rare, and most patients typically respond to therapy. However, a subfraction of patients relapse, and approximately 30% of relapsed tumors harbor mutant p53. Moreover, patients with p53 mutant tumors are less likely to enter a second remission compared to patients with relapsed tumors harboring wild-type p53 (Diccianni, M. B., et al., Blood 84, 3105-12 1994; Hsiao, M. H., et al., Blood 83, 2922-30 1994). It is now known that most anticancer agents induce apoptosis, a genetically-regulated form of cell death (reviewed in Kerr, J. F. R. et al., Cancer 73:2013-2026, 1994). Since drugs with distinct primary targets can induce apoptosis through similar mechanisms, mutations in apoptotic programs can produce multiple drug resistance (Dive, C., and Hickman, J. A., Br. J. Cancer 64:192-196, 1991). These observations raise the possibility that the chemosensitivity of human tumors is determined, in part, by the combined effects of oncogenic mutations on apoptosis (Lowe, S. W. et al., Cell 74:957-967, 1993). Web site: http://www.delphion.com/details?pn=US06583333__ •
Method and reagent for treatment of diseases by expression of the c-Myc gene Inventor(s): Draper; Kenneth G. (Boulder, CO), Thompson; James D. (Boulder, CO) Assignee(s): Ribozyme Pharmaceuticals, Inc. (Boulder, CO) Patent Number: 6,544,755 Date filed: February 7, 1994 Abstract: An enzymatic RNA molecule which cleaves mRNA associated with development or maintenance of Burkitt's lymphoma or acute lymphocytic leukemia. Excerpt(s): This invention relates to methods for inhibition of growth of transformed cells, and inhibition of progression to a transformed phenotype in pre-neoplastic cells. Transformation is a cumulative process whereby normal control of cell growth and differentiation is interrupted, usually through the accumulation of mutations affecting the expression of genes that regulate cell growth and differentiation. Scanlon WO91/18625, WO91/18624, and WO91/18913 describes a ribozyme effective to cleave oncogene RNA from the H-ras gene. This ribozyme is said to inhibit H-ras expression in response to exogenous stimuli. Reddy WO92/00080 describes use of ribozymes as therapeutic agents for leukemias, such as CML by targeting specific portions of the BCRABL gene transcript. Web site: http://www.delphion.com/details?pn=US06544755__
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Method of detecting a chromosomal rearrangement involving a breakpoint in the ALK or NPM gene Inventor(s): Look; A. Thomas (Memphis, TN), Morris; Stephan W. (Memphis, TN) Assignee(s): St. Jude Children's Research Hospital (Memphis, TN) Patent Number: 6,174,674 Date filed: June 19, 1998 Abstract: The present invention is based on the identification and sequence determination of a novel gene, ALK, which is fused to the gene encoding nucleophosmin (NPM) in translocations present in t(2;5) lymphoma cells. Based on homologies to other proteins, the amino acid sequence of the polypeptide encoded by the ALK (Anaplastic Lymphoma Kinase) gene is a membrane-spanning protein tyrosine kinase (PTK)/receptor. Antibodies to the ALK PTK/receptor and methods utilizing such antibodies are described, as are methods of using the ALK gene to isolate ligands for the ALK PTK/receptor. Excerpt(s): The present invention is directed to the field of molecular genetics of cancer. Specifically, the present invention relates to human lymphomas in which a translocation between chromosomes 2 and 5 (referred to in the art as "t(2;5)") has occurred. On a molecular level, the DNA rearrangement in t(2;5) results in the fusion of the known NPM gene with a novel gene named ALK (Anaplastic Lymphoma Kinase) that encodes a protein tyrosine kinase (PTK). Chromosomal abnormalities are frequently associated with malignant diseases. In a number of instances, specific chromosomal translocations have been characterized, which generate fusion genes encoding proteins with oncogenic properties (Sawyers et al., Cell 64:337-350 (1991)). Perhaps the best example of genetic characterization of a malignant disease is provided by the analysis of the chromosomal abnormalities unique to different subsets of non-Hodgkin's lymphoma (NHL). The NHL subset commonly referred to as large cell lymphoma (which comprises.about.25% and 40% of NHL in children and adults, respectively) has historically been the most illdefined because of its marked cytological, immunological and clinical heterogeneity. Approximately one-third of large cell lymphomas (10% of all NHL) contain the t(2;5)(p23;q35), usually as the only cytogenetic abnormality (R. Rimokh et al., Br. J. Haematol. 71:31-36 (1989); D. Mason et al., Br. J. Haematol. 74:161-168 (1990); H. Stein and F. Dallenbach, in Neoplastic Hematopathology, D. M. Knowles, ed., Williams & Wilkins, Baltimore (1992), pp. 675-714), suggesting that rearrangement of cellular protooncogenes on these chromosomes contributes to lymphomagenesis. Web site: http://www.delphion.com/details?pn=US06174674__
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Method of prophylaxis or treatment of antigen presenting cell driven skin conditions using inhibitors of the CD2/LFA-3 interaction Inventor(s): Cooper; Kevin D. (Ann Arbor, MI), Wallner; Barbara P. (Weston, MA) Assignee(s): Biogen, Inc. (Cambridge, MA), The Regents of The University of Michigan (Ann Arbor, MI) Patent Number: 6,162,432 Date filed: June 6, 1995 Abstract: Methods of using inhibitors of the CD2/LFA-3 interaction in treating skin conditions characterized by increased T cell activation and abnormal antigen
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presentation in the dermis and epidermis in mammals, including humans. Such conditions include psoriasis, UV damage, e.g., photoaging, atopic dermatitis, cutaneous T cell lymphoma such as mycosis fungoides, allergic and irritant contact dermatitis, lichen planus, alopecia areata, pyoderma gangrenosum, vitiligo, ocular cicatricial pemphigoid, and urticaria. Excerpt(s): This invention relates to methods of using inhibitors of the CD2/LFA-3 interaction in treating skin conditions characterized by increased T cell activation and abnormal antigen presentation in the dermis and epidermis in mammals, including humans. Such conditions include psoriasis, UV damage, e.g., photoaging, atopic dermatitis, cutaneous T cell lymphoma such as mycosis fungoides, allergic and irritant contact dermatitis, lichen planus, alopecia areata, pyodermna gangrenosum, vitiligo, ocular cicatricial pemphigoid, and urticaria. There are numerous skin conditions characterized by increased T cell activation and abnormal antigen presentation in the dermis and epidermis. The pathophysiologic mechanisms involved in the evolution of such inflammatory processes are poorly understood. However, it has become apparent that skin cells are important in the generation of a cutaneous inflammatory response (Kupper, "Immune and Inflammatory Processes in Cutaneous Tissues", J. Clin. Invest., 86, pp. 1783-89 (1990)). The normal adult epidermal population contains 1-2% Langerhans' cells and about 98% keratinocytes. Keratinocytes and other nonhematopoietically-derived cells resident in skin contribute to immune homeostasis and can produce various cytokines which influence migration of T cells and expression of adhesion molecules. Web site: http://www.delphion.com/details?pn=US06162432__ •
Method of treating lymphoproliferative syndrome Inventor(s): Bihari; Bernard (29 W. 15th St., New York, NY 10011) Assignee(s): none reported Patent Number: 6,288,074 Date filed: November 15, 1999 Abstract: Lymphoproliferative syndrome, including such diseases as malignant lymphoma, chronic lymphocytic leukemia, Hodgkin's lymphoma, and non-Hodgkin's lymphoma, is treated in human patients by the administration by a pharmacologically effective mode or route of an essentially pure opiate receptor antagonist, typified by Naltrexone and Naloxone, exerting substantially higher blocking action for Mu opiate receptor sites than against Delta opiate receptor sites at a low dose concentration which produces therapeutic results corresponding to those obtained by the administration of Naltrexone at a low dosage level in the range of 1.0 mg. to 10 mg. and at which Delta receptor blocking activity is at most small and Mu receptor blocking activity is significant and most preferably substantially exclusive. Naltrexone is suitable for oral administration and is preferred. Excerpt(s): This invention relates to the treatment of lymphoproliferative syndrome and is concerned specifically with treatment of this syndrome, including by such diseases as malignant lymphoma, chronic lymphocytic leukemia, Hodgkin's lymphoma, and nonHodgkin's lymphoma, by administration of an essentially pure opiate receptor antagonist such as Naltrexone and Naloxone at a low level dosage. The use of an essentially pure opiate receptor antagonist in the treatment of several diseases has already been disclosed in patents in which I am named as an inventor. In U.S. Pat. No.
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4,888,346, issued Dec. 19, 1989, the treatment was for the acquired immune deficiency syndrome (or AIDS) in any of its known states, including AIDS-related complex. In U.S. Pat. No. 5,013,739, issued May 7, 1991, the disease treated was chronic fatigue syndrome while in U.S. Pat. No. 5,346,900, issued Oct. 18, 1994, the disease was chronic herpes virus infections. In the latter patent, examples of treatment of multiple sclerosis was also disclosed. For the treatment of all these diseases, the amount of the essentially pure opiate receptor antagonist was required to be at a quite low level corresponding in results to those obtained by the administration of Naltrexone at a dosage level of from 1.0 mg. to 10 mg., preferably at a dosage level of 1.0 mg. to about 5 mg., and most preferably up to about 3.0 mg. At dosage levels above about 10 mg., not only were the desired therapeutic results not obtained but the effect of the treatment appeared to be negative in acerbating the disease. Web site: http://www.delphion.com/details?pn=US06288074__ •
Methods and compositions for modulating cell proliferation and cell death Inventor(s): Au; Jessie L. -S. (2287 Palmleaf Ct., Columbus, OH 43235), Wientjes; Guillaume (2287 Palmleaf Ct., Columbus, OH 43235) Assignee(s): none reported Patent Number: 6,599,912 Date filed: June 5, 2000 Abstract: Methods and compositions for modulating the FGF effect on the sensitivity of malignant and normal cells to anticancer agents are provided. In particular, methods and compositions for inhibiting FGF-induced resistance to a broad spectrum of anticancer agents in solid and soft-tissue tumors, metastatic lesions, leukemia and lymphoma are provided. Preferably, the compositions include at least one FGF inhibitor in combination with a cytotoxic agents, e.g., antimicrotubule agents, topoisomerase I inhibitors, topoisomerase II inhibitors, antimetabolites, mitotic inhibitors, alkylating agents, intercalating agents, agents capable of interfering with a signal transduction pathway (e.g., g., a protein kinase C inhibitor, e.g., an anti-hormone, e.g., an antibody against growth factor receptors), an agent that promotes apoptosis and/or necrosis, and interferon, an interleukin, a tumor necrosis factor, and radiation.In other embodiments, methods and composition for protecting a cell in a subject, from one or more of killing, inhibition of growth or division or other damage caused, e.g., by a cytotoxic agent, are provided. Preferably, the method includes: administering, to the subject, an effective amount of at least one FGF agonist, thereby treating the cell, e.g., protecting or reducing the damage to the dividing cell from said cytotoxic agent. Excerpt(s): Resistance of tumor cells to cancer therapy, limited efficacy of cancer therapy in metastatic disease, and undesired host toxicity of cancer therapy are three significant challenges in patient management. A common resistance mechanism to chemotherapy observed in preclinical studies is the overexpression of drug efflux proteins (Lum, B. L. et al. (1993) Cancer 72, 3502-3514; Barrand, M. A. et al. (1997) Gen. Pharmacol. 28, 639645; Fidler, I. J. (1999) Cancer Chemother. Pharmacol. 43:S3-S10.). However, at least some clinical studies show that inhibition of the drug efflux proteins does not significantly improve the effectiveness of chemotherapy in patients (Ferry, D. R., et al. (1996) Eur. J. Cancer 32:1070-1081; Broxterman, H. J., et al. (1996) Eur. J. Cancer. 32:10241033), suggesting the existence of other resistance mechanisms. Cancer therapy, such as chemotherapy and radiation, targets proliferating cells and thereby causes undesired toxicity to normal host tissues that undergo continuous renewal, including the
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hematopoietic cells, cells in the lining of the gastrointestinal tract, and hair follicles. Bone marrow suppression induced by cancer therapy is, at least in part, overcome by the use of hematopoietic growth factors, including erythropoietin, granulocytes colonystimulating factor, and granulocyte-macrophage colony-stimulating factor (Gabrilove, J. L. and Goldie, D. W. (1993) In: Cancer, Principles & Practice of Oncology (eds. DeVita, V. T. et al., J. B. Lippincott Co., Philadelphia). On the other hand, no treatment is available to overcome the gastrointestinal toxicity and alopecia induced by anticancer agents. Web site: http://www.delphion.com/details?pn=US06599912__ •
Modulation of IAPs for the diagnosis and antisense treatment of proliferative disease Inventor(s): Baird; Stephen (Ottawa, CA), Korneluk; Robert G. (Ontario, CA), Liston; Peter (Ottawa, CA), Mackenzie; Alexander E. (Ontario, CA), Pratt; Christine (Nepean, CA), Tsang; Benjamin K. (Nepean, CA) Assignee(s): Aegera Therapeutics Inc. (Verdum, CA) Patent Number: 6,300,492 Date filed: July 14, 2000 Abstract: Disclosed are diagnostic and prognostic kits for the detection and treatment of proliferative diseases such as ovarian cancer, breast cancer, and lymphoma. Also disclosed are cancer therapeutics utilizing IAP antisense nucleic acids IAP fragments, and antibodies which specifically bind IAP polypeptides. Excerpt(s): The invention relates to the diagnosis and treatment of cancer. One way by which cells die is referred to as apoptosis, or programmed cell death. Apoptosis often occurs a normal part of the development and maintenance of health tissues. The process occurs so rapidly that it is difficult to detect. This may help to explain why the involvement of apoptosis in a wide spectrum of biological processes has only recently been recognized. The apoptosis pathway is now known to play a critical role in embryonic development, viral pathogenesis, cancer, autoimmune disorders, and neurodegenerative disease. The failure of an apoptotic response has been implicated in the development of cancer, autoimmune disorders, such as lupus erythematosis and multiple sclerosis, and in viral infections, including those associated with herpes virus, poxvirus, and adenovirus. Web site: http://www.delphion.com/details?pn=US06300492__
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Monoclonal antibody antagonists to IL-3 Inventor(s): Lopez; Angel F (Adelaide, AU) Assignee(s): Medvet Science Pty Limited (AU) Patent Number: 6,177,078 Date filed: June 29, 1998 Abstract: Anti IL-3 Receptor alpha chain monoclonal antibody (MoAb) is the product of a hybridoma cell line designated 7G3. The MoAb acts as an antagonist to IL-3 in vitro activity. The MoAb binds to the N terminal domain of the IL-3 receptor alpha chain and does so competitively with IL-3 which indicates that this is, at least in part, involved in IL-3 binding. Treatment with the MoAb or fragment thereof, whether recombinant or
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otherwise, may be suitable for the treatment of one or more of the following conditions: myeloid leukemias, lymphomas such as follicular B cell lymphoma, or the alleviation of allergies. Excerpt(s): The present invention relates to monoclonal antibodies (MoAb) and reagents derived therefrom which are reactive with Haemopoietic Growth Factors, and especially with human interleukin 3 (IL-3) receptor.alpha.-chain and function as an antagonist to the Haemopoietic Growth Factors. Human interleukin-3 is a pleiotropic cytokine that stimulates the production of hemopoietic cells from multiple lineages including neutrophils, eosinophils, monocytes, megakaryocytes, erythroid cells, basophils and B cells. Recently IL-3 has also been shown to regulate vascular endothelial cell functions; enhancing adhesion molecule expression, neutrophil transmigration and cytokine production. Although some of the effects of IL-3 may be desirable and have prompted its clinical use in bone marrow reconstitution following chemotherapy, it is also apparent that abnormal or excessive production of IL-3 has the potential to lead to disease states. For example, some acute myeloid leukaemias proliferate in response to IL-3, and cells from follicular B cell lymphomas produce and depend on IL-3 for their growth. IL-3 has also been implicated in allergy not only for its ability to stimulate eosinophil and basophil production but also for being a strong stimulus of histamine release from basophils in vitro. The detection of elevated amounts of IL-3 mRNA in the skin and bronchi of allergic individuals further suggests an in vivo role in allergy. The structure of the extracellular domain of human IL-3R.alpha. has not yet been elucidated. Since IL-3R.alpha. belongs to the cytokine receptor family, it is predicted to contain a cytokine receptor module (CRM) with two discrete folding domains.sup.20 In addition there is also an N-terminal domain which, interestingly, has sequence similarities with the human GM-CSF and IL-5 receptor.alpha. chains.sup.21 This feature distinguishes these receptors from the other members of the cytokine receptor family. The functions of the CRM and N-terminal domain of the IL-3R.alpha. chain are not known, nor is it known where the IL-3 binding regions lie in the receptor. Web site: http://www.delphion.com/details?pn=US06177078__ •
Mouse MTS2 gene Inventor(s): Jiang; Ping (Salt Lake City, UT), Kamb; Alexander (Salt Lake City, UT), Stone; Steven (Midvale, UT) Assignee(s): Myriad Genetics, Inc. (Salt Lake City, UT) Patent Number: 6,210,949 Date filed: November 30, 1998 Abstract: The present invention relates to the Multiple Tumor Suppressor (MTS) genes in mice, their expression products, and their homology to the human MTS genes. The human MTS genes are involved in human cancers. The invention is further related to the use of the MTS genes in the therapy, diagnosis and prognosis of human cancer. The invention further relates to mutations in the MTS gene and their use in the diagnosis of predisposition to melanoma, leukemia, astrocytoma, glioblastoma, lymphoma, glioma, Hodgkin's lymphoma, CLL, and cancers of the pancreas, breast, thyroid, ovary, uterus, testis, kidney, stomach and rectum. The invention also relates to the therapy of human cancers which have a mutation in the MTS gene, including gene therapy, protein replacement therapy and protein mimetics. Finally, the invention relates to the screening of drugs for cancer therapy.
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Excerpt(s): The present invention relates to the Multiple Tumor Suppressor (MTS) genes in mice and to somatic mutations in the Multiple Tumor Suppressor gene in human cancers and their use in the diagnosis and prognosis of human cancer. The invention further relates to germline mutations in the MTS gene and their use in the diagnosis of predisposition to cancer, such as melanoma, ocular melanoma, leukemia, astrocytoma, glioblastoma, lymphoma, glioma, Hodgkin's lymphoma, multiple myeloma, sarcoma, myosarcoma, cholangiocarcinoma, squamous cell carcinoma, CLL, and cancers of the pancreas, breast, brain, prostate, bladder, thyroid, ovary, uterus, testis, kidney, stomach, colon and rectum. The invention also relates to the therapy of human cancers which have a mutation in the MTS gene, including gene therapy, protein replacement therapy and protein mimetics. The invention also relates to the screening of drugs for cancer therapy. Finally, the invention relates to mouse MTS genes corresponding the human MTS genes. The publications and other materials used herein to illuminate the background of the invention, and in particular, cases to provide additional details respecting the practice, are incorporated herein by reference, and for convenience are referenced in the following text and respectively grouped in the appended List of References. The genetics of cancer is complicated, involving multiple dominant, positive regulators of the transformed state (oncogenes) as well as multiple recessive, negative regulators (tumor suppressor genes). Over one hundred oncogenes have been characterized. Fewer than a dozen tumor suppressor genes have been identified, but the number is expected to increase beyond fifty (Knudson, 1993). Web site: http://www.delphion.com/details?pn=US06210949__ •
Non-myeloablative/lymphoablative conditioning regimen to induce patient antidonor unresponsiveness in stem cell transplantation Inventor(s): Slavin; Shimon (Jerusalem, IL) Assignee(s): Baxter International Inc. (Deerfield, IL), Hadash Medical Research Services and Development Ltd. (Jerusalem, IL) Patent Number: 6,544,787 Date filed: November 14, 1997 Abstract: Serious hematologic malignancies are treated through high dose or lethal chemotherapy and/or radiation therapy conditioning regimens followed by rescue with allogeneic stem cell transplantation (allo-SCT) or autologous stem cell transplantation (ASCT). These myeloablative/lymphoablative (M/L) treatment regimens involve the elimination of both the patient's hematopoietic stem cells and T-lymphocytes, often leading to serious complications including graft versus host disease (GVHD). The claimed invention addresses some of these problems by providing a conditioning regimen that is designed to eliminate the patient's T-lymphocytes while retaining a functional population of hematopoietic stem cells (HSC). This nonmyeloablative/lymphoablative (-/L) conditioning regimen involves the administration of one or more agents such as purine analogs (e.g., fludarabine), alkylating agents (e.g., bisulfan, cyclophosphamide), or anti-leukocyte globulins (e.g., anti-T lymphocyte globulin). After this, a donor-derived allogeneic stem cell preparation is administered to the patient. Patients treated according to the claimed invention develop donor-specific unresponsiveness and relatively fewer complications as compared to standard M/L conditioning regimens. The claimed methodologies should prove useful in the treatment of a number of hematologic malignancies such as chronic myelogenous leukemia, acute myelogenous leukemia, acute lymphoblastic leukemia, and non-Hodgkin's lymphoma.
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Excerpt(s): High dose or lethal conditioning regimens using chemotherapy and/or radiation therapy followed by rescue with allogeneic stem cell transplantation (alloSCT) or autologous stem cell transplantation (ASCT) have been the treatments of choice for patients with a variety of hematologic malignancies and chemosensitive solid tumors resistant to conventional doses of chemotherapy. A common source of stem cells for such procedures has been the bone marrow. Recently, peripheral blood stem cells (PBSC) have also been used. As such, the terms "allogeneic bone marrow transplantation" (allo-BMT) and "autologous bone marrow transplantation" (ABMT) are widely used in the literature to refer to particular types of allo-SCT and ASCT, respectively, whether the rescue is with bone marrow or PBSC. Current procedures typically employ allo-SCT or ASCT after myeloablative/lymphoablative (M/L) conditioning. As the name implies, M/L conditioning involves elimination, through cell killing, blocking, and/or down-regulation, of substantially all the hematopoietic stem cells and lymphocytes of the patient. Patients treated by allo-SCT or ASCT can develop major complications due to the M/L conditioning. In addition, patients receiving alloSCT are susceptible to graft versus host disease (GVHD), as well as to graft rejection. Moreover, relapse is still a frequent problem in these patients. Several attempts to improve disease-free survival by increasing the intensity of the M/L conditioning have failed due to unacceptable toxicity. Furthermore, increasing the intensity of the M/L conditioning does not appear to improve the outcome by decreasing the rate of relapse. A wide variety of protocols of varying intensities have been used among greater than 30,000 transplants worldwide reported to the International Bone Marrow Transplant Registry. Despite these numerous attempts to vary the intensity of the conditioning regimens, there have not been any documented significant differences in the over-all patient outcomes. Web site: http://www.delphion.com/details?pn=US06544787__ •
Nucleic acids encoding a heptahelix receptor, and methods of using them Inventor(s): Owman; Christer (Lund, SE) Assignee(s): Owman Invest, Ltd. (Lund, SE) Patent Number: 6,468,769 Date filed: November 15, 2000 Abstract: A full-length cDNA encoding a 375-amino-acid protein contains seven regions of hydrophobic amino acids representing membrane-spanning domains of a heptahelix receptor, tentatively named CMKRL2. It shows nearly 30% overall identity with the high-affinity IL8 receptor and similar degree of homology with other chemoattractant receptors, including the coreceptors for HIV-1. Receptor expression was ubiquitous in brain and in peripheral tissue as well as in Burkitt's lymphoma (irrespective of EBV status). The receptor and the gene encoding the receptor are useful for detecting Burkitt's lymphoma. Excerpt(s): This invention relates to a new chemoattractant receptor and its use. More particularly, this invention relates to cDNA encoding a novel heptahelix receptor widely distributed in brain and peripheral tissues. This invention also relates to the use of the receptor for detecting Burkitt's lymphoma cells. The G-protein coupled (heptahelix) membrane receptors (1) receive chemical signals in cell communication both in CNS and in the peripheral tissues. Interest has recently focused also on the immune system because this receptor type is recognized by many chemoattractant peptides, the model substances being IL8 (2,3), and heptahelix receptors are now recognized also among
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cluster determinant antigens in immune cells, i.e., CDw78 (4) and CD97 (5). In addition, the G-protein coupled receptors may be involved in other functional mechanisms, such as viral pathogenesis. Thus, the human cytomegalovirus shows structural homology with heptahelix receptors (6) and encodes a functional chemokine receptor (7), and Herpesvirus saimiri exerts "molecular piracy" of the IL8B receptor (8). It has recently been shown that the entry of HIV-1 into CD4-positive cells is mediated by two distinct chemoattractant receptors (9-10). Herpesvirus saimiri is closely related to the B lymphotropic Epstein-Barr virus (EBV). This is implicated in several human malignancies, such as Burkitt's lymphoma, which expresses BLR1, the first example of a heptahelix (chemokine-like) receptor identified specifically in the lymphocyte lineage of the hematopoietic system (11). Web site: http://www.delphion.com/details?pn=US06468769__ •
Prophylactic or therapeutic agent for diseases attributable to infection with helicobacters Inventor(s): Hirayama; Fumihiro (Fukuoka, JP), Sakurai; Nobuhiro (Fukuoka, JP), Sano; Mitsuharu (Fukuoka, JP), Yokoyama; Yoshito (Fukuoka, JP) Assignee(s): Welfide Corporation (Osaka, JP) Patent Number: 6,221,864 Date filed: December 23, 1999 Abstract: The present invention relates to an agent for the prophylaxis and treatment of diseases caused by Helicobacter infections, which comprises (S)-1-cyclopropyl-1,4dihydro-7-[2-(N,N-dimethylaminomethyl)morpholino]-6fluoro-8-methoxy-4oxoquinoline-3-carboxylic acid or a pharmaceutically acceptable salt thereof. The prophylactic and therapeutic agent of the present invention is effective even when used alone in a small dose for a short time, is almost free of problematic side effects such as tolerance and diarrhea, and is low toxic and capable of safe and ensured bacterial eradication. It is useful for the prophylaxis and treatment of diseases caused by Helicobacter infections, particularly, gastritis, gastric ulcer, duodenal ulcer, malignant lymphoma and gastric cancer. Excerpt(s): The present invention relates to a pharmaceutical agent containing (S)-1cyclopropyl-1,4-dihydro-7-[2-(N,N-dimethylaminomethyl)morpholino]-6fluoro-8methoxy-4-oxoquinoline-3-carboxylic acid or a pharmaceutically acceptable salt thereof, which agent is useful for the prophylaxis and treatment of diseases caused by Helicobacter infections, particularly gastritis, gastric ulcer, duodenal ulcer, gastric malignant lymphoma and gastric cancer. By the development of antisecretory drugs, such as histamine H.sub.2 antagonist and proton pump inhibitor, peptic ulcers, inclusive of a number of ulcers that heretofore required an operation, can now be cured by drug therapy. In view of the fact that most of the ulcers once cured are subject to recurrence and relapse, however, a maintenance therapy over a long period of time is considered to be necessary even after a complete cure, and even during the maintenance therapy, recurrence and relapse are highly frequently observed. In 1988, Marrshall B. J. et. al. (Lancet ii: 1437-42, 1988) applied eradication of Helicobacter pylori (H. pylori) to H. pylori positive gastric/duodenal ulcer cases, and reported a noticeable decrease in the relapse of duodenal ulcer. Thereafter in 1992, Graham D. Y. et. al. (Ann. Intern. Med. 116:705-708, 1992.) and in 1993, Hentschel E. et. al. (N. Engl. J. Med. 328:308-312, 1993) successively reported that relapse of peptic ulcer decreased significantly in the group subjected to eradication of H. pylori. Given the strong suggestion of the relationship
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between H. pylori infection, and gastritis and gastric/duodenal ulcer, a bacterial eradication therapy has been tentatively applied to patients with gastric/duodenal ulcer. Web site: http://www.delphion.com/details?pn=US06221864__ •
Purging leukemia cells from hematopoietic stem cells Inventor(s): Kolls; Jay (New Orleans, LA), Schwarzenberger; Paul (New Orleans, LA) Assignee(s): Board of Supervisors of Louisiana State University and Agricultural and (Baton Rouge, LA) Patent Number: 6,461,869 Date filed: July 20, 1999 Abstract: A gene therapy system is disclosed that selectively kills leukemia cells in bone marrow, while leaving stem cells unaffected. All cells in a mixture of stem cells and leukemia cells are transfected with a high efficiency gene transfer vector. The vector carries a eukaryotic expression construct encoding a toxin gene. This toxin gene is expressed only in leukemia cells, not in stem cells. Differential expression of the toxin gene in leukemia cells and stem cells may be achieved by placing the coding sequence under the control of an appropriate promoter, such as the RSV promoter or the SV40 promoter. High gene expression has been demonstrated in a panel of transformed leukemia cell lines, but no gene expression in transformed, CD34-selected, primary human stem cells. The treatment will be useful not only for leukemia patients, but also for other cancer patients undergoing autologous bone marrow transplants (e.g., breast or lymphoma cancers). Excerpt(s): This invention pertains to a method and composition for purging leukemia cells from hematopoietic stem cells. For many leukemia patients, the only hope for cure or long term survival is a bone marrow transplant from a donor. The cells for these "allogeneic" transplants are generally obtained from a sibling or from an unrelated, HLA-matched donor. However only a small fraction of potential patients receive such transplants due to constraints such as advanced age or the lack of a matching donor. Therefore, "autologous" marrow transplants are also used at times, the re-infusion of cells from the patient's own bone marrow following chemotherapy or radiation therapy that otherwise destroys the patient's marrow. Bone marrow is taken from a patient prior to high dose chemotherapy or radiation therapy, and is later reinfused to "rescue" the patient following the otherwise lethal therapy. However, there is currently no effective procedure to completely remove contaminating leukemia cells from bone marrow or other stem cell preparations. On the one hand, an autologous transplant does not carry the risk of short- or long-term graft-versus-host-disease, since the patient receives back his or her own bone marrow. However, a major drawback of existing autologous techniques is the lack of an effective way to remove all contaminating cancer cells from the bone marrow ex vivo. Relapses frequently result from such contaminating cancer cells. In principle, autologous transplants should be superior to allogeneic transplants if a method could be found to completely purge the transplanted cells of contaminating leukemia cells, because the risk of host-versus-graft disease would be eliminated. Progress has been made in reducing relapse rates in autologous transplants. Various purging procedures have been used to selectively remove leukemia cells from bone marrow, such as ex vivo chemotherapy with 4-hydrocyclophosphamide, or fractionation of cells by size. The combination of these two techniques, ex vivo chemotherapy with fractionation of cells by size, would probably be considered the current state-of-the art
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purging procedure by most researchers. However, this combination therapy often does not completely purge leukemic cells from the transplanted material. Web site: http://www.delphion.com/details?pn=US06461869__ •
Radioimmunotherapy of lymphoma using anti-CD20 antibodies Inventor(s): Butchko; Gregory M. (Lake Forest, IL), Glenn; Stephan D. (Sunnyvale, CA), Kaminski; Mark S. (Ann Arbor, MI), Wahl; Richard L. (Ann Arbor, MI) Assignee(s): Coulter Pharmaceutical, Inc. (South San Francisco, CA), The Regents of the University of Michigan (Ann Arbor, MI) Patent Number: 6,287,537 Date filed: May 29, 1998 Abstract: Methods for the treatment of lymphoma by adminstration of a B cell-specific antibody are described. The invention encompasses providing to a patient both unlabeled antibodies and antibodies labeled with a radioisotope. A principal advantage of the method is that tumor responses can be obtained in a radiometric dose range that does not require hematopoietic stem cell replacement as an adjunct therapy. Excerpt(s): The invention relates to therapy of lymphoma using antibodies directed to an antigen present on the surface of the lymphoma cells. The antibody demonstrates a therapeutic effect when administered per se, however, greatly enhanced therapeutic effect is seen when the antibody is labeled with a toxic substance, e.g. radioactively labeled. The amount of radioactivity used to label the antibody is preferably low enough that toxicity to bone marrow and other tissues is avoided, yet high enough to effect complete remission of the lymphoma. Although significant advances have been made in the treatment of non-Hodgkin's lymphoma over the past two decades, a curative regimen for patients with low-grade B cell lymphomas has yet to be developed. In addition, durable remission in patients treated with various regimens for refractory intermediate- and high-grade lymphomas have been relatively rare (1). Recent attempts utilizing supralethal chemotherapy combined with radiotherapy followed by bone marrow transplantation have resulted in an approximately 20% long term disease-free survival rate (2). However, most patients treated in this manner die of lymphoma or treatment related complications. Therefore, new strategies for the treatment of nonHodgkin's lymphomas are needed. These strategies should have as their goal the maximization of therapeutic effect coupled with the minimization of toxicity. One approach involves the use of monoclonal antibodies which recognize tumor-associated antigens as a means of targeting drugs or radioisotopes to tumor cells. This approach is particularly attractive in the case of non-Hodgkin's lymphomas as the tumor cells of these lymphomas display a variety of tumor-restricted antigens on their cell surfaces which would be available for targeting (3). Web site: http://www.delphion.com/details?pn=US06287537__
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Rhadino virus LANA acts in trans on a unit of rhadino virus DNA to mediate efficient episome persistance Inventor(s): Ballestas; Mary E. (Beverly, MA), Kaye; Kenneth M. (Weston, MA), Kieff; Elliott D. (269 Lee St., Brookline, MA 02445) Assignee(s): Kieff; Elliott D. (Brookline, MA) Patent Number: 6,322,792 Date filed: April 21, 1999 Abstract: Primary effusion lymphoma (PEL) cells harbor Kaposi's sarcoma-associated herpesvirus (KSHV) episomes and express a KSHV encoded latency-associated nuclear antigen (LANA). In PEL cells, LANA and KSHV DNA co-localized in dots in interphase nuclei and along mitotic chromosomes. In the absence of KSHV DNA, LANA was diffusely distributed in the nucleus or on mitotic chromosomes. In lymphoblasts, LANA was necessary and sufficient for the persistence of episomes containing a specific KSHV DNA fragment. Furthermore, LANA co-localized with the artificial KSHV DNA episomes in nuclei and along mitotic chromosomes. The KSHV DNA segment that provides for efficient persistence in LANA positive cells has been identified as the rhodino virus cis-acting element (RVCAE). These results support a model in which LANA tethers episomes containing the KSHV RVCAE DNA to chromosomes during mitosis to enable efficient segregation to progeny cells. The products and methods of the invention are useful in identifying compounds for modulating (especially including interfering with) the persistance of rhodino virus DNA in mammalian cells, and disease states associated therewith, as well as such compounds themselves. The products and methods of the invention are also useful in modulating (especially including enabling or improving) the efficient persistence of a heterologous DNA containing RVCAE and a selected DNA in mammalian cells in which LANA is expressed for use in gene therapies and related techniques based on the selected DNA. Excerpt(s): The present invention relates to a class of viruses called rhadino viruses, or gamma-2 herpes viruses. By way of example, but not by way of limitation, one commonly studied rhadino virus is Kaposi's Sarcoma-Associated Herpes Virus (KSHV), which is also known as Human Herpes Virus 8 (HHV8). More specifically, the invention relates to a rhadino virus protein known as LANA and to a segment of rhadino virus DNA known as the rhodino virus cis-acting element (RVCAE). The LANA protein is encoded by open reading frame (ORF) 73 and is expressed in mammalian cells that are latently infected with KSHV. The present invention relates to the discovery that LANA is necessary and sufficient for the efficient presistence of rhadino virus DNA in mammalian cells. The invention encompasses methods and assays for determining whether a compound of interest can modulate the ability of LANA to enable the efficient persistence of rhadino virus DNA in a mammalian cell, the binding of LANA to rhadino virus RVCAE DNA, the binding of LANA to mammalian chromosomes, or the tethering by LANA of rhadino virus RVCAE DNA to mammalian chromosomes, as well as such compounds themselves. Because persistent rhadino virus infection is linked to diseases such as Kaposi's Sarcoma (KS) and Primary Effusion Lymphoma (PEL), the invention also encompasses methods and assays for determining whether a compound of interest can modulate rhadino virus-associated disease states, including but not limited to KS and PEL, as well as such compounds themselves. Web site: http://www.delphion.com/details?pn=US06322792__
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Treatment of AIDS-associated non-Hodgkin's lymphoma by gallium nitrate Inventor(s): Rubin; Alan A. (207 Hitching Post Dr., Wilmington, DE 19803), Von Hoff; Daniel D. (226 Branch Oak Way, San Antonio, TX 78230) Assignee(s): none reported Patent Number: 6,562,870 Date filed: September 14, 1995 Abstract: The present invention comprises an improved method of treatment of AIDSassociated non-Hodgkin's lymphoma by administering gallium nitrate in a pharmaceutically acceptable vehicle. Excerpt(s): This invention relates to an improvement in the treatment of certain malignant lymphomas associated with acquired immunodeficiency syndrome (AIDS), and in particular, non-Hodgkin's lymphoma (NHL). More specifically, the present invention is directed to the therapeutic use of gallium nitrate in AIDS-associated NHL. The occurrence of NHL in HIV-infected individuals has increased dramatically since the onset of the AIDS epidemic. Projections of AIDS-associated NHL incidence based on the National Cancer Institute's program of Surveillance, Epidemiology and End Results (SEER) suggest that between 2900 (8%) and 9800 (27%) of all NHL cases that occurred in the US in 1992 are related to HIV infection (Gall, M. H. et al., J. Natl. Cancer Inst., 83:695, 1991). NHL incidence has been found to increase exponentially with increasing duration of HIV infection. Accordingly, improvements in AIDS therapy that prolong survival may result in even more AIDS-associated NHL than predicted from current epidemiologic studies. Treatment of AIDS-associated NHL has relied primarily upon drug combinations previously found to be effective in HIV(-)NHL. Some examples of these regimens include the: following: CHOP (cyclophosphamide, doxorubicin, vincristine, prednisone); M-BACOD (methotrexate, bleomycin, doxorubicin, cyclophospharmide, vincristine, dexamethasone); PROMACE-MOPP (prednisone, methotrexate, doxorubicin, cyclophosphamide, epipodophyllotoxin administered in alternating cycles with nitrogen mustard, vincristine, procarbazine, prednisone); and COMET-A (cyclophosphamide, vincristine, methotrexate with leucovorin calcium rescue, etoposide, cytarabine). Web site: http://www.delphion.com/details?pn=US06562870__
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Use of betulinic acid derivatives for inhibiting cancer growth Inventor(s): Jaggi; Manu (Haryana, IN), Khanna; Achla B. (Delhi, IN), Ramadoss; Sunder (Delhi, IN), Siddiqui; Mohammad Jamshed Ahmed (Ghaziabad, IN) Assignee(s): Dabur Research Foundation (Ghaziabad, IN) Patent Number: 6,214,814 Date filed: February 17, 1999 Abstract: The invention relates to the use of betulinic acid and its derivatives for the inhibition and/or prevention or cancer growth. The invention also relates to novel betulinic acid derivatives useful for the inhibition of tumor/cancer cells and a process for the preparation of the derivatives. The invention also relates to the antileukemic, and anti-lymphoma activity of the betulinic acid derivatives, and the use of the derivatives for the treatment of prostate, ovarian and lung cancer.
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Excerpt(s): Under the auspices of a National Cooperative Natural Product Drug Discovery Group supported by the National Cancer Institute, the potential antitumor activity of approximately 2500 extracts derived from globally collected plants was evaluated in a panel of enzyme based assays and in a battery of cultured human tumor cell lines. One such extract, prepared from the stem bark of Ziziphus mauritiana Lam. (Rhamnaceae), displayed selective cytotoxicity against cultured human melanoma cells (Nature Medicine, Vo. 1 (10), 1995, WO 96/29068). As a result of bioactivity guided fractionation, betulinic acid, a pentacyclic triterpene, was identified as a melanomaspecific cytotoxic agent. In follow-up studies conducted with a thymic mice carrying human melanomas, tumor growth was completely inhibited without toxicity. As judged by a variety of cellular responses, antitumor activity was mediated by the induction of apoptosis. A number of triterpenoids, including betulinic acid, have several known medical applications, including use as anticancer drugs. Anderson et al., in WO 95/04526, have discussed the derivatives of triterpenoids which have been used in cancer therapy, including their activity against polyamines which are required by cells to grow at an optimal rate. Some of these triterpenoids have been found to interfere with enzymatic synthesis of polyamines required for optimal cell growth, and thus inhibit the growth of cancer cells, particularly by inhibiting ornithine decarboxylase (Yasukawa, K. et al., Oncology 48: 72-76, 1991), The anti-cancer activity of betulinic acid and some derivatives has been demonstrated using mouse sarcoma 180 cells implanted subcutaneously in nude mice (JP 87,301,580). Choi et al have shown that betulinic acid 3monoacetate, and betulinic acid methyl ester exhibit ED.sub.50 values of 10.5 and 6.8.mu.g/ml, respectively, against p388 lymphocytic leukemia cells (Choi, Y-H et al., Planta Medical vol. XLVII, pages 511-513, 1988). Web site: http://www.delphion.com/details?pn=US06214814__
Patent Applications on Lymphoma As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to lymphoma: •
Antibodies against tumor necrosis factor delta (APRIL) Inventor(s): Ruben, Steven M.; (Brookeville, MD) Correspondence: Human Genome Sciences Inc; 9410 Key West Avenue; Rockville; MD; 20850 Patent Application Number: 20030059862 Date filed: May 22, 2002 Excerpt(s): This application claims the benefit of priority under 35 U.S.C.sctn.119(e) based on U.S. Provisional Application Serial No. 60/293,100 filed May 24, 2001. The present invention relates to antibodies and related molecules that immunospecifically bind to Tumor Necrosis Factor Delta (TNF-delta; APRIL). The present invention also relates to methods and compositions for detecting, diagnosing, prognosing, treating, preventing, or ameliorating a disease or disorder associated with aberrant APRIL or APRIL receptor expression or aberrant function of APRIL or APRIL receptor,
10
This has been a common practice outside the United States prior to December 2000.
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comprising antibodies or fragments or variants thereof, or related molecules, that immunospecifically bind to APRIL. In particular, the present invention further relates to methods and compositions for detecting, diagnosing, prognosing, preventing, treating or ameliorating autoimmune diseases or disorder, such as systemic lupus erythematosus Rheumatoid arthritis, and Sjogren's syndrome, or cancers of the immune system, particularly B cell cancers such as non-Hodgkin's lymphoma and multiple myeloma, comprising administering to an animal, preferably a human, an effective amount of one or more antibodies or fragments or variants thereof, or related molecules, that immunospecifically bind to APRIL. Tumor Necrosis Factor delta (TNF-delta; APRIL) is a member of the tumor necrosis factor ("TNF") superfamily that induces both in vivo and in vitro B cell proliferation and differentiation (See e.g. U.S. Patent Application Nos. 60/016,812; 60/211,537; 60/241,952; 60/254,875; 60/277,978; and 08/815,783; and International Publication No. WO97/33902; and Yu et al., Nature Immunol. 1(3):252-256 (2000)). APRIL is distinguishable from other B cell growth and differentiation factors such as IL-2, IL-4, IL-5, IL-6, IL-7, IL-13, IL-15, CD40L, or CD27L (CD70) by its monocyte-specific gene and protein expression pattern and its specific receptor distribution and biological activity on B lymphocytes. APRIL expression is not detected in natural killer ("NK") cells, T cells or B cells, but is restricted to cells of myeloid origin. The gene encoding APRIL has been mapped to chromosome 17p13. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Anti-CD80 antibody having ADCC activity for ADCC mediated killing of B cell lymphoma cells alone or in combination with other therapies Inventor(s): Hanna, Nabil; (Rancho Santa Fe, CA), Hariharan, Kandasamy; (San Diego, CA) Correspondence: Pillsbury Winthrop Llp; Intellectual Property Group; P.O. Box 10500; Mclean; VA; 22102; US Patent Application Number: 20030180290 Date filed: November 12, 2002 Abstract: Methods for treating B cell malignancies, in particular B cell leukemia and lymphoma, using an anti-CD80 antibody alone or in combination with an anti-CD20 antibody or chemotherapy is provided. These methods result in a synergistic anti-tumor response. Excerpt(s): This application claims priority to provisional application U.S. Serial No. 60/331,187 filed Nov. 9, 2001 which is incorporated by reference in its entirety herein. Additionally, this application is a continuation-in-part of U.S. Ser. No. 09/758,173 filed Jan. 12, 2001 which is a divisional of U.S. Ser. No. 09/383,916 filed Aug. 26, 1999 which is a divisional of U.S. Ser. No. 08/487,950 filed Jun. 7, 1995, now U.S. Pat. No. 6,113,898 all of which are incorporated by reference in their entirety herein. The present invention relates to the discovery that a PRIMATIZED.RTM. IgG.sub.1 antibody that shows specificity to the human CD80 molecule and which is referred to by the subject assignee, IDEC Pharmaceuticals Corporation, as IDEC-114 possesses antibody dependent cellular cytotoxicty (ADCC) against CD80 positive cells, especially CD80 positive cells of B cell lineage, and more particularly B cell lymphoma cells. (The sequence of this PRIMATIZED.RTM. antibody is disclosed in U.S. Pat. No. 6,113,898 which is incorporated by reference in its entirety herein). (This primatized antibody is referred to as 16C10 therein). The present invention also relates to the discovery that the use of IDEC-114 in combination with Rituxan.RTM., a chimeric anti-CD20 antibody approved
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by the FDA for treatment of non-Hodgkin's lymphoma, and/or chemotherapy yields a synergistic anti-tumor response against B cell lymphoma in vivo. IDEC-114 or 16C10 as it is referred to in an earlier patent and applications by the inventors is a PRIMATIZED.RTM. anti-CD80 IgG.sub.1 lambda monoclonal antibody (mAb) containing human constant regions and primate (cynomolgus macaque) variable regions. This antibody binds specifically to human CD80 (B7.1), which is membraneassociated 60 KDa glycoprotein expressed an activated B cells, activated antigen presenting cells, and activated T cells. (Freeman et al., J. Immunol. 1043:2714-22 (1989); Razi-Wolf et al., Proc. Natl Acad. Sci., USA 89:4210-4 (1992); and Azuma et al., J. Exp. Med. 177:845-50 (1993)) As noted above, the DNA and amino acid sequences that contain the variable heavy and light regions of IDEC-114 are disclosed in U.S. Pat. No. 6,113,898, which are identified therein as the 16C10 and heavy and light variable sequences, and which patent is incorporated by reference in its entirety herein. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Apparatus and method for debilitating or killing microorganisms within the body Inventor(s): Ganz, Robert A.; (Minnetonka, MN), Melgaard, Hans L.; (North Oaks, MN) Correspondence: James V. Harmon; Pillsbury Center, Suite 2000; 220 South Sixth Street; Minneapolis; MN; 55402; US Patent Application Number: 20030191459 Date filed: April 9, 2002 Abstract: A surgical apparatus has a body portion that includes a shaft terminating in a distal head or tip and a means for directing light radiation from the apparatus onto the lining of a body cavity for treating an ailment in a body cavity of a patient as for example a gastrointestinal ailment of a patient such as gastritis, gastric ulcer, duodenal ulcer, gastric cancer, gastric lymphoma, ulcerative colitis, or Crohn's disease as well as for treating diseases of the circulatory system, urogenital systems and other body cavities. The method of use of the apparatus comprises inserting the shaft of the apparatus into a body cavity, e.g., stomach or colon, of the patient to place the distal tip of the shaft in the desired position. The body cavity of the patient is then irradiated with light radiation so as to kill or debilitate microorganisms lining the body cavity without serious destruction of the body tissue of the patient to thereby improve or alleviate one or more of the symptoms of the ailment. A probiotic comprising innocuous bacteria can be administered to the patient to reestablish the growth of normal microbial flora when used in the gastrointestinal tract. Excerpt(s): This invention relates to an apparatus and method for the destruction of micro-organisms on or within a body cavity of a patient through the use of radiation. Infections involving the human gastrointestinal tract are extremely common, involving many millions of people on an annual basis. These infections include bacteria, viruses, and fungi, and are responsible for significant illness, morbidity and, in many cases, death. While the invention has utility in destroying microorganisms in various parts of the body, e.g., the stomach, bowel, lungs, peritoneal cavity, urinary tract, etc., it is particularly useful in the treatment of gastrointestinal infections. It has recently been shown that the most common gastrointestinal infection in the world is due to Helicobacter pylori, a bacterial pathogen that infects the stomach and duodenum. In the United States, for example, Helicobacter pylori is found in approximately 20% of the adult population. It is a chronic gut infection and, once acquired, is notoriously difficult to cure. Most infectious bacteria can be readily destroyed by the human immune system;
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however, Helicobacter pylori lives in the lumen of the stomach and on the surfaces of the stomach and duodenal cells, making it relatively resistant to a host immune response, even if vigorous. Its position has, however, been taken advantage of in the treatment method and apparatus employed in the present invention. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
B-cell lymphoma specific antigen for use in diagnosis and treatment of B-cell malignancies Inventor(s): Hu, Guanghui; (Houston, TX), Li, Yucheng; (Houston, TX), Wang, ShenWu; (Sugar Land, TX), Yao, Zhengbin; (Sugar Land, TX) Correspondence: Tanox, INC.; 10301 Stella Link; Houston; TX; 77025; US Patent Application Number: 20030147887 Date filed: November 2, 2002 Abstract: The present invention provides vaccines, antibodies, and diagnostic tools for the diagnosis and/or treatment of B-cell mediated diseases, particularly B-cell lymphomas. Excerpt(s): This application claims priority to U.S. Provisional Application No. 60/337,542, filed Nov. 2, 2001. This invention relates generally to molecules, e.g., peptides and antibodies, that interact with B-cell Lymphoma Specific Antigen ("BLSA"). Malignant tumors often express characteristic antigens or "markers" which offer a mechanism for tumor prevention, resistance or treatment. The antigens which are characteristic of the tumor may be purified and formulated into vaccines. This may stimulate an antibody response and a cellular immune response which are helpful in controlling tumor growth. At a minimum, the antibodies raised by these antigens can be used as detection tools to monitor the level of lymphoma-associated marker in the host to track the course of the disease, identify patients that have an early stage of the disease that are currently asymptomatic, or to monitor the effectiveness of treatment. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Cytostatic agents Inventor(s): Ayscough, Andrew Paul; (Oxford, GB), Drummond, Alan Hastings; (Oxford, GB), Pratt, Lisa Marie; (Oxford, GB) Correspondence: Greenberg Traurig, Llp; 885 3rd Avenue; New York; NY; 10022; US Patent Application Number: 20030149084 Date filed: December 10, 2002 Abstract: This invention provides a method of inhibiting proliferation of tumor cells in a subject by administering to the subject an effective amount of ester and thioester compounds containing an N-formyl hydroxylamine group.The compounds with which this invention is concerned thus represent a selection of a subclass from the compounds known in the art as MMP inhibitors, for a specific and previously unrecognized pharmaceutical utility in the inhibition of proliferation of rapidly dividing cells, including such tumor cells as lymphoma, leukemia, myeloma, adenocarcinoma, carcinoma, mesothelioma, teratocarcinoma, choriocarcinoma, small cell carcinoma, large
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cell carcinoma, melanoma, retinoblastoma, fibrosarcoma, endothelioma cells by a mechanism other than MMP inhibition.
leiomyosarcoma
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Excerpt(s): The present invention relates to N-formyl hydroxylamine derivatives, to processes for their preparation, to pharmaceutical compositions containing them, and to the use of such compounds in medicine. In particular, the compounds are inhibitors of the proliferation of a range of rapidly dividing tumour cells, for example melanoma and/or lymphoma cells. There is a need in cancer therapy for therapeutic compounds which are inhibitors of the proliferation of tumour cells. One compound which is known to have such activity is 5-fluorouracil (5FU). Patent publication WO 98/11063 describes and claims the use of certain hydroxamic acid derivatives as inhibitors of tumour cell proliferation, and also describes and claims certain novel hydroxamic acids useful for that purpose. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Detection of extracellular tumor-associated nucleic acid in blood plasma or serum using nucleic acid amplification assays Inventor(s): Benko, Floyd A.; (Palmyra, PA), Gocke, Christopher D.; (Ellicott City, MD), Kopreski, Michael S.; (Long Valley, NJ) Correspondence: Mcdonnell Boehnen Hulbert & Berghoff; 300 South Wacker Drive; Suite 3200; Chicago; IL; 60606; US Patent Application Number: 20030143600 Date filed: November 18, 2002 Abstract: This invention relates to detection of specific extracellular nucleic acid in plasma or serum fractions of human or animal blood associated with neoplastic or proliferative disease. Specifically, the invention relates to detection of nucleic acid derived from mutant oncogenes or other tumor-associated DNA, and to those methods of detecting and monitoring extracellular mutant oncogenes or tumor-associated DNA found in the plasma or serum fraction of blood by using rapid DNA extraction followed by nucleic acid amplification with or without enrichment for mutant DNA. In particular, the invention relates to the detection, identification, or monitoring of the existence, progression or clinical status of benign, premalignant, or malignant neoplasms in humans or other animals that contain a mutation that is associated with the neoplasm through detection of the mutated nucleic acid of the neoplasm in plasma or serum fractions. The invention permits the detection of extracellular, tumor-associated nucleic acid in the serum or plasma of humans or other animals recognized as having a neoplastic or proliferative disease or in individuals without any prior history or diagnosis of neoplastic or proliferative disease. The invention provides the ability to detect extracellular nucleic acid derived from genetic sequences known to be associated with neoplasia, such as oncogenes, as well as genetic sequences previously unrecognized as being associated with neoplastic or proliferative disease. The invention thereby provides methods for early identification of colorectal, pancreatic, lung, breast, bladder, ovarian, lymphoma and all other malignancies carrying tumor-related mutations of DNA and methods for monitoring cancer and other neoplastic disorders in humans and other animals. Excerpt(s): This application is a continuation-in-part of U.S. Provisional Application, Serial No. 60/028,180, filed Oct. 15, 1996, which is a continuation-in-part of U.S. Provisional Application, Serial No. 60/026,252, filed Sep. 17, 1996, which is a
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continuation-in-part of U.S. Provisional Application, Serial No. 60/013,497, filed Mar. 15, 1996, the entire disclosure of each of which is hereby incorporated by reference. This invention relates to methods for detecting specific extracellular nucleic acid in plasma or serum fractions of human or animal blood associated with neoplastic or proliferative disease. Specifically, the invention relates to detection of nucleic acid derived from mutant oncogenes or other tumor-associated DNA, and to methods of detecting and monitoring extracellular mutant oncogenes or tumor-associated DNA found in the plasma or serum fraction of blood by using rapid DNA extraction and nucleic acid amplification. In particular, the invention relates to the detection, identification, or monitoring of the existence, progression or clinical status of benign, premalignant, or malignant neoplasms in humans or other animals that contain a mutation that is associated with the neoplasm, through detection of the mutated nucleic acid of the neoplasm in plasma or serum fractions. The invention permits the detection of extracellular, tumor-associated nucleic acid in the serum or plasma of humans or other animals recognized as having a neoplastic or proliferative disease or in individuals without any prior history or diagnosis of neoplastic or proliferative disease. The invention provides the ability to detect extracellular nucleic acid derived from genetic sequences known to be associated with neoplasia, such as oncogenes, as well as genetic sequences previously unrecognized as being associated with neoplastic or proliferative disease. The invention thereby provides methods for early identification of colorectal, pancreatic, lung, breast, bladder, ovarian, lymphoma and all other malignancies carrying tumor-related mutations of DNA, and methods for monitoring cancer and other neoplastic disorders in humans and other animals. Neoplastic disease, including most particularly that collection of diseases known as cancer are a significant part of morbidity and mortality in adults in the developed world, being surpassed only by cardiovascular disease as the primary cause of adult death. Although improvements in cancer treatment have increased survival times from diagnosis to death, success rates of cancer treatment are more closely related to early detection of neoplastic disease that enable aggressive treatment regimes to be instituted before either primary tumor expansion or metastatic growth can ensue. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Deuterated rapamycin compounds, method and uses thereof Inventor(s): Foster, Robert T.; (Edmonton, CA), Naicker, Selvaraj; (Edmonton, CA), Yatscoff, Randall W.; (Edmonton, CA) Correspondence: Mary Ann Dillahunty; Burns, Doane, Swecker & Mathis, L.L.P.; P.O. Box 1404; Alexandria; VA; 22313-1404; US Patent Application Number: 20030139440 Date filed: November 20, 2002 Abstract: The synthesis of deuterated analogues of rapamycin is disclosed together with a method for use for inducing immunosupression and in the treatment of transplantation rejection, graft vs host disease, autoimmune diseases, diseases of inflammation leukemia/lymphoma, solid tumors, fungal infections, hyperproliferative vascular disorders. Also described is a method for the synthesis of water soluble deuteratred rapamycin compounds and their use as described above. Excerpt(s): This application is a continuation-in-part of U.S. patent application Ser. No. 09/148,623, which is based on provisional patent application No. 60/057,632, both of which are relied on and incorporated herein by reference. This invention relates to
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deuterated derivatives of rapamycin and a method for using them in the treatment of transplantation rejection, host vs. graft disease, graft vs. host disease, leukemia/lymphoma, hyperproliferative vascular disorders, autoimmune diseases, diseases of inflammation, solid tumors, and fungal infections. Rapamycin, known as sirolimusis, is a 31-membered macrolide lactone, C.sub.51H.sub.79NO.sub.13, with a molecular mass of 913.6 Da. In solution, sirolimus forms two conformational trans-, cisisomers with a ratio of 4:1 (chloroform) due to hindered rotation around the pipecolic acid amide bond. It is sparingly soluble in water, aliphatic hydrocarbons and diethyl ether, whereas it is soluble in alcohols, halogenated hydrocarbons and dimethyl sulfoxide. Rapamycin is unstable in solution and degrades in plasma and low-, and neuteral -pH buffers at 37.degree. C. with half-life of <10 h. the structures of the degradation products have recently been characterized. Rapamycin is a macrocyclic triene antibiotic produced by Streptomyces hygroscopicus, which was found to have antifungal activity, particularly against Candida albicans, both in vitro and in vivo (C. Vezina et al., J. Antibiot. 28, 721 (1975); S. N. Seh{overscore (g)}al et al., J. Antibiot. 28, 727 (1975); H. A. Baker et al., J. Antibiot. 31, 539 (1978); U.S. Pat. No. 3,929,992; and U.S. Pat. No. 3,993,749]. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Diagnosis and treatment of diseases caused by mutations in CD72 Inventor(s): Yang, Bing; (Saginaw, MI) Correspondence: Brooks & Kushman; 1000 Town Center 22nd FL; Southfield; MI; 48075 Patent Application Number: 20030077644 Date filed: September 27, 2002 Abstract: Mutants of the CD72 gene and their protein products are disclosed. Methods of diagnosing various diseases such as thyroid follicular carcinoma, renal cancer, endometrial adenocarcinoma, leukemia, ovarian cancer, lymphoma and lupus erythematosus by detecting particular mutations in human CD72 are also disclosed. Methods for supplying wild-type to cells which have lost normal CD72 function is additionally disclosed. CD72 associated diseases are additionally disclosed. Excerpt(s): This application claims the benefit of U.S. provisional application Serial No. 60/325,946, filed Sep. 28, 2001. The present invention relates to diseases resulting from hyperproliferation or hyperactivity of cells. In human thyroid follicular carcinoma, leukemia, renal cancer, endometrial adenocarcinoma, ovarian cancer, chondrosarcoma, lymphoma and human lupus erythematosus, expression of mutated forms of CD72 is described. Four different alleles have been identified for CD72 in mice. Sequence analysis of CD72 between mouse strains revealed that the cytoplasmic domain of CD72 is highly conserved while the extracellular domain is highly polymorphic, especially at the membrane-distal portion of the protein (Robinson et al., supra). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Diffuse large cell lymphoma diagnosis and outcome prediction by expression analysis Inventor(s): Aster, Jon C.; (Lexington, MA), Golub, Todd R.; (Newton, MA), Lander, Eric S.; (Cambridge, MA), Shipp, Margaret; (Wellesley, MA), Tamayo, Pablo; (Cambridge, MA) Correspondence: Lisa M. Treannie, ESQ.; Hamilton, Brook, Smith & Reynolds, P.C.; 530 Virginia Road; P.O. Box 9133; Concord; MA; 01742-9133; US Patent Application Number: 20030194701 Date filed: November 20, 2001 Abstract: Methods for predicting phenotypic classes of lymphomas, such as lymphoma type or treatment outcome, for lymphoma samples based on gene expression profiles are described. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/252,142, filed on Nov. 20, 2000, and U.S. Provisional Application No. 60/254,458, filed on Dec. 8, 2000. The entire teachings of the above applications are incorporated herein by reference. Classification of biological samples from individuals is not an exact science. In many instances, accurate diagnoses and safe and effective treatment of a disorder depend on being able to discern biological distinctions among morphologically similar samples, such as, for example, tumor samples. The classification of a sample from an individual into particular disease classes has proven to be difficult, incorrect or equivocal. Typically, using traditional methods such as histochemical analyses, immunophenotyping and cytogenetic analyses, only one or two characteristics of the sample are analyzed to determine the sample's classification, resulting in inconsistent and sometimes inaccurate results. Such results can lead to incorrect diagnoses and potentially ineffective or harmful treatment. Furthermore, important biological distinctions are likely to exist that have yet to be identified due to the lack of systematic and unbiased approaches for identifying or recognizing such classes. Thus, a need exists for an accurate and efficient method for identifying biological classes and classifying samples. The present invention relates to one or more sets of informative genes whose expression levels correlate with a class distinction between samples. In a particular embodiment, the class distinction is a lymphoma class distinction, such as a NonHodgkin's lymphoma class distinction (e.g., folicular lymphoma (FL) or diffuse large cell lymphoma (DLCL)). In another embodiment the class distinction can be a treatment outcome or survival class distinction. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Double-stranded RNA (dsRNA) and method of use for inhibiting expression of a fusion gene Inventor(s): Heidenreich, Olaf; (Tubgingen, DE), Kreutzer, Roland; (Weidenberg, DE), Limmer, Stefan; (Neudrossenfeld, DE), Vornlocher, Hans-Peter; (Bayreuth, DE) Correspondence: Palmer & Dodge, Llp; Kathleen M. Williams; 111 Huntington Avenue; Boston; MA; 02199; US Patent Application Number: 20030190654 Date filed: January 22, 2003
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Abstract: The present invention relates to the specific inhibition of expression of a fusion gene in mammals using a short double stranded RNA. The dsRNA is approximately 1924 nucleotides in length, and has a nucleotide sequence which is complementary to at least a part of the target gene. The dsRNAs of the present invention are useful for treating diseases caused by chromosomal aberrations, particularly malignant diseases such as lymphoma and leukemia. Excerpt(s): This application claims priority under 35 U.S.C.sctn. 119 to German Application No. DE 102 02 419.7, which is incorporated by reference herein. Chromosomal aberrations play a central role in the pathogenesis of many human malignant diseases, including hematologic neoplasms such as lymphoma and leukemia. Chromosomal abnormalities, characterized by structural changes or defects in one or more chromosomes, generally involve translocation, wherein a chromosome fragment is switched between non-homologous chromosomes; inversion, wherein the nucleotide sequence of a chromosome fragment is reversed; deletion (loss of a chromosomal fragment); insertion (incorporation of genetic material); duplication (repetition of an individual chromosome segment); or ring formation. These acquired genetic anomalies usually result in either activation of a quiescent gene or creation of a hybrid gene encoding a chimeric fusion oncoprotein, which triggers the malignant transformation. The chimeric fusion proteins created by cancer-associated chromosomal anomalies are ideal therapeutic targets because they are unique to the disease; they only exist in the malignant cells, not in the patient's normal cells (Cobaleda, C. et al., Bioassays (1995) 23:922). A number of therapeutic agents which target expression of chimeric fusion genes are known in the art, including zinc-finger proteins (Choo, Y., et al., Nature (1994) 372:642), hammerhead-based ribozymes (James, H. A, and I. Gibson, Blood (1998) 91:371), and antisense RNA (Skorski, T. et al., Proc. Natl. Acad. Sci. USA (1994) 91:45044508). Each of these agents have inherent limitations. Zinc-finger proteins act at the DNA level, interacting with the target sequence and blocking transcription. However, gene fusions occur randomly and within introns, hence requiring a unique or "custom" zinc-finger for each patient. Antisense approaches, using either single-stranded RNA or DNA, act in a 1:1 stoichiometric relationship and thus have low efficacy, as well as questionable specificity (Skorski et al., supra). Hammerhead ribozymes, which because of their catalytic activity can degrade a higher number of target molecules, have been used to overcome the stoichiometry problem associated with antisense RNA. However, hammerhead ribozymes require specific nucleotide sequences in the target gene, which are not always present. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Euphorbia antiquorum extract, a pharmaceutical composition containing the same and methods for treatment of cancers Inventor(s): Cheng, Wen-Ching; (Taipei, TW), Lin, Chih-Hui; (Taichung, TW) Correspondence: Lariviere, Grubman & Payne, Llp; P.O. Box 3140; Monterey; CA; 93942; US Patent Application Number: 20030165579 Date filed: February 27, 2002 Abstract: An herbal extract of Euphorbia antiquorum is provided. The herbal extract of the invention demonstrates in vitro inhibition of growth of hepatoma cells, colorectal adenocarcinoma cells, monocyte-like lymphoma and leukemia cells. This invention also
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provides a pharmaceutical composition containing the same and a method for treatments for cancers. Excerpt(s): This invention relates to herbal extracts from Euphorbia antiquorum, and more particularly, to a single-herb based pharmaceutical composition and method having therapeutic effects for treating cancers. According to the invention, the extracts from Euphorbia antiquorum have been found to show inhibitory effect on several different cancer cell lines. The extracts are useful in effective treatment of cancers, particularly hepatoma, colon cancer, leukemia and lymphocytoma. Cancer is the second leading cause of death in the United States (CA Cancer J. Clin. 43:7). The occurrence of cancer for any one individual is correlated with numerous risk factors. Some risk factors are believed to include age, genetics, diet and environmental exposure (e.g., to mutagenic chemicals, radiation, transforming viruses, etc.). According to an estimation by World Health Organization, about 10 million new cancer cases are now occurring annually around the world. The number is expected to reach 15 million by the year 2015, with two thirds of these new cases occurring in developing countries (World Health 48:22, 1995). For example, Hepatoma is much more prevalent in many of the developing countries than in the industrialized world. Although relatively uncommon in the Western world, an estimated 300 cases will occur annually in Missouri, USA. Statistics show that about 20,000 new patients are diagnosed every year in United States. It is not known exactly what causes hepatoma. However, certain risk factors have been identified. The risk factors are: a history of cirrhosis of the liver, certain types of viral hepatitis infection, chronic inflammatory conditions, exposure to the following substances aflatoxin, vinyl chloride, thorium dioxide, arsenic, long-term use of anabolic steroids and tabacco. In general, surgical resection is the treatment of choice for patients with hepatoma and can be curative, provided the tumor is confined to the liver and is completely removed. Unfortunately, many patients are not candidates for resection due to large tumor size, multiple tumors or severe cirrhosis of the liver. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Human-derived bradeion proteins, DNA coding for the proteins, and uses thereof Inventor(s): Tanaka, Manami; (Ibaraki, JP), Tanaka, Tomoo; (Kanagawa, JP) Correspondence: Foley And Lardner; Suite 500; 3000 K Street NW; Washington; DC; 20007; US Patent Application Number: 20030113753 Date filed: July 10, 2002 Abstract: This invention relates to a human-derived bradeion protein having the following properties:(i) it is a transmembranous protein;(ii) it has a transmembranous portion, an extracellular portion, and a cytoplasmic portion in its molecule as determined by a hydrophobicity analysis according to Kyte-Doolittle method;(iii) it is expressed in the human adult normal brain and heart, the expression level thereof in the heart being about 10% or lower of that in the brain, while it is not expressed in other adult normal organs of spleen, lung, liver, skeletal muscle, kidney and pancreas, and in fetal brain, lung, heart and kidney;(iv) it induces programmed cell death when overexpressed in a cultured human brain-derived undifferentiated nerve cell line;(v) it induces termination of cell division and aging when over-expressed in a cultured human brain-derived differentiated nerve cell;(vi) it is located in cytoplasm in the course of the induced cell death, and forms an intracellular aggregate when overexpressed; and(vii) it is expressed in a human colorectal cancer cell line or in a human malignant
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melanoma cell line, but not in leukemia, lymphoma and lung carcinoma,to a DNA encoding said bradeion protein, to a vector comprising said DNA, to a host cell comprising said vector, and to a method for detecting a cancer such as colorectal cancer or malignant melanoma. Excerpt(s): Japan Priority Application 325380/1998, filed Nov. 16, 1998, including the specification, drawings, claims and abstract, is incorporated herein by reference in its entirety. U.S. Priority application Ser. No. 09/440,936, filed Nov. 16, 1999, including the specification, drawings, claims and abstract, is incorporated herein by reference in its entirety. The present invention relates to a protein involved in long-term survival of cranial nerve cell, to DNA encoding the protein, and to uses thereof. More particularly, the present invention relates to human-derived bradeion protein or derivatives thereof, to DNA encoding the protein or the derivatives thereof, to a vector containing the DNA, to a host cell transformed or transfected with the vector, to an antibody immunologically reactive with the protein or the derivatives thereof, and to uses of the DNA or the antibody for detecting a cancer. Cranial nerve cells (neurons) are main elements for controlling survival of higher order animals. Once the neurons are produced, they do not divide at all and only gradually exfoliate or go through necrosis. Exfoliation of the neurons occurs in the normal state but is particularly accelerated by genetic diseases, brain ischemia, or status epilepticus, or under conditions of poor nutrition and low oxygen. Some disorders of cranial nerves associated with aging (e.g., dementia) result from deficiency of an absolute amount of functional neurons caused by accumulation of exfoliated neurons. Thus, the monitoring and control of the exfoliation, as well as regeneration of the functions of neurons, are the most demanding subject to be solved among the aging problems. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Identification of genes whose expression patterns distinguish benign lymphoid tissue and mantle cell, follicular, and small lymphocytic lymphoma Inventor(s): Koehler, Karen M.; (Brier, WA), LeVasseur, Robert J.; (Seattle, WA), Sabath, Daniel E.; (Seattle, WA), Schmechel, Stephen C.; (Seattle, WA), Yang, Kathleen H.; (Woodinville, WA) Correspondence: Greenlee Winner And Sullivan P C; 5370 Manhattan Circle; Suite 201; Boulder; CO; 80303; US Patent Application Number: 20030175761 Date filed: December 6, 2002 Abstract: Provided are genes whose expression patterns allow differentiation between benign lymph node tissue, follicular lymphoma tissue, mantle cell lymphoma tissue and small lymphocytic lymphoma tissue. These genes are useful as diagnostic markers for lymphoma. The protein products of these genes are useful in diagnostic and therapeutic applications, including monoclonal antibodies, lymphoma-specific chemotherapeutic agents, and gene therapies. Excerpt(s): This application takes priority to U.S. provisional application Serial No. 60/337,862, filed Dec. 7, 2001 which is incorporated herein to the extent not inconsistent with the disclosure herewith. The identification of genes whose patterns of expression are cancer-specific will lead to better management of cancer patients. New tests fall into four areas: (a) tests designed to classify a patient's cancer (diagnosis), (b) tests designed to predict a patient's clinical course (prognosis), (c) tests designed to determine which
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subset of patients with a particular type of cancer will respond to particular drugs (pharmacogenomics), and (c) tests to monitor patient response to therapy (monitoring). Genes identified as over- or under-expressed in cancer also serve as important targets for the process of drug discovery and have utility as gene therapy agents. DNA array technology (Schena, Shalon et al. 1995; Wodicka, Dong et al. 1997) provides the means to analyze the expression of hundreds to thousands of biomarkers in parallel. A DNA array is a device containing probes on a solid support that are designed to detect a large number of different DNA sequences. These devices allow quantification of the expression of thousands of distinct genes. Each gene generally encodes a single protein, which is the functional product of the gene. In the process of gene expression, each gene is copied into an intermediate form known as messenger RNA (mRNA). Genes that are expressed at high levels give rise to many copies of mRNA, whereas genes that are not expressed or expressed at low levels express few to no mRNA copies. DNA arrays facilitate the quantitative measurement of thousands of different mRNAs simultaneously. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Immunoconjugates and humanized antibodies specific for B-cell lymphoma and leukemia cells Inventor(s): Hansen, Hans; (Mystic Island, NJ), Leung, Shui-on; (Madison, NJ) Correspondence: Foley And Lardner; Suite 500; 3000 K Street NW; Washington; DC; 20007; US Patent Application Number: 20030103979 Date filed: November 16, 2001 Abstract: A chimeric LL2 monoclonal antibody is described in which the complementarity determining regions (CDRs) of the light and heavy chains of the murine LL2 anti-B-lymphoma, anti-leukemia cell monoclonal antibody has been recombinantly joined to the human kappa and IgG.sub.1 constant region domains, respectively, which retains the immunospecificity and B-cell lymphoma and leukemia cell internalization capacity of the parental murine LL2 monoclonal antibody, and which has the potential of exhibiting reduced human anti-mouse antibody production activity. A humanized LL2 monoclonal antibody is described in which the CDRs of the light and heavy chains have been recombinantly joined to a framework sequence of human light and heavy chains variable regions, respectively, and subsequently linked to human kappa and IgG.sub.1 constant region domains, respectively, which retains the immunospecificity and B-lymphoma and leukemia cell internalization capacities of the parental murine and chimeric LL2 monoclonal antibodies, and which has the potential for exhibiting reduced human anti-mouse antibody production activity. Vectors for producing recombinant chimeric and humanized chimeric monoclonal antibodies are provided. Isolated DNAs encoding the amino acid sequences of the LL2 variable light and heavy chain and CDR framework regions are described. Conjugates of chimeric and humanized chimeric LL2 antibodies with cytotoxic agents or labels find use in therapy and diagnosis of B-cell lymphomas and leukemias. Excerpt(s): This application claims benefit of priority to U.S. Ser. No. 09/741,843 filed on Dec. 22, 2000, which claims benefit of priority to U.S. Ser. No. 09/127,902 filed on Aug. 3, 1999, now U.S. Pat. No. 6,187,287, which claims benefit of priority to U.S. Ser. No. 08/690,102 filed on Jul. 31, 1996, now U.S. Pat. No. 5,789,554, which claims benefit of priority to U.S. Ser. No. 081289,576 filed on Aug. 12, 1994, now abandoned. The
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invention relates generally to immunoconjugates for diagnostic and therapeutic uses in cancer. In particular, the invention relates to recombinantly produced chimeric and humanized monoclonal antibodies directed against B-cell lymphoma and leukemia cells, which antibodies can be covalently conjugated to a diagnostic or therapeutic reagent without loss of antibody binding and internalization function and with reduced production of human anti-mouse antibodies. Non-Hodgkins lymphoma (NHL) and chronic lymphocytic leukemia are B-cell malignancies that remain important contributors to cancer mortality. The response of these malignancies to various forms of treatment is mixed. They respond reasonably well to chemotherapy, and, in cases where adequate clinical staging of NHL is possible, as for patients with localized disease, satisfactory treatment may be provided using field radiation therapy (Hall et al., Radiology for the Radiologist, Lippincott, Philadelphia, 1989, pp 365-376). However, the toxic side effects associated with chemotherapy and the toxicity to the hematopoietic system from local, as well as whole body, radiotherapy, limits the use of these therapeutic methods. About one-half of the patients die from the disease (Posner et al., Blood, 61: 705 (1983)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Immunogenic ALK peptides Inventor(s): Gambacorti-Passerini, Carlo; (Milano, IT), Passoni, Lorena; (Milano, IT) Correspondence: Alston & Bird Llp; Bank OF America Plaza; 101 South Tryon Street, Suite 4000; Charlotte; NC; 28280-4000; US Patent Application Number: 20030157101 Date filed: November 15, 2001 Abstract: There are disclosed immunogenic peptides from Anaplastic Lymphoma Kinase (ALK), methods in vivo or in vitro for activating ALK-specific CTLs and for stimulating an immune response against tumors, and pharmaceutical compositions containing ALK peptides for tumor immunotherapy. Excerpt(s): The present invention relates to immunogenic peptides derived from Anaplastic Lymphoma Kinase (ALK) that can be used in the immunotherapy of tumors. More specifically, the invention provides cytotoxic T-lymphocyte (CTL)-epitopes from ALK protein, in vivo and in vitro methods, using the ALK peptides of the invention, for activating ALK-specific CTLs and for stimulating an immune response against ALK positive tumors, and pharmaceutical compositions suitable for use in such methods. The discovery of tumor-associated antigens (TAAs) demonstrated that tumor cells can be specifically recognized by the immune system raising the hypothesis that most if not all tumors express antigens that cytotoxic T-lymphocytes can potentially attack (Renkvist N et al., (2001) Cancer Immunol Immunother., 50: 3-15). The identification of immunogenic epitopes led to their use as targets to mediate the specific clearance of neoplastic cells by TAA targeting strategies including vaccination, such as but not limited to allele-specific peptide-based vaccination. (Bremers A J et al., (2000) Eur J Surg Oncol., 26: 418-424; Kugler A. et al.,(2000) Nat Med., 6: 332-336; Nestle F O et al.,(1989) Nat Med., 4: 328-332). A major issue in the development of efficient vaccination protocols is the identification of the appropriate and effective TAAs, able to induce an immune response that will affect tumor growth. The ideal target for immune destruction is a tumor specific protein that is not expressed in normal cells and is essential for the malignant phenotype (Gilboa E., (1999) Immunity, 11: 263-270).
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Immunotherapy of B-cell malignancies using anti-CD22 antibodies Inventor(s): Goldenberg, David M.; (Mendham, NJ) Correspondence: Foley And Lardner; Suite 500; 3000 K Street NW; Washington; DC; 20007; US Patent Application Number: 20030124058 Date filed: December 9, 2002 Abstract: B-cell malignancies, such as the B-cell subtype of non-Hodgkin's lymphoma and chronic lymphocytic leukemia, are significant contributors to cancer mortality. The response of B-cell malignancies to various forms of treatment is mixed. Traditional methods of treating B-cell malignancies, including chemotherapy and radiotherapy, have limited utility due to toxic side effects. Immunotherapy with anti-CD20 antibodies have also provided limited success. The use of antibodies that bind with the CD22 or CD19 antigen, however, provides an effective means to treat B-cell malignancies such as indolent and aggressive forms of B-cell lymphomas, and acute and chronic forms of lymphatic leukemias. Moreover, immunotherapy with anti-CD22 and/or anti-CD19 antibodies requires comparatively low doses of antibody protein, and can be used effectively in multimodal therapies. Excerpt(s): The present application is a continuation-in-part application of U.S. patent application Ser. No. 09/038,995. The present invention relates to immunotherapeutic methods for treating B-cell malignancies. In particular, this invention is directed to methods for treating B-cell malignancies by administering comparatively low doses of antibody that binds to the CD22 antigen or antibody that binds to the CD19 antigen. The present invention also is directed to multimodal therapeutic methods in which antiCD22 or anti-CD19 administration is supplemented with chemotherapy, or by administration of therapeutic proteins, such as immunoconjugates and antibody fusion proteins. B-Cell lymphomas, such as the B-cell subtype of non-Hodgkin's lymphoma, are significant contributors to cancer mortality. The response of B-cell malignancies to various forms of treatment is mixed. For example, in cases in which adequate clinical staging of non-Hodgkin's lymphoma is possible, field radiation therapy can provide satisfactory treatment. Still, about one-half of the patients die from the disease. Devesa et al., J. Nat'l Cancer Inst. 79:701 (1987). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Inhibition of Bcl-2 protein expression by liposomal antisense oligodeoxynucleotides Inventor(s): Lopez-Berestein, Gabriel; (Bellaire, TX), Tari, Ana M.; (Houston, TX), Tormo, Mar; (Valencia, ES) Correspondence: Fulbright & Jaworski L.L.P.; 600 Congress AVE.; Suite 2400; Austin; TX; 78701; US Patent Application Number: 20030219474 Date filed: March 12, 2003 Abstract: The present invention provides novel compositions and methods for use in the treatment of Bcl-2-associated diseases like cancer, specifically, in the treatment of
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follicular lymphoma (FL). The compositions contain antisense oligonucleotides that hybridize to Bcl-2 nucleic acids, the gene products of which are known to interact with the tumorigenic protein Bcl-2. Used alone, or in conjunction with other antisense oligonucleotides, these compositions inhibit the proliferation of FL cancer cells. Excerpt(s): Bcl-2 has been linked to a wide variety of diseases such as hematologic malignancies, both leukemias and lymphomas, including follicular and nonfollicular lymphomas, chronic lymphocytic leukemia, and plasma cell dyscrasias (Campos et al., 1994); solid tumors like those associated with breast, prostate and colon cancer; and immune disorders. One particular Bcl-2-related disease is Follicular non-Hodgkin Lymphoma (FL). FL is the most common lymphoid malignancy in Europe and the United States. Typically it is an indolent, low grade disease consisting of an accumulation of small, resting B cells. Although the response to chemotherapy is initially good, relapses are inevitable with the transformation to a more aggressive histological type and the development of drug resistance (Aisenberg, 1995; Johnson et. at, 1995). In over 90% of FL patients, a t(14;18) translocation is found, which results in the juxtaposition of the bcl-2 gene from chromosome 18q21 with the immunoglobulin heavy chain gene locus on chromosome 14q323 (Tsujimoto et. at, 1985; Graninger et. al, 1987). As a consequence, the bcl-2 gene is under the influence of immunoglobulin heavy chain enhancer, and the Bcl-2 protein is overexpressed (Bakhshi et. at, 1985; Tsujimoto et. at, 1987). Bcl-2 tumorigenic potential is related to its capacity of interfering with physiological death responses, thereby enhancing the longevity of the cell (Nuez et. at, 1990). The Bcl-2 protein blocks apoptotic stimuli such as growth factor deprivation, radiation, heat-shock, virus, and most of the chemotherapeutic agents (Reed, 1995; Hockenbery et. at, 1990). In bcl-2-Ig-transgenic mice, a polyclonal follicular lymphoproliferation consisting of an expansion of mature B lymphocytes is initially observed (McDonnell et. al, 1989). Subsequently, a monoclonal high grade large immunoblastic type lymphomas develop with 50% of them presenting rearrangement of C-MYC. This suggests that a second genetic alteration is necessary for the development and progression of malignant lymphoma (McDonnell and Korsmeyer, 1991). Recently, an expanding family of Bcl-2-related proteins has been identified. This includes Bax, BCl-X.sub.L, Bcl-X.sub.S, Bad, Bak, Mcl-1, A-1, and several open reading frames in DNA viruses (Oltvai et. al, 1993; Boise et. al, 1993; Yang et. al, 1995; Chittenden et. al, 1995; Kiefer et. al, 95; Kozopas et. al, 1993; Lin et. al, 1993; Pearson et. al, 1987; Neilan et. al, 1993). Membership in the Bcl-2 family of proteins is principally defined by homology within the BH1 and BH2 domains, which help regulate dimerization between the members (Sato et. al, 1994). Bax, which shares 21% amino-acid identity with Bcl-2, can bind to Bcl-2 protein and neutralize its ability to block cell death. Thus, the ratio of Bcl-2 to Bax is thought to determine the cell's susceptibility to death following an apoptotic stimulus (Oltvai et. al, 1993; Yin et. al, 1994). Phosphodiester antisense oligodeoxynucleotides complementary to specific sequences of the translationinitiation site of Bcl-2 mRNA are able to inhibit the production of the Bcl-2 protein and the growth of t(14;18) translocation bearing cells (Kitada et. al, 1993). However, the therapeutic use of antisense oligonucleotides has been hampered by their low cellular uptake and their rapid degradation by nucleases and other serum or cellular components. Phosphorothioate oligonucleotides, which are resistant to nuclease degradation, were found to inhibit FL cell growth at concentrations 10 times lower than phosphodiester oligonucleotides (Reed et. al, 1990a; Cotter et. al, 1994). However, this approach suffers from low cellular uptake of the oligonucleotides. For example, Reed et. al had to use concentrations of greater than 25.mu.M of phosphorothioates to achieve 50% growth inhibitions of cell lines derived from B-cell lymphomas, such as 697 and SuDhl-4 cells. Liposomal incorporation has led to enhanced uptake of oligonucleotides into
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leukemic cells (Akhtar et. al, 1991; Tari et. al, 1994). The use of cationic lipids by Reed et. al to deliver phosphorothioate antisense oligonucleotides allowed them to reduce the concentration of oligonucleotides to 0.075 to 0.3.mu.M and still induce growth inhibition in Su-Dhl-4 cells. However, there has been no reported use of liposomes to deliver Bcl-2 antisense oligonucleotides and no proof of this as a method of treating Bcl-2 mediated disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method for treating cancer Inventor(s): Mermelstein, Fred H.; (Upper Montclair, NJ), Yurkow, Edward J.; (Hillsborough, NJ) Correspondence: Licata & Tyrrell P.C.; 66 East Main Street; Marlton; NJ; 08053; US Patent Application Number: 20030036513 Date filed: August 26, 2002 Abstract: A method of treating lymphoma, ovarian cancer, colorectal cancer, or gastric cancer by administering an effective amount of Mesna to a patient is provided. A method for treating and reducing the effective dose of an anti-cancer agent by administering Mesna in conjunction with an anti-cancer agent is also provided. Excerpt(s): This Application is a continuation-in-part of U.S. application Ser. No. 09/913,435 filed Feb. 2, 2002 which was the National stage of International Application No. PCT/US00/03878 filed Feb. 15, 2000, which claims the benefit of U.S. Provisional Application No. 60/120,128 filed Feb. 16, 1999. Sodium-2-mercaptoethane sulphonate, known as Mesna, was approved for the prevention of the urotoxic effects of oxazaphosphorine cytotoxic agents, cyclosphosphamide and ifosfamide. Mesna is traditionally given to patients undergoing chemotherapy, to offset the toxic effects of chemotherapy on the bladder. Mesna is pharmacologically and toxicologically a relatively inert substance, even in very high dose, i.e. 1000 mg/kg. It is particularly striking that even high Mesna doses do not interfere with the curative potency of the oxazaphosphorines or cytostatics. In the body Mesna is rapidly inactivated to form inert Mesna disulfide (diMesna). Within a few minutes after administration, more than 90% of the administered dose has been transformed into Mesna disulphide which remains in the vascular system and is rapidly eliminated via the kidneys. After glomerular filtration, a considerable part of Mesna disulphide is reduced to a third compound which reacts and detoxifies the urotoxic oxazaphosphorine metabolites in the urine. The reaction with glutathione plays a particular role in the reduction of Mesna disulphide to Mesna in the renal epithelia, suggesting a three stage reaction. The first reactions are catalyzed by thiol transferase, the last by glutathione reductase. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of isolating extract from the euphorbaciae obesa plant and methods for using the same Inventor(s): Donato, Nicholas D.; (San Marcos, CA), Donato, Nicholas J.; (Sugarland, TX), McMurray, John S.; (Houston, TX), Newman, Robert A.; (Sugarland, TX), Perez, Margot; (Houston, TX), Sample, David C.; (Porter, TX) Correspondence: Foley & Lardner; P.O. Box 80278; San Diego; CA; 92138-0278; US Patent Application Number: 20030118677 Date filed: December 12, 2001 Abstract: The present invention is directed to a process of isolating an extract from a Euphorbaciae obesa (EO) plant by: preparing a sample of said plant comprising removal of the latex material; dissolving said sample with first solvent to form a solution; seperating said solution into a liquid and a pulp fraction; and purifying said pulp fraction. The isolated EO extract induces apoptosis and inhibits growth of a cancerous cell. Thus, the present invention is also directed to a method for inducing apoptosis and growth inhibition of a cancerous cell by contacting the cell with an effective amount of the EO extract by the process of the invention. Preferably, the extract is administered both to the tumor directly and intravenously. The preferred lines of cancerous cells are melanoma, non-small cell lung cancer, prostate cancer, breast carcinoma, ovarian cancer, lymphoma and leukemia cells. Excerpt(s): This invention generally relates to compounds for treating cancer that are derived from plants and, in particular, the isolation and use of an extract from a Euphorbaciae obesa plant having anti-tumor effects on a variety of cancerous cells. Plants and marine organisms provide a rich source of compounds that have been investigated and exploited for a variety of medicinal and biological applications. The Euphorbiaceae family is one of the largest families of plants with about 300 genera and 7,500 species, mostly monoecious herbs, shrubs and trees, sometimes succulent and cactus-like, that are further frequently characterized by a milky sap or latex material. Members of the Euphorbiaceae family have been investigated as providing potential treatments for cancers, tumors and warts. Active components found in members of this plant family may be common to several genera or species of the family or may be limited to a particular genus or species. Certain Euphorbiaceae species have been shown to synthesize phorbol ester and diterpene diester compounds having therapeutic effects on certain cancers. For instance, the isolation and characterization of antileukemic properties from Euphorbia esula L and Croton tiglium L. have been reported. S. M. Kupchan et al., Science 191: 571-572 (1976). The fractionation of an active extract led to the characterization of the antileukemic component from Euphorbia esula L as a diterpene diester. Fractionation of croton oil led to the characterization of the active component known as a phorbol diester, phorbol 12-tiglate 13-decanoate. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of treating tumors Inventor(s): Burke, Patricia A.; (Sacramento, CA), DeNardo, Gerald L.; (El Macerco, CA), DeNardo, Sally J.; (El Macerco, CA), Goodman, Simon; (Darmstadt, DE), Matzku, Siegfried; (Zwingenberg, DE) Correspondence: Olson & Hierl, LTD.; 36th Floor; 20 North Wacker Drive; Chicago; IL; 60606; US Patent Application Number: 20030143157 Date filed: July 31, 2002 Abstract: A method of treating tumors, such as prostate tumors, breast tumors, nonHodgkin's lymphoma, and the like, includes the sequential steps of administering to the patient at least one dose of an antiangiogenic cyclo-arginine-glycine-aspartic acidcontaining pentapeptide (cRGD pentapeptide); administering to the patient an antitumor effective amount of a radioimmunotherapeutic agent (RIT); and then administering to the patient at least one additional dose of cRGD pentapeptide. The cRGD pentapeptide is preferably cyclo-(Arg-Gly-Asp-D-Phe-[N-Me]-Val), and the RIT is preferably a radionuclide-labeled chelating agent-ligand complex in which chelating agent is chemically bonded to a tumor-targeting molecule, such as a monoclonal antibody. Excerpt(s): This application is a continuation-in-part of co-pending U.S. patent application Ser. No. 09/787,374, filed on Sep. 9, 1999. The invention relates to methods of treating tumors. More particularly the invention relates to treatment of tumors with a combination of radioimmunotherapy and an integrin receptor antagonist. Novel and synergistic therapeutic combinations are desirable for the treatment of metastatic breast cancer, prostate cancer, Hodgkin's lymphoma, and other cancers, many of which are currently incurable with standard multimodality therapy. High incidence of p53 mutations and bcl-2 protein over-expression in breast cancer increase resistance to chemotherapy and radiotherapy. Systemic, tumor-targeted radioimmunotherapy (RIT) has the potential to target tissue specifically and to deliver cancer-specific cytotoxic antibodies to widespread metastatic foci. However, studies in a human breast cancer xenograft model demonstrate that RIT, as a single agent, typically does not cure the tumors. Tumor penetration of radiolabeled antibodies may be non-uniform and may not be sufficient in all regions of the tumor to provide cure. The combination of RIT with other therapeutic modalities is currently being utilized, but the additional chemotherapy or external radiotherapy increases the risk of bone marrow toxicity, the major doselimiting factor in RIT. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods and compositions for determining neoplastic disease responsiveness to antibody therapy Inventor(s): Bohen, Sean P.; (Mountain View, CA), Botstein, David; (Belmont, CA), Brown, Patrick O.; (Stanford, CA), Levy, Ronald; (Stanford, CA) Correspondence: Bozicevic, Field & Francis Llp; 200 Middlefield RD; Suite 200; Menlo Park; CA; 94025; US Patent Application Number: 20030219818 Date filed: May 9, 2003
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Abstract: Methods are provided for determining whether a subject suffering from a neoplastic condition, e.g., non-Hodgkin's lymphoma (NHL), such as follicular lymphoma, is responsive to antineoplastic therapy, such as antibody therapy, e.g., Rituximab. In practicing the subject methods, an expression profile is obtained from the subject suffering from NHL and employed to determine whether the subject is responsive to antineoplastic therapy. In addition, reagents and kits thereof that find use in practicing the subject methods are provided. Excerpt(s): This application claims priority (pursuant to 35 U.S.C.sctn.119 (e)) to the filing date of the U.S. Provisional Patent Application Serial No. 60/379,847 filed May 10, 2002; the disclosure of which is herein incorporated by reference. The field of this invention is non-Hodgkin's lymphoma and the treatment therapy thereof, particularly using antibody therapeutics, e.g., rituximab. In the fall of 1997, the anti-CD20 monoclonal antibody, rituximab (currently sold under the brand name RITUXAN.RTM.), was approved for the treatment of refractory or relapsed low-grade B-cell non-Hodgkin's lymphoma (NHL). Rituximab has since become a mainstay of treatment for low-grade NHL and over 400,000 patients worldwide have been treated with rituximab. Despite this extensive clinical experience, the mechanism of action of rituximab remains unclear, as does the nature of resistance. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods for diagnosis and treatment of diseases associated with altered expression of JAK1 Inventor(s): Martin, Javier Hernandez; (Aarhus N, DK), Pedersen, Finn Skou; (Aarhus V, DK), Soerensen, Annette Balle; (Aarhus N, DK) Correspondence: Robin M. Silva, ESQ.; Flehr Hohbach Test Albritton & Herbert Llp; Suite 3400; Four Embarcadero Center; San Francisco; CA; 94111-4187; US Patent Application Number: 20030044803 Date filed: September 24, 2001 Abstract: The present invention relates to novel compositions and methods related to JAKI for use in diagnosis and treatment of lymphoma and leukemia. In addition, the present invention describes the use of such novel compositions for use in screening methods. Excerpt(s): This application is a continuing application of U.S. Ser. No. 09/668,644, filed Sep. 22, 2000, which is expressly incorporated herein by reference. The present invention relates to novel compositions for use in diagnosis and treatment of lymphoma and leukemia, as well as the use of these novel compositions in screening methods. Lymphomas are a collection of cancers involving the lymphatic system and are generally categorized as Hodgkin's disease and Non-Hodgkin lymphoma. Hodgkin's lymphomas are of B lymphocyte origin. Non-Hodgkin lymphomas are a collection of over 30 different types of cancers including T and B lymphomas. Leukemia is a disease of the blood forming tissues and includes B and T cell lymphocytic leukemias. It is characterized by an abnormal and persistent increase in the number of leukocytes and the amount of bone marrow, with enlargement of the spleen and lymph nodes. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods of inhibiting Pin1-associated states using a fredericamycin a compound Inventor(s): Fischer, Gunter; (Halle, DE), Lu, Kun Ping; (Newton, MA) Correspondence: Lahive & Cockfield; 28 State Street; Boston; MA; 02109; US Patent Application Number: 20030055072 Date filed: December 21, 2001 Abstract: This invention provides a method for treating a Pin1-associated state in a subject including administering to a subject an effective amount of a fredericamycin A compound such that the Pin1-associated state is treated. In another aspect, this invention includes the above described method, wherein the Pin1-associated state is a cyclin D1 elevated state, neoplastic transformation, and/or tumor growth. In an embodiment, this invention provides the above described methods, wherein the Pin1associated state is colon cancer, breast cancer, a sarcoma, a malignant lymphoma, and/or esophageal cancer. This invention also provides a method for treating cyclin D1 overexpression in a subject including administering to a subject an effective amount of a combination of a fredericamycin A compound and a hyperplastic inhibitory agent such that the cyclin D1 overexpression is treated. Excerpt(s): This application claims priority to U.S. Provisional Patent Application No. ______, filed on Dec. 20, 2001, entitled "Methods of Inhibiting Pin1-Associated States Using a Fredericamycin A Compound;" and U.S. Provisional Patent Application No. 60/257,412, filed on Dec. 22, 2000. This application is related to U.S. patent application Ser. No. 09/726,464, filed Nov. 29, 2000; U.S. application Ser. No. 08/988,842, filed Dec. 11, 1997; and WO 99/12962, published Mar. 8, 1999. The entire contents of each of the aforementioned applications are hereby incorporated herein by reference. At the center of the cell cycle are the cyclin dependent kinases (cdks). The cdks are a family of structurally related small protein (.about.34-40 kD) kinase catalytic subunits whose activation requires association with a cyclin regulatory subunit. In most cases, full activation also requires phosphorylation of a threonine near the kinase active site. Cdk function has been well conserved during evolution. For example, yeast cells can divide normally when their cdk1 gene is replaced with the human cdk1 gene. The cdks form unique complexes with cyclins and those complex promote cell proliferation by phosphorylating specific substrates in a cell cycle dependent fashion to ensure progression through various cell cycle transitions. The precise timing of cyclin-cdk activity during the cell cycle determines whether the cell cycle continues or becomes blocked. Morgan 1997. Annu. Rev. Cell. Dev. Biol 13:261-291. There are at least 11 different mammalian cyclins including cyclins A, B1, B2, C, D1, D2, D3, E, F, G, and H. The different cyclins reach peak activity during different phases of the cell cycle. Cyclin D1 is a protein derived from the PRAD1, CCND1, or bc1-1 gene on chromosome 11q13. The cyclin D1 gene spans about 15 kb and has 5 exons. Its upstream region has Sp1 binding sites, a potential E2F binding motif, and no obvious TATA box. Cyclin D1 reaches its maximum activity during mid G.sub.1 phase, decreases during S-phase, and remains low throughout the rest of the cycle. Cyclin D1 appears to regulate the transition from the G.sub.1 to S phase of the cell cycle. Donnellan, et al. 1998. J. Clin. Pathol: Mol. Pathol. 51:1-7. In normal cells, the level of cyclin D1 protein fluctuates in response to external stimuli. In contrast, expression is unscheduled in transformed cell lines and may occur throughout the cycle. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods of therapy and diagnosis using immunotargeting of cells expressing VpreB1 protein Inventor(s): Chen, Huang-Tsu; (Cupertino, CA), Dedera, Douglas A.; (Castro Valley, CA), Wan, Ching-Yi; (Alviso, CA) Correspondence: Luisa Bigornia; Hyseq, INC.; 670 Almanor Avenue; Sunnyvale; CA; 94085; US Patent Application Number: 20030215453 Date filed: May 14, 2002 Abstract: Certain cells, including types of cancer cells such as B-cell lymphoma, T-cell lymphoma, T-cell leukemia, and non-Hodgkin's lymphoma, are capable of expressing VpreB1 RNA. Immunotargeting using VpreB1 polypeptides, nucleic acids encoding for VpreB1 polypeptides and anti-VpreB1 antibodies provides a method of killing or inhibiting that growth of cancer cells that express the VpreB1 protein. Methods of immunotherapy and diagnosis of disorders associated with VpreB1 protein-expressing cells, such as B-cell lymphoma, T-cell lymphoma, T-cell leukemia, and non-Hodgkin's lymphoma, are described. Excerpt(s): This invention relates to compositions and methods for targeting VpreB1 protein-expressing cells and their use in the therapy and diagnosis of various pathological states, including cancer, autoimmune disease, organ transplant rejection, and allergic reactions. Antibody therapy for cancer involves the use of antibodies, or antibody fragments, against a tumor antigen to target antigen-expressing cells. Antibodies, or antibody fragments, may have direct or indirect cytotoxic effects or may be conjugated or fused to cytotoxic moieties. Direct effects include the induction of apoptosis, the blocking of growth factor receptors, and anti-idiotype antibody formation. Indirect effects include antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-mediated cellular cytotoxicity (CMCC). When conjugated or fused to cytotoxic moieties, the antibodies, or fragments thereof, provide a method of targeting the cytotoxicity towards the tumor antigen expressing cells. (Green, et al., Cancer Treatment Reviews, 26:269-286 (2000)). Because antibody therapy targets cells expressing a particular antigen, there is a possibility of cross-reactivity with normal cells or tissue. Although some cells, such as hematopoietic cells, are readily replaced by precursors, cross-reactivity with many tissues can lead to detrimental results. Thus, considerable research has gone towards finding tumor-specific antigens. Such antigens are found almost exclusively on tumors or are expressed at a greater level in tumor cells than the corresponding normal tissue. Tumor-specific antigens provide targets for antibody targeting of cancer, or other disease-related cells, expressing the antigen. Antibodies specific to such tumor-specific antigens can be conjugated to cytotoxic compounds or can be used alone in immunotherapy. Immunotoxins target cytotoxic compounds to induce cell death. For example, anti-CD22 antibodies conjugated to deglycosylated ricin A may be used for treatment of B cell lymphoma that has relapsed after conventional therapy (Amlot, et al., Blood 82:2624-2633 (1993)) and has demonstrated encouraging responses in initial clinical studies. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods of therapy for non-hodgkin's lymphoma Inventor(s): Hurst, Deborah; (Piedmont, CA), Milan, Sandra; (Orinda, CA), Wolin, Maurice J.; (Piedmont, CA) Correspondence: Chiron Corporation; Intellectual Property - R440; P.O. Box 8097; Emeryville; CA; 94662-8097; US Patent Application Number: 20030185796 Date filed: November 12, 2002 Abstract: Methods for treating a human with lymphoma using a combination of interleukin-2 and at least one anti-CD20 antibody are provided. These therapeutic agents are administered as two separate pharmaceutical compositions, one containing IL-2, the other containing at least one anti-CD20 antibody, according to a dosing regimen. Administering of these two therapeutic agents together potentiates the effectiveness of either agent alone, resulting in a positive therapeutic response that is improved with respect to that observed with either agent alone. The therapeutic effects of these agents can be achieved using lower dosages of IL-2, thereby lessening the toxicity of prolonged IL-2 administration and the potential for tumor escape. Excerpt(s): This application is a continuation-in-part of U.S. application Ser. No. 09/815,597, filed Mar. 23, 2001, which claims the benefit of U.S. Provisional application Serial No. 60/192,047, filed Mar. 24, 2000, the contents of which are herein incorporated by reference in their entirety. The present invention is directed to methods of therapy for non-Hodgkin's lymphoma, more particularly to concurrent therapy with interleukin-2 and monoclonal antibodies targeting the CD20 B-cell surface antigen. The nonHodgkin's lymphomas are a diverse group of malignancies that are predominately of Bcell origin. In the Working Formulation classification scheme, these lymphomas been divided into low-, intermediate-, and high-grade categories by virtue of their natural histories (see "The Non-Hodgkin's Lymphoma Pathologic Classification Project," Cancer 49(1982):2112-2135). The low-grade lymphomas are indolent, with a median survival of 5 to 10 years (Horning and Rosenberg (1984) N. Engl. J. Med. 311:1471-1475). Although chemotherapy can induce remissions in the majority of indolent lymphomas, cures are rare and most patients eventually relapse, requiring further therapy. The intermediateand high-grade lymphomas are more aggressive tumors, but they have a greater chance for cure with chemotherapy. However, a significant proportion of these patients will relapse and require further treatment. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods of treating cancer using an FPT inhibitor and antineoplastic Inventor(s): Baum, Charles; (Westfield, NJ), Cutler, David L.; (Moorestown, NJ), Meyers, Michael L.; (Hastings-on-Hudson, NY), Zaknoen, Sara L.; (Hoboken, NJ) Correspondence: Schering-plough Corporation; Patent Department (k-6-1, 1990); 2000 Galloping Hill Road; Kenilworth; NJ; 07033-0530; US Patent Application Number: 20030185831 Date filed: November 25, 2002 Abstract: Disclosed is a method of treating cancer in a patient in need of such treatment comprising administering a therapeutically effective amount of an FPT inhibitor and therapeutically effective amounts of one or more antineoplastic agents. Methods of
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treating non small cell lung cancer, CML, AML, non-Hodgkin's lymphoma and multiple myeloma are disclosed. Excerpt(s): This application claims the benefit of Provisional Application Serial No. 60/334411 filed on Nov. 30, 2001. WO 98/54966 published Dec. 10, 1998 discloses methods of treating cancer by administering at least two therapeutic agents selected from a group consisting of a compound which is an antineoplastic agent and a compound which is an inhibitor of prenyl-protein transferase (e.g., a farnesyl protein transferase inhibitor). Farnesyl Protein Transferase (FPT) Inhibitors are known in the art, see for example U.S. Pat. No. 5,874,442 issued Feb. 23, 1999. Methods of treating proliferative diseases (e.g., cancers) by administering an FPT inhibitor in conjunction with an antineoplastic agent and/or radiation therapy are also known, see for example U.S. Pat. No. 6,096,757 issued Aug. 1, 2000. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Modulating lymphoid commitment and survival Inventor(s): Allman, David; (Havertown, PA), Aster, Jon C.; (Lexington, MA), He, Yiping; (Philadelphia, PA), Izon, David J.; (Wembley, AU), Pear, Warren S.; (Philadelphia, PA) Correspondence: Evelyn H. Mcconathy; Dilworth Paxson Llp; 3200 Mellon Bank Center; 1735 Market Street; Philadelphia; PA; 19103; US Patent Application Number: 20030181380 Date filed: March 10, 2003 Abstract: Provided are methods for manipulating aspects of lymphopoiesis by modulating and controlling Notch signaling, thereby providing treatment for diseases of the immune system. Accordingly, there are provided methods for selectively modulating T cell fate commitment of a common lymphoid progenitor at the expense of B cell fate commitment, and in the converse for selectively modulating B cell fate commitment of a common lymphoid progenitor at the expense of T cell fate commitment. Also provided are methods for treating patients suffering from a disease or disorder of T cell origin, or conversely of B cell origin. Further provided are methods for selectively killing B cells in a committed population of B cells, such as in a patient suffering from B cell leukemia or lymphoma; as well as methods for selectively killing T cells in a committed population of T cells such as in a patient suffering from diseases of T cell origin. Excerpt(s): This application claims priority to U.S. Provisional Application Nos. 60/363,018, filed Mar. 8, 2002, and 60/277,422, filed Mar. 21, 2001, the content of which is herein incorporated by reference. The present invention relates to compositions and methods useful in the treatment and prevention of diseases of the immune system, such as leukemias, specifically relating to controlling the effect of Notch signaling on lymphoid differentiation and cell fate decisions. B cell development begins in the bone marrow (BM), where the earliest B cells derive from a common lymphocyte progenitor, that is also capable of producing T and NK cells (Kondo et al., Cell 91:661-672. (1997); Izon et al., J. Immunol. 167:1387-1392. (2001b); Gounari et al., Nat. Immunol. 3:489-96. (2002); Igarashi et al., Immunity 17:117-130. (2002)). B cell development in the BM occurs in successive stages during which the immunoglobulin (Ig) genes are rearranged and expressed to produce a naive B cell that expresses surface immunoglobulin of a single antigen specificity (Hardy et al., Immunol. Rev 175:23-32. (2002); Janeway et al., (2001)
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Immunobiology, 5th ed., New York: Garland Publishing; Rolink et al., Curr. Opin. Immunol. 13:202-207. (2001)). The earliest B lineage cells, originating from a subset of hematopoietic stem cells known as early lymphoid progenitors (ELPs), are termed pro-B cells, and it is in these cells that Ig rearrangement begins (Igarashi et al., 2002). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Molecular characterization of chromosome translocation t(11;18)(q21;q21) and its correlation to carcinogenesis Inventor(s): Baens, Mathijs; (Lubbeek, BE), Dierlamm, Judith; (Hamburg, DE), Marijnen, Peter; (Herent, BE) Correspondence: Trask Britt; P.O. Box 2550; Salt Lake City; UT; 84110; US Patent Application Number: 20030176682 Date filed: January 28, 2003 Abstract: Methods for determining whether a tissue sample or an analogue and/or derivative thereof comprises a cell with a chromosome (11:18) translocation associated with malignancies such as mucosa-associated lymphoid tissue (MALT) lymphomas. The invention further provides insight into a novel mechanism of transformation of primary cells. The mechanism involves expression of a fusion proteinaceous molecule comprising at least apoptosis inhibitor 2 (API2) or a functional part, derivative and/or analogue thereof fused to at least One other proteinaceous molecule. The invention also provides a novel nucleic acid sequence and proteinaceous molecule expressed from the sequence termed "MALT-lymphoma associated Translocation (MLT) protein." Excerpt(s): This application is a continuation of U.S. patent application Ser. No. 09/579,692, filed Mar. 26, 2000, which claims priority from Provisional Patent Application No. 60/138,834, filed Jun. 9, 1999. The invention relates to the fields of medicine and diagnostics. More in particular, the invention relates to medicine and the diagnosis of tumors. Since biopsies of these lymphomas are relatively rarely subjected to cytogenetic analysis and their in vitro proliferation is often poor, abnormal karyotypic data have been published for only 46 low-grade MALT lymphomas,.sup.9-17 5 extranodal small lymphocytic lymphomas of probable marginal zone origin,.sup.18-20 and 23 high-grade gastric MALT lymphomas.sup.14,15 Recurrent abnormalities in these cases include trisomies of chromosomes 3, 7, 12, and 18,.sup.11,17,21 the t(1;14)(p22;q32) which has been described in two cases.sup.17 and the t(11;18)(q21;q21). The t(11;18)(q21;q21) has been detected in 15 out of the 51 low-grade lymphomas arising from various extranodal sites.sup.9,12,14,18-20 but in none of the high-grade MALT lymphomas or any other subtype of NHL. In the largest cytogenetic series, this translocation has been found in 7 out of 13 cases of low-grade MALT lymphomas with an abnormal karyotype.sup.14 These data clearly indicate that the t(11;18) represents the most frequent structural abnormality in low-grade MALT lymphomas and seems to specifically characterize this disease entity. An attempt to delineate the breakpoint at 18q21.1 has been described by Akagi et al. (Genes, Chromosomes and Cancer, 24 (1999): 315-321). A detailed characterization, however, is urgently needed. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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New clinical parameters radioimmunotherapy
for
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Inventor(s): Rastetter, William H.; (Rancho Santa Fe, CA), White, Christine A.; (Rancho Santa Fe, CA) Correspondence: Pillsbury Winthrop, Llp; P.O. Box 10500; Mclean; VA; 22102; US Patent Application Number: 20030211038 Date filed: July 16, 2002 Abstract: New clinical parameters are reported which may serve as predictors of the hematological toxicity associated with therapeutic radiolabeled antibodies, particularly those antibodies which target lymphoma cells which have a tendency to localize to the bone marrow. Excerpt(s): The present invention reports new clinical parameters for predicting the hematological toxicity which can be expected upon administering a therapeutic radiolabeled anti-CD20 antibody, as well as other therapeutic antibodies which have the potential to target immune cells. The clinical parameters of the present invention are useful alternatives to performing dosimetry trials with gamma-emitting radiolabeled antibodies prior to therapy. The immune system of vertebrates (for example, primates, which include humans, apes, monkeys, etc.) consists of a number of organs and cell types which have evolved to: accurately and specifically recognize foreign microorganisms ("antigen") which invade the vertebrate-host; specifically bind to such foreign microorganisms; and, eliminate/destroy such foreign microorganisms. Lymphocytes, as well as other types of cells, are critical to the immune system. Lymphocytes are produced in the thymus, spleen and bone marrow (adult) and represent about 30% of the total white blood cells present in the circulatory system of humans (adult). There are two major sub-populations of lymphocytes: T cells and B cells. T cells are responsible for cell mediated immunity, while B cells are responsible for antibody production (humoral immunity). However, T cells and B cells can be considered interdependent--in a typical immune response, T cells are activated when the T cell receptor binds to fragments of an antigen that are bound to major histocompatability complex ("MHC") glycoproteins on the surface of an antigen presenting cell; such activation causes release of biological mediators ("interleukins") which, in essence, stimulate B cells to differentiate and produce antibody ("immunoglobulins") against the antigen. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Oligonucleotide compositions and their use to induce differentiation of cells Inventor(s): Filion, Mario C.; (Laval, CA), Phillips, Nigel C.; (Pointe-Clarie, CA) Correspondence: John S. Pratt, Esq; Kilpatrick Stockton, Llp; 1100 Peachtree Street; Suite 2800; Atlanta; GA; 30309; US Patent Application Number: 20030045493 Date filed: April 22, 2002 Abstract: The present invention provides compositions comprising a 3'-OH, 5'-OH, chemically unmodified, synthetic phosphodiester nucleotide sequence selected from the group consisting of SEQ ID NO: 1, SEQ ID NO: 2, SEQ ID NO: 3, and SEQ ID NO: 4, and a pharmaceutically acceptable carrier, wherein the compositions are useful to induce
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differentiation of cells or to stimulate differentiation or production of pluripotent cells. The present invention provides methods of using these compositions to induce differentiation of pluripotent cells, including bone marrow derived cells, and to treat disease associated with insufficient differentiation of cells in animals and humans, including but not limited to leukemia, lymphoma, non-malignant blood disorders such as hemoglobinopathies, sickle cell disease, myelodysplastic syndrome, pancytopenia, anemia, thrombocytopenia and leukopenia. Excerpt(s): The present application claims priority to U.S. provisional patent application serial No. 60/286,158 filed Apr. 24, 2001. The present invention provides compositions comprising specific oligonucleotides combined with a pharmaceutically acceptable carrier, wherein the compositions are useful to induce differentiation of cells, including pluripotent cells, leukemic cells, lymphoma cells and bone marrow-derived cells, and to treat diseases such as leukemia, lymphoma and disorders associated with insufficient differentiation of cells. Numerous diseases and conditions in animals and humans are associated with insufficient differentiation of cells or with an insufficiency of cells. Many of these cells are derived from bone marrow. Such diseases and conditions include but are not limited to leukemia, lymphoma, and non-malignant blood disorders such as hemoglobinopathies, sickle cell disease, myelodysplastic syndrome and insufficient production of bone marrow derived cells following therapies such as radiation and chemotherapy. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Prediction of cancer by detection of ATM mutations Inventor(s): Gilad, Shlomit; (Gedera, IL), Yahalom, Joachim; (New York, NY) Correspondence: John P. White; Cooper & Dunham Llp; 1185 Avenue OF The Americas; New York; NY; 10036; US Patent Application Number: 20030162195 Date filed: September 20, 2002 Abstract: There is provided a method of testing a subject to determine if the subject has a predisposition for developing a cancer, a cancer of epithelial origin such as lung cancer, colon cancer, prostate cancer, ovarian cancer, bladder cancer, and cancer of the pancreas, and also a lymphoproliferative malignancy such as Hodgkin's disease and nonHodgkin's lymphoma. This method includes the steps of detecting a mutation in the open reading frame of the ATM gene (SEQ.ID.NO:1) in a cDNA sample or a genomic DNA sample from the subject, which mutation is selected from the group consisting of the mutations set forth in Table 3 and Table 4; or, detecting a mutation in the mRNA corresponding to the open reading frame of the ATM gene (SEQ.ID.NO:1) in a mRNA sample from the subject, which mutation is selected from the group consisting of RNA complementary to the mutations set forth in Table 3 and Table 4, wherein the presence of such a mutation indicates that the subject has a predisposition for developing cancer. Also provided is an isolated cDNA molecule having a nucleotide sequence which differs from the sequence set forth in SEQ.ID.NO:1 by a mutation selected from the group consisting of mutations 378 T.fwdarw.A, 3383 A.fwdarw.G, 1636 C.fwdarw.G, 2614 C.fwdarw.T, 6437 G.fwdarw.C, 2932 T.fwdarw.C, 2289 T.fwdarw.A, 6096 A.fwdarw.T, 6176 C.fwdarw.T, 6919 C.fwdarw.T, 2442 C.fwdarw.A, 3925 G.fwdarw.A, 6067 G.fwdarw.A, 2119 T.fwdarw.C, 1810 C.fwdarw.T, and 4388 T.fwdarw.G. An oligonucleotide probe which is capable of detecting a mutation in the open reading
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frame of the ATM gene is also provided. Additionally, kits for detection and prediction of cancer are provided. Excerpt(s): This invention is a continuation-in-part and claims the benefit of U.S. Provisional Application No. 60/323,766, filed Sep. 20, 2001, the contents of which are hereby incorporated by reference into this application. The present invention generally relates to the relationship of ATM germine point mutations to cancer, in particular cancers of epithelial origin such as lung cancer, colon cancer, prostate cancer, ovarian cancer, bladder cancer, and cancer of the pancreas. The present invention also relates to the relationship of an ATM germline point mutation to a lymphoproliferative malignancy such as Hodgkin's disease and non-Hodgkin's lymphoma. More specifically, the present invention relates to the use of this relationship in prediction and detection of cancers prior to large tumor growth. Ataxia Telangiectasia (A-T) is a pleiotrophic inherited disease characterized by neurodegeneration, cancer, immunodeficiencies, radiation sensitivity, and genetic instability. The gene, a mutation in which is responsible for A-T, is called ATM, and it was discovered by Shiloh et al. in 1995 (Savitsky, K et al., 1995). The ATM gene extends over 150 kb of genomic DNA (Uziel, T et al., 1996) and is transcribed into a large transcript of about 13 kb, representing 66 exons (Uziel, T et al., 1996; Savitsky, K et al., 1995; Savitsky, K et al., 1997). The open reading frame of this transcript predicts a 370 kDa protein composed of 3,056 amino acids. The ATM product is homologous to several cell cycle checkpoint proteins from other organisms and is thought to play a crucial role in a signal transduction network that modulates cell cycle checkpoints, genetic recombination, apoptosis and other cellular responses to DNA damage (Meyn, MS, 1999). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Process for producing arsenic trioxide formulations and methods for treating cancer using arsenic trioxide or melarsoprol Inventor(s): Ellison, Ralph; (Palm Beach, FL), Gabrilove, Janice L.; (New York, NY), Pandolfi, Pier P.; (New York, NY), Soignet, Steven; (New York, NY), Warrell, Raymond P. JR.; (Westfield, NJ) Correspondence: Stephen A. Bent; Foley & Lardner, Washington Harbour; Suite 500; 3000 K Street, N.W.; Washington; DC; 20007-5143; US Patent Application Number: 20030099719 Date filed: September 30, 2002 Abstract: The invention relates to the use of arsenic compounds to treat a variety of leukemia, lymphoma and solid tumors. Further, the arsenic compounds may be used in combination with other therapeutic agents, such as a retinoid. The invention also provides a process for producing arsenic trioxide formulations. Excerpt(s): The present invention relates to methods and compositions for the treatment of leukemia, lymphoma, and certain other cancers. More specifically, the present invention relates to the novel uses of arsenic trioxide and an organic arsenic compound for treating acute leukemia and chronic leukemia. Cancer is characterized primarily by an increase in the number of abnormal cells derived from a given normal tissue, invasion of adjacent tissues by these abnormal cells, and lymphatic or blood-borne spread of malignant cells to regional lymph nodes and to distant sites (metastasis). Clinical data and molecular biologic studies indicate that cancer is a multistep process
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that begins with minor preneoplastic changes, which may under certain conditions progress to neoplasia. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Retrovirus isolated from mantle histiocytes in mantle cell lymphoma Inventor(s): Herndier, Brian; (Burlingame, CA), McGrath, Michael S.; (Burlingame, CA) Correspondence: Bozicevic, Field & Francis Llp; 200 Middlefield RD; Suite 200; Menlo Park; CA; 94025; US Patent Application Number: 20030104009 Date filed: August 15, 2002 Abstract: The present invention features an isolated, intact virus associated with human lymphoma, and originally isolated from a mantle cell lymphoma, referred to herein as a mantle histiocyte retrovirus (MHRV). The invention also features compositions and methods for detecting MHRV, as well as methods and compositions for propagating MHRV in vitro, screening for anti-MHRV agents, and generation of attenuated MHRV strains. Excerpt(s): The present invention relates to a human retrovirus, particularly to a human retrovirus isolated from a human, non-Hodgkins lymphoma, specifically a mantle cell lymphoma. As human beings age, they begin to develop a variety of chronic diseases the etiologies of which remain unclear at this time. These chronic diseases affect virtually all organ systems of the body. Several animal models of chronic disease involve viral infection, especially retroviral infection. For example, murine leukemia viruses have been implicated in causing lymphoma, autoimmune and immunodeficiency diseases. The study of these types of animal models suggested that retroviruses play significant roles in those disease states. However, the extrapolation of findings within animal models to humans have not proven very successful in the identification of fully infectious retroviruses associated with chronic immunologic diseases outside of HTLV (with lymphoma), HIV (with AIDS), and HuLAV (with human B-cell, non-Hodgkins lymphoma (U.S. Pat. No. 5,108,920). In searching for potential agents associated with other chronic diseases a vast array of human endogenous retroviral elements were discovered and characterized (Lower et al. Proc Natl Acad Sci 93:5177-5184 (1996); Tonjes et al. J Virol 73(11):9187-9195 (1999); Sverdlov Bioessays 22(2):161-171 (2000)). The closest class of endogenous retroviral element identified in humans to those associated with chronic disease in mouse disease models are the human endogenous retroviruses (HERV) (Wilier et al. Virus Genes 15(2):123-133 (1997)). Evidence for expression of HERV related genes or antibodies to HERV elements have been identified in a variety of chronic diseases such as terato carcinoma (Boller et al. J Virol 71:4581-4588 (1997); Boller et al. Virology 196:349-353 (1993)), lymphoma (Lower et al., (1996) supra), multiple sclerosis (Clerici et al. J Neuroimmunol 99(2):173182 (1999); Trabattoni et al. J Neurovirol 6(Suppl 2):S38-41 (2000)), autoimmune rheumatic diseases (Nelson et al. Immunol Invest 28(4):277-289 (1999)), and most recently schizophrenia (Yolken et al. Brain Res Rev 31(2-3):193-199 (2000)). However, as human endogenous retroviral elements make up almost 1% of the human genome and each of these elements is highly related to other endogenous elements, their role in the pathogenesis of disease has been difficult to assess. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Self antigen vaccines for treating B cell lymphomas and other cancers Inventor(s): Lindbo, John A.; (Vacaville, CA), McCormick, Alison A.; (Vacaville, CA), Reinl, Stephen J.; (Sacramento, CA), Turpen, Thomas H.; (Vacaville, CA), Tuse, Daniel; (Menlo Park, CA) Correspondence: Roylance, Abrams, Berdo & Goodman, L.L.P.; 1300 19th Street, N.W.; Suite 600; Washington,; DC; 20036; US Patent Application Number: 20030035807 Date filed: February 8, 2002 Abstract: A polypeptide self-antigen useful in a tumor-specific vaccine mimics one or more epitopes of an antigen uniquely expressed by cells of the tumor. The polypeptide is preferably produced in a plant that has been transformed or transfected with nucleic acid encoding the polypeptide and is obtainable from the plant in correctly folded, preferably soluble form without a need for denaturation and renaturation. This plantproduced polypeptide is immunogenic without a need for exogenous adjuvants or other immunostimulatory materials. The polypeptide is preferably an scFv molecule that bears the idiotype of the surface immunoglobulin of a non-Hodgkin's (or B cell) lymphoma. Upon administration to a subject with lymphoma, the plant-produced, tumor-unique scFv polypeptide induces an idiotype-specific antibody or cell-mediated immune response against the lymphoma. Excerpt(s): This invention, in the field of molecular biology, immunology and medicine, relates to a polypeptide vaccine, produced in plants, for inducing an immune response to a self-antigen (which is normally clonally expressed) on the surface of certain tumor cells. In a preferred embodiment, the tumor is a B cell lymphoma, the self antigen is a B cell idiotype, and the vaccine composition is a soluble single chain antibody polypeptide (scFv) than includes the V.sub.L and V.sub.H domains of the surface immunoglobulin of the lymphoma. Malignancies of B lymphocytes, primarily non-Hodgkin's lymphomas ("NHL") also called B cell lymphomas, are generally treated by standard antitumor regimens of radiation therapy and chemotherapy, optionally in combination with stem cell transplantation. Unfortunately, in a significant number of cases, none of these modalities is completely successful. As a result, most B-cell lymphomas, which are increasing in frequency in industrial nations, are incurable (Ries, L. et al. (1996) SEER Cancer Statistics Review, 1973-1993: Tables and graphs (Natl. Cancer Inst., Bethesda); Parker, S L et al., (1997) CA Cancer J Clin. 47:5-27). Although responses of B-cell lymphomas to treatment vary widely as do the patients' prognoses (Armitage, J O (1997) CA Cancer J Clin. 47:323-325), these tumors nevertheless share a common feature: each B cell lymphoma is clonal, made up of descendents of a single malignant B cell each of which expresses a unique surface immunoglobulin (Ig) molecule that is characteristic of that clone and serves as a tumor-specific marker. Intact immunoglobulin (Ig) molecules (or antibodies) are proteins that generally consist of two identical heavy (H) and two identical light (L) chains. An L chain has a molecular mass of about 25 kDa whereas an H chain is about 50-70 kDa. The amino-termini of H and L chains are the variable (V) regions or domains, which are about 100 to 110 amino acid residues in length. The combination of the V region of the H chain (V.sub.H) and L chain (V.sub.L) results in a structure that forms the antigen-combining site (also termed antigen-binding or antigen-recognition site) of the Ig molecule. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Therapeutic compositions and methods useful in modulating protein tyrosine phosphatases Inventor(s): Yi, Taolin; (Solon, OH) Correspondence: Benesch, Friedlander, Coplan & Aronoff Llp; Attn: IP Department Docket Clerk; 2300 BP Tower; 200 Public Square; Cleveland; OH; 44114; US Patent Application Number: 20030072738 Date filed: September 9, 2002 Abstract: In one embodiment, a therapeutic composition containing a pentavalent antimonial is provided. The pentavalent antimonial can be sodium stibogluconate, levamisole, ketoconazole, and pentamidine and biological equivalents of said compounds. Additionally, pentavalent antimonials that can be used in accordance with the present invention may be any such compounds which are anti-leishmaniasis agents. The therapeutic composition of this embodiment contains an effective amount of pentavalent antimonial that can be used in treating infectious diseases. The types of diseases that can be treated with the present invention include, but are not limited to, the following: diseases associated with PTPase activity, immune deficiency, cancer, infections (such as viral infections), hepatitis B, and hepatitis C. The types of cancers that the present embodiment can be used to treat include those such as lymphoma, multiple myeloma, leukemia, melanoma, prostate cancer, breast cancer, renal cancer, bladder cancer. The therapeutic composition enhances cytokine activity. The therapeutic composition may include a cytokine, such as interferon.alpha., interferon.beta., interferon.gamma., or granulocyte/macrophage colony stimulating factor. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/317,993 filed Sep. 7, 2001. Intercellular protein tyrosine phosphorylation is regulated by extracellular stimuli, such as cytokines, to control cell growth, differentiation and functional activities. This signaling mechanism depends on the interplay of protein tyrosine kinases, which initiate signaling cascades through phosphorylating tyrosine residues in protein substrates, and by protein tyrosine phosphatases that terminate signaling via substrate dephosphorylation. Chemical compounds that modulate the activity of protein tyrosine kinases or phosphatases can induce cellular changes through affecting the balance of intracellular protein tyrosine phosphorylation and redirecting signaling. Such compounds can be of value as experimental tools and, importantly, as potent therapeutic reagents. So far, few specific inhibitors of protein tyrosine phosphatases have been reported despite extensive efforts in the last decade to identify them. Although a number of chemicals that broadly inhibit protein tyrosine phosphatases are known, including sodium orthovanadate and iodoacetic acid, their usefulness as therapeutic agents is severely limited due to their general toxicity in vivo. Recently, it has been reported that Suramin, a polysulfonated naphthylurea compound, can act in vitro as a competitive and reversible inhibitor of several protein tyrosine phosphatases. Such an inhibitory activity of Suramin against protein tyrosine phosphatases is consistent with its activity in augmenting tyrosine phosphorylation of cellular proteins and may explain its antitumor activity and its therapeutic effect in treating trypanosomiasis and onchocerciasis. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Therapeutic compounds Inventor(s): Fatih, M. Uckun; (White Bear Lake, MN) Correspondence: Merchant & Gould PC; P.O. Box 2903; Minneapolis; MN; 55402-0903; US Patent Application Number: 20030149045 Date filed: August 2, 2002 Abstract: The invention provides novel JAK-3 inhibitors that are useful for treating leukemia and lymphoma. The compounds are also useful to treat or prevent skin cancer, as well as sunburn and UVB-induced skin inflammation. In addition, the compounds of the present invention prevent the immunosuppressive effects of UVB radiation, and are useful to treat or prevent autoimmune diseases, inflammation, and transplant rejection. The invention also provides pharmaceutical compositions comprising compounds of the invention, as well as therapeutic methods for their use. Excerpt(s): This application is a continuation-in-part, claiming priority under 35 U.S.C.sctn.120, of U.S. application Ser. No. 09/812,098, filed Mar. 19, 2001 which is a continuation of U.S. application Ser. No. 09/378,093 filed Aug. 20, 1999, now U.S. Pat. No. 6,313,129, and claims priority under 35 U.S.C.sctn.119(e) from U.S. Provisional application No. 60/309,557 and from U.S. Provisional application No. 60/309,558, each filed Aug. 2, 2001, the disclosures of which are hereby incorporated by reference. Bone marrow transplantation (BMT) has become one of the standard treatment modalities offered to high-risk leukemia patients. Very intensive "supralethal" myeloablative chemotherapy or radiochemotherapy regimens can be applied in the context of BMT with a curative intent to overcome the drug resistance of residual leukemia cells of certain leukemia patients who are unlikely to be cured by standard chemotherapy. In addition, leukemia patients undergoing allogeneic BMT may benefit from the graftversus-leukemia (GVL) effect of the marrow allograft. Graft-Versus-Host Disease (GVHD), a donor T-cell initiated highly complex pathologic condition that frequently follows allogeneic BMT, especially in the context of a major-HLA disparity, is associated with significant morbidity and mortality. Severe GVHD remains a major obstacle to a more successful outcome of allogeneic BMT using HLA-matched unrelated donors as well as partially HLA-mismatched related donors. Therefore, GVHD prophylaxis aimed at reducing the risk of severe GVHD is an integral component of all BMT programs. On the other hand, there is a widely accepted notion in the BMT community that leukemia patients who develop GVHD after BMT have a reduced risk of relapse indicating that alloreactive T cells participating in GVHD are major contributors of the GVL function of the marrow allografts. In certain subsets of leukemia patients who relapsed after BMT (e.g. chronic myelogenous leukemia patients), infusions of donor T-cells resulted in remissions, thereby providing direct evidence that host leukemia cells can be killed by alloreactive T-cells. Therefore, several groups involved in the treatment of leukemia patients are currently exploring alternative methods of inducing mixed chimerism with non-myeloablative conditioning regimens followed by donor lymphocyte infusions to achieve a GVL effect without severe GVHD. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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ZAP-70 expression as a marker for chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) Inventor(s): Barry, Todd S.; (Seattle, WA), Rosenwald, Andreas; (Bethesda, MD), Staudt, Louis M.; (Silver Spring, MD), Wiestner, Adrian; (Bethesda, MD), Wilson, Wyndham; (Washington, DC) Correspondence: Klarquist Sparkman, Llp; One World Trade Center; Suite 1600; 121 S.W. Salmon Street; Portland; OR; 97204; US Patent Application Number: 20030203416 Date filed: December 3, 2002 Abstract: It has been surprisingly found that ZAP-70 expression, both at the protein and mRNA levels, is indicative of clinical subgroups of CLL/SLL patients. In particular, high ZAP-70 expression is indicative of Ig-unmutated CLL/SLL. Methods are provided for discriminating between clinical subgroups of CLL/SLL, by determining whether subjects overexpress ZAP-70 mRNA mRNA or protein. Excerpt(s): Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is a malignancy of B-lymphocytes in the blood, bone marrow, and lymph nodes with a characteristic immunophenotype. The recent WHO classification discusses CLL/SLL as an entity but notes that the term SLL is restricted to cases with the tissue morphology and immunophenotype of CLL, but which are non-leukemic (WHO Classification of Tumours. Tumours of Haemotopoietic and Lymphoid Tissue. Edited by Jaffe, Harris, Stein, Vardiman. IARC Press 2001). The clinical course of CLL is quite varied. While some patients have a chronic lymphocytosis without any need for therapeutic interventions, other patients may die rapidly despite aggressive treatment. The classic staging systems provide only limited prognostic information in newly diagnosed patients. Recently, the presence or absence of somatic mutations in the immunoglobulin (Ig) variable region genes has been shown to distinguish between two disease subsets conferring important prognostic information. A median survival of 95 months was found in patients with unmutated Ig genes versus 293 months in patients with mutated Ig genes (Hamblin, Blood 94(6):1848-1854, 1999). Unfortunately, the ability to sequence Ig genes is not available in most clinical laboratories. In addition to mutated Ig genes, several other potential diagnostic or prognostic markers have been identified for CLL, as well as for other small B-cell lymphomas. By way of example, these include CD10, CD20, CD21, CD23 (including serum CD23), CD38, CD69, CD43, FMC-7, and BCL-6. The research and medical communities are actively searching for good prognostic markers, but as yet no definitive markers have been identified. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Keeping Current In order to stay informed about patents and patent applications dealing with lymphoma, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “lymphoma” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on lymphoma.
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You can also use this procedure to view pending patent applications concerning lymphoma. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.
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CHAPTER 7. BOOKS ON LYMPHOMA Overview This chapter provides bibliographic book references relating to lymphoma. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on lymphoma include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.
Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “lymphoma” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on lymphoma: •
Low Dose Chemotherapy With CNS Prophylaxis and Zidovudine (AZT) Maintenance for AIDS - Related Lymphoma: Preliminary Results of A Multi - Institutional Study Source: 25th Proceedings of Annual Meeting of the American Society of Clinical Oncology; Vol., March 1989. p. 5. Contact: US Department of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Division of AIDS, 6700-B Rockledge Dr, Bethesda, MD, 20892-7620, (301) 496-0545, http://www.niaid.nih.gov. Summary: Use of intensive, multi-agent chemotherapy (chemo) in AIDS-related lymphoma may be associated with severe marrow suppression and early demise due to infection. In an attempt to ascertain if lower dose chemo, with CNS prophylaxis, would improve response rates, the following regimen was used: Day 1: Cytoxan, 300 mg/m2; Adriamycin 25 mg/m2; vincristine 1.4 mg/m2; bleomycin 4 u/m2; Decadron 3 mg/m2
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po day 1-5. Day 15: methotrexate 500 mg/m2 with folinic acid 50 mg q 6 hr x 8. With absence of CNS or marrow involvement, Ara-C, 30 mg IT was given on days 1, 8, 15, 21 of cycle 1. With CNS or marrow involvement, 2400 rads to whole brain was also given. At completion of 4-6 mo of total chemo, AZT (200 mg q 4 hr) x 1 yr was begun. This prospective trial began in 6/87; 38 patients (pts) are registered; 31 are now evaluable. Complete response (CR) occurred in 14 (45 percent), with an additional 2 pts in early clinical CR (total CR = 52 percent). No response or progressive disease occurred in 14 (45 percent), and 1 had PR. Of 16 CR pts, 4 subsequently died, 2 of opportunistic infection. In 68 chemo cycles, a nadir granulocyte count of less than 1000 was seen in 16 (24 percent), and less than 500 in 19 percent of these. Nadir platelet count less than 100K was seen in 5/68 (7 percent). Fever occurred in 13/68 cycles, with granulocyte count greater than 500 in 12 of these, and documented sepsis in 2/13. Other toxicity was minimal. We conclude: (1) Low dose chemo with CNS therapy may be effective in approx half of these pts; (2) Details are presented.
Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “lymphoma” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “lymphoma” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “lymphoma” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •
100 Questions and Answers About Lymphoma by Jodi Garrett, et al (2003); ISBN: 0763720399; http://www.amazon.com/exec/obidos/ASIN/0763720399/icongroupinterna
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21st Century Complete Medical Guide to AIDS-Related Cancer (Kaposi's Sarcoma and AIDS-related Lymphoma) - Authoritative Government Documents and Clinical References for Patients and Physicians with Practical Information on Diagnosis and Treatment Options by PM Medical Health News; ISBN: 1592480276; http://www.amazon.com/exec/obidos/ASIN/1592480276/icongroupinterna
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A Comprehensive guide to the therapeutic use of methotrexate in poor-prognosis non-Hodgkin's lymphoma; ISBN: 0919839002; http://www.amazon.com/exec/obidos/ASIN/0919839002/icongroupinterna
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A Genetic Profile of Marginal Zone B-Cell Lymphoma (Acta Biomedica Lovaniensia, 200) by Judith Dierlamm (1999); ISBN: 906186965X; http://www.amazon.com/exec/obidos/ASIN/906186965X/icongroupinterna
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Advances in Lymphoma Research (Cancer Treatment and Research, Vol 85) by Fernando, Md. Cabanillas (Editor), M. Alma, MD Rodriguez (Editor) (1997); ISBN: 0792339290; http://www.amazon.com/exec/obidos/ASIN/0792339290/icongroupinterna
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An Atlas and Textbook of Malignant Lymphomas: Cytology, Histopathology and Immunochemistry by P. van Heerde MD PhD, et al; ISBN: 1874545723; http://www.amazon.com/exec/obidos/ASIN/1874545723/icongroupinterna
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An Illustrated Guide to Skin Lymphoma by Lorenzo Cerroni, et al; ISBN: 0632050829; http://www.amazon.com/exec/obidos/ASIN/0632050829/icongroupinterna
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Atlas and Textbook of Malignant Lymphomas: Cytology, Histopathology & Immunochemistry by P. Van Heerde, et al; ISBN: 019521269X; http://www.amazon.com/exec/obidos/ASIN/019521269X/icongroupinterna
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Atlas of Lymphoid Hyperplasia and Lymphoma by Judith A. Ferry, et al; ISBN: 0721659071; http://www.amazon.com/exec/obidos/ASIN/0721659071/icongroupinterna
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Autologous Bone Marrow Transplantation for Hodgkin's Disease, Non-Hodgkin's Lymphoma and Multiple Myeloma by A.R. Zander, B. Barlogie (Editor); ISBN: 0387561307; http://www.amazon.com/exec/obidos/ASIN/0387561307/icongroupinterna
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Autologous Bone Marrow Transplantation for Hodgkin's Disease, Non-Hodgkin's Lymphoma and Multiple Myeloma; ISBN: 3540561307; http://www.amazon.com/exec/obidos/ASIN/3540561307/icongroupinterna
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Biological Response Modifiers-Leukemias and Lymphomas (International Cancer Congress, Lectures and Symposia, Vol 10) by K. Lapis, S. Eckhardt (Editor) (1987); ISBN: 380554426X; http://www.amazon.com/exec/obidos/ASIN/380554426X/icongroupinterna
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Burkitt Lymphoma, Hemostasis & Intercellular Matrix: Barbara Robert Memorial by L. Robert (Editor) (1976); ISBN: 3805523262; http://www.amazon.com/exec/obidos/ASIN/3805523262/icongroupinterna
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Burkitt's Lymphoma by D P Burkitt, D H Wright; ISBN: 0443007004; http://www.amazon.com/exec/obidos/ASIN/0443007004/icongroupinterna
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Burkitt's Lymphoma: A Human Cancer Model (Larc Scientific Pubns, No 60) by G. Lenoir (Editor), G. O'Conor (Editor); ISBN: 0197230571; http://www.amazon.com/exec/obidos/ASIN/0197230571/icongroupinterna
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Cell Proliferation Lymphomas by J. Crocker; ISBN: 0632029250; http://www.amazon.com/exec/obidos/ASIN/0632029250/icongroupinterna
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Chronic Leukemias and Lymphomas: Clinical Management by Gary J., MD Schiller (Editor); ISBN: 0896039072; http://www.amazon.com/exec/obidos/ASIN/0896039072/icongroupinterna
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Clinical Morphological Immunophenotypic and Genetic Characterisation of Follicle Mantle Lymphomas by E. Vandenberghe (1992); ISBN: 9061864909; http://www.amazon.com/exec/obidos/ASIN/9061864909/icongroupinterna
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Clinical radiology of the lymphomas by Henry Ngan; ISBN: 0407137157; http://www.amazon.com/exec/obidos/ASIN/0407137157/icongroupinterna
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Controversies in the Management of Lymphomas: Including Hodgkin's Disease by John M. Bennett (Editor) (1983); ISBN: 0898385865; http://www.amazon.com/exec/obidos/ASIN/0898385865/icongroupinterna
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Copper and Lymphomas by Martin J. Hrgovcic, C. Shullenberger (1984); ISBN: 0849363314; http://www.amazon.com/exec/obidos/ASIN/0849363314/icongroupinterna
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Current concepts in the management of lymphoma and leukemia; ISBN: 0387053093; http://www.amazon.com/exec/obidos/ASIN/0387053093/icongroupinterna
274 Lymphoma
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Current Issues in Lymphoma (Diagnostic Oncology; Vol 4, No 1) by R. L. Katz (Editor), W.C. Pugh (Editor) (1994); ISBN: 3805560141; http://www.amazon.com/exec/obidos/ASIN/3805560141/icongroupinterna
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Cutaneous Lymphoma (Current Problems in Dermatology, Vol 19) by W.A. Van Vloten (Editor) (1989); ISBN: 3805550588; http://www.amazon.com/exec/obidos/ASIN/3805550588/icongroupinterna
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Cutaneous Lymphomas, Pseudolymphomas, and Related Disorders by O. BraunFalco, Gunter Burg; ISBN: 0387104674; http://www.amazon.com/exec/obidos/ASIN/0387104674/icongroupinterna
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Cutaneous Lymphomas: Unusual Cases by G. Burg (Editor), et al; ISBN: 3798512507; http://www.amazon.com/exec/obidos/ASIN/3798512507/icongroupinterna
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Cutaneous t Cell Lymphoma: Basic and Clinically Relevant Biology (Annals of the New York Academy of Sciences, Vol 941) by Richard Edelson (Editor) (2001); ISBN: 1573313394; http://www.amazon.com/exec/obidos/ASIN/1573313394/icongroupinterna
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Diagnosis and therapy of malignant lymphoma; ISBN: 0387067043; http://www.amazon.com/exec/obidos/ASIN/0387067043/icongroupinterna
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Drug Resistance in Leukemia and Lymphoma II (Advances in Blood Disorders) by G. J. Kaspers (Editor), et al; ISBN: 3718659344; http://www.amazon.com/exec/obidos/ASIN/3718659344/icongroupinterna
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Drug Resistance in Leukemia and Lymphoma: The Clinical Value of Laboratory Studies by G. J. L. Kaspers (Editor), et al (1993); ISBN: 3718653877; http://www.amazon.com/exec/obidos/ASIN/3718653877/icongroupinterna
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Epidemiology of Leukemia and Lymphoma: Report of the Leukemia Research Fund International Workshop, Oxford, Uk, September 1984 by L.C. Chan (Editor), et al; ISBN: 0080320023; http://www.amazon.com/exec/obidos/ASIN/0080320023/icongroupinterna
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Extranodal Lymphomas by Peter G. Isaacson, Andrew J. Norton; ISBN: 0443040397; http://www.amazon.com/exec/obidos/ASIN/0443040397/icongroupinterna
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Fourth International Symposium on Hodgkin's Lymphoma by ENGERT, A. Engert; ISBN: 905702361X; http://www.amazon.com/exec/obidos/ASIN/905702361X/icongroupinterna
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Gastrointestinal Lymphoma. Future Perspectives (Recent Results in Cancer Research Vol. 156) by W. Fischbach (Author) (2000); ISBN: 3540653244; http://www.amazon.com/exec/obidos/ASIN/3540653244/icongroupinterna
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Histopathology Non-Hodgkin's Lymphomas by Karl. Lennert; ISBN: 0387104453; http://www.amazon.com/exec/obidos/ASIN/0387104453/icongroupinterna
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Histopathology of Non-Hodgkin-Lymphomas (1992); ISBN: 3540512705; http://www.amazon.com/exec/obidos/ASIN/3540512705/icongroupinterna
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Histopathology of Non-Hodgkin's Lymphomas by Karl Lennert, A. C. Feller; ISBN: 0387512705; http://www.amazon.com/exec/obidos/ASIN/0387512705/icongroupinterna
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Histopathology of Non-Hodgkin's Lymphomas (Based on the Updated Kiel Classification) by Alfred C. Feller, et al; ISBN: 3540638016; http://www.amazon.com/exec/obidos/ASIN/3540638016/icongroupinterna
Books
275
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Hodgkin Lymphoma: Studies of Advanced Stages, Relapses & the Relation to NonHodgkin Lymphomas (Comprehensive Summaries of Uppsala Dissertations from the Faculty of mediciNe, 1132) by Rose-Marie Amini (2002); ISBN: 9155452655; http://www.amazon.com/exec/obidos/ASIN/9155452655/icongroupinterna
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Hodgkin's and Non-Hodgkin's Lymphomas (Seminars in Oncology) by Coltman Jr, Golomb; ISBN: 0808913549; http://www.amazon.com/exec/obidos/ASIN/0808913549/icongroupinterna
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Hodgkin's Disease & Non-Hodgkin's Lymphoma: New Perspectives in Immunopathology, Diagnosis, & Treatment by Richard J. Ford (Editor), Clinical Conference on Cancer (1984); ISBN: 0608006289; http://www.amazon.com/exec/obidos/ASIN/0608006289/icongroupinterna
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Hodgkin's Disease and Non-Hodgkin's Lymphoma: New Perspectives in Immunopathology, Diagnosis, and Treatment (Ut M. D. Anderson Clinical Conference O) by Richard J. Ford (Editor); ISBN: 0881670391; http://www.amazon.com/exec/obidos/ASIN/0881670391/icongroupinterna
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Hodgkin's Disease and Non-Hodgkin's Lymphomas in Adults and Children by Lillian M. Fuller (Editor), et al; ISBN: 0890047952; http://www.amazon.com/exec/obidos/ASIN/0890047952/icongroupinterna
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Hodgkin's Disease and the Lymphomas (ARR) by C R Taylor; ISBN: 0443018014; http://www.amazon.com/exec/obidos/ASIN/0443018014/icongroupinterna
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Human Cell Culture, Volume III: Cancer Cell Lines, Part 3: Leukemias and Lymphomas by John R. W. Masters (Editor), Bernhard O. Palsson (Editor); ISBN: 079236225X; http://www.amazon.com/exec/obidos/ASIN/079236225X/icongroupinterna
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Human Lymphoma: Clinical Implications of the Real Classification by David Y. Mason (Editor), Nancy L. Harris (Editor) (1999); ISBN: 1852331291; http://www.amazon.com/exec/obidos/ASIN/1852331291/icongroupinterna
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Human T-Cell Leukemia Lymphoma Virus by Robert C. Gallo (Editor); ISBN: 0879691700; http://www.amazon.com/exec/obidos/ASIN/0879691700/icongroupinterna
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Ibritumomab Tiuxetan (Zevalin) in Non-Hodgkin's Lymphoma: Clinical Background, Practical Considerations, and Case Studies by Bruce D. Cheson (Editor) (2003); ISBN: 1891483196; http://www.amazon.com/exec/obidos/ASIN/1891483196/icongroupinterna
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Immunologic Approaches to the Classification and Management of Lymphomas and Leukemias (Cancer Treatment and Research) by John M. Bennett, Kenneth A. Foon (Editor) (1988); ISBN: 0898383552; http://www.amazon.com/exec/obidos/ASIN/0898383552/icongroupinterna
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Immunology of the Lymphomas (CRC Series in Immunology and Lymphoid Cell Biology) by Simon B. Sutcliffe (Editor) (1985); ISBN: 0849363713; http://www.amazon.com/exec/obidos/ASIN/0849363713/icongroupinterna
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Keeping Up in the Fragmented Lymphoma Competitive Environment [DOWNLOAD: PDF] by BioSeeker Group AB (Author); ISBN: B0000BZ3ZG; http://www.amazon.com/exec/obidos/ASIN/B0000BZ3ZG/icongroupinterna
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Leukemia and Lymphoma by J.M. Chessells, I.M. Hann; ISBN: 0702020753; http://www.amazon.com/exec/obidos/ASIN/0702020753/icongroupinterna
276 Lymphoma
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Leukemia and Lymphoma by Emil J. Freireich; ISBN: 080891166X; http://www.amazon.com/exec/obidos/ASIN/080891166X/icongroupinterna
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Leukemia and lymphoma; ISBN: 0808908588; http://www.amazon.com/exec/obidos/ASIN/0808908588/icongroupinterna
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Leukemia and Lymphoma Reviews 2 by A Polliack (Author); ISBN: 3718653745; http://www.amazon.com/exec/obidos/ASIN/3718653745/icongroupinterna
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Leukemia and Lymphoma Reviews 3 (Leukemia & Lymphoma Reviews Series) by Aaron Polliack (Editor); ISBN: 3718654903; http://www.amazon.com/exec/obidos/ASIN/3718654903/icongroupinterna
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Leukemia and Lymphoma Reviews 7 (Leukemia & Lymphoma Reviews Series) by Aaron Polliack, Aaron Polliack; ISBN: 9057021994; http://www.amazon.com/exec/obidos/ASIN/9057021994/icongroupinterna
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Leukemia and Lymphoma Reviews, Vol. 1 by Aaron Polliack (Editor), A. Polliack; ISBN: 371865251X; http://www.amazon.com/exec/obidos/ASIN/371865251X/icongroupinterna
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Leukemia and Lymphoma Supplement by Michael J. Keating; ISBN: 3718656647; http://www.amazon.com/exec/obidos/ASIN/3718656647/icongroupinterna
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Leukemia and Lymphoma: Detection of Minimal Residual Disease by Theodore F., Ph.D., Md. Zipf (Editor), et al (2002); ISBN: 0896039668; http://www.amazon.com/exec/obidos/ASIN/0896039668/icongroupinterna
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Leukemia and Non-Hodgkin Lymphoma by D. G. Crowther (1979); ISBN: 0080243908; http://www.amazon.com/exec/obidos/ASIN/0080243908/icongroupinterna
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Leukemia-lymphoma; a collection of papers; ISBN: 0815102070; http://www.amazon.com/exec/obidos/ASIN/0815102070/icongroupinterna
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Leukemias and Lymphomas (Contemporary Issues in Clinical Oncology Vol 4) by Peter H. Wiernik (Editor); ISBN: 0443083452; http://www.amazon.com/exec/obidos/ASIN/0443083452/icongroupinterna
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Leukemias, Lymphomas and Papillomas: Comparative Aspects. Ed by P.A. Bachmann Proc of Symp Held June, 1980 Org by Who Collab Ctr for Coll and Eval O by Munich Symposium on Microbiology (1980); ISBN: 0850662133; http://www.amazon.com/exec/obidos/ASIN/0850662133/icongroupinterna
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Lymphocyte membrane markers in human leukemias and lymphomas by Maxime Seligmann; ISBN: 0950223026; http://www.amazon.com/exec/obidos/ASIN/0950223026/icongroupinterna
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Lymphoma by A.C. Wotherspoon (Editor), Imperial Cancer Research Fund (1997); ISBN: 0879695196; http://www.amazon.com/exec/obidos/ASIN/0879695196/icongroupinterna
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LYMPHOMA - THE NEXT QUESTIONS by POLLIACK; ISBN: 3718654067; http://www.amazon.com/exec/obidos/ASIN/3718654067/icongroupinterna
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Lymphoma (Hematology Series, Unit 4); ISBN: 0683159240; http://www.amazon.com/exec/obidos/ASIN/0683159240/icongroupinterna
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Lymphoma of the Nervous System by Tracy Batchelor (Editor); ISBN: 0750674067; http://www.amazon.com/exec/obidos/ASIN/0750674067/icongroupinterna
Books
277
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Lymphoma Project Report: Current Issues in Research and Treatment of AIDSAssociated Lymphoma by Michael Marco (1995); ISBN: 0788118412; http://www.amazon.com/exec/obidos/ASIN/0788118412/icongroupinterna
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Lymphoma: Cancer in AIDS Gynecologic Cancer by Larry Ward (Illustrator), et al (1994); ISBN: 1859226221; http://www.amazon.com/exec/obidos/ASIN/1859226221/icongroupinterna
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Lymphomas by J.M. Bennett (Editor) (1981); ISBN: 9024724791; http://www.amazon.com/exec/obidos/ASIN/9024724791/icongroupinterna
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Lymphomas and Miscellaneous Tumors (M.D. Anderson Pediatric Tumor Board Series) by R. Beverly Raney (Editor) (1999); ISBN: 0412144212; http://www.amazon.com/exec/obidos/ASIN/0412144212/icongroupinterna
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Lymphomas Bimr Hematology by Bennett, Rees (1995); ISBN: 0407023372; http://www.amazon.com/exec/obidos/ASIN/0407023372/icongroupinterna
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Lymphomas Other Then Hodgkins Disease by A. E. Stuart; ISBN: 0192612964; http://www.amazon.com/exec/obidos/ASIN/0192612964/icongroupinterna
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Lymphomas: Current Concepts in Pathogenesis and Management by 17042002753, Daniel C. Idhe; ISBN: 0160222168; http://www.amazon.com/exec/obidos/ASIN/0160222168/icongroupinterna
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Malignant Lymphoma by Barry W. Hancock (Editor), et al; ISBN: 0340742070; http://www.amazon.com/exec/obidos/ASIN/0340742070/icongroupinterna
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Malignant lymphoma; ISBN: 9290180374; http://www.amazon.com/exec/obidos/ASIN/9290180374/icongroupinterna
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Malignant Lymphoma (Monographs in Pathology, No 29) by Ronald F. Dorfman, et al; ISBN: 0683006010; http://www.amazon.com/exec/obidos/ASIN/0683006010/icongroupinterna
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Malignant Lymphoma: Biology, Natural History and Treatment by Alan Clifford Aisenberg (1991); ISBN: 0812113829; http://www.amazon.com/exec/obidos/ASIN/0812113829/icongroupinterna
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Malignant Lymphoma: Diagnosis, Biology and Treatment by Wendy N. Erber (Editor), et al (1990); ISBN: 3718650584; http://www.amazon.com/exec/obidos/ASIN/3718650584/icongroupinterna
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Malignant lymphoma: nodal and extranodal diseases by Yeu-Tsu N. Lee; ISBN: 0808908243; http://www.amazon.com/exec/obidos/ASIN/0808908243/icongroupinterna
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Malignant Lymphomas by Michael L. Grossbard (Editor), American Cancer Society (2002); ISBN: 1550091522; http://www.amazon.com/exec/obidos/ASIN/1550091522/icongroupinterna
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Malignant Lymphomas by John A. Habeshaw, Ian Lauder (Editor) (1988); ISBN: 0443034087; http://www.amazon.com/exec/obidos/ASIN/0443034087/icongroupinterna
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Malignant Lymphomas and Hodgkin's Disease: Experimental and Therapeutic Advances (Developments in Oncology) by Franco Cavalli (Editor), et al (1986); ISBN: 0898387272; http://www.amazon.com/exec/obidos/ASIN/0898387272/icongroupinterna
278 Lymphoma
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Malignant Lymphomas, Including Hodgkin's Disease: Diagnosis, Management, and Special Problems (Cancer Treatment and Research) by Bruce W. Dana (Editor) (1993); ISBN: 0792321715; http://www.amazon.com/exec/obidos/ASIN/0792321715/icongroupinterna
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Malignant Lymphomas: A Pathology Annual Monograph by Paul Peter Rosen, Sheldon C. Sommers; ISBN: 0838561136; http://www.amazon.com/exec/obidos/ASIN/0838561136/icongroupinterna
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Malignant Lymphomas: Biology and Treatment: An Update by Gerassimos A. Pangalis (Editor) (1995); ISBN: 3540601228; http://www.amazon.com/exec/obidos/ASIN/3540601228/icongroupinterna
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Malignant Lymphomas: Etiology, Immunology, Pathology, Treatment by Saul Rosenberg (Editor), Henry S. Kaplan (Editor); ISBN: 0125971206; http://www.amazon.com/exec/obidos/ASIN/0125971206/icongroupinterna
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Malt Lymphomas by Francesco Bertoni (2004); ISBN: 1587061635; http://www.amazon.com/exec/obidos/ASIN/1587061635/icongroupinterna
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Management of Intermediate & High Grade Lymphomas; ISBN: 0849085284; http://www.amazon.com/exec/obidos/ASIN/0849085284/icongroupinterna
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Management of Intermediate and High Grade Lymphomas by Joseph M. Connors (1993); ISBN: 0160422906; http://www.amazon.com/exec/obidos/ASIN/0160422906/icongroupinterna
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Management of intermediate and high grade lymphomas (SuDoc HE 20.3173/3:OT92/03) by Judith Illy; ISBN: B00010JZWS; http://www.amazon.com/exec/obidos/ASIN/B00010JZWS/icongroupinterna
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Molecular Biology of Hematopoiesis and Treatment of Leukemias and Lymphomas: 10th Symposium, Hamburg, July 1997, Proceedings (Acta Heamatologica , Vol 99, No 3) by Abraham N.G. (Editor), et al (1998); ISBN: 3805566816; http://www.amazon.com/exec/obidos/ASIN/3805566816/icongroupinterna
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Non Hodgkins Lymphomas: New Techniques and Treatments by J. J. Sotto (Editor), et al (1985); ISBN: 3805540647; http://www.amazon.com/exec/obidos/ASIN/3805540647/icongroupinterna
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Non-Hodgkin's Lymphomas by Peter M. Md. Mauch (Editor), et al (2003); ISBN: 0781735262; http://www.amazon.com/exec/obidos/ASIN/0781735262/icongroupinterna
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Non-Hodgkin's Lymphomas by David Mason Y., et al; ISBN: 1874545073; http://www.amazon.com/exec/obidos/ASIN/1874545073/icongroupinterna
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Non-Hodgkin's lymphomas in children; ISBN: 0893520683; http://www.amazon.com/exec/obidos/ASIN/0893520683/icongroupinterna
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Non-Hodgkin's Lymphomas: Making Sense of Diagnosis, Treatment and Options by Lorraine Johnston; ISBN: 1565924444; http://www.amazon.com/exec/obidos/ASIN/1565924444/icongroupinterna
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Pathogenesis of Leukemias and Lymphomas Environmental Influences by Ian T. Magrath (Editor); ISBN: 0890049017; http://www.amazon.com/exec/obidos/ASIN/0890049017/icongroupinterna
Books
279
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Pathology and Management of Lymphoma by John G. Allison (Editor); ISBN: 0879932074; http://www.amazon.com/exec/obidos/ASIN/0879932074/icongroupinterna
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Radiology of Lymphomas by M. Schneider, et al (1986); ISBN: 0387159517; http://www.amazon.com/exec/obidos/ASIN/0387159517/icongroupinterna
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Radiology of Lymphomas (1986); ISBN: 3540159517; http://www.amazon.com/exec/obidos/ASIN/3540159517/icongroupinterna
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Recent Advances in Leukemia and Lymphoma (UCLA Symposia on Molecular and Cellular Biology, New Ser, Vol 61) by Robert Peter Gale (Editor), David W. Golde (Editor); ISBN: 0471602566; http://www.amazon.com/exec/obidos/ASIN/0471602566/icongroupinterna
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Roentgenology of the Lymphomas and Leukemias: A Seminars in Roentgenology Reprint, July and October 1980 by Benjamin Felson; ISBN: 0808913336; http://www.amazon.com/exec/obidos/ASIN/0808913336/icongroupinterna
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Selected Papers Fourth International Conference on Malignant Lymphoma, June 6-9, 1990, Iugano by J. E. Ultmann (Editor) (1993); ISBN: 0792311167; http://www.amazon.com/exec/obidos/ASIN/0792311167/icongroupinterna
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Serological and flow cytometric DNA studies on etiology and pathogenesis of malignant lymphomas by Tuula Lehtinen; ISBN: 9514424492; http://www.amazon.com/exec/obidos/ASIN/9514424492/icongroupinterna
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Slide Atlas of Solid Tumors, Leukemias, and Lymphomas of Childhood by Steven Sallan MD; ISBN: 1563750449; http://www.amazon.com/exec/obidos/ASIN/1563750449/icongroupinterna
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Text Atlas of Lymphomas by James O., Md. Armitage, et al; ISBN: 1853177059; http://www.amazon.com/exec/obidos/ASIN/1853177059/icongroupinterna
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The Geographical Epidemiology of Childhood Leukemia and Non-Hodgkin Lymphomas in Great Britain, 1966-83 (Studies on Medical and Population Subjects) by Gerald Draper (1991); ISBN: 0116913576; http://www.amazon.com/exec/obidos/ASIN/0116913576/icongroupinterna
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The histopathology of lymphomas and pseudolymphomas by J. R. Jackson; ISBN: 0839113242; http://www.amazon.com/exec/obidos/ASIN/0839113242/icongroupinterna
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The Leukemia-Lymphoma Cell Line Factsbook by Hans Drexler (Author) (2000); ISBN: 0122219708; http://www.amazon.com/exec/obidos/ASIN/0122219708/icongroupinterna
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The Lymphomas by George P. Canellos (Editor), et al; ISBN: 0721650309; http://www.amazon.com/exec/obidos/ASIN/0721650309/icongroupinterna
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The Lymphomas: Etiology, Pathology, Genetics and Treatment by Raju Chaganti, et al (2003); ISBN: 0121663701; http://www.amazon.com/exec/obidos/ASIN/0121663701/icongroupinterna
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The Management of Non-Hodgkin's Lymphomas in Europe; ISBN: 3540522972; http://www.amazon.com/exec/obidos/ASIN/3540522972/icongroupinterna
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The Management of Non-Hodgkin's Lymphomas in Europe (Eso Intercity Report) by S. Monfardini (Editor), U. Veronesi (Editor); ISBN: 0387522972; http://www.amazon.com/exec/obidos/ASIN/0387522972/icongroupinterna
280 Lymphoma
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The Non-Hodgkin's Lymphomas by Ian T. Magrath (Editor) (1997); ISBN: 0340557931; http://www.amazon.com/exec/obidos/ASIN/0340557931/icongroupinterna
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The Official Patient's Sourcebook on Non-Hodgkin's Lymphoma During Pregnancy: A Revised and Updated Directory for the Internet Age by Icon Health Publications (2002); ISBN: 0597834792; http://www.amazon.com/exec/obidos/ASIN/0597834792/icongroupinterna
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The Pocket Guide to Lymphoma Classification by David Mason, Kevin Gatter; ISBN: 0632050969; http://www.amazon.com/exec/obidos/ASIN/0632050969/icongroupinterna
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Understanding Non-Hodgkin's Lymphomas (1999); ISBN: 190127635X; http://www.amazon.com/exec/obidos/ASIN/190127635X/icongroupinterna
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Vaccine Intervention Against Virus-Induced Tumors (Leukemia and Lymphoma Research) by John M. Goldman (Editor) (1986); ISBN: 0943818931; http://www.amazon.com/exec/obidos/ASIN/0943818931/icongroupinterna
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What you need to know about non-Hodgkin's lymphoma (SuDoc HE 20.3152:L 98/999) by U.S. Dept of Health and Human Services; ISBN: B00011287G; http://www.amazon.com/exec/obidos/ASIN/B00011287G/icongroupinterna
The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “lymphoma” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 •
Burkitt's lymphoma; a bibliography. Author: Nadanasabapathy, V.; Year: 1968; Kampala, Uganda, Albert Cook Library, 1972
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Current problems in the epidemiology of cancer and lymphomas, edited by E. Grundmann and H. Tulinius. Author: Grundmann, E. (Ekkehard); Year: 1968; Berlin, New York, Springer-Verlag, 1972; ISBN: 3540058605
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Leukemia & lymphoma [by] Joseph H. Burchenal [and] Henry D. Diamond. Author: Burchenal, Joseph Holland,; Year: 1963; Chicago, Year Book Publishers, 1958
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Lymphomas; regression, carcinogenesis, and prevention. Author: Lampkin-Asam, Julia McCain,; Year: 1952; Miami, Fla., c1966]
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Malignant lymphoma of the testis. Author: Massey, Ben D.,; Year: 1966; [Minneapolis] 1966
11
In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.
Books
281
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Malignant lymphomas and their management. Author: Jacobs, Meville L.; Year: 1969; Berlin, New York, Springer, 1968
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Possible relationships between the African lymphoma and acute leukaemia: third guest lecture delivered by invitation. Author: Burkitt, D. P. (Denis P.); Year: 1970; London: Queen Anne Press for the Leukaemia Research Fund, 1967
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Primary localized malignant lymphomas of the colon and appendix. Author: Glick, Dallas Donald,; Year: 1964; [Minneapolis] 1964
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Symposium on changing concepts in Hodgkin's disease, lymphomas, and leukemias. Philip Rubin, Malcolm A. Bagshaw, guest editors. Author: Rubin, Philip,; Year: 1969; Philadelphia, London, Saunders [c1968]
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The roentgenologic diagnosis of lymphoma primary in the small intestine. Author: Cupps, Roger Ellis,; Year: 1965; [Minneapolis] 1965
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The roentgenologic diagnosis of primary gastric lymphoma. Author: Sherrick, Donald William,; Year: 1964; [Minneapolis] 1963
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Treatment of lymphomatous diseases with triethylene melamine, by Leo M. Meyer [and others]. Author: Meyer, Leo M.; Year: 1965; Stockholm, 1952
Chapters on Lymphoma In order to find chapters that specifically relate to lymphoma, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and lymphoma using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “lymphoma” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on lymphoma: •
Lymphoma in Inflammatory Bowel Disease Source: in Bayless, T.M. and Hanauer, S.B. Advanced Therapy of Inflammatory Bowel Disease. Hamilton, Ontario: B.C. Decker Inc. 2001. p. 645-648. Contact: Available from B.C. Decker Inc. 20 Hughson Street South, P.O. Box 620, L.C.D. 1 Hamilton, Ontario L8N 3K7. (905) 522-7017 or (800) 568-7281. Fax (905) 522-7839. Email:
[email protected]. Website: www.bcdecker.com. PRICE: $129.00 plus shipping and handling. ISBN: 1550091220. Summary: This chapter on lymphoma (a tumor of the lymphoid tissue, usually malignant) in inflammatory bowel disease (IBD) is from the second edition of a book devoted to the details of medical, surgical, and supportive management of patients with Crohn's disease (CD) and ulcerative colitis (UC), together known as IBD. Lymphoma may either mimic or complicate ulcerative colitis UC and CD, and the understanding of this relationship is of importance to physicians. There is significant overlap between the symptoms, signs, and the radiologic and endoscopic appearance of intestinal lymphoma and IBD. Small intestinal lymphoma may mimic CD and colonic lymphoma may mimic both colitis and colonicadnocarcinoma (cancer). The authors conclude that intestinal lymphomas are uncommon but both intestinal and extraintestinal lymphomas appear to be of increased incidence in chronic inflammatory bowel disease states, including IBD. The relationship between immune modifying therapy used in IBD and the development
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of lymphoma remains controversial. The differential diagnosis between IBD and lymphoma, either complicating IBD or occurring independently, is difficult. Most intestinal lymphomas diagnosed in the setting of IBD have been unanticipated and were found incidentally at the time of surgery performed for IBD indications or only subsequently in the histopathology of the resected specimen. Intestinal lymphoma also may complicate IBD; therefore, awareness of its association, clues to its presence, and knowledge of appropriate diagnostic investigations (and their shortcomings) are critical to patient management. 10 references.
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CHAPTER 8. MULTIMEDIA ON LYMPHOMA Overview In this chapter, we show you how to keep current on multimedia sources of information on lymphoma. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.
Video Recordings An excellent source of multimedia information on lymphoma is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “lymphoma” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “lymphoma” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on lymphoma: •
Issues of Dementia: In - Service Training With Brian Smith Contact: Shanti, 730 Polk St, San Francisco, CA, 94109-7813, (415) 674-4700, http://www.shanti.org. Summary: In this videorecording, the moderator and participants in a volunteer training program discuss the cognitive and motor problems resulting from neurological diseases and disorders associated with Acquired immunodeficiency syndrome (AIDS). Psychologically, potential dementia and other disorders pose one of the most frightening prospects for Persons with AIDS (PWA's). The symptoms may include seizures, headaches, and short-term memory loss. Specific diagnoses, including meningitis, lymphoma of the brain, PML, and toxoplasmosis are discussed. Volunteers are given some guidance on what to expect from clients in terms of denial, confusion, and personality changes; they are urged to attempt to breach communication barriers with their clients and talk about the possibility of Human immunodeficiency virus (HIV) infection of the brain. The videorecording briefly describes the apparent effect of Azidothymidine (AZT) on the manifestations of HIV-brain infection.
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Audio Recordings The Combined Health Information Database contains abstracts on audio productions. To search CHID, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find audio productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Sound Recordings.” Type “lymphoma” (or synonyms) into the “For these words:” box. The following is a typical result when searching for sound recordings on lymphoma: •
AIDS - Related Lymphoma & Kaposi's Sarcoma: National Conference on Today's Clinical Issues; September 12 - 14, 1990; Anaheim, CA Contact: Convention Recorders, 2645 Financial Ct Ste P, Ste C, San Diego, CA, 92117, (619) 274-7100. Summary: This sound recording discusses the types of lymphomas that are related to varying degrees of immune dysfunction and AIDS. It defines the ranges of HIV infection up to the development of AIDS. The history, epidemiology, pathogenesis, subfactors and histology of Kaposi's sarcoma, high grade non-Hodgkins lymphoma, intermediate grade lymphoma, and primary central nervous system (CNS) lymphoma are explained. Classification of lesions, management issues, and therapies are also discussed.
Bibliography: Multimedia on Lymphoma The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in lymphoma (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on lymphoma: •
A Clinical approach to canine malignant lymphoma [slide] Source: [presented by] Purdue Comparative Oncology Program; Medical Illustration & Communications, School of Veterinary Medicine, Purdue University; Year: 1983; Format: Slide; West Lafayette, Ind.: Purdue Research Foundation, c1983
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Adults with lymphoma [videorecording] Source: University of Texas System Cancer Center; Year: 1976; Format: Videorecording; Houston: The Center, 1976
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Bone marrow transplant for lymphoma and leukemia [videorecording] Source: Marshfield Medical Foundation, in cooperation with Marshfield Clinic & St. Joseph's Hospital; Year: 1983; Format: Videorecording; Marshfield, WI: Marshfield Regional Video Network, [1983]
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Classification of malignant lymphomas [slide] Source: Richard S. Neiman, John M. Bennett; Year: 9999; Format: Slide; Garden Grove, Calif.: Medcom, c1986-
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Clinical relevance of lymphocyte surface markers in malignant lymphoma [videorecording] Source: Department of Medicine, Emory University, School of Medicine; Year: 1980; Format: Videorecording; Atlanta: Emory Medical Television Network: [for loan or sale by A. W. Calhoun Medical Library], 1980
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Cutaneous lymphoma, dermatologic appearance and management [slide] Source: Radiological Society of North America; Year: 1983; Format: Slide; [Chicago, Ill.]: RSNA, c1983
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Cutaneous lymphoma, electron beam therapy [slide] Source: Radiological Society of North America; Year: 1983; Format: Slide; [Chicago, Ill.]: RSNA, c1983
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Cutaneous lymphoma, histopathologic features [slide] Source: Radiological Society of North America; Year: 1983; Format: Slide; [Chicago, Ill.]: RSNA, c1983
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Gastrointestinal lymphoma [videorecording] Source: WRAMC Television; Year: 1977; Format: Videorecording; Washington: WRAMC-TV, [1977]
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Malignant lymphoma [slide] Source: American Society of Hematology; Year: 1974; Format: Slide; [Seattle: The Society: for sale by University of Washington Health Sciences Center for Educational Resources, 1974]
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Malignant lymphomas: chest involvement [slide] Source: T. J. Wachowski and E. J. Liebner; Year: 1965; Format: Slide; [Urbana, Ill.: Wachowski; Chicago: for sale by Micro X-Ray Recorder, Inc., Medical Film Slide Division, 196-?]
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Medical management of cutaneous lymphomas [slide] Source: Radiological Society of North America; Year: 1983; Format: Slide; [Chicago, Ill.]: RSNA, c1983
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Non-Hodgkin's lymphomas [videorecording] Source: American Society of Clinical Pathologists; Year: 1976; Format: Videorecording; Chicago: The Society, c1976
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Non-Hodgkin's lymphomas [videorecording] Source: author, Robert E. Reed; faculty consultant, Roland Hiss; Biomedical Media Production Unit, the University of Michigan Medical Center, Office of Educational Resources & Research; Year: 1979; Format: Videorecording; Ann Arbor, Mich.: The University, c1979
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Noni[n]vasive evaluation of lymphoma, nuclear medicine [slide] Source: Radiological Society of North America; Year: 1983; Format: slide; [Chicago, Ill.]: RSNA, c1983
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Noninvasive evaluation of lymphoma, radiologic techniques [slide] Source: Radiological Society of North America; Year: 1983; Format: Slide; [Chicago, Ill.]: RSNA, c1983
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Physics of radiation treatment in lymphoma [slide] Source: Radiological Society of North America; Year: 1983; Format: Slide; [Chicago, Ill.]: RSNA, c1983
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Radiation therapy of cutaneous lymphomas [slide] Source: Radiological Society of North America; Year: 1983; Format: Slide; [Chicago, Ill.]: RSNA, c1983
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Surgical staging of lymphoma [slide] Source: Radiological Society of North America; Year: 1983; Format: Slide; [Chicago, Ill.]: RSNA, c1983
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The Classification of malignant lymphomas [slide] Source: John M. Bennett, Richard J. Werner; Year: 1973; Format: Slide; [New York]: Medcom, c1973
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The Malignant lymphomas [slide] Source: McMaster University Health Sciences; Year: 1971; Format: Slide; [Hamilton, Ont.: Health Sciences McMaster Univ., 1971]
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Treatment of pediatric lymphoma [slide] Source: Radiological Society of North America; Year: 1983; Format: Slide; [Chicago, Ill.]: RSNA, c1983
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X-ray findings in lymphoma, part 1 [videorecording] Source: M. I. Goldstein; produced by Ohio State University, Medical Audio-visual and Television Center; Year: 1972; Format: Videorecording; [Columbus, Ohio]: The Center, c1972
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X-ray findings in lymphoma, part 2 [videorecording] Source: M.I. Goldstein; produced by Ohio State University Medical Audiovisual and Television Center; Year: 1972; Format: Videorecording; [Columbus, Ohio]: The Center, c1972
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CHAPTER 9. PERIODICALS AND NEWS ON LYMPHOMA Overview In this chapter, we suggest a number of news sources and present various periodicals that cover lymphoma.
News Services and Press Releases One of the simplest ways of tracking press releases on lymphoma is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “lymphoma” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to lymphoma. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “lymphoma” (or synonyms). The following was recently listed in this archive for lymphoma: •
Non-purged bone marrow transplant improves survival in lymphoma Source: Reuters Industry Breifing Date: November 24, 2003
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Study links psoriasis to lymphoma cancers. Source: Reuters Health eLine Date: November 17, 2003
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Psoriasis increases risk of lymphoma Source: Reuters Medical News Date: November 17, 2003
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Topical bexarotene gel effective in early-stage cutaneous T-cell lymphoma Source: Reuters Industry Breifing Date: November 13, 2003
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Rituxan meets goal in non-Hodgkin's lymphoma trial Source: Reuters Medical News Date: November 13, 2003
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Early Genentech, Idec data lackluster on Rituxan for aggressive lymphoma Source: Reuters Industry Breifing Date: November 05, 2003
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Early data lackluster on rituximab for aggressive lymphoma Source: Reuters Medical News Date: November 05, 2003
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Higher mortality persists decades after Hodgkin's lymphoma remission Source: Reuters Medical News Date: October 08, 2003
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HAART usually unhindered by lymphoma chemotherapy Source: Reuters Medical News Date: October 06, 2003
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Mononucleosis-related EBV infection may cause Hodgkin's lymphoma Source: Reuters Medical News Date: October 01, 2003
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Painkillers may raise lymphoma risk for women Source: Reuters Health eLine Date: September 12, 2003
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NSAIDs tied to non-Hodgkin lymphoma risk in women Source: Reuters Industry Breifing Date: September 12, 2003
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HAART prolongs survival after diagnosis of AIDS-related CNS lymphoma Source: Reuters Medical News Date: August 29, 2003
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Watch and wait policy suitable for some lymphomas Source: Reuters Health eLine Date: August 15, 2003
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HAART prolongs survival in AIDS-related primary CNS lymphoma Source: Reuters Medical News Date: July 31, 2003
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Britain's NICE set to back Roche's MabThera for lymphoma Source: Reuters Medical News Date: July 30, 2003
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Chromosome linked to deafness, lymphomas sequenced Source: Reuters Health eLine Date: July 09, 2003
Periodicals and News
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No association found between presence of SV40 and lymphoma Source: Reuters Medical News Date: July 08, 2003
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Radiation for Hodgkin lymphoma before age 30 ups breast cancer risk: study Source: Reuters Medical News Date: June 30, 2003
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Glaxo, Corixa get U.S. nod for lymphoma drug Source: Reuters Industry Breifing Date: June 30, 2003
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Glaxo, Corixa get U.S. approval for lymphoma drug Source: Reuters Medical News Date: June 30, 2003
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HAART not necessary for effective treatment of AIDS-related lymphoma Source: Reuters Medical News Date: June 17, 2003
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High endostatin levels linked to poor outcome in non-Hodgkin lymphoma Source: Reuters Medical News Date: June 16, 2003
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Kaposi sarcoma and lymphoma risk linked to CD4+ count at AIDS onset Source: Reuters Medical News Date: May 12, 2003
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Epstein-Barr virus not the sole etiologic agent in Hodgkin's lymphoma Source: Reuters Medical News Date: April 25, 2003
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Increased malignant lymphoma risk observed in RA patients Source: Reuters Medical News Date: April 24, 2003
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Praecis files to test fumagillin compound for non-Hodgkin's lymphoma Source: Reuters Industry Breifing Date: April 16, 2003
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SSRI antidepressants kill lymphoma cells in vitro Source: Reuters Medical News Date: April 15, 2003
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Prozac kills lymphoma cancer cells -- scientists Source: Reuters Industry Breifing Date: April 15, 2003
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Prozac kills Burkitt's lymphoma cells: scientists Source: Reuters Health eLine Date: April 15, 2003
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Instance of gastric lymphoma remission reported with H. pylori eradication alone Source: Reuters Medical News Date: April 14, 2003
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Study links hepatitis C to type of lymphoma Source: Reuters Health eLine Date: April 07, 2003
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HCV infection linked to non-Hodgkin's lymphoma risk in U.S. Source: Reuters Medical News Date: April 07, 2003
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Hodgkin's lymphoma cells have distinct gene expression profiles Source: Reuters Medical News Date: February 19, 2003
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Viral tagging method identifies 19 possible lymphoma oncogenes in mice Source: Reuters Medical News Date: February 14, 2003
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Prognostic score for primary CNS lymphoma may allow risk-adjusted treatment Source: Reuters Medical News Date: February 12, 2003
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HAART improves outcome of HIV-associated Hodgkin's lymphoma Source: Reuters Medical News Date: January 22, 2003
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Combination chemotherapy not necessarily advantageous in follicular lymphomas Source: Reuters Industry Breifing Date: January 21, 2003
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Etanercept and infliximab may be associated with development of lymphoma Source: Reuters Medical News Date: December 23, 2002
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FDA advisors back non-Hodgkin's lymphoma drug Source: Reuters Health eLine Date: December 18, 2002
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Idec antibody induces tumor reduction in non-Hodgkin's lymphoma study Source: Reuters Industry Breifing Date: December 10, 2002
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High-dose therapy in primary treatment of aggressive lymphoma not effective Source: Reuters Industry Breifing Date: December 06, 2002
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Proteasome inhibitor exhibits safe anti-myeloma, anti-lymphoma activity Source: Reuters Industry Breifing Date: November 26, 2002 The NIH
Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine.
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Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “lymphoma” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests. Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “lymphoma” (or synonyms). If you know the name of a company that is relevant to lymphoma, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/. BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “lymphoma” (or synonyms).
Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “lymphoma” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on lymphoma: •
Salivary Gland Biopsy for Sjogren's Syndrome Source: Moisture Seekers Newsletter. 17(7): 1-3. October 1999.
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Contact: Available from Sjogren's Syndrome Foundation, Inc. 8120 Woodmont Avenue, Suite 530, Bethesda, MD 20814-1437. (301) 718-0300 or (800) 475-6473. Fax (301) 718-0322. Website: www.sjogrens.org. Summary: This article from a newsletter for people with Sjogren's syndrome (SS) describes the use of salivary gland biopsy for diagnostic purposes. The author notes that the salivary gland biopsy demonstrates the extent of salivary gland involvement, the extent of cellular infiltration, and how much normal tissue remains in the gland of the patient with SS. Many conditions, therapies, and medications can cause dry mouth (xerostomia) and decreased salivary function. The most definitive way of attributing the changes that take place in SS is to examine a sample of the salivary tissue microscopically (with a biopsy). The author reviews the three types of salivary glands (parotid, submandibular, and sublingual), characteristic changes in SS, classification and grading systems for describing salivary gland changes, what to expect during the biopsy procedure itself, and the role of other diagnostic methods in SS. The author stresses the importance of salivary gland biopsy, noting that a biopsy cannot be considered optional in the case of an individual with chronically enlarged salivary glands because of the risk of lymphoma. •
Celiac Disease: How to Manage Gluten Intolerance Source: Mayo Clinic Health Letter. 18(11): 7. November 2000. Contact: Available from Mayo Clinic Health Letter. Subscription Services, P.O. Box 53889, Boulder, CO 80322-3889. (800) 333-9037 or (303) 604-1465. Summary: This newsletter article offers strategies for dealing with celiac disease (an inherited intolerance to gluten that results in intestinal and other disorders). Gluten proteins are found in a variety of grains, including wheat, barley, and rye, so that a diet that is gluten free can be somewhat challenging. The article describes how the immune system of people with celiac disease reacts whenever they eat food containing gluten; this reaction causes the lining of the small intestine to become swollen and inflamed. The result is nutritional deficiencies and digestive problems, as well as a greater chance of developing small bowel cancer, especially intestinal lymphoma. Celiac disease can become active at any age, but sometimes follows a disruptive event, such as a viral infection, severe stress, pregnancy, or physical trauma. Symptoms vary greatly, and the disease can resemble other conditions, such as irritable bowel syndrome. Symptoms can include fatigue, abdominal pain, intermittent diarrhea, bloating and excessive passing of gas, weight loss, or foul smelling stools that float. The primary treatment for celiac disease is a lifelong gluten free diet. There are still many foods that can be eaten, including plain meats, fruits, vegetables, rice, potatoes, and most dairy products. The author encourages readers to work with their health care provider to set up a balanced, gluten free diet that incorporates individual preferences and needs. Once the gluten is completely eliminated from the patient's diet, inflammation in the small intestine begins to subside in just a few days. Most people who maintain the diet experience complete healing within several months to 2 to 3 years. One sidebar explains the diagnosis of celiac disease, which may include a small intestine biopsy for confirmation of the clinical diagnosis.
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Dry Eyes Source: EDucator, The. p. 3-4. November-December 2000.
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Contact: Available from National Foundation for Ectodermal Dysplasias. 410 East Main Street, P.O. Box 114, Mascoutah, IL 62258-0114. (618) 566-2020. Fax (618) 566-4718. Website: www.nfed.org. Summary: This newsletter article provides people who have dry eyes with information on the causes, categories, and treatment of this condition. Various environmental influences, medical disorders, and medications may cause dry eyes, which can be divided into two major groups: those in which there is inadequate production of the watery component of tears and those in which there is adequate watery tear production. Inadequate production of the watery component of tears results from an undersecreting tear gland. Conditions associated with tear deficiency include congenital alacrima, lymphoma, sarcoidosis, amyloidosis, severe vitamin A deficiency, neurologic conditions, and Sjogren's syndrome. One cause of dry eyes with adequate watery tear production is abnormal functioning of the oil glands in the eyelids that produce the protective oily layer on the outside of the tear film. Other conditions that increase tear film evaporation include increased width of the eyelids and inadequate lid closure. The treatment of irritation with dry eyes is mainly directed at symptom relief. The usual treatment for decreased aqueous tear production is topically applied lubricants and ointments. Other treatment options include humidifying the indoor environment, placing side panels and moisture chambers around the frame of eyeglasses, covering the eyes at night to reduce tear evaporation, and occluding the punctum with small collagen plugs. •
Sjogren's Syndrome in Systemic Lupus Erythematosus Source: Lupus News: A Newsletter of the Western Pennsylvania Chapter of the Lupus Foundation. 25(3): 1, 7-8. Fall 1997. Contact: Available from Western Pennsylvania Chapter of the Lupus Foundation. Suite 200, 1323 Forbes Avenue, Pittsburgh, PA 15219. (412)261-5886. Summary: This newsletter article summarizes the occurrence of Sjogren's syndrome (SS) in systemic lupus erythematosus (SLE). Sjogren's syndrome (SS) is a condition characterized by malfunction of the tear and saliva producing glands and the Bartholin's glands in the vagina. The result is the feeling of dryness of the eyes, mouth, and vagina. SS is caused by the accumulation of activated lymphocytes in the affected glands and the ducts which drain the glands. These lymphocytes produce substances which damage moisture producing tissues. The article describes the symptoms of SS, then outlines the potential complications of the disease, including those affecting the eyes, mouth, nervous system, respiratory tract, vasculitis, kidney, skin, pregnancy, and lymphoma. The author then briefly notes the diagnostic tests that are used to confirm the presence of SS. Treatment options are then described, including those for dry mouth: sips of water throughout the day or over the counter saliva substitutes or gels; sugar free chewing gum or candies to stimulate saliva flow; treatment for oral candidiasis; a saliva stimulant oral medication containing the active ingredient pilocarpine; and good oral hygiene to prevent dental cares. The article concludes with a brief section describing how SS is related to scleroderma.
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Case for the Gluten-Free Diet Or One Dietitian's Journey In the Gluten-Free Diet Maze Source: Lifeline. 19(1): 1-4. Winter 2000. Contact: Available from Celiac Sprue Association-United States of America, Inc. P.O. Box 31700, Omaha, NE 68131. (402) 558-0600. Website: www.csaceliacs.org.
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Summary: This newsletter article, written by a pediatric clinical dietitian, explores the use of the gluten free diet for the treatment of celiac disease (CD). Gluten is the substance that gives bread elasticity; structurally, gluten contains high glutamine and high proline storage proteins (prolamins) and is composed of two protein fractions, gliadin and glutenin. Gliadin is a toxic protein fraction in gluten; glutenin is found only in wheat, while gliadin is found in other grains and grasses. The author explains how toxic amino acid sequences are identified and discusses the role of total protein content in determining toxicity. The author then explores the variance in the recommendations for a safe gluten intake. One major reason for this variation is the unique response of each individual with CD; some patients are more sensitive to a lower level of gluten than others. Although clinical studies are very expensive to undertake, their results have demonstrated the need for dietary compliance, particularly to ensure adequate growth in children with CD. For adults, strict adherence to a diet free of toxic prolamins can reduce the risk for reduced bone mineralization, lymphoma, and other forms of cancer associated with CD. The author briefly reviews three hypotheses about how CD occurs: enzyme deficiency, lectin interaction, and immune mechanisms. The author concludes by proposing a different name for the CD diet therapy, since gluten free does not encompass the many other aspects that must be taken into consideration. 2 tables.
Academic Periodicals covering Lymphoma Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to lymphoma. In addition to these sources, you can search for articles covering lymphoma that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”
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CHAPTER 10. RESEARCHING MEDICATIONS Overview While a number of hard copy or CD-ROM resources are available for researching medications, a more flexible method is to use Internet-based databases. Broadly speaking, there are two sources of information on approved medications: public sources and private sources. We will emphasize free-to-use public sources.
U.S. Pharmacopeia Because of historical investments by various organizations and the emergence of the Internet, it has become rather simple to learn about the medications recommended for lymphoma. One such source is the United States Pharmacopeia. In 1820, eleven physicians met in Washington, D.C. to establish the first compendium of standard drugs for the United States. They called this compendium the U.S. Pharmacopeia (USP). Today, the USP is a nonprofit organization consisting of 800 volunteer scientists, eleven elected officials, and 400 representatives of state associations and colleges of medicine and pharmacy. The USP is located in Rockville, Maryland, and its home page is located at http://www.usp.org/. The USP currently provides standards for over 3,700 medications. The resulting USP DI Advice for the Patient can be accessed through the National Library of Medicine of the National Institutes of Health. The database is partially derived from lists of federally approved medications in the Food and Drug Administration’s (FDA) Drug Approvals database, located at http://www.fda.gov/cder/da/da.htm. While the FDA database is rather large and difficult to navigate, the Phamacopeia is both user-friendly and free to use. It covers more than 9,000 prescription and over-the-counter medications. To access this database, simply type the following hyperlink into your Web browser: http://www.nlm.nih.gov/medlineplus/druginformation.html. To view examples of a given medication (brand names, category, description, preparation, proper use, precautions, side effects, etc.), simply follow the hyperlinks indicated within the United States Pharmacopeia (USP). Below, we have compiled a list of medications associated with lymphoma. If you would like more information on a particular medication, the provided hyperlinks will direct you to ample documentation (e.g. typical dosage, side effects, drug-interaction risks, etc.). The
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following drugs have been mentioned in the Pharmacopeia and other sources as being potentially applicable to lymphoma: Bexarotene •
Systemic - U.S. Brands: Targretin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500095.html
Bleomycin •
Systemic - U.S. Brands: Blenoxane http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202093.html
Denileukin Diftitox •
Systemic - U.S. Brands: Ontak http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500010.html
Ifosfamide •
Systemic - U.S. Brands: IFEX http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202293.html
Interferons, Alpha •
Systemic - U.S. Brands: Alferon N; Intron A; Roferon-A http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202299.html
Leucovorin •
Systemic - U.S. Brands: Wellcovorin http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202321.html
Methoxsalen •
Extracorporeal-Systemic - U.S. Brands: Uvadex http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/500002.html
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Systemic - U.S. Brands: 8-MOP; Oxsoralen-Ultra http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202357.html
Rituximab •
Systemic - U.S. Brands: Rituxan http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203423.html
Teniposide •
Systemic - U.S. Brands: Vumon http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/203661.html
Vinblastine •
Systemic - U.S. Brands: Velban http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202593.html
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Commercial Databases In addition to the medications listed in the USP above, a number of commercial sites are available by subscription to physicians and their institutions. Or, you may be able to access these sources from your local medical library.
Mosby’s Drug Consult Mosby’s Drug Consult database (also available on CD-ROM and book format) covers 45,000 drug products including generics and international brands. It provides prescribing information, drug interactions, and patient information. Subscription information is available at the following hyperlink: http://www.mosbysdrugconsult.com/.
PDRhealth The PDRhealth database is a free-to-use, drug information search engine that has been written for the public in layman’s terms. It contains FDA-approved drug information adapted from the Physicians’ Desk Reference (PDR) database. PDRhealth can be searched by brand name, generic name, or indication. It features multiple drug interactions reports. Search PDRhealth at http://www.pdrhealth.com/drug_info/index.html. Other Web Sites Drugs.com (www.drugs.com) reproduces the information in the Pharmacopeia as well as commercial information. You may also want to consider the Web site of the Medical Letter, Inc. (http://www.medletter.com/) which allows users to download articles on various drugs and therapeutics for a nominal fee.
Researching Orphan Drugs Although the list of orphan drugs is revised on a daily basis, you can quickly research orphan drugs that might be applicable to lymphoma by using the database managed by the National Organization for Rare Disorders, Inc. (NORD), at http://www.rarediseases.org/. Scroll down the page, and on the left toolbar, click on “Orphan Drug Designation Database.” On this page (http://www.rarediseases.org/search/noddsearch.html), type “lymphoma” (or synonyms) into the search box, and click “Submit Query.” When you receive your results, note that not all of the drugs may be relevant, as some may have been withdrawn from orphan status. Write down or print out the name of each drug and the relevant contact information. From there, visit the Pharmacopeia Web site and type the name of each orphan drug into the search box at http://www.nlm.nih.gov/medlineplus/druginformation.html. You may need to contact the sponsor or NORD for further information. NORD conducts “early access programs for investigational new drugs (IND) under the Food and Drug Administration’s (FDA’s) approval ‘Treatment INDs’ programs which allow for a limited number of individuals to receive investigational drugs before FDA marketing approval.” If the orphan product about which you are seeking information is approved for
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marketing, information on side effects can be found on the product’s label. If the product is not approved, you may need to contact the sponsor. The following is a list of orphan drugs currently listed in the NORD Orphan Drug Designation Database for lymphoma: •
Pentostatin (trade name: Nipent) http://www.rarediseases.org/nord/search/nodd_full?code=1005
•
Hypericin http://www.rarediseases.org/nord/search/nodd_full?code=1023
•
Interferon beta (recombinant) (trade name: R-IFN-beta) http://www.rarediseases.org/nord/search/nodd_full?code=103
•
Hu1D10, humanized monoclonal antibody (trade name: Remitogen) http://www.rarediseases.org/nord/search/nodd_full?code=1165
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Hu1D10, humanized monoclonal antibody (trade name: Remitogen) http://www.rarediseases.org/nord/search/nodd_full?code=1220
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Ibritumomab Tiuxetan (Trade Name: Zevalin) http://www.rarediseases.org/nord/search/nodd_full?code=1295
•
Iodine I 131 murine monoclonal antibody IgG2a to B (trade name: Immurait, L1-2-I131) http://www.rarediseases.org/nord/search/nodd_full?code=146
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Peldesine http://www.rarediseases.org/nord/search/nodd_full?code=507
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APL 400-020 http://www.rarediseases.org/nord/search/nodd_full?code=510
•
Technetium Tc-99m murine monoclonal antibody (IgG2 (trade name: LymphoScan) http://www.rarediseases.org/nord/search/nodd_full?code=311
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Elliott's B solution http://www.rarediseases.org/nord/search/nodd_full?code=330
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Prednimustine (trade name: Sterecyt) http://www.rarediseases.org/nord/search/nodd_full?code=424
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Allopurinol sodium (trade name: Zyloprim for Injection) http://www.rarediseases.org/nord/search/nodd_full?code=520
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Chimeric (murine variable human constant) MAb (C2B http://www.rarediseases.org/nord/search/nodd_full?code=628
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In-111 murine Mab(2b8-mx-dtpa) & Y-90 murine Mab(2 (trade name: Melimmune) http://www.rarediseases.org/nord/search/nodd_full?code=63
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Cladribine (trade name: Leustatin Injection) http://www.rarediseases.org/nord/search/nodd_full?code=647
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Buffered intrathecal electrolyte/dextrose injectio (trade name: Elliotts B Solution) http://www.rarediseases.org/nord/search/nodd_full?code=805
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LymphoCIDE http://www.rarediseases.org/nord/search/nodd_full?code=930
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•
Ricin (blocked) conjugated murine monoclonal antib http://www.rarediseases.org/nord/search/nodd_full?code=7
•
Fludarabine phosphate (trade name: Fludara) http://www.rarediseases.org/nord/search/nodd_full?code=705
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Aldesleukin (trade name: Proleukin) http://www.rarediseases.org/nord/search/nodd_full?code=949
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I-131 radiolabeled B1 monoclonal antibody http://www.rarediseases.org/nord/search/nodd_full?code=772
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Iodine I 131 murine monoclonal antibody IgG2a to B (trade name: Immurait, L1-2-I131) http://www.rarediseases.org/nord/search/nodd_full?code=782
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DAB389IL2 http://www.rarediseases.org/nord/search/nodd_full?code=787
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Mitoguazone (trade name: Zyrkamine) http://www.rarediseases.org/nord/search/nodd_full?code=81
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Murine MAb (Lym-1) and Iodine 131-I radiolabled mu (trade name: Oncolym) http://www.rarediseases.org/nord/search/nodd_full?code=954
If you have any questions about a medical treatment, the FDA may have an office near you. Look for their number in the blue pages of the phone book. You can also contact the FDA through its toll-free number, 1-888-INFO-FDA (1-888-463-6332), or on the World Wide Web at www.fda.gov.
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APPENDICES
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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.
NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute12: •
Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm
•
National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/
•
National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html
•
National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25
•
National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm
•
National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm
•
National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375
•
National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/
12
These publications are typically written by one or more of the various NIH Institutes.
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•
National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm
•
National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/
•
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm
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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm
•
National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/
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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/
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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm
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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html
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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm
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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm
•
National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm
•
National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html
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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm
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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp
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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/
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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp
•
Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html
•
Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm
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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.13 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:14 •
Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html
•
HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html
•
NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html
•
Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/
•
Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html
•
Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html
•
Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/
•
Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html
•
Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html
•
Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html
•
MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html
13
Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 14 See http://www.nlm.nih.gov/databases/databases.html.
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•
Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html
•
Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html The Combined Health Information Database
A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “lymphoma” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “lymphoma” (or synonyms) into the “For these words:” box. The following is a sample result: •
Research Report on Dermatitis Herpetiformis Source: Seattle, WA: Gluten Intolerance Group of North America. 1993. 17 p. Contact: Available from Gluten Intolerance Group of North America. P.O. Box 23053, Seattle, WA 98102-0353. (206) 325-6980. PRICE: $5; plus shipping and handling. Summary: This document provides an overview of dermatitis herpetiformis (DH), a common complication in people with celiac disease or gluten intolerance. Written in a question-and-answer format, the document discusses the appearance of DH; the body areas most likely to have DH eruptions; variations in severity; relationship between hormone levels and DH eruptions; demographics; diagnosis; other IgA skin disorders that mimic DH; treatment options for DH; medications used and side effects of each, including dapsone, sulphapyridine, and sulphamethoxy-pyridazine; choosing diet versus medication; other substances that can trigger an outbreak of DH, including cleaning products; the use of elemental diets in DH; tests for antibodies as diagnostic tools; recent research on diagnosis; advances in drug therapy, including the use of cyclosporin; epidemiological information; and disorders or conditions associated with DH, including thyroid disease, other autoimmune disorders, low gastric acid secretion, lymphoma, and dental enamel defects. One chart lists toll-free telephone numbers for the major manufacturers of cleaning products. 21 references.
•
Manual of HIV/AIDS Therapy Contact: Current Clinical Strategies Publishing, 9550 Warner Ave Ste 250, Fountain Valley, CA, 92708-2822, (714) 965-9400. Summary: This handbook is a guide to the management of adult patients with HIV infections and AIDS. It is designed as a reference aid for attending physicians, house officers, and medical students involved in day-to-day patient care. The first section discusses the epidemiology, natural history, and clinical management of HIV infection. Subsequent chapters cover in detail infectious diseases that occur commonly in patients with AIDS. The last section includes diseases that are not unique to AIDS, but differ from their usual presentation in the setting of HIV infection. Neoplastic disorders such
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as Kaposi's sarcoma and lymphoma are covered as they occur in the differential diagnosis of various AIDS-related disorders. •
Clinical Manual for Care of the Adult Patient With HIV Infection Contact: Boston City Hospital, Department of Medicine, 818 Harrison Ave, Boston, MA, 02118. Summary: This manual provides information crucial to providing high-quality health care to adult patients who have Human immunodeficiency virus (HIV) infection or Acquired immunodeficiency sydnrome (AIDS). Divided into four sections, it opens with an overview that looks at the natural history of the illness, its diagnosis, and available laboratory tests. Symptoms and signs of AIDS are examined in Section II; these include fever, weight loss, persistent generalized lymphadenopathy, and oral, ocular, dermatologic, pulmonary, neurological, gastrointestinal, hematologic, renal, and psychological signs. In the third section, the manual looks at the many associated opportunistic infections, such as pneumocystis carinii pneumonia (PCP), mycobacterial infections, cryptococcal meningitis, toxoplasmosis, syphilis, cytomegalovirus infection, herpes simplex, varicella zoster, candidiasis, bacterial infections, Kaposi's sarcoma, and AIDS-related lymphoma. The final section studies a variety of topics; they include education and prevention, antiretroviral therapy, treatment of the asymptomatic patient, infection control, reluctance to provide care, dealing with the homosexual or bisexual patient, and legal issues. The supplement updates 17 chapters, in addition to adding three chapters on AIDS in women, in minorities, and in drug-using populations.
•
Adult T-Cell Leukemia Associated With Human T-Lymphotropic Virus Type I (HTLV-I) Infection - North Carolina Source: Morbidity and Mortality Weekly Report; Vol. 36, no. 49. Contact: US Government Printing Office, PO Box 371954, Pittsburgh, PA, 15250-7954, (202) 512-1800, http://www.access.gpo.gov. Massachusetts Medical Society, Medical Publishing Group, CSPO Box 9121, Waltham, MA, 02254, (800) 843-6356. Summary: This report contains epidemiologic notes and reports related to adult T-Cell Leukemia/Lymphoma associated with Human T-cell lymphotropic virus type I (HTLV I) infection in North Carolina. The article focuses on a patient who developed jaundice in December 1986 after several weeks of anorexia, fatigue, and fever. The patient's history throughout hospitalization is then reported.
•
Oral Health Care for Adults With HIV Infection Contact: New York State Department of Health, Statewide AIDS Service Delivery Consortium, AIDS Institute, 5 Penn Plz, New York, NY, 10001, (212) 268-6235, http://www.health.state.ny.us/. Summary: This report reviews the principles of, and considerations for, dentistry in patients with HIV. It explains that patients with HIV may have soft-tissue and periodontal disease requiring frequent evaluations. The report considers HIV and tuberculosis infection control in the dentistry setting and ethical and legal issues of interest to dentists caring for HIV-positive patients. Topics addressed include patient evaluation, treatment planning, diagnosis, and management of soft-tissue lesions and oral ulcers, hairy leukoplakia, papillomavirus infections, Kaposi's sarcoma, lymphoma, and mucosal melanin pigmentation. Gingival and periodontal disease, endodontic
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treatment, oral and maxillofacial surgery, and restorative and prosthetic dental care are also reviewed. •
Changing Issues in the Management of HIV Infection: Chronic Therapy of Early HIV Infection Contact: World Health Communications Incorporated, 41 Madison Ave 40th Fl, New York, NY, 10010, (212) 679-6200, http://www.whci.com. British Overseas Development Administration, 94 Victoria St, London. Summary: This report summarizes the discussion of a panel of physicians, nurses, and healthcare professionals involved in clinical studies of azidothymidine (AZT), also known as retrovir. The report opens with a section looking at the effectiveness of therapy with AZT. Side effects, including anemia, myopathy, lymphoma, headache, nausea, and fatigue are studied in the second section. The final two sections look at maintaining patients on continued therapy and tracking clinical and other information during therapy.
The NLM Gateway15 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.16 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “lymphoma” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total
Items Found 138156 676 1157 970 1 140960
HSTAT17 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.18 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as
15
Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.
16
The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 17 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 18
The HSTAT URL is http://hstat.nlm.nih.gov/.
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AHRQ’s Put Prevention Into Practice.19 Simply search by “lymphoma” (or synonyms) at the following Web site: http://text.nlm.nih.gov.
Coffee Break: Tutorials for Biologists20 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.21 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.22 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.
Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •
CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.
•
Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.
The Genome Project and Lymphoma In the following section, we will discuss databases and references which relate to the Genome Project and lymphoma.
19 Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations. 20 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 21
The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 22 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.
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Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).23 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “lymphoma” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for lymphoma: •
Anaplastic Lymphoma Kinase Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?105590
•
B-cell Cll/lymphoma 10 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?603517
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B-cell Cll/lymphoma 11a Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606557
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B-cell Cll/lymphoma 11b Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606558
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B-cell Cll/lymphoma 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?151430
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B-cell Cll/lymphoma 7a Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601406
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B-cell Cll/lymphoma 7b Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605846
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B-cell Cll/lymphoma 7c Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605847
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B-cell Cll/lymphoma 8 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601889
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B-cell Cll/lymphoma 9 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?602597
•
B-cell Leukemia/lymphoma 3 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?109560
•
B-cell Lymphoma 6 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?109565
•
Burkitt Lymphoma Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?113970
23 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.
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Burkitt Lymphoma Receptor 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601613
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Frequently Rearranged in Advanced T-cell Lymphomas Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?602503
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Gastric Lymphoma, Primary Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?137245
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Hodgkin Lymphoma Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?236000
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Leukemia/lymphoma, Chronic B-cell, 5 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?151441
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Lymphoma, Non-hodgkin, Familial Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605027
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Mucosa-associated Lymphoid Tissue Lymphoma Translocation Gene 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604860
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Pancreatic Lymphoma, Familial Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?602596
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T-cell Leukemia/lymphoma 1a Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?186960
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T-cell Leukemia/lymphoma 4 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?186860
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T-cell Leukemia/lymphoma 6 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604412
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T-cell Lymphoma Invasion and Metastasis 1 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600687
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T-cell Lymphoma Invasion and Metastasis 2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?604709
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T-cell Lymphoma/leukemia 1b Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?603769
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Genes and Disease (NCBI - Map) The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed: •
Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html
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Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html
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Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html
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Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html
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Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html
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Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html
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Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html Entrez
Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: •
3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books
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Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome
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NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/
Physician Resources
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Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide
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OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM
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PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset
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ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo
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Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein
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PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
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Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure
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Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy
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To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “lymphoma” (or synonyms) into the search box and click “Go.” Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database24 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html. The Genome Database25 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing 24
Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html. 25 Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.
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on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “lymphoma” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).
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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on lymphoma can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.
Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to lymphoma. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to lymphoma. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “lymphoma”:
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Guides on lymphoma Lymphoma http://www.nlm.nih.gov/medlineplus/lymphoma.html
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Other guides Hodgkin's Disease http://www.nlm.nih.gov/medlineplus/hodgkinsdisease.html
Within the health topic page dedicated to lymphoma, the following was listed: •
General/Overviews Non-Hodgkin Lymphoma Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_page?item_id=7087 Non-Hodgkin's Lymphoma Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=DS00350 What Is Non-Hodgkin's Lymphoma? Source: American Cancer Society http://www.cancer.org/docroot/cri/content/cri_2_4_1x_what_is_non_hodgkins_l ymphoma_32.asp
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Diagnosis/Symptoms Can Non-Hodgkin's Lymphoma Be Found Early? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_3X_Can_nonHodgkins_lymphoma_be_found_early_32.asp Gene Chips Accurately Diagnose Four Complex Childhood Cancers Source: National Human Genome Research Institute http://www.nih.gov/news/pr/may2001/nhgri-30.htm How Is Non-Hodgkin's Lymphoma Diagnosed? Source: American Cancer Society http://www.cancer.org/docroot/cri/content/cri_2_4_3x_how_is_nonhodgkins_lymphoma_diagnosed_32.asp Understanding Blood Counts Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9452
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Treatment Adult Non-Hodgkin's Lymphoma (PDQ): Treatment Source: National Cancer Institute http://www.cancer.gov/cancerinfo/pdq/treatment/adult-non-hodgkins/patient/
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AIDS-Related Lymphoma (PDQ): Treatment Source: National Cancer Institute http://www.cancer.gov/cancerinfo/pdq/treatment/AIDS-relatedlymphoma/patient/ Biological Therapies: Using the Immune System to Treat Cancer Source: National Cancer Institute http://cis.nci.nih.gov/fact/7_2.htm Blood and Marrow Stem Cell Transplantation Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=2443 Cord Blood FAQs Source: National Marrow Donor Program http://www.marrow.org/FAQS/cord_blood_faqs.html FDA Approves First Radiopharmaceutical Product to Treat Non-Hodgkin's Lymphoma Source: Food and Drug Administration http://www.fda.gov/bbs/topics/ANSWERS/2002/ANS01138.html Long Term and Late Effects of Treatment for Blood-Related Cancers Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9965 Mycosis Fungoides and the Sezary Syndrome (PDQ): Treatment Source: National Cancer Institute http://www.cancer.gov/cancerinfo/pdq/treatment/mycosisfungoides/patient/ New Approaches to Treatment Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_page?item_id=4702 Non-Hodgkin's Lymphoma during Pregnancy (PDQ) Source: National Cancer Institute http://www.cancer.gov/cancerinfo/pdq/treatment/non-hodgkins-duringpregnancy/patient/ Primary CNS Lymphoma (PDQ): Treatment Source: National Cancer Institute http://www.cancer.gov/cancerinfo/pdq/treatment/primary-CNSlymphoma/patient/ Treatment of Extranodal Non-Hodgkin's Lymphoma Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_4X_Treatment_of_Extrano dal_Non-Hodgkins_Lymphoma_32.asp Treatment of Intermediate Grade Non-Hodgkin's Lymphoma -- Stages I and II Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_4X_Treatment_of_Interme diate_Grade_Non-Hodgkins_Lymphoma_--_Stages_I_and_II_32.asp?sitearea= Treatment of Intermediate Grade Non-Hodgkin's Lymphoma -- Stages III and IV and High Grade Lymphomas Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_4X_Treatment_of_Interme
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diate_Grade_Non-Hodgkins_Lymphoma_-_Stages_III_and_IV_and_High_Grade_Lymphomas_32.asp?sitearea= Treatment of Waldenstrom's Macroglobulinemia Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_4X_Treatment_of_Walden stroms_Macroglobulinemia_32.asp What if the Lymphoma Doesn't Respond or Comes Back After Treatment? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_4X_What_if_the_Lympho ma_Doesnt_Respond_or_Comes_Back_After_Treatment_32.asp •
Alternative Therapy Complementary & Alternative Therapies for Leukemia, Lymphoma, Hodgkin's Disease, & Myeloma Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9882
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Specific Conditions/Aspects Choosing a Treatment Facility Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9877 Choosing and Communicating with a Cancer Specialist Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9872 Mantle Cell Lymphoma Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_mat_toc.adp?item_id=9651 Waldenstrom's Macroglobulinemia Source: National Cancer Institute http://cis.nci.nih.gov/fact/6_4.htm
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Children Bone Marrow Transplantation (BMT) and Peripheral Blood Stem Cell Transplantation (PBSCT) Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_4x_Bone_Marrow_Transp lantation_and_Peripheral_Blood_Stem_Cell_Transplantation_9.asp Childhood Cancer: Lymphoma Source: Nemours Foundation http://kidshealth.org/parent/medical/cancer/cancer_lymphoma.html Childhood Non-Hodgkin's Lymphoma (PDQ): Treatment Source: National Cancer Institute http://www.cancer.gov/cancerinfo/pdq/treatment/child-non-hodgkins/patient/
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How Is Childhood Non-Hodgkin's Lymphoma Diagnosed? Source: American Cancer Society http://www.cancer.org/docroot/cri/content/cri_2_4_3x_how_is_childhood_non_ hodgkins_lymphoma_diagnosed_9.asp How Is Childhood Non-Hodgkin's Lymphoma Staged Source: American Cancer Society http://www.cancer.org/docroot/cri/content/cri_2_4_3x_how_is_childhood_non_ hodgkins_lymphoma_staged_9.asp How Is Childhood Non-Hodgkin's Lymphoma Treated? Source: American Cancer Society http://www.cancer.org/docroot/cri/content/cri_2_2_4x_how_is_childhood_nonhodgkins_lymphoma_treated_9.asp What Are the Key Statistics for Childhood Non-Hodgkin's Lymphoma? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_1x_What_are_the_key_sta tistics_for_childhood_non_Hodgkins_lymphoma_9.asp What Are the Risk Factors for Childhood Non-Hodgkin's Lymphoma? Source: American Cancer Society http://www.cancer.org/docroot/cri/content/cri_2_4_2x_what_are_the_risk_factor s_for_childhood_non_hodgkins_lymphoma_9.asp What's New in Childhood Non-Hodgkin's Lymphoma Research and Treatment? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_6x_Whats_new_in_childh ood_non_hodgkins_lymphoma_research_and_treatment_9.asp •
From the National Institutes of Health What You Need to Know about Non-Hodgkin's Lymphomas Source: National Cancer Institute http://www.cancer.gov/cancerinfo/wyntk/non-hodgkins-lymphoma
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Journals/Newsletter Blood & Marrow Transplant Newsletter Source: BMT InfoNet http://www.bmtnews.org/newsletters/
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Latest News Study Links Psoriasis to Lymphoma Cancers Source: 11/17/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14715 .html
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Organizations American Cancer Society http://www.cancer.org/
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Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/hm_lls Lymphoma Research Foundation http://www.lymphoma.org/ National Cancer Institute http://www.cancer.gov/ National Marrow Donor Program http://www.marrow.org/ •
Pictures/Diagrams Atlas of the Body: The Lymphatic System Source: American Medical Association http://www.medem.com/medlb/article_detaillb.cfm?article_ID=/ZZZG0S6CGJC &sub_cat=198
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Prevention/Screening Can Non-Hodgkin's Lymphoma Be Prevented? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_2X_Can_nonHodgkins_lymphoma_be_prevented_32.asp What Are the Risk Factors for Non-Hodgkin's Lymphoma? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_2X_What_are_the_risk_fa ctors_for_non-Hodgkins_lymphoma_32.asp
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Research Gene Expression Profiles Predict Survival of Lymphoma Patients After Chemotherapy Source: National Cancer Institute http://www.nih.gov/news/pr/jun2002/nci-19.htm Researchers Identify Shift Towards More Treatable AIDS-Related Lymphomas Source: National Cancer Institute http://www.nih.gov/news/pr/jun2003/nci-10.htm What's New in Non-Hodgkin's Lymphoma Research and Treatment? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_6X_Whats_new_in_nonHodgkins_lymphoma_research_and_treatment_32.asp
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Statistics Cancer Facts & Figures-2002 Source: American Cancer Society http://www.cancer.org/downloads/STT/CancerFacts&Figures2002TM.pdf Facts and Statistics Source: Leukemia & Lymphoma Society http://www.leukemia-lymphoma.org/all_page?item_id=12486
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What Are the Key Statistics about Non-Hodgkin's Lymphoma? Source: American Cancer Society http://www.cancer.org/docroot/CRI/content/CRI_2_4_1X_What_are_the_key_sta tistics_for_non-Hodgkins_lymphoma_32.asp You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on lymphoma. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •
Cutaneous T-Cell Lymphoma Source: Schaumberg, IL: American Society for Dermatologic Surgery. 2002. 10 p. Contact: Available from American Academy for Dermatologic Surgery. P.O. Box 4014 Schaumberg, IL 60168-4014. Website: www.aboutskinsurgery.com. Summary: This brochure discusses cutaneous T-cell lymphoma (CTCL), a type of cancer of the white blood cells that affects skin and blood. The two main types of CTCL are mycosis fungoides (MF)and Sezary syndrome. MF is the more common condition and primarily affects the skin. It can appear anywhere on the body and usually occurs in stages: a flat, red, scaly patch; a thicker raised plaque, or a larger, ulcerated, mushroomshaped tumor. Sezary syndrome is a more advanced form of MF affecting the blood and characterized by redness all over the body and itchy, hot, sore skin. Treatment includes topical creams, such as cortisone, nitrogen mustard ointment and liquid, and retinoids; oral medications such as corticosteroids, retinoids, and methotrexate; chemotherapy; light therapy; and radiation. These treatments seek to alleviate itching and burning and to eliminate the skin patches and tumors in MF. In Sezary syndrome, the goal of treatment is to reduce skin redness and abnormal lymphocytes in the blood. 6 figures.
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HIV-Positive Patients Talk About. Non-Hodgkins Lymphoma Contact: Ortho Pharmaceutical Corporation, Biotech Division, PO Box 300, Raritan, NJ, 08869-0602, (908) 218-7010. Summary: This brochure discusses non-Hodgkins lymphoma and how it can affect a person with the human immunodeficiency virus (HIV). The brochure uses the personal anecdotal statements of HIV-positive persons at various points throughout the brochure to give the reader a sense of what this disease is like from a non-medical view, thereby letting the reader know that he or she is not alone in this experience. It describes non-
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Hodgkins lymphoma and its symptoms. The brochure explains how this form of cancer can affect the life span of an HIV-positive person, and how this lymphoma is treated. The side effects and adverse reactions that persons with HIV and non-Hodgkins lymphoma may experience due to chemotherapy and other medical treatments are listed. It describes the reasons why someone with HIV and lymphoma is especially prone to fatigue and anemia and how to avoid these adverse reactions. •
Cutaneous T-Cell Lymphoma, Mycosis Fungoides Source: Kirksville, MO: American Osteopathic College of Dermatology (AOCD). 2001. 2 p. Contact: Available online from American Osteopathic College of Dermatology. 1501 East Illinois Street, P.O. Box 7525, Kirksville, MO 63501. (800) 449-2623 or (660) 665-2184. Fax (660) 627-2623. E-mail:
[email protected]. Website: www.aocd.org/skin/dermatologic_diseases/ index.html. Summary: This fact sheet provides people who have cutaneous T cell lymphoma (CTCL) with information on this collection of related cancers of the lymphatic system. In CTCL, some of the body's white blood cells become malignant, are drawn to the skin, and are deposited there. CTCL is a subtype of non-Hodgkin's lymphoma that develops slowly. The most common type of CTCL is mycosis fungoides (MF). Other types are the Sezary syndrome, hypopigmented MF, or lymphomatoid papulosis. If CTCL progresses unchecked, raised growths may form on the skin after a period of years. Although most cancers are treated with surgery and chemotherapy, slow growing forms are less curable with chemotherapy, and surgery is usually not an option. Treatment is based mainly on the size, extent, and location of CTCL, as well as the patient's age and general health. Early, very limited CTCL can be treated with a potent topical steroid cream. Phototherapy is useful if larger body areas are affected. Topical chemotherapy is more aggressive and less widely used. A systemic therapy is used if other options fail or if CTCL is more advanced. These options include Bexarotene capsules, intravenous fusion protein, interferon alpha, or methotrexate. Systemic treatments may be combined for better results. Total skin electron beam radiation therapy may also be used for advanced CTCL. Experimental treatments include chemotherapy with Leustatin or Nipent alone or in combination with interleukin-2. Prognosis is good for people diagnosed at early stages. 2 figures.
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Lymphoma Contact: University of New Mexico School of Medicine, New Mexico AIDS Education and Training Center, New Mexico AIDS InfoNet, PO Box 810, Arroyo Seco, NM, 87514, (505) 776-8032, http://www.aidsinfonet.org. Summary: This information sheet, for individuals with the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS), provides information about lymphoma. It explains that lymphoma refers to cancers that involve a type of white blood cell. AIDS-related lymphoma is sometimes called Non-Hodgkin's Lymphoma (NHL). The information sheet discusses the diagnosis, cause, and treatment of lymphoma and reports that the use of combination anti-viral therapy has reduced the number of new cases of lymphoma, particularly central nervous system lymphoma.
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Patient Education: Cutaneous T-Cell Lymphoma Source: Nurse Practitioner. 25(4): 97. April 2000.
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Summary: This journal article uses a question and answer format to provide people who have cutaneous T cell lymphoma (CTCL) with information on the signs, symptoms, diagnosis, and treatment of this malignant lymphoma, which is often mistaken for common skin conditions such as eczema and psoriasis. Malignant cells in the lymph tissue appear on the skin in increasing numbers. Mycosis fungoides (MF) and Sezary syndrome are the main types of CTCL. The skin manifestations of MF are flat, pink to yellowish-tan lesions that may itch. Over time, the lesions may become raised and darker red than patches, thus becoming plaques. They may already be tumors or become tumors. Sezary syndrome begins as reddened skin that resembles a rash all over the body. The diagnosis of CTCL is based on a person's symptoms, a physical examination, and laboratory findings. Treatment depends on the extent of the disease. Early stages may be treated with topical steroids or biologic response modifiers. Chemotherapy and radiation therapy may be used in later stages. The article offers skin care tips and suggestions on fighting the disease. •
People With AIDS Are 60 - 100 Times More Likely to Contract Non - Hodgkin's Lymphoma (NHL) Contact: Interscience Communications Limited, 1615 L St NW Ste 1150, Washington, DC, 20036, (800) 243-7645. Summary: This volunteer recruitment package contains information related to a clinical trial of a drug for treatment of relapsed or refractory AIDS-related non-Hodgkin's lymphoma. The folder includes a five-page list of sites across the United States where the efficacy of mitoguazone dihydrochloride (MGBG) is being tested. Each listing includes the name of the physician, research administrator, and research nurse. A summary of patient characteristics, inclusion criteria, exclusion criteria, and a treatment plan are also included. The folder also contains three papers that examine the potential anti-tumor activity of MGBG and initial results from the study of its application among patients with AIDS-related lymphoma. Healthfinder™
Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: •
Leukemia, Lymphomas, and Myeloma: About the Diseases Summary: Browse this site for patient information about leukemia, lymphomas, and myeloma. Source: Leukemia & Lymphoma Society http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2292
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Lymphoma Focus Summary: Lymphoma Focus delivers information that represents the most current body of knowledge on lymphoma, enabling patients to make informed treatment and quality of life decisions and also assisting Source: Lymphoma Research Foundation of America http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6329
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What You Need To Know About™ Non-Hodgkin's Lymphoma Summary: This booklet discusses symptoms, diagnosis, and treatment. It also has information about resources and sources of support for people with non-Hodgkin's lymphoma. Source: Cancer Information Service, National Cancer Institute http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7124 The NIH Search Utility
The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to lymphoma. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/specific.htm
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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/
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Med Help International: http://www.medhelp.org/HealthTopics/A.html
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Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/
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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/
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WebMDHealth: http://my.webmd.com/health_topics
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Associations and Lymphoma The following is a list of associations that provide information on and resources relating to lymphoma: •
Leukemia and Lymphoma Society Telephone: (914) 949-5213 Toll-free: (800) 955-4572 Fax: (914) 949-6691 Email:
[email protected] Web Site: http://www.leukemia-lymphoma.org Background: The Leukemia and Lymphoma Society is a national voluntary health agency dedicated to curing leukemia, lymphoma, Hodgkin's disease and myeloma, and to improving the quality of life of patients and their families. The Society was established in 1949 as the de Villiers Foundation. In 2000, the Society changed its name from The Leukemia Society of America to The Leukemia and Lymphoma Society to emphasize its commitment to fighting all blood-related cancers. Today, the Society supports the following major programs: research, patient services, public and professional education, advocacy and community services. With headquarters in White Plains, NY, the Society has chapter offices across the United States and is a single corporation doing business under New York State not-for-profit corporate laws. Relevant area(s) of interest: Lymphoma
•
Lymphoma Research Foundation Telephone: (212) 349-2910 Toll-free: (800) 235-6848 Fax: (212) 349-2886 Email:
[email protected] Web Site: http://www.lymphoma.org Background: The Lymphoma Research Foundation of America (LRFA) and Cure for Lymphoma Foundation merged to become the Lymphoma Research Foundation. This is a national voluntary nonprofit organization dedicated to funding lymphoma research and providing comprehensive educational and support programs to increase awareness and knowledge of lymphoma nationwide. Lymphoma refers to cancer of the lymphatic system, which is a network of glands and vessels that circulate a thin, watery fluid known as lymph throughout the body. A network of small organs called lymph nodes produce and store certain infection-fighting white blood cells; play a role in manufacturing antibodies; and filter out microorganisms and other foreign bodies within lymph. Lymphoma is classified into two major categories that are distinguished by cell type: Hodgkin's disease and non-Hodgkin's lymphoma. Both may be characterized by similar symptoms including night sweats, painless swelling of lymph nodes, fever, fatigue, itching, and weight loss. The Lymphoma Research Foundation of America was established in 1991 and currently has approximately 17,050 members. The Foundation's primary mission is to fund lymphoma research at universities and cancer centers across the nation through annual research grants and fellowship awards. In addition, the LRFA provides a one-on-one 'phone buddy support program' that matches affected individuals by cell type, stage and grade, or treatment plan; offers a lymphoma helpline that directs affected individuals and family members to cancer resources and clinical trial information; and conducts free support groups. The Foundation also holds an annual patient education forum; conducts an annual educational drive to inform the
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public about lymphoma; and has a web site on the Internet that features news on research and clinical trials and provides links to additional resources. The LRFA also publishes 'Lymphoma Update,' a quarterly newsletter that is circulated to over 30,000 patients, family members, and health care providers. Relevant area(s) of interest: Lymphoma •
Lymphoma Research Foundation Canada Fax: (604) 631-3232 Email:
[email protected] Web Site: http://www.lymphoma.ca Background: The Lymphoma Research Foundation Canada (LRFC) is a not-for-profit organization that was founded in 1998 to provide support for those affected by lymphoma and for individuals who conduct research in the diagnosis, treatment, and cure of these diseases. Lymphoma is a group of cancers affecting the lymphatic system, which is a network of glands and vessels that collect the thin, watery fluid known as lymph from different areas of the body and drain it into the bloodstream. The lymphatic system also functions as an essential part of the immune system. Lymphoma may be classified into two major categories that are distinguished by cell type: Hodgkin's disease and non-Hodgkin's lymphoma. Both may be characterized by similar symptoms including night sweats, painless swelling of lymph nodes, fever, fatigue, itching, and weight loss. The focus of the Lymphoma Research Foundation Canada is on lymphoma issues and treatment in Canada. The LRCF provides information on research currently being conducted in Canada; offers understandable reports on the lymphatic system and the incidence, classification, causes, diagnosis, staging, and treatment of lymphomas; and has a web site on the Internet.
Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to lymphoma. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with lymphoma. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about lymphoma. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at
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http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “lymphoma” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “lymphoma”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “lymphoma” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months. The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “lymphoma” (or a synonym) into the search box, and click “Submit Query.”
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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.
Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.26
Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.
Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of
26
Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.
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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)27: •
Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/
•
Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)
•
Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm
•
California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html
•
California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html
•
California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html
•
California: Gateway Health Library (Sutter Gould Medical Foundation)
•
California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/
•
California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp
•
California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html
•
California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/
•
California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/
•
California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/
•
California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html
•
California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/
•
Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/
•
Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/
•
Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/
27
Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.
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•
Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml
•
Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm
•
Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html
•
Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm
•
Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp
•
Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/
•
Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm
•
Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html
•
Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/
•
Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm
•
Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/
•
Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/
•
Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/
•
Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm
•
Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html
•
Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm
•
Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/
•
Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/
•
Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10
•
Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/
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•
Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html
•
Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp
•
Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp
•
Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/
•
Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html
•
Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm
•
Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp
•
Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/
•
Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html
•
Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/
•
Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm
•
Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/
•
Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html
•
Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm
•
Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330
•
Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)
•
National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html
•
National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/
•
National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/
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•
Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm
•
New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/
•
New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm
•
New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm
•
New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/
•
New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html
•
New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/
•
New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html
•
New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/
•
Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm
•
Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp
•
Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/
•
Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/
•
Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml
•
Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html
•
Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html
•
Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml
•
Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp
•
Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm
•
Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/
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•
South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp
•
Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/
•
Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/
•
Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72
335
ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •
ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html
•
MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp
•
Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/
•
Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html
•
On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/
•
Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp
•
Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm
Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a).
Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •
Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical
•
MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html
•
Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/
•
Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine
337
LYMPHOMA DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 3-dimensional: 3-D. A graphic display of depth, width, and height. Three-dimensional radiation therapy uses computers to create a 3-dimensional picture of the tumor. This allows doctors to give the highest possible dose of radiation to the tumor, while sparing the normal tissue as much as possible. [NIH] Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal Pain: Sensation of discomfort, distress, or agony in the abdominal region. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Ablation: The removal of an organ by surgery. [NIH] Abscess: Accumulation of purulent material in tissues, organs, or circumscribed spaces, usually associated with signs of infection. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acitretin: An oral retinoid effective in the treatment of psoriasis. It is the major metabolite of etretinate with the advantage of a much shorter half-life when compared with etretinate. [NIH]
Acquired Immunodeficiency Syndrome: An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive Tlymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993. [NIH] Actin: Essential component of the cell skeleton. [NIH] Acute leukemia: A rapidly progressing cancer of the blood-forming tissue (bone marrow). [NIH]
Acute lymphoblastic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphocytic leukemia. [NIH] Acute lymphocytic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphoblastic leukemia. [NIH] Acute myelogenous leukemia: AML. A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myeloid leukemia or acute nonlymphocytic leukemia. [NIH] Acute myeloid leukemia: AML. A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myelogenous leukemia or acute nonlymphocytic leukemia. [NIH]
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Acute nonlymphocytic leukemia: A quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. Also called acute myeloid leukemia or acute myelogenous leukemia. [NIH] Acute renal: A condition in which the kidneys suddenly stop working. In most cases, kidneys can recover from almost complete loss of function. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenosylmethionine Decarboxylase: An enzyme that catalyzes the decarboxylation of Sadenosyl-L-methionine to yield 5'-deoxy-(5'-),3-aminopropyl-(1), methylsulfonium salt. It is one of the enzymes responsible for the synthesis of spermidine from putrescine. EC 4.1.1.50. [NIH]
Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adnexa: The appendages of the eye, as the lacrimal apparatus, the eyelids, and the extraocular muscles. [NIH] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adrenal Glands: Paired glands situated in the retroperitoneal tissues at the superior pole of each kidney. [NIH] Adrenal insufficiency: The reduced secretion of adrenal glands. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerosol: A solution of a drug which can be atomized into a fine mist for inhalation therapy. [EU]
Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]
Dictionary 339
Age-Adjusted: Summary measures of rates of morbidity or mortality in a population using statistical procedures to remove the effect of age differences in populations that are being compared. Age is probably the most important and the most common variable in determining the risk of morbidity and mortality. [NIH] Agenesis: Lack of complete or normal development; congenital absence of an organ or part. [NIH]
Aggressiveness: The quality of being aggressive (= characterized by aggression; militant; enterprising; spreading with vigour; chemically active; variable and adaptable). [EU] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] Alkylating Agents: Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases. [NIH]
Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allergen: An antigenic substance capable of producing immediate-type hypersensitivity (allergy). [EU] Allium: A genus of liliaceous herbs containing onions (Allium cepa), garlic (Allium sativum), and others; many produce pungent, often bacteriostatic and physiologically active compounds and are used as food, condiment, and medicament, the latter in traditional medicine. [NIH] Allo: A female hormone. [NIH] Allogeneic: Taken from different individuals of the same species. [NIH] Allogeneic bone marrow transplantation: A procedure in which a person receives stem cells, the cells from which all blood cells develop, from a compatible, though not genetically identical, donor. [NIH] Allograft: An organ or tissue transplant between two humans. [NIH] Alopecia: Absence of hair from areas where it is normally present. [NIH]
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Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Aluminum: A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98. [NIH] Alveolar Bone Loss: The resorption of bone in the supporting structures of the maxilla or mandible as a result of periodontal disease. [NIH] Alveolar Process: The thickest and spongiest part of the maxilla and mandible hollowed out into deep cavities for the teeth. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or accident from becoming as bad as it otherwise would. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Ampulla: A sac-like enlargement of a canal or duct. [NIH] Amyloidosis: A group of diseases in which protein is deposited in specific organs (localized amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (with no known cause) or secondary (caused by another disease, including some types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands. [NIH] Anabolic: Relating to, characterized by, or promoting anabolism. [EU] Anabolic Steroids: Chemical derivatives of testosterone that are used for anabolic promotion of growth and repair of body tissues and the development of male sexual characteristics. [NIH]
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Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anaplastic: A term used to describe cancer cells that divide rapidly and bear little or no resemblance to normal cells. [NIH] Anaplastic large cell lymphoma: A rare agressive form of lymphoma (cancer that begins in cells of the lymphatic system) that is usually of T-cell origin. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anergy: Absence of immune response to particular substances. [NIH] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angiogenesis inhibitor: A substance that may prevent the formation of blood vessels. In anticancer therapy, an angiogenesis inhibitor prevents the growth of blood vessels from surrounding tissue to a solid tumor. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Annealing: The spontaneous alignment of two single DNA strands to form a double helix. [NIH]
Anogenital: Pertaining to the anus and external genitals. [EU] Anoikis: Apoptosis triggered by loss of contact with the extracellular matrix. [NIH] Anomalies: Birth defects; abnormalities. [NIH] Anorexia: Lack or loss of appetite for food. Appetite is psychologic, dependent on memory and associations. Anorexia can be brought about by unattractive food, surroundings, or company. [NIH] Anterior chamber: The space in front of the iris and behind the cornea. [NIH] Anthracycline: A member of a family of anticancer drugs that are also antibiotics. [NIH] Antiangiogenic: Having to do with reducing the growth of new blood vessels. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms.
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[NIH]
Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Antibody therapy: Treatment with an antibody, a substance that can directly kill specific tumor cells or stimulate the immune system to kill tumor cells. [NIH] Antibody-Dependent Cell Cytotoxicity: The phenomenon of antibody-mediated target cell destruction by non-sensitized effector cells. The identity of the target cell varies, but it must possess surface IgG whose Fc portion is intact. The effector cell is a "killer" cell possessing Fc receptors. It may be a lymphocyte lacking conventional B- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Antidote: A remedy for counteracting a poison. [EU] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]
Antifungal: Destructive to fungi, or suppressing their reproduction or growth; effective against fungal infections. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Antigen-presenting cell: APC. A cell that shows antigen on its surface to other cells of the immune system. This is an important part of an immune response. [NIH] Anti-infective: An agent that so acts. [EU] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Antimetabolite: A chemical that is very similar to one required in a normal biochemical reaction in cells. Antimetabolites can stop or slow down the reaction. [NIH] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antineoplastic Agents: Substances that inhibit or prevent the proliferation of neoplasms. [NIH]
Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH]
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Antiproliferative: Counteracting a process of proliferation. [EU] Antiserum: The blood serum obtained from an animal after it has been immunized with a particular antigen. It will contain antibodies which are specific for that antigen as well as antibodies specific for any other antigen with which the animal has previously been immunized. [NIH] Antiviral: Destroying viruses or suppressing their replication. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Apheresis: Components plateletpheresis. [NIH]
being
separated
out,
as
leukapheresis,
plasmapheresis,
Aplasia: Lack of development of an organ or tissue, or of the cellular products from an organ or tissue. [EU] Apnea: A transient absence of spontaneous respiration. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Aptitude: The ability to acquire general or special types of knowledge or skill. [NIH] Aqueous: Having to do with water. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arginine butyrate: A substance that is being studied as a treatment for cancer. [NIH] Arsenic trioxide: An anticancer drug that induces programmed cell death (apoptosis) in certain cancer cells. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Asbestos: Fibrous incombustible mineral composed of magnesium and calcium silicates with or without other elements. It is relatively inert chemically and used in thermal insulation and fireproofing. Inhalation of dust causes asbestosis and later lung and gastrointestinal neoplasms. [NIH] Asparaginase: A hydrolase enzyme that converts L-asparagine and water to L-aspartate and NH3. EC 3.5.1.1. [NIH] Aspartate: A synthetic amino acid. [NIH] Aspartic: The naturally occurring substance is L-aspartic acid. One of the acidic-amino-acids is obtained by the hydrolysis of proteins. [NIH] Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter. [NIH] Aspiration: The act of inhaling. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU]
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Astringents: Agents, usually topical, that cause the contraction of tissues for the control of bleeding or secretions. [NIH] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Astrocytoma: A tumor that begins in the brain or spinal cord in small, star-shaped cells called astrocytes. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atopic: Pertaining to an atopen or to atopy; allergic. [EU] Atrial: Pertaining to an atrium. [EU] Atrial Flutter: Rapid, irregular atrial contractions due to an abnormality of atrial excitation. [NIH]
Atrioventricular: Pertaining to an atrium of the heart and to a ventricle. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuated: Strain with weakened or reduced virulence. [NIH] Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Autoantibodies: Antibodies that react with self-antigens (autoantigens) of the organism that produced them. [NIH] Autoantigens: Endogenous tissue constituents that have the ability to interact with autoantibodies and cause an immune response. [NIH] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autologous: Taken from an individual's own tissues, cells, or DNA. [NIH] Autologous bone marrow transplantation: A procedure in which bone marrow is removed from a person, stored, and then given back to the person after intensive treatment. [NIH]
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Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH] Autopsy: Postmortem examination of the body. [NIH] Avian: A plasmodial infection in birds. [NIH] Avian Leukosis: A group of transmissible viral diseases of chickens and turkeys. Liver tumors are found in most forms, but tumors can be found elsewhere. [NIH] Avidity: The strength of the interaction of an antiserum with a multivalent antigen. [NIH] Backcross: A cross between a hybrid and either one of its parents. [NIH] Bacteremia: The presence of viable bacteria circulating in the blood. Fever, chills, tachycardia, and tachypnea are common acute manifestations of bacteremia. The majority of cases are seen in already hospitalized patients, most of whom have underlying diseases or procedures which render their bloodstreams susceptible to invasion. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Infections: Infections by bacteria, general or unspecified. [NIH] Bacterial toxin: A toxic substance, made by bacteria, that can be modified to kill specific tumor cells without harming normal cells. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacteriostatic: 1. Inhibiting the growth or multiplication of bacteria. 2. An agent that inhibits the growth or multiplication of bacteria. [EU] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Base Pair Mismatch: The presence of an uncomplementary base in double-stranded DNA caused by spontaneous deamination of cytosine or adenine, mismatching during homologous recombination, or errors in DNA replication. Multiple, sequential base pair
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mismatches lead to formation of heteroduplex DNA (nucleic acid heteroduplexes). [NIH] Basophil: A type of white blood cell. Basophils are granulocytes. [NIH] BCL-1: Codes for cyclin D1, a stimulatory component of the cell cycle clock. Involved in breast, head and neck cancers. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]
Bewilderment: Impairment or loss of will power. [NIH] Bexarotene: An anticancer drug used to decrease the growth of some types of cancer cells. Also called LGD1069. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile Ducts: Tubes that carry bile from the liver to the gallbladder for storage and to the small intestine for use in digestion. [NIH] Bile Pigments: Pigments that give a characteristic color to bile including: bilirubin, biliverdine, and bilicyanin. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Tract: The gallbladder and its ducts. [NIH] Binding Sites: The reactive parts of a macromolecule that directly participate in its specific combination with another molecule. [NIH] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biopsy specimen: Tissue removed from the body and examined under a microscope to determine whether disease is present. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived
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constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotin: Hexahydro-2-oxo-1H-thieno(3,4-d)imidazole-4-pentanoic acid. Growth factor present in minute amounts in every living cell. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk.The biotin content of cancerous tissue is higher than that of normal tissue. [NIH] Bladder: The organ that stores urine. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [NIH] Bleomycin: A complex of related glycopeptide antibiotics from Streptomyces verticillus consisting of bleomycin A2 and B2. It inhibits DNA metabolism and is used as an antineoplastic, especially for solid tumors. [NIH] Bloating: Fullness or swelling in the abdomen that often occurs after meals. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]
Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blotting and transferred to strips of nitrocellulose paper. The blots are then detected by radiolabeled antibody probes. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone marrow biopsy: The removal of a sample of tissue from the bone marrow with a needle for examination under a microscope. [NIH] Bone Marrow Cells: Cells contained in the bone marrow including fat cells, stromal cells, megakaryocytes, and the immediate precursors of most blood cells. [NIH] Bone Marrow Transplantation: The transference of bone marrow from one human or animal to another. [NIH] Bone metastases: Cancer that has spread from the original (primary) tumor to the bone. [NIH]
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Bone scan: A technique to create images of bones on a computer screen or on film. A small amount of radioactive material is injected into a blood vessel and travels through the bloodstream; it collects in the bones and is detected by a scanner. [NIH] Boron: A trace element with the atomic symbol B, atomic number 5, and atomic weight 10.81. Boron-10, an isotope of boron, is used as a neutron absorber in boron neutron capture therapy. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [NIH] Brain Hypoxia: Lack of oxygen leading to unconsciousness. [NIH] Brain Infarction: The formation of an area of necrosis in the brain, including the cerebral hemispheres (cerebral infarction), thalami, basal ganglia, brain stem (brain stem infarctions), or cerebellum secondary to an insufficiency of arterial or venous blood flow. [NIH] Brain Ischemia: Localized reduction of blood flow to brain tissue due to arterial obtruction or systemic hypoperfusion. This frequently occurs in conjuction with brain hypoxia. Prolonged ischemia is associated with brain infarction. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]
Breakdown: A physical, metal, or nervous collapse. [NIH] Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Buffers: A chemical system that functions to control the levels of specific ions in solution. When the level of hydrogen ion in solution is controlled the system is called a pH buffer. [NIH]
Bullous: Pertaining to or characterized by bullae. [EU] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Cachexia: General ill health, malnutrition, and weight loss, usually associated with chronic disease. [NIH] Calcineurin: A calcium- and calmodulin-binding protein present in highest concentrations in the central nervous system. Calcineurin is composed of two subunits. A catalytic subunit, calcineurin A, and a regulatory subunit, calcineurin B, with molecular weights of about 60 kD and 19 kD, respectively. Calcineurin has been shown to dephosphorylate a number of phosphoproteins including histones, myosin light chain, and the regulatory subunit of cAMP-dependent protein kinase. It is involved in the regulation of signal transduction and is the target of an important class of immunophilin-immunosuppressive drug complexes in T-lymphocytes that act by inhibiting T-cell activation. EC 3.1.3.-. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with
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phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calmodulin: A heat-stable, low-molecular-weight activator protein found mainly in the brain and heart. The binding of calcium ions to this protein allows this protein to bind to cyclic nucleotide phosphodiesterases and to adenyl cyclase with subsequent activation. Thereby this protein modulates cyclic AMP and cyclic GMP levels. [NIH] Camptothecin: An alkaloid isolated from the stem wood of the Chinese tree, Camptotheca acuminata. This compound selectively inhibits the nuclear enzyme DNA topoisomerase. Several semisynthetic analogs of camptothecin have demonstrated antitumor activity. [NIH] Candidiasis: Infection with a fungus of the genus Candida. It is usually a superficial infection of the moist cutaneous areas of the body, and is generally caused by C. albicans; it most commonly involves the skin (dermatocandidiasis), oral mucous membranes (thrush, def. 1), respiratory tract (bronchocandidiasis), and vagina (vaginitis). Rarely there is a systemic infection or endocarditis. Called also moniliasis, candidosis, oidiomycosis, and formerly blastodendriosis. [EU] Candidosis: An infection caused by an opportunistic yeasts that tends to proliferate and become pathologic when the environment is favorable and the host resistance is weakened. [NIH]
Canonical: A particular nucleotide sequence in which each position represents the base more often found when many actual sequences of a given class of genetic elements are compared. [NIH] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carboplatin: An organoplatinum compound that possesses antineoplastic activity. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]
Cardiac: Having to do with the heart. [NIH] Cardiotoxicity: Toxicity that affects the heart. [NIH] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH]
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Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group. [NIH] Caspase: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Castor Oil: Oil obtained from seeds of Ricinus communis that is used as a cathartic and as a plasticizer. [NIH] Cauda Equina: The lower part of the spinal cord consisting of the lumbar, sacral, and coccygeal nerve roots. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cecum: The beginning of the large intestine. The cecum is connected to the lower part of the small intestine, called the ileum. [NIH] Celiac Disease: A disease characterized by intestinal malabsorption and precipitated by gluten-containing foods. The intestinal mucosa shows loss of villous structure. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Adhesion: Adherence of cells to surfaces or to other cells. [NIH] Cell Communication: Any of several ways in which living cells of an organism communicate with one another, whether by direct contact between cells or by means of chemical signals carried by neurotransmitter substances, hormones, and cyclic AMP. [NIH] Cell Count: A count of the number of cells of a specific kind, usually measured per unit volume of sample. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell Extracts: Preparations of cell constituents or subcellular materials, isolates, or substances. [NIH] Cell Lineage: The developmental history of cells as traced from the first division of the original cell or cells in the embryo. [NIH]
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Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Size: The physical dimensions of a cell. It refers mainly to changes in dimensions correlated with physiological or pathological changes in cells. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cell Transplantation: Transference of cells within an individual, between individuals of the same species, or between individuals of different species. [NIH] Cellular metabolism: The sum of all chemical changes that take place in a cell through which energy and basic components are provided for essential processes, including the synthesis of new molecules and the breakdown and removal of others. [NIH] Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Central Nervous System Infections: Pathogenic infections of the brain, spinal cord, and meninges. DNA virus infections; RNA virus infections; bacterial infections; mycoplasma infections; Spirochaetales infections; fungal infections; protozoan infections; helminthiasis; and prion diseases may involve the central nervous system as a primary or secondary process. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral hemispheres: The two halves of the cerebrum, the part of the brain that controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. The right hemisphere controls muscle movement on the left side of the body, and the left hemisphere controls muscle movement on the right side of the body. [NIH] Cerebrospinal: Pertaining to the brain and spinal cord. [EU] Cerebrospinal fluid: CSF. The fluid flowing around the brain and spinal cord. Cerebrospinal fluid is produced in the ventricles in the brain. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the
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relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemokines: Class of pro-inflammatory cytokines that have the ability to attract and activate leukocytes. They can be divided into at least three structural branches: C (chemokines, C), CC (chemokines, CC), and CXC (chemokines, CXC), according to variations in a shared cysteine motif. [NIH] Chemoprevention: The use of drugs, vitamins, or other agents to try to reduce the risk of, or delay the development or recurrence of, cancer. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chloroform: A commonly used laboratory solvent. It was previously used as an anesthetic, but was banned from use in the U.S. due to its suspected carcinogenecity. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Chondrosarcoma: A type of cancer that forms in cartilage. [NIH] Choriocarcinoma: A malignant tumor of trophoblastic epithelium characterized by secretion of large amounts of chorionic gonadotropin. It usually originates from chorionic products of conception (i.e., hydatidiform mole, normal pregnancy, or following abortion), but can originate in a teratoma of the testis, mediastinum, or pineal gland. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chromosome Aberrations: Deviations from the normal number or structure of chromosomes, not necessarily associated with disease. [NIH] Chromosome Abnormalities: Defects in the structure or number of chromosomes resulting in structural aberrations or manifesting as disease. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic Fatigue Syndrome: Fatigue caused by the combined effects of different types of prolonged fatigue. [NIH] Chronic granulocytic leukemia: A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myelogenous leukemia or chronic myeloid leukemia. [NIH] Chronic leukemia: A slowly progressing cancer of the blood-forming tissues. [NIH] Chronic lymphocytic leukemia: A slowly progressing disease in which too many white blood cells (called lymphocytes) are found in the body. [NIH] Chronic myelogenous leukemia: CML. A slowly progressing disease in which too many white blood cells are made in the bone marrow. Also called chronic myeloid leukemia or chronic granulocytic leukemia. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or
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transplantation to replace the work of the kidneys. [NIH] Cicatricial: Ectropion due to scar tissue on the margins or the surrounding surfaces of the eyelids. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [NIH] Ciliary Body: A ring of tissue extending from the scleral spur to the ora serrata of the retina. It consists of the uveal portion and the epithelial portion. The ciliary muscle is in the uveal portion and the ciliary processes are in the epithelial portion. [NIH] Circulatory system: The system that contains the heart and the blood vessels and moves blood throughout the body. This system helps tissues get enough oxygen and nutrients, and it helps them get rid of waste products. The lymph system, which connects with the blood system, is often considered part of the circulatory system. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner, and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Cisplatin: An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle. [NIH] Claviceps: A genus of ascomycetous fungi, family Clavicipitaceae, order Hypocreales, parasitic on various grasses. The sclerotia contain several toxic alkaloids. Claviceps purpurea on rye causes ergotism. [NIH] Cleave: A double-stranded cut in DNA with a restriction endonuclease. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]
Clinical Protocols: Precise and detailed plans for the study of a medical or biomedical problem and/or plans for a regimen of therapy. [NIH] Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Clone: The term "clone" has acquired a new meaning. It is applied specifically to the bits of inserted foreign DNA in the hybrid molecules of the population. Each inserted segment originally resided in the DNA of a complex genome amid millions of other DNA segment. [NIH]
Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Codons: Any triplet of nucleotides (coding unit) in DNA or RNA (if RNA is the carrier of primary genetic information as in some viruses) that codes for particular amino acid or signals the beginning or end of the message. [NIH] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Cognition: Intellectual or mental process whereby an organism becomes aware of or obtains knowledge. [NIH]
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Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics. [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colony-Stimulating Factors: Glycoproteins found in a subfraction of normal mammalian plasma and urine. They stimulate the proliferation of bone marrow cells in agar cultures and the formation of colonies of granulocytes and/or macrophages. The factors include interleukin-3 (IL-3), granulocyte colony-stimulating factor (G-CSF), macrophage colonystimulating factor (M-CSF), and granulocyte-macrophage colony-stimulating factor (GMCSF). [NIH] Colorectal: Having to do with the colon or the rectum. [NIH] Colorectal Cancer: Cancer that occurs in the colon (large intestine) or the rectum (the end of the large intestine). A number of digestive diseases may increase a person's risk of colorectal cancer, including polyposis and Zollinger-Ellison Syndrome. [NIH] Colorectal Neoplasms: Tumors or cancer of the either the colon or rectum or both. The most frequent malignant tumor in the United States. Etiological factors which increase the risk of colorectal cancer include chronic ulcerative colitis, familial polyposis of the colon, exposure to asbestos, irradiation of the cervix. [NIH] Combination chemotherapy: Treatment using more than one anticancer drug. [NIH] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Combined Modality Therapy: The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, radioimmunotherapy, chemoradiotherapy, cryochemotherapy, and salvage therapy are seen most frequently, but their combinations with each other and surgery are also used. [NIH] Communication Barriers: Those factors, such as language or sociocultural relationships, which interfere in the meaningful interpretation and transmission of ideas between individuals or groups. [NIH] Communis: Common tendon of the rectus group of muscles that surrounds the optic foramen and a portion of the superior orbital fissure, to the anterior margin of which it is attached at the spina recti lateralis. [NIH] Comorbidity: The presence of co-existing or additional diseases with reference to an initial diagnosis or with reference to the index condition that is the subject of study. Comorbidity may affect the ability of affected individuals to function and also their survival; it may be used as a prognostic indicator for length of hospital stay, cost factors, and outcome or survival. [NIH]
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Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementarity Determining Regions: Three regions (CDR1, CDR2 and CDR3) of amino acid sequence in theimmunoglobulin variable region that are highly divergent. Together the CDRs from the light and heavy immunoglobulin chains form a surface that is complementary to the antigen. These regions are also present in other members of the immunoglobulin superfamily, for example, T-cell receptors (receptors, antigen, T-cell). [NIH] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementation: The production of a wild-type phenotype when two different mutations are combined in a diploid or a heterokaryon and tested in trans-configuration. [NIH] Complete remission: The disappearance of all signs of cancer. Also called a complete response. [NIH] Complete response: The disappearance of all signs of cancer in response to treatment. This does not always mean the cancer has been cured. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body,
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taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized axial tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called CAT scan, computed tomography (CT scan), or computerized tomography. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Concomitant: Accompanying; accessory; joined with another. [EU] Confounding: Extraneous variables resulting in outcome effects that obscure or exaggerate the "true" effect of an intervention. [NIH] Confusion: A mental state characterized by bewilderment, emotional disturbance, lack of clear thinking, and perceptual disorientation. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Consolidation: The healing process of a bone fracture. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Contact dermatitis: Inflammation of the skin with varying degrees of erythema, edema and vesinculation resulting from cutaneous contact with a foreign substance or other exposure. [NIH]
Continuous infusion: The administration of a fluid into a blood vessel, usually over a prolonged period of time. [NIH] Contractility: Capacity for becoming short in response to a suitable stimulus. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [NIH] Conventional therapy: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional treatment. [NIH] Conventional treatment: A currently accepted and widely used treatment for a certain type of disease, based on the results of past research. Also called conventional therapy. [NIH] Cooperative group: A group of physicians, hospitals, or both formed to treat a large number
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of persons in the same way so that new treatment can be evaluated quickly. Clinical trials of new cancer treatments often require many more people than a single physician or hospital can care for. [NIH] Coordination: Muscular or motor regulation or the harmonious cooperation of muscles or groups of muscles, in a complex action or series of actions. [NIH] Core biopsy: The removal of a tissue sample with a needle for examination under a microscope. [NIH] Coreceptors: Invariant receptor of the helper T-cells. [NIH] Cornea: The transparent part of the eye that covers the iris and the pupil and allows light to enter the inside. [NIH] Corneum: The superficial layer of the epidermis containing keratinized cells. [NIH] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroids: Hormones that have antitumor activity in lymphomas and lymphoid leukemias; in addition, corticosteroids (steroids) may be used for hormone replacement and for the management of some of the complications of cancer and its treatment. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Cranial Nerves: Twelve pairs of nerves that carry general afferent, visceral afferent, special afferent, somatic efferent, and autonomic efferent fibers. [NIH] Craniocerebral Trauma: Traumatic injuries involving the cranium and intracranial structures (i.e., brain; cranial nerves; meninges; and other structures). Injuries may be classified by whether or not the skull is penetrated (i.e., penetrating vs. nonpenetrating) or whether there is an associated hemorrhage. [NIH] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Croton Oil: Viscous, nauseating oil obtained from the shrub Croton tiglium (Euphorbaceae). It is a vesicant and skin irritant used as pharmacologic standard for skin inflammation and allergy and causes skin cancer. It was formerly used as an emetic and cathartic with frequent
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mortality. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Curcumin: A dye obtained from tumeric, the powdered root of Curcuma longa Linn. It is used in the preparation of curcuma paper and the detection of boron. Curcumin appears to possess a spectrum of pharmacological properties, due primarily to its inhibitory effects on metabolic enzymes. [NIH] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclin: Molecule that regulates the cell cycle. [NIH] Cyclin-Dependent Kinases: Protein kinases that control cell cycle progression in all eukaryotes and require physical association with cyclins to achieve full enzymatic activity. Cyclin-dependent kinases are regulated by phosphorylation and dephosphorylation events. [NIH]
Cyclophosphamide: Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the liver to form the active aldophosphamide. It is used in the treatment of lymphomas, leukemias, etc. Its side effect, alopecia, has been made use of in defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer. [NIH] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]
Cytarabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Cytidine: A pyrimidine nucleoside that is composed of the base cytosine linked to the fivecarbon sugar D-ribose. [NIH] Cytidine Deaminase: An enzyme that catalyzes the deamination of cytidine, forming uridine. EC 3.5.4.5. [NIH] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytogenetic Analysis: Examination of chromosomes to diagnose, classify, screen for, or manage genetic diseases and abnormalities. Following preparation of the sample, karyotyping is performed and/or the specific chromosomes are analyzed. [NIH] Cytogenetics: A branch of genetics which deals with the cytological and molecular behavior
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of genes and chromosomes during cell division. [NIH] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [NIH] Cytomegalovirus Infections: Infection with Cytomegalovirus, characterized by enlarged cells bearing intranuclear inclusions. Infection may be in almost any organ, but the salivary glands are the most common site in children, as are the lungs in adults. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytosine: A pyrimidine base that is a fundamental unit of nucleic acids. [NIH] Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm. [NIH] Cytotoxic: Cell-killing. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Cytotoxins: Substances elaborated by microorganisms, plants or animals that are specifically toxic to individual cells; they may be involved in immunity or may be contained in venoms. [NIH]
Dairy Products: Raw and processed or manufactured milk and milk-derived products. These are usually from cows (bovine) but are also from goats, sheep, reindeer, and water buffalo. [NIH] Databases, Bibliographic: Extensive collections, reputedly complete, of references and citations to books, articles, publications, etc., generally on a single subject or specialized subject area. Databases can operate through automated files, libraries, or computer disks. The concept should be differentiated from factual databases which is used for collections of data and facts apart from bibliographic references to them. [NIH] Daunorubicin: Very toxic anthracycline aminoglycoside antibiotic isolated from Streptomyces peucetius and others, used in treatment of leukemias and other neoplasms. [NIH]
De novo: In cancer, the first occurrence of cancer in the body. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decision Making: The process of making a selective intellectual judgment when presented with several complex alternatives consisting of several variables, and usually defining a course of action or an idea. [NIH] Decubitus: An act of lying down; also the position assumed in lying down. [EU] Decubitus Ulcer: An ulceration caused by prolonged pressure in patients permitted to lie too still for a long period of time. The bony prominences of the body are the most frequently affected sites. The ulcer is caused by ischemia of the underlying structures of the skin, fat, and muscles as a result of the sustained and constant pressure. [NIH] Defense Mechanisms: Unconscious process used by an individual or a group of individuals
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in order to cope with impulses, feelings or ideas which are not acceptable at their conscious level; various types include reaction formation, projection and self reversal. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Denaturation: Rupture of the hydrogen bonds by heating a DNA solution and then cooling it rapidly causes the two complementary strands to separate. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Dendritic: 1. Branched like a tree. 2. Pertaining to or possessing dendrites. [EU] Dendritic cell: A special type of antigen-presenting cell (APC) that activates T lymphocytes. [NIH]
Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Dental Care: The total of dental diagnostic, preventive, and restorative services provided to meet the needs of a patient (from Illustrated Dictionary of Dentistry, 1982). [NIH] Dental Caries: Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp. The three most prominent theories used to explain the etiology of the disase are that acids produced by bacteria lead to decalcification; that micro-organisms destroy the enamel protein; or that keratolytic micro-organisms produce chelates that lead to decalcification. [NIH]
Dentists: Individuals licensed to practice dentistry. [NIH] Deoxyglucose: 2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity. [NIH] Depigmentation: Removal or loss of pigment, especially melanin. [EU] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Deprivation: Loss or absence of parts, organs, powers, or things that are needed. [EU] Depsipeptide: Anticancer drugs obtained from microorganisms. [NIH] Dermal: Pertaining to or coming from the skin. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Dermatitis Herpetiformis: Rare, chronic, papulo-vesicular disease characterized by an intensely pruritic eruption consisting of various combinations of symmetrical, erythematous, papular, vesicular, or bullous lesions. The disease is strongly associated with the presence of HLA-B8 and HLA-DR3 antigens. A variety of different autoantibodies has been detected in small numbers in patients with dermatitis herpetiformis. [NIH] Detergents: Purifying or cleansing agents, usually salts of long-chain aliphatic bases or acids, that exert cleansing (oil-dissolving) and antimicrobial effects through a surface action
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that depends on possessing both hydrophilic and hydrophobic properties. [NIH] Developing Countries: Countries in the process of change directed toward economic growth, that is, an increase in production, per capita consumption, and income. The process of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures. [NIH] Dexamethasone: (11 beta,16 alpha)-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4diene-3,20-dione. An anti-inflammatory glucocorticoid used either in the free alcohol or esterified form in treatment of conditions that respond generally to cortisone. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnostic Imaging: Any visual display of structural or functional patterns of organs or tissues for diagnostic evaluation. It includes measuring physiologic and metabolic responses to physical and chemical stimuli, as well as ultramicroscopy. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diaphragm: The musculofibrous partition that separates the thoracic cavity from the abdominal cavity. Contraction of the diaphragm increases the volume of the thoracic cavity aiding inspiration. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Dietitian: An expert in nutrition who helps people plan what and how much food to eat. [NIH]
Diffusion: The tendency of a gas or solute to pass from a point of higher pressure or concentration to a point of lower pressure or concentration and to distribute itself throughout the available space; a major mechanism of biological transport. [NIH] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dilatation: The act of dilating. [NIH] Dimerization: The process by which two molecules of the same chemical composition form a condensation product or polymer. [NIH] Dimethyl: A volatile metabolite of the amino acid methionine. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis. [NIH] Disease-Free Survival: Period after successful treatment in which there is no appearance of the symptoms or effects of the disease. [NIH] Disorientation: The loss of proper bearings, or a state of mental confusion as to time, place, or identity. [EU]
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Disparity: Failure of the two retinal images of an object to fall on corresponding retinal points. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Dissociative Disorders: Sudden temporary alterations in the normally integrative functions of consciousness. [NIH] Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Disulphide: A covalent bridge formed by the oxidation of two cysteine residues to a cystine residue. The-S-S-bond is very strong and its presence confers additional stability. [NIH] Docetaxel: An anticancer drug that belongs to the family of drugs called mitotic inhibitors. [NIH]
Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dormancy: The period when an organism (i. e., a virus or a bacterium) is in the body but not producing any ill effects. [NIH] Dorsal: 1. Pertaining to the back or to any dorsum. 2. Denoting a position more toward the back surface than some other object of reference; same as posterior in human anatomy; superior in the anatomy of quadrupeds. [EU] Dose-limiting: Describes side effects of a drug or other treatment that are serious enough to prevent an increase in dose or level of that treatment. [NIH] Dosimetry: All the methods either of measuring directly, or of measuring indirectly and computing, absorbed dose, absorbed dose rate, exposure, exposure rate, dose equivalent, and the science associated with these methods. [NIH] Doxorubicin: Antineoplastic antibiotic obtained from Streptomyces peucetics. It is a hydroxy derivative of daunorubicin and is used in treatment of both leukemia and solid tumors. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from drug tolerance which is the progressive diminution of the susceptibility of a human or animal to the effects
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of a drug, as a result of continued administration. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duct: A tube through which body fluids pass. [NIH] Duodenal Ulcer: An ulcer in the lining of the first part of the small intestine (duodenum). [NIH]
Duodenum: The first part of the small intestine. [NIH] Dura mater: The outermost, toughest, and most fibrous of the three membranes (meninges) covering the brain and spinal cord; called also pachymeninx. [EU] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Ectopic: Pertaining to or characterized by ectopia. [EU] Eczema: A pruritic papulovesicular dermatitis occurring as a reaction to many endogenous and exogenous agents (Dorland, 27th ed). [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Effector cell: A cell that performs a specific function in response to a stimulus; usually used to describe cells in the immune system. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Effusion: The escape of fluid into a part or tissue, as an exudation or a transudation. [EU] Ejection fraction: A measure of ventricular contractility, equal to normally 65 8 per cent; lower values indicate ventricular dysfunction. [EU] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electrocardiogram: Measurement of electrical activity during heartbeats. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]
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Elementary Particles: Individual components of atoms, usually subatomic; subnuclear particles are usually detected only when the atomic nucleus decays and then only transiently, as most of them are unstable, often yielding pure energy without substance, i.e., radiation. [NIH] Emaciation: Clinical manifestation of excessive leanness usually caused by disease or a lack of nutrition. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Emetic: An agent that causes vomiting. [EU] Emollient: Softening or soothing; called also malactic. [EU] Emulsion: A preparation of one liquid distributed in small globules throughout the body of a second liquid. The dispersed liquid is the discontinuous phase, and the dispersion medium is the continuous phase. When oil is the dispersed liquid and an aqueous solution is the continuous phase, it is known as an oil-in-water emulsion, whereas when water or aqueous solution is the dispersed phase and oil or oleaginous substance is the continuous phase, it is known as a water-in-oil emulsion. Pharmaceutical emulsions for which official standards have been promulgated include cod liver oil emulsion, cod liver oil emulsion with malt, liquid petrolatum emulsion, and phenolphthalein in liquid petrolatum emulsion. [EU] Enamel: A very hard whitish substance which covers the dentine of the anatomical crown of a tooth. [NIH] Encapsulated: Confined to a specific, localized area and surrounded by a thin layer of tissue. [NIH]
Encephalopathy: A disorder of the brain that can be caused by disease, injury, drugs, or chemicals. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocarditis: Exudative and proliferative inflammatory alterations of the endocardium, characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but sometimes affecting the inner lining of the cardiac chambers or the endocardium elsewhere. It may occur as a primary disorder or as a complication of or in association with another disease. [EU] Endocardium: The innermost layer of the heart, comprised of endothelial cells. [NIH] Endocytosis: Cellular uptake of extracellular materials within membrane-limited vacuoles or microvesicles. Endosomes play a central role in endocytosis. [NIH] Endogenous Retroviruses: Retroviruses that have integrated into the germline (Proviruses) that have lost infectious capability but retained the capability to transpose. [NIH] Endometrial: Having to do with the endometrium (the layer of tissue that lines the uterus). [NIH]
Endometrium: The layer of tissue that lines the uterus. [NIH] Endoscope: A thin, lighted tube used to look at tissues inside the body. [NIH] Endoscopic: A technique where a lateral-view endoscope is passed orally to the duodenum for visualization of the ampulla of Vater. [NIH] Endostatin: A drug that is being studied for its ability to prevent the growth of new blood vessels into a solid tumor. Endostatin belongs to the family of drugs called angiogenesis inhibitors. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph
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vessels, and the heart. [NIH] Endotoxin: Toxin from cell walls of bacteria. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Enteropeptidase: A specialized proteolytic enzyme secreted by intestinal cells. It converts trypsinogen into its active form trypsin by removing the N-terminal peptide. EC 3.4.21.9. [NIH]
Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]
Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Eosinophil: A polymorphonuclear leucocyte with large eosinophilic granules in its cytoplasm, which plays a role in hypersensitivity reactions. [NIH] Eosinophilia: Abnormal increase in eosinophils in the blood, tissues or organs. [NIH] Eosinophilic: A condition found primarily in grinding workers caused by a reaction of the pulmonary tissue, in particular the eosinophilic cells, to dust that has entered the lung. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiologic Studies: Studies designed to examine associations, commonly, hypothesized causal relations. They are usually concerned with identifying or measuring the effects of risk factors or exposures. The common types of analytic study are case-control studies, cohort studies, and cross-sectional studies. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU] Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epidermoid carcinoma: A type of cancer in which the cells are flat and look like fish scales. Also called squamous cell carcinoma. [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epirubicin: An anthracycline antibiotic which is the 4'-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA. Clinical studies indicate activity in breast cancer, non-Hodgkin's lymphomas, ovarian
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cancer, soft-tissue sarcomas, pancreatic cancer, gastric cancer, small-cell lung cancer and acute leukemia. It is equal in activity to doxorubicin but exhibits less acute toxicities and less cardiotoxicity. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]
Ergot: Cataract due to ergot poisoning caused by eating of rye cereals contaminated by a fungus. [NIH] Erythema: Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythropoietin: Glycoprotein hormone, secreted chiefly by the kidney in the adult and the liver in the fetus, that acts on erythroid stem cells of the bone marrow to stimulate proliferation and differentiation. [NIH] Escalation: Progressive use of more harmful drugs. [NIH] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]
Essential Tremor: A rhythmic, involuntary, purposeless, oscillating movement resulting from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Estrogen: One of the two female sex hormones. [NIH] Ether: One of a class of organic compounds in which any two organic radicals are attached directly to a single oxygen atom. [NIH] Etoposide: A semisynthetic derivative of podophyllotoxin that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle. [NIH] Etretinate: An oral retinoid used in the treatment of keratotic genodermatosis, lichen planus, and psoriasis. Beneficial effects have also been claimed in the prophylaxis of epithelial neoplasia. The compound may be teratogenic. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Evacuation: An emptying, as of the bowels. [EU] Evaluable patients: Patients whose response to a treatment can be measured because enough information has been collected. [NIH] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH]
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Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Exercise Therapy: Motion of the body or its parts to relieve symptoms or to improve function, leading to physical fitness, but not physical education and training. [NIH] Exfoliation: A falling off in scales or layers. [EU] Exocrine: Secreting outwardly, via a duct. [EU] Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the cell membrane. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exons: Coding regions of messenger RNA included in the genetic transcript which survive the processing of RNA in cell nuclei to become part of a spliced messenger of structural RNA in the cytoplasm. They include joining and diversity exons of immunoglobulin genes. [NIH]
Extensor: A muscle whose contraction tends to straighten a limb; the antagonist of a flexor. [NIH]
External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracorporeal: Situated or occurring outside the body. [EU] Extraction: The process or act of pulling or drawing out. [EU] Extraocular: External to or outside of the eye. [NIH] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] Facial: Of or pertaining to the face. [EU] Facial Nerve: The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and salivary glands, and convey afferent information for taste from the anterior two-thirds of the tongue and for touch from the external ear. [NIH] Fallopian Tubes: Two long muscular tubes that transport ova from the ovaries to the uterus. They extend from the horn of the uterus to the ovaries and consist of an ampulla, an infundibulum, an isthmus, two ostia, and a pars uterina. The walls of the tubes are composed of three layers: mucosal, muscular, and serosal. [NIH] Familial polyposis: An inherited condition in which numerous polyps (tissue masses) develop on the inside walls of the colon and rectum. It increases the risk for colon cancer. [NIH]
Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Farnesyl: Enzyme which adds 15 carbon atoms to the Ras precursor protein. [NIH] Fat: Total lipids including phospholipids. [NIH]
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Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]
Feces: The excrement discharged from the intestines, consisting of bacteria, cells exfoliated from the intestines, secretions, chiefly of the liver, and a small amount of food residue. [EU] Fetal Hemoglobin: The major component of hemoglobin in the fetus. This hemoglobin has two alpha and two gamma polypeptide subunits in comparison to normal adult hemoglobin, which has two alpha and two beta polypeptide subunits. Fetal hemoglobin concentrations can be elevated (usually above 0.5%) in children and adults affected by leukemia and several types of anemia. [NIH] Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fever of Unknown Origin: Fever in which the etiology cannot be ascertained. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibrosarcoma: A type of soft tissue sarcoma that begins in fibrous tissue, which holds bones, muscles, and other organs in place. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Filgrastim: A colony-stimulating factor that stimulates the production of neutrophils (a type of white blood cell). It is a cytokine that belongs to the family of drugs called hematopoietic (blood-forming) agents. Also called granulocyte colony-stimulating factor (G-CSF). [NIH] Filtration: The passage of a liquid through a filter, accomplished by gravity, pressure, or vacuum (suction). [EU] Fine-needle aspiration: The removal of tissue or fluid with a needle for examination under a microscope. Also called needle biopsy. [NIH] Fixation: 1. The act or operation of holding, suturing, or fastening in a fixed position. 2. The condition of being held in a fixed position. 3. In psychiatry, a term with two related but distinct meanings : (1) arrest of development at a particular stage, which like regression (return to an earlier stage), if temporary is a normal reaction to setbacks and difficulties but if protracted or frequent is a cause of developmental failures and emotional problems, and (2) a close and suffocating attachment to another person, especially a childhood figure, such as one's mother or father. Both meanings are derived from psychoanalytic theory and refer to 'fixation' of libidinal energy either in a specific erogenous zone, hence fixation at the oral, anal, or phallic stage, or in a specific object, hence mother or father fixation. 4. The use of a fixative (q.v.) to preserve histological or cytological specimens. 5. In chemistry, the process whereby a substance is removed from the gaseous or solution phase and localized, as in carbon dioxide fixation or nitrogen fixation. 6. In ophthalmology, direction of the gaze so that the visual image of the object falls on the fovea centralis. 7. In film processing, the chemical removal of all undeveloped salts of the film emulsion, leaving only the developed silver to form a permanent image. [EU] Flatus: Gas passed through the rectum. [NIH] Flavodoxin: A low-molecular-weight (16,000) iron-free flavoprotein containing one
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molecule of flavin mononucleotide (FMN) and isolated from bacteria grown on an irondeficient medium. It can replace ferredoxin in all the electron-transfer functions in which the latter is known to serve in bacterial cells. [NIH] Flavopiridol: Belongs to the family of anticancer drugs called flavinols. [NIH] Flexor: Muscles which flex a joint. [NIH] Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake. [NIH] Fludarabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fluorescent Dyes: Dyes that emit light when exposed to light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags. They are used as markers in biochemistry and immunology. [NIH] Fluorine: A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as flouride to prevent dental caries. [NIH] Fluorouracil: A pyrimidine analog that acts as an antineoplastic antimetabolite and also has immunosuppressant. It interferes with DNA synthesis by blocking the thymidylate synthetase conversion of deoxyuridylic acid to thymidylic acid. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Folic Acid: N-(4-(((2-Amino-1,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-Lglutamic acid. A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia. [NIH] Follicles: Shafts through which hair grows. [NIH] Follicular large cell lymphoma: A rare type of non- Hodgkin's lymphoma (cancer of the lymphatic system) with large cells that look cleaved (split) or non-cleaved under the microscope. It is an indolent (slow-growing) type of lymphoma. [NIH] Follow-Up Studies: Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease. [NIH]
Foramen: A natural hole of perforation, especially one in a bone. [NIH] Fovea: The central part of the macula that provides the sharpest vision. [NIH] Fractionation: Dividing the total dose of radiation therapy into several smaller, equal doses delivered over a period of several days. [NIH] Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites,
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including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Fungus: A general term used to denote a group of eukaryotic protists, including mushrooms, yeasts, rusts, moulds, smuts, etc., which are characterized by the absence of chlorophyll and by the presence of a rigid cell wall composed of chitin, mannans, and sometimes cellulose. They are usually of simple morphological form or show some reversible cellular specialization, such as the formation of pseudoparenchymatous tissue in the fruiting body of a mushroom. The dimorphic fungi grow, according to environmental conditions, as moulds or yeasts. [EU] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gallium: A rare, metallic element designated by the symbol, Ga, atomic number 31, and atomic weight 69.72. [NIH] Gallium nitrate: A drug that lowers blood calcium. Used as treatment for hypercalcemia (too much calcium in the blood) and for cancer that has spread to the bone (bone metastases). [NIH] Gamma Rays: Very powerful and penetrating, high-energy electromagnetic radiation of shorter wavelength than that of x-rays. They are emitted by a decaying nucleus, usually between 0.01 and 10 MeV. They are also called nuclear x-rays. [NIH] Ganciclovir: Acyclovir analog that is a potent inhibitor of the Herpesvirus family including cytomegalovirus. Ganciclovir is used to treat complications from AIDS-associated cytomegalovirus infections. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] Gap Junctions: Connections between cells which allow passage of small molecules and electric current. Gap junctions were first described anatomically as regions of close apposition between cells with a narrow (1-2 nm) gap between cell membranes. The variety in the properties of gap junctions is reflected in the number of connexins, the family of proteins which form the junctions. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Acid: Hydrochloric acid present in gastric juice. [NIH] Gastric Juices: Liquids produced in the stomach to help break down food and kill bacteria. [NIH]
Gastric Mucosa: Surface epithelium in the stomach that invaginates into the lamina propria, forming gastric pits. Tubular glands, characteristic of each region of the stomach (cardiac, gastric, and pyloric), empty into the gastric pits. The gastric mucosa is made up of several different kinds of cells. [NIH] Gastric Resection: An operation to remove part or all of the stomach. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid.
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[NIH]
Gastritis: Inflammation of the stomach. [EU] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gels: Colloids with a solid continuous phase and liquid as the dispersed phase; gels may be unstable when, due to temperature or other cause, the solid phase liquifies; the resulting colloid is called a sol. [NIH] Gemcitabine: An anticancer drug that belongs to the family of drugs called antimetabolites. [NIH]
Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]
Gene Deletion: A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus. [NIH] Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Fusion: Fusion of structural genes to analyze protein behavior or fusion of regulatory sequences with structural genes to determine mechanisms of regulation. [NIH] Gene Rearrangement: The ordered rearrangement of gene regions by DNA recombination such as that which occurs normally during development. [NIH] Gene Silencing: Interruption or suppression of the expression of a gene at transcriptional or translational levels. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic Markers: A phenotypically recognizable genetic trait which can be used to identify a genetic locus, a linkage group, or a recombination event. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genitourinary: Pertaining to the genital and urinary organs; urogenital; urinosexual. [EU] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Germ cell tumors: Tumors that begin in the cells that give rise to sperm or eggs. They can occur virtually anywhere in the body and can be either benign or malignant. [NIH]
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Germ Cells: The reproductive cells in multicellular organisms. [NIH] Germinal Center: The activated center of a lymphoid follicle in secondary lymphoid tissue where B-lymphocytes are stimulated by antigens and helper T cells (T-lymphocytes, helperinducer) are stimulated to generate memory cells. [NIH] Germline mutation: A gene change in the body's reproductive cells (egg or sperm) that becomes incorporated into the DNA of every cell in the body of offspring; germline mutations are passed on from parents to offspring. Also called hereditary mutation. [NIH] Gestational: Psychosis attributable to or occurring during pregnancy. [NIH] Gestational trophoblastic disease: A rare cancer in women of child-bearing age in which cancer cells grow in the tissues that are formed in the uterus after conception. Also called gestational trophoblastic tumor, gestational trophoblastic neoplasia, molar pregnancy, or choriocarcinoma. [NIH] Gestational trophoblastic neoplasia: A rare cancer in women of child-bearing age in which cancer cells grow in the tissues that are formed in the uterus after conception. Also called gestational trophoblastic disease, gestational trophoblastic tumor, molar pregnancy, or choriocarcinoma. [NIH] Gestational trophoblastic tumor: A rare cancer in women of child-bearing age in which cancer cells grow in the tissues that are formed in the uterus after conception. Also called gestational trophoblastic disease, gestational trophoblastic neoplasia, molar pregnancy, or choriocarcinoma. [NIH] Giant Cells: Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus. [NIH] Ginger: Deciduous plant rich in volatile oil (oils, volatile). It is used as a flavoring agent and has many other uses both internally and topically. [NIH] Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Gliadin: Simple protein, one of the prolamines, derived from the gluten of wheat, rye, etc. May be separated into 4 discrete electrophoretic fractions. It is the toxic factor associated with celiac disease. [NIH] Glioblastoma: A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures. [NIH] Glioma: A cancer of the brain that comes from glial, or supportive, cells. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]
Glomerulus: A tiny set of looping blood vessels in the nephron where blood is filtered in the kidney. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally
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occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH]
Glutamine: A non-essential amino acid present abundantly throught the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. [NIH] Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]
Gluten: The protein of wheat and other grains which gives to the dough its tough elastic character. [EU] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycolysis: The pathway by which glucose is catabolized into two molecules of pyruvic acid with the generation of ATP. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Goats: Any of numerous agile, hollow-horned ruminants of the genus Capra, closely related to the sheep. [NIH] Gonadal: Pertaining to a gonad. [EU] Gonadotropin: The water-soluble follicle stimulating substance, by some believed to originate in chorionic tissue, obtained from the serum of pregnant mares. It is used to supplement the action of estrogens. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Grading: A system for classifying cancer cells in terms of how abnormal they appear when examined under a microscope. The objective of a grading system is to provide information about the probable growth rate of the tumor and its tendency to spread. The systems used to grade tumors vary with each type of cancer. Grading plays a role in treatment decisions. [NIH]
Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the recipient. [NIH] Graft vs Host Disease: The clinical entity characterized by anorexia, diarrhea, loss of hair, leukopenia, thrombocytopenia, growth retardation, and eventual death brought about by the graft vs host reaction. [NIH] Graft vs Host Reaction: An immunological attack mounted by a graft against the host because of tissue incompatibility when immunologically competent cells are transplanted to an immunologically incompetent host; the resulting clinical picture is that of graft vs host disease. [NIH]
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Graft-versus-host disease: GVHD. A reaction of donated bone marrow or peripheral stem cells against a person's tissue. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Granisetron: A serotonin receptor (5HT-3 selective) antagonist that has been used as an antiemetic for cancer chemotherapy patients. [NIH] Granule: A small pill made from sucrose. [EU] Granulocyte Colony-Stimulating Factor: A glycoprotein of MW 25 kDa containing internal disulfide bonds. It induces the survival, proliferation, and differentiation of neutrophilic granulocyte precursor cells and functionally activates mature blood neutrophils. Among the family of colony-stimulating factors, G-CSF is the most potent inducer of terminal differentiation to granulocytes and macrophages of leukemic myeloid cell lines. [NIH] Granulocyte-Macrophage Colony-Stimulating Factor: An acidic glycoprotein of MW 23 kDa with internal disulfide bonds. The protein is produced in response to a number of inflammatory mediators by mesenchymal cells present in the hemopoietic environment and at peripheral sites of inflammation. GM-CSF is able to stimulate the production of neutrophilic granulocytes, macrophages, and mixed granulocyte-macrophage colonies from bone marrow cells and can stimulate the formation of eosinophil colonies from fetal liver progenitor cells. GM-CSF can also stimulate some functional activities in mature granulocytes and macrophages. [NIH] Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Habitual: Of the nature of a habit; according to habit; established by or repeated by force of habit, customary. [EU] Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [NIH] Hairy cell leukemia: A type of chronic leukemia in which the abnormal white blood cells appear to be covered with tiny hairs when viewed under a microscope. [NIH] Half-Life: The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary
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disease process are referred to as headache disorders (e.g., migraine). [NIH] Headache Disorders: Common conditions characterized by persistent or recurrent headaches. Headache syndrome classification systems may be based on etiology (e.g., vascular headache, post-traumatic headaches, etc.), temporal pattern (e.g., cluster headache, paroxysmal hemicrania, etc.), and precipitating factors (e.g., cough headache). [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Helix-loop-helix: Regulatory protein of cell cycle. [NIH] Hematologic Diseases: Disorders of the blood and blood forming tissues. [NIH] Hematologic malignancies: Cancers of the blood or bone marrow, including leukemia and lymphoma. Also called hematologic cancers. [NIH] Hematopoiesis: The development and formation of various types of blood cells. [NIH] Hematopoietic growth factors: A group of proteins that cause blood cells to grow and mature. [NIH] Hematopoietic Stem Cell Transplantation: The transference of stem cells from one animal or human to another (allogeneic), or within the same individual (autologous). The source for the stem cells may be the bone marrow or peripheral blood. Stem cell transplantation has been used as an alternative to autologous bone marrow transplantation in the treatment of a variety of neoplasms. [NIH] Hematopoietic Stem Cells: Progenitor cells from which all blood cells derive. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobin H: An abnormal hemoglobin composed of four beta chains. It is caused by the reduced synthesis of the alpha chain. This abnormality results in alpha-thalassemia. [NIH] Hemoglobin M: A group of abnormal hemoglobins in which amino acid substitutions take place in either the alpha or beta chains but near the heme iron. This results in facilitated oxidation of the hemoglobin to yield excess methemoglobin which leads to cyanosis. [NIH] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH] Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] Hemolytic: A disease that affects the blood and blood vessels. It destroys red blood cells, cells that cause the blood to clot, and the lining of blood vessels. HUS is often caused by the Escherichia coli bacterium in contaminated food. People with HUS may develop acute renal failure. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation.
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[NIH]
Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [NIH] Hepatoma: A liver tumor. [NIH] Hepatomegaly: Enlargement of the liver. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Hereditary mutation: A gene change in the body's reproductive cells (egg or sperm) that becomes incorporated into the DNA of every cell in the body of offspring; hereditary mutations are passed on from parents to offspring. Also called germline mutation. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Herpes: Any inflammatory skin disease caused by a herpesvirus and characterized by the formation of clusters of small vesicles. When used alone, the term may refer to herpes simplex or to herpes zoster. [EU] Herpes virus: A member of the herpes family of viruses. [NIH] Herpes Zoster: Acute vesicular inflammation. [NIH] Herpetiformis: Duhring's disease a recurring, inflammatory disease of the skin of unknown etiology characterized by erythematous, papular, pustular, or vesicular lesions which tend to group and are accompanied by itching and burning. [NIH] Heterodimers: Zippered pair of nonidentical proteins. [NIH] Heteroduplex Analysis: A method of detecting gene mutation by mixing PCR-amplified mutant and wild-type DNA followed by denaturation and reannealing. The resultant products are resolved by gel electrophoresis, with single base substitutions detectable under optimal electrophoretic conditions and gel formulations. Large base pair mismatches may also be analyzed by using electron microscopy to visualize heteroduplex regions. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]
Heterotrophic: Pertaining to organisms that are consumers and dependent on other organisms for their source of energy (food). [NIH] Heterozygotes: Having unlike alleles at one or more corresponding loci on homologous chromosomes. [NIH] High-grade lymphomas: Includes large cell, immunoblastic, lymphoblastic, and small noncleaved cell lymphomas. These lymphomas grow quickly but have a better response to anticancer drugs than that seen with low-grade lymphomas. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histamine Release: The secretion of histamine from mast cell and basophil granules by exocytosis. This can be initiated by a number of factors, all of which involve binding of IgE, cross-linked by antigen, to the mast cell or basophil's Fc receptors. Once released, histamine binds to a number of different target cell receptors and exerts a wide variety of effects. [NIH]
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Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Histology: The study of tissues and cells under a microscope. [NIH] Homeobox: Distinctive sequence of DNA bases. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homodimer: Protein-binding "activation domains" always combine with identical proteins. [NIH]
Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Homotypic: Adhesion between neutrophils. [NIH] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Horny layer: The superficial layer of the epidermis containing keratinized cells. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Humour: 1. A normal functioning fluid or semifluid of the body (as the blood, lymph or bile) especially of vertebrates. 2. A secretion that is itself an excitant of activity (as certain hormones). [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hybridoma: A hybrid cell resulting from the fusion of a specific antibody-producing spleen cell with a myeloma cell. [NIH] Hydatidiform Mole: A trophoblastic disease characterized by hydrops of the mesenchymal portion of the villus. Its karyotype is paternal and usually homozygotic. The tumor is indistinguishable from chorioadenoma destruens or invasive mole ( = hydatidiform mole, invasive) except by karyotype. There is no apparent relation by karyotype to choriocarcinoma. Hydatidiform refers to the presence of the hydropic state of some or all of the villi (Greek hydatis, a drop of water). [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxamic Acids: A class of weak acids with the general formula R-conhoh. [NIH]
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Hydroxylamine: A colorless inorganic compound (HONH2) used in organic synthesis and as a reducing agent, due to its ability to donate nitric oxide. [NIH] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hygienic: Pertaining to hygiene, or conducive to health. [EU] Hyperbilirubinemia: Pathologic process consisting of an abnormal increase in the amount of bilirubin in the circulating blood, which may result in jaundice. [NIH] Hypercalcemia: Abnormally high level of calcium in the blood. [NIH] Hyperplasia: An increase in the number of cells in a tissue or organ, not due to tumor formation. It differs from hypertrophy, which is an increase in bulk without an increase in the number of cells. [NIH] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hypoglycemia: Abnormally low blood sugar [NIH] Hypoplasia: Incomplete development or underdevelopment of an organ or tissue. [EU] Hypopyon: An accumulation of pus in the anterior chamber of the eye associated with infectious diseases of the cornea, the iris, and the ciliary body. [NIH] Ibritumomab tiuxetan: An anticancer drug that is a combination of a monoclonal antibody and a radioisotope (yttrium-90). Also called IDEC-Y2B8 monoclonal antibody. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Idiopathic: Describes a disease of unknown cause. [NIH] Idiotype: The unique antigenic determinant in the variable region. [NIH] Ifosfamide: Positional isomer of cyclophosphamide which is active as an alkylating agent and an immunosuppressive agent. [NIH] Ileum: The lower end of the small intestine. [NIH] Imaging procedures: Methods of producing pictures of areas inside the body. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immortal: Stage when the mother cell and its descendants will multiply indefinitely. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]
Immune Sera: Serum that contains antibodies. It is obtained from an animal that has been immunized either by antigen injection or infection with microorganisms containing the antigen. [NIH] Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH]
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Immunity: Nonsusceptibility to the invasive or pathogenic microorganisms or to the toxic effect of antigenic substances. [NIH]
effects
of
foreign
Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunoblotting: Immunologic methods for isolating and quantitatively measuring immunoreactive substances. When used with immune reagents such as monoclonal antibodies, the process is known generically as western blot analysis (blotting, western). [NIH]
Immunocompromised: Having a weakened immune system caused by certain diseases or treatments. [NIH] Immunoconjugates: Combinations of diagnostic or therapeutic substances linked with specific immune substances such as immunoglobulins, monoclonal antibodies or antigens. Often the diagnostic or therapeutic substance is a radionuclide. These conjugates are useful tools for specific targeting of drugs and radioisotopes in the chemotherapy and radioimmunotherapy of certain cancers. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodeficiency syndrome: The inability of the body to produce an immune response. [NIH]
Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulin: A protein that acts as an antibody. [NIH] Immunoglobulin Variable Region: That region of the immunoglobulin (antibody) molecule that varies in its amino acid sequence and composition, confers the antigenic specificity, and is thought to comprise the binding site for the antigen. It is located at the N-terminus of the Fab fragment of the immunoglobulin. It includes hypervariable regions (complementarity determining regions) and framework regions. [NIH] Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents. [NIH] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunologic Diseases: Disorders caused by abnormal or absent immunologic mechanisms, whether humoral, cell-mediated or both. [NIH] Immunology: The study of the body's immune system. [NIH] Immunophenotyping: Process of classifying cells of the immune system based on structural and functional differences. The process is commonly used to analyze and sort Tlymphocytes into subsets based on CD antigens by the technique of flow cytometry. [NIH] Immunophilin: A drug for the treatment of Parkinson's disease. [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH] Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to
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prevent graft rejection. [NIH] Immunotoxin: An antibody linked to a toxic substance. Some immmunotoxins can bind to cancer cells and kill them. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [NIH] Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] In situ: In the natural or normal place; confined to the site of origin without invasion of neighbouring tissues. [EU] In Situ Hybridization: A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Incubation: The development of an infectious disease from the entrance of the pathogen to the appearance of clinical symptoms. [EU] Incubation period: The period of time likely to elapse between exposure to the agent of the disease and the onset of clinical symptoms. [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU] Indolent: A type of cancer that grows slowly. [NIH] Indolent lymphoma: Lymphoma that grows slowly and has few symptoms. [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Induction therapy: Treatment designed to be used as a first step toward shrinking the cancer and in evaluating response to drugs and other agents. Induction therapy is followed by additional therapy to eliminate whatever cancer remains. [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]
Infection Control: Programs of disease surveillance, generally within health care facilities, designed to investigate, prevent, and control the spread of infections and their causative microorganisms. [NIH]
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Infectious Mononucleosis: A common, acute infection usually caused by the Epstein-Barr virus (Human herpesvirus 4). There is an increase in mononuclear white blood cells and other atypical lymphocytes, generalized lymphadenopathy, splenomegaly, and occasionally hepatomegaly with hepatitis. [NIH] Infiltration: The diffusion or accumulation in a tissue or cells of substances not normal to it or in amounts of the normal. Also, the material so accumulated. [EU] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]
Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Inlay: In dentistry, a filling first made to correspond with the form of a dental cavity and then cemented into the cavity. [NIH] Innervation: 1. The distribution or supply of nerves to a part. 2. The supply of nervous energy or of nerve stimulus sent to a part. [EU] Inorganic: Pertaining to substances not of organic origin. [EU] Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] Insertional: A technique in which foreign DNA is cloned into a restriction site which occupies a position within the coding sequence of a gene in the cloning vector molecule. Insertion interrupts the gene's sequence such that its original function is no longer expressed. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insulator: Material covering the metal conductor of the lead. It is usually polyurethane or silicone. [NIH] Integrins: A family of transmembrane glycoproteins consisting of noncovalent heterodimers. They interact with a wide variety of ligands including extracellular matrix glycoproteins, complement, and other cells, while their intracellular domains interact with the cytoskeleton. The integrins consist of at least three identified families: the cytoadhesin receptors, the leukocyte adhesion receptors, and the very-late-antigen receptors. Each family contains a common beta-subunit combined with one or more distinct alpha-subunits. These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development, hemostasis, thrombosis, wound healing, immune and nonimmune defense mechanisms, and oncogenic transformation. [NIH] Intercalating Agents: Agents that are capable of inserting themselves between the successive bases in DNA, thus kinking, uncoiling or otherwise deforming it and therefore preventing its proper functioning. They are used in the study of DNA. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and -
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gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-10: Factor that is a coregulator of mast cell growth. It is produced by T-cells and B-cells and shows extensive homology with the Epstein-Barr virus BCRFI gene. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Interleukin-3: A multilineage cell growth factor secreted by lymphocytes, epithelial cells, and astrocytes which stimulates clonal proliferation and differentiation of various types of blood and tissue cells. Also called multi-CSF, it is considered one of the hematopoietic colony stimulating factors. [NIH] Interleukins: Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH] Interphase: The interval between two successive cell divisions during which the chromosomes are not individually distinguishable and DNA replication occurs. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestinal: Having to do with the intestines. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intraepithelial: Within the layer of cells that form the surface or lining of an organ. [NIH] Intraperitoneal: IP. Within the peritoneal cavity (the area that contains the abdominal organs). [NIH] Intrathecal: Describes the fluid-filled space between the thin layers of tissue that cover the brain and spinal cord. Drugs can be injected into the fluid or a sample of the fluid can be removed for testing. [NIH] Intravascular: Within a vessel or vessels. [EU]
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Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Introns: Non-coding, intervening sequences of DNA that are transcribed, but are removed from within the primary gene transcript and rapidly degraded during maturation of messenger RNA. Most genes in the nuclei of eukaryotes contain introns, as do mitochondrial and chloroplast genes. [NIH] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]
Involuntary: Reaction occurring without intention or volition. [NIH] Iodine: A nonmetallic element of the halogen group that is represented by the atomic symbol I, atomic number 53, and atomic weight of 126.90. It is a nutritionally essential element, especially important in thyroid hormone synthesis. In solution, it has anti-infective properties and is used topically. [NIH] Iodoacetic Acid: Iodoacetic acid and its salts and derivatives. Iodoacetic acid reacts with cysteine (-SH) groups to form a carboxymethylated protein and is used as an enzyme inhibitor in biochemical research. [NIH] Ionization: 1. Any process by which a neutral atom gains or loses electrons, thus acquiring a net charge, as the dissociation of a substance in solution into ions or ion production by the passage of radioactive particles. 2. Iontophoresis. [EU] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ionomycin: A divalent calcium ionophore that is widely used as a tool to investigate the role of intracellular calcium in cellular processes. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Irinotecan: An anticancer drug that belongs to a family of anticancer drugs called topoisomerase inhibitors. It is a camptothecin analogue. Also called CPT 11. [NIH] Iris: The most anterior portion of the uveal layer, separating the anterior chamber from the posterior. It consists of two layers - the stroma and the pigmented epithelium. Color of the iris depends on the amount of melanin in the stroma on reflection from the pigmented epithelium. [NIH] Irradiation: The use of high-energy radiation from x-rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Irradiation is also called radiation therapy, radiotherapy, and x-ray therapy. [NIH] Irritable Bowel Syndrome: A disorder that comes and goes. Nerves that control the muscles in the GI tract are too active. The GI tract becomes sensitive to food, stool, gas, and stress. Causes abdominal pain, bloating, and constipation or diarrhea. Also called spastic colon or mucous colitis. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU]
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Isoelectric: Separation of amphoteric substances, dissolved in water, based on their isoelectric behavior. The amphoteric substances are a mixture of proteins to be separated and of auxiliary "carrier ampholytes". [NIH] Isoelectric Point: The pH in solutions of proteins and related compounds at which the dipolar ions are at a maximum. [NIH] Jaundice: A clinical manifestation of hyperbilirubinemia, consisting of deposition of bile pigments in the skin, resulting in a yellowish staining of the skin and mucous membranes. [NIH]
Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Karyotype: The characteristic chromosome complement of an individual, race, or species as defined by their number, size, shape, etc. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keratin: A class of fibrous proteins or scleroproteins important both as structural proteins and as keys to the study of protein conformation. The family represents the principal constituent of epidermis, hair, nails, horny tissues, and the organic matrix of tooth enamel. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms an alpha-helix, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. [NIH] Keratinocytes: Epidermal cells which synthesize keratin and undergo characteristic changes as they move upward from the basal layers of the epidermis to the cornified (horny) layer of the skin. Successive stages of differentiation of the keratinocytes forming the epidermal layers are basal cell, spinous or prickle cell, and the granular cell. [NIH] Ketoconazole: Broad spectrum antifungal agent used for long periods at high doses, especially in immunosuppressed patients. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Transplantation: The transference of a kidney from one human or animal to another. [NIH] Killer Cells: Lymphocyte-like effector cells which mediate antibody-dependent cell cytotoxicity. They kill antibody-coated target cells which they bind with their Fc receptors. [NIH]
Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lacrimal: Pertaining to the tears. [EU] Lacrimal Apparatus: The tear-forming and tear-conducting system which includes the lacrimal glands, eyelid margins, conjunctival sac, and the tear drainage system. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning
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secondarily as the organ of voice. [NIH] Latency: The period of apparent inactivity between the time when a stimulus is presented and the moment a response occurs. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Lectin: A complex molecule that has both protein and sugars. Lectins are able to bind to the outside of a cell and cause biochemical changes in it. Lectins are made by both animals and plants. [NIH] Leiomyosarcoma: A tumor of the muscles in the uterus, abdomen, or pelvis. [NIH] Leishmaniasis: A disease caused by any of a number of species of protozoa in the genus Leishmania. There are four major clinical types of this infection: cutaneous (Old and New World), diffuse cutaneous, mucocutaneous, and visceral leishmaniasis. [NIH] Lentivirus: A genus of the family Retroviridae consisting of non-oncogenic retroviruses that produce multi-organ diseases characterized by long incubation periods and persistent infection. Lentiviruses are unique in that they contain open reading frames (ORFs) between the pol and env genes and in the 3' env region. Five serogroups are recognized, reflecting the mammalian hosts with which they are associated. HIV-1 is the type species. [NIH] Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Leucocyte: All the white cells of the blood and their precursors (myeloid cell series, lymphoid cell series) but commonly used to indicate granulocytes exclusive of lymphocytes. [NIH]
Leucovorin: The active metabolite of folic acid. Leucovorin is used principally as its calcium salt as an antidote to folic acid antagonists which block the conversion of folic acid to folinic acid. [NIH] Leukaemia: An acute or chronic disease of unknown cause in man and other warm-blooded animals that involves the blood-forming organs, is characterized by an abnormal increase in the number of leucocytes in the tissues of the body with or without a corresponding increase of those in the circulating blood, and is classified according of the type leucocyte most prominently involved. [EU] Leukapheresis: The preparation of leukocyte concentrates with the return of red cells and leukocyte-poor plasma to the donor. [NIH] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukopenia: A condition in which the number of leukocytes (white blood cells) in the blood is reduced. [NIH] Leukoplakia: A white patch that may develop on mucous membranes such as the cheek, gums, or tongue and may become cancerous. [NIH] Levamisole: An antiparasitic drug that is also being studied in cancer therapy with fluorouracil. [NIH] Levo: It is an experimental treatment for heroin addiction that was developed by German scientists around 1948 as an analgesic. Like methadone, it binds with opioid receptors, but it is longer acting. [NIH] Library Services: Services offered to the library user. They include reference and circulation. [NIH]
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Lichen Planus: An inflammatory, pruritic disease of the skin and mucous membranes, which can be either generalized or localized. It is characterized by distinctive purplish, flattopped papules having a predilection for the trunk and flexor surfaces. The lesions may be discrete or coalesce to form plaques. Histologically, there is a "saw-tooth" pattern of epidermal hyperplasia and vacuolar alteration of the basal layer of the epidermis along with an intense upper dermal inflammatory infiltrate composed predominantly of T-cells. Etiology is unknown. [NIH] Life cycle: The successive stages through which an organism passes from fertilized ovum or spore to the fertilized ovum or spore of the next generation. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Ligands: A RNA simulation method developed by the MIT. [NIH] Ligation: Application of a ligature to tie a vessel or strangulate a part. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Lipid: Fat. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Liposomal: A drug preparation that contains the active drug in very tiny fat particles. This fat-encapsulated drug is absorbed better, and its distribution to the tumor site is improved. [NIH]
Liposome: A spherical particle in an aqueous medium, formed by a lipid bilayer enclosing an aqueous compartment. [EU] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver cancer: A disease in which malignant (cancer) cells are found in the tissues of the liver. [NIH]
Liver Neoplasms: Tumors or cancer of the liver. [NIH] Liver scan: An image of the liver created on a computer screen or on film. A radioactive substance is injected into a blood vessel and travels through the bloodstream. It collects in the liver, especially in abnormal areas, and can be detected by the scanner. [NIH] Local therapy: Treatment that affects cells in the tumor and the area close to it. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside
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diameter) and used in transferring microorganisms. [NIH] Low-grade lymphomas: Lymphomas that tend to grow and spread slowly, including chronic lymphocytic lymphoma and follicular small cleaved cell lymphoma. Also called indolent lymphomas. [NIH] Lubricants: Oily or slippery substances. [NIH] Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] Lumen: The cavity or channel within a tube or tubular organ. [EU] Lupus: A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the nasal, buccal, and conjunctival mucosa. [NIH] Lupus Nephritis: Glomerulonephritis associated with systemic lupus erythematosus. It is classified into four histologic types: mesangial, focal, diffuse, and membranous. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]
Lymphadenopathy: Disease or swelling of the lymph nodes. [NIH] Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphoblastic: One of the most aggressive types of non-Hodgkin lymphoma. [NIH] Lymphoblasts: Interferon produced predominantly by leucocyte cells. [NIH] Lymphocyte: A white blood cell. Lymphocytes have a number of roles in the immune system, including the production of antibodies and other substances that fight infection and diseases. [NIH] Lymphocyte Count: A count of the number of lymphocytes in the blood. [NIH] Lymphocyte Transformation: Morphologic alteration of small lymphocytes in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by interleukins, mitogens such as phytohemagglutinins, and by specific antigens. It may also occur in vivo, as in graft rejection and chronic myelogenous leukemia. [NIH] Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphocytosis: Excess of normal lymphocytes in the blood or in any effusion. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Lymphoma, Follicular: Malignant lymphoma in which the lymphomatous cells are clustered into identifiable nodules within the lymph nodes. The nodules resemble to some extent the germinal centers of lymph node follicles and most likely represent neoplastic proliferation of lymph node-derived follicular center B-lymphocytes. This class of lymphoma usually occurs in older persons, is commonly multinodal, and possibly extranodal. Patients whose lymphomas present a follicular or nodular pattern generally
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have a more indolent course than those presenting with a diffuse pattern. [NIH] Lymphoma, Lymphoblastic: A high-grade malignant lymphoma composed of a diffuse, relatively uniform proliferation of cells with round or convoluted nuclei and scanty cytoplasm. The cells are cytologically similar to the lymphoblasts seen in acute lymphocytic leukemia, and in some cases, the disease may evolve into a leukemic phase morphologically indistinguishable from acute T-lymphocytic leukemia. Lymphoblastic lymphoma represents approximately one-third of the cases of non-Hodgkin's lymphomas in children and 5% of the cases in adults. It is more prevalent in males. [NIH] Lymphomatoid Papulosis: Clinically benign, histologically malignant, recurrent cutaneous eruption characterized by an infiltration of large atypical cells surrounded by inflammatory cells. The atypical cells resemble Reed-Sternberg cells of Hodgkin's disease or the malignant cells of cutaneous T-cell lymphoma. In some cases, lymphomatoid papulosis progresses to lymphomatous conditions including mycosis fungoides, Hodgkin's disease, cutaneous T-cell lymphoma, or Ki-1 lymphoma. [NIH] Lymphoproliferative: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lymphoproliferative Disorders: Disorders characterized by proliferation of lymphoid tissue, general or unspecified. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Lysosome: A sac-like compartment inside a cell that has enzymes that can break down cellular components that need to be destroyed. [NIH] Lytic: 1. Pertaining to lysis or to a lysin. 2. Producing lysis. [EU] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Magnetic Resonance Spectroscopy: Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (magnetic resonance imaging). [NIH] Maintenance therapy: Treatment that is given to help a primary (original) treatment keep working. Maintenance therapy is often given to help keep cancer in remission. [NIH] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant mesothelioma: A rare type of cancer in which malignant cells are found in the sac lining the chest or abdomen. Exposure to airborne asbestos particles increases one's risk of developing malignant mesothelioma. [NIH] Malignant tumor: A tumor capable of metastasizing. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]
Mammary: Pertaining to the mamma, or breast. [EU] Mandible: The largest and strongest bone of the face constituting the lower jaw. It supports
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the lower teeth. [NIH] Mastication: The act and process of chewing and grinding food in the mouth. [NIH] Maxillary: Pertaining to the maxilla : the irregularly shaped bone that with its fellow forms the upper jaw. [EU] Maxillary Sinus: One of the paired paranasal sinuses, located in the body of the maxilla, communicating with the middle meatus of the nasal cavity. [NIH] Meatus: A canal running from the internal auditory foramen through the petrous portion of the temporal bone. It gives passage to the facial and auditory nerves together with the auditory branch of the basilar artery and the internal auditory veins. [NIH] Mechlorethamine: A vesicant and necrotizing irritant destructive to mucous membranes. It was formerly used as a war gas. The hydrochloride is used as an antineoplastic in Hodgkin's disease and lymphomas. It causes severe gastrointestinal and bone marrow damage. [NIH] Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Mediastinum: The area between the lungs. The organs in this area include the heart and its large blood vessels, the trachea, the esophagus, the bronchi, and lymph nodes. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Oncology: A subspecialty of internal medicine concerned with the study of neoplasms. [NIH] Medical Records: Recording of pertinent information concerning patient's illness or illnesses. [NIH] Medicament: A medicinal substance or agent. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Megakaryocytes: Very large bone marrow cells which release mature blood platelets. [NIH] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Melarsoprol: Arsenical used in trypanosomiases. It may cause fatal encephalopathy and other undesirable side effects. [NIH] Melphalan: An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - melphalan, the racemic mixture - merphalan, and the dextro isomer medphalan; toxic to bone marrow, but little vesicant action; potential carcinogen. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH]
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Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Meningeal: Refers to the meninges, the tissue covering the brain and spinal cord. [NIH] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Meningitis: Inflammation of the meninges. When it affects the dura mater, the disease is termed pachymeningitis; when the arachnoid and pia mater are involved, it is called leptomeningitis, or meningitis proper. [EU] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mentors: Senior professionals who provide guidance, direction and support to those persons desirous of improvement in academic positions, administrative positions or other career development situations. [NIH] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenchymal: Refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue. [NIH] Mesothelioma: A benign (noncancerous) or malignant (cancerous) tumor affecting the lining of the chest or abdomen. Exposure to asbestos particles in the air increases the risk of developing malignant mesothelioma. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metaphase: The second phase of cell division, in which the chromosomes line up across the equatorial plane of the spindle prior to separation. [NIH] Metaplasia: A condition in which there is a change of one adult cell type to another similar adult cell type. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Metastatic: Having to do with metastasis, which is the spread of cancer from one part of the body to another. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] Methoxsalen: A naturally occurring furocoumarin compound found in several species of plants, including Psoralea corylifolia. It is a photoactive substance that forms DNA adducts in the presence of ultraviolet A irradiation. [NIH]
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Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Mice Minute Virus: The type species of parvovirus prevalent in mouse colonies and found as a contaminant of many transplanted tumors or leukemias. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Micro-organism: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microscopy: The application of microscope magnification to the study of materials that cannot be properly seen by the unaided eye. [NIH] Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein tubulin. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Mineralization: The action of mineralizing; the state of being mineralized. [EU] Miotic: 1. Pertaining to, characterized by, or producing miosis : contraction of the pupil. 2. An agent that causes the pupil to contract. 3. Meiotic: characterized by cell division. [EU] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitoguazone: Antineoplastic agent effective against myelogenous leukemia in experimental animals. Also acts as an inhibitor of animal S-adenosylmethionine decarboxylase. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mitotic: Cell resulting from mitosis. [NIH] Mitotic inhibitors: Drugs that kill cancer cells by interfering with cell division (mitostis). [NIH]
Mitoxantrone: An anthracenedione-derived antineoplastic agent. [NIH] Mobility: Capability of movement, of being moved, or of flowing freely. [EU] Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [EU] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molar pregnancy: A rare cancer in women of child-bearing age in which cancer cells grow in the tissues that are formed in the uterus after conception. Also called gestational
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trophoblastic disease, gestational trophoblastic neoplasia, gestational trophoblastic tumor, or choriocarcinoma. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecular mass: The sum of the atomic masses of all atoms in a molecule, based on a scale in which the atomic masses of hydrogen, carbon, nitrogen, and oxygen are 1, 12, 14, and 16, respectively. For example, the molecular mass of water, which has two atoms of hydrogen and one atom of oxygen, is 18 (i.e., 2 + 16). [NIH] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocyte: A type of white blood cell. [NIH] Mononuclear: A cell with one nucleus. [NIH] Mononucleosis: The presence of an abnormally large number of mononuclear leucocytes (monocytes) in the blood. The term is often used alone to refer to infectious mononucleosis. [EU]
Monophosphate: So called second messenger for neurotransmitters and hormones. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motility: The ability to move spontaneously. [EU] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucocutaneous: Pertaining to or affecting the mucous membrane and the skin. [EU] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucositis: A complication of some cancer therapies in which the lining of the digestive system becomes inflamed. Often seen as sores in the mouth. [NIH] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multicenter study: A clinical trial that is carried out at more than one medical institution. [NIH]
Multiple Myeloma: A malignant tumor of plasma cells usually arising in the bone marrow; characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones
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proteinuria, and anemia. [NIH] Multiple sclerosis: A disorder of the central nervous system marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis is thought to be an autoimmune disease in which the body's immune system destroys myelin. Myelin is a substance that contains both protein and fat (lipid) and serves as a nerve insulator and helps in the transmission of nerve signals. [NIH] Multivalent: Pertaining to a group of 5 or more homologous or partly homologous chromosomes during the zygotene stage of prophase to first metaphasis in meiosis. [NIH] Muscle Fibers: Large single cells, either cylindrical or prismatic in shape, that form the basic unit of muscle tissue. They consist of a soft contractile substance enclosed in a tubular sheath. [NIH] Muscular Atrophy: Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Mutagenic: Inducing genetic mutation. [EU] Mycosis: Any disease caused by a fungus. [EU] Mycosis Fungoides: A chronic malignant T-cell lymphoma of the skin. In the late stages the lymph nodes and viscera are affected. [NIH] Myelin: The fatty substance that covers and protects nerves. [NIH] Myelodysplasia: Abnormal bone marrow cells that may lead to myelogenous leukemia. [NIH]
Myelodysplastic syndrome: Disease in which the bone marrow does not function normally. Also called preleukemia or smoldering leukemia. [NIH] Myelofibrosis: A disorder in which the bone marrow is replaced by fibrous tissue. [NIH] Myelogenous: Produced by, or originating in, the bone marrow. [NIH] Myeloid Cells: Cells which include the monocytes and the granulocytes. [NIH] Myeloma: Cancer that arises in plasma cells, a type of white blood cell. [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myopathy: Any disease of a muscle. [EU] Myosin: Chief protein in muscle and the main constituent of the thick filaments of muscle fibers. In conjunction with actin, it is responsible for the contraction and relaxation of muscles. [NIH] Myotonic Dystrophy: A condition presenting muscle weakness and wasting which may be progressive. [NIH] Nadir: The lowest point; point of greatest adversity or despair. [EU] Naive: Used to describe an individual who has never taken a certain drug or class of drugs (e. g., AZT-naive, antiretroviral-naive), or to refer to an undifferentiated immune system cell. [NIH] Nasopharynx: The nasal part of the pharynx, lying above the level of the soft palate. [NIH] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense
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pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Needle biopsy: The removal of tissue or fluid with a needle for examination under a microscope. Also called fine-needle aspiration. [NIH] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephropathy: Disease of the kidneys. [EU] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nerve Growth Factor: Nerve growth factor is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neurotransmitters: Endogenous signaling molecules that alter the behavior of neurons or effector cells. Neurotransmitter is used here in its most general sense, including not only messengers that act directly to regulate ion channels, but also those that act through second messenger systems, and those that act at a distance from their site of release. Included are neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not acting at synapses. [NIH] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are
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unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutropenia: An abnormal decrease in the number of neutrophils, a type of white blood cell. [NIH] Neutrophil: A type of white blood cell. [NIH] Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Non-Hodgkin's lymphoma: A group of cancers of the lymphoid system, including acute lymphoblastic leukemia, B-cell lymphoma, Burkitt's lymphoma, diffuse cell lymphoma, follicular lymphoma, immunoblastic large cell lymphoma, lymphoblastic lymphoma, mantle cell lymphoma, mycosis fungoides, post-transplantation lymphoproliferative disorder, small non-cleaved cell lymphoma, and T-cell lymphoma. [NIH] Non-small cell lung cancer: A group of lung cancers that includes squamous cell carcinoma, adenocarcinoma, and large cell carcinoma. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclear Medicine: A specialty field of radiology concerned with diagnostic, therapeutic, and investigative use of radioactive compounds in a pharmaceutical form. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleolus: A small dense body (sub organelle) within the nucleus of eukaryotic cells, visible by phase contrast and interference microscopy in live cells throughout interphase. Contains RNA and protein and is the site of synthesis of ribosomal RNA. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Occult: Obscure; concealed from observation, difficult to understand. [EU] Ocular: 1. Of, pertaining to, or affecting the eye. 2. Eyepiece. [EU] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Ointments: Semisolid preparations used topically for protective emollient effects or as a vehicle for local administration of medications. Ointment bases are various mixtures of fats, waxes, animal and plant oils and solid and liquid hydrocarbons. [NIH]
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Omega-3 fatty acid: A type of fat obtained in the diet and involved in immunity. [NIH] Onchocerciasis: Infection with nematodes of the genus Onchocerca. Characteristics include the presence of firm subcutaneous nodules filled with adult worms, pruritus, and ocular lesions. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Oncogenic Viruses: Viruses that produce tumors. [NIH] Oncology: The study of cancer. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Open Reading Frames: Reading frames where successive nucleotide triplets can be read as codons specifying amino acids and where the sequence of these triplets is not interrupted by stop codons. [NIH] Operon: The genetic unit consisting of a feedback system under the control of an operator gene, in which a structural gene transcribes its message in the form of mRNA upon blockade of a repressor produced by a regulator gene. Included here is the attenuator site of bacterial operons where transcription termination is regulated. [NIH] Ophthalmology: A surgical specialty concerned with the structure and function of the eye and the medical and surgical treatment of its defects and diseases. [NIH] Ophthalmoplegia: Paralysis of one or more of the ocular muscles due to disorders of the eye muscles, neuromuscular junction, supporting soft tissue, tendons, or innervation to the muscles. [NIH] Opportunistic Infections: An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression. [NIH] Oral Health: The optimal state of the mouth and normal functioning of the organs of the mouth without evidence of disease. [NIH] Oral Hygiene: The practice of personal hygiene of the mouth. It includes the maintenance of oral cleanliness, tissue tone, and general preservation of oral health. [NIH] Orbit: One of the two cavities in the skull which contains an eyeball. Each eye is located in a bony socket or orbit. [NIH] Orbital: Pertaining to the orbit (= the bony cavity that contains the eyeball). [EU] Organ Culture: The growth in aseptic culture of plant organs such as roots or shoots, beginning with organ primordia or segments and maintaining the characteristics of the organ. [NIH] Organ Transplantation: Transference of an organ between individuals of the same species or between individuals of different species. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Ornithine: An amino acid produced in the urea cycle by the splitting off of urea from arginine. [NIH] Ornithine Decarboxylase: A pyridoxal-phosphate protein, believed to be the rate-limiting compound in the biosynthesis of polyamines. It catalyzes the decarboxylation of ornithine to form putrescine, which is then linked to a propylamine moiety of decarboxylated S-
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adenosylmethionine to form spermidine. EC 4.1.1.17. [NIH] Osteogenic sarcoma: A malignant tumor of the bone. Also called osteosarcoma. [NIH] Osteosarcoma: A cancer of the bone that affects primarily children and adolescents. Also called osteogenic sarcoma. [NIH] Outpatient: A patient who is not an inmate of a hospital but receives diagnosis or treatment in a clinic or dispensary connected with the hospital. [NIH] Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily. [NIH] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overall survival: The percentage of subjects in a study who have survived for a defined period of time. Usually reported as time since diagnosis or treatment. Often called the survival rate. [NIH] Overexpress: An excess of a particular protein on the surface of a cell. [NIH] Oxaliplatin: An anticancer drug that belongs to the family of drugs called platinum compounds. [NIH] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]
Oxidative Phosphorylation: Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds. [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] P53 gene: A tumor suppressor gene that normally inhibits the growth of tumors. This gene is altered in many types of cancer. [NIH] Pacemaker: An object or substance that influences the rate at which a certain phenomenon occurs; often used alone to indicate the natural cardiac pacemaker or an artificial cardiac pacemaker. In biochemistry, a substance whose rate of reaction sets the pace for a series of interrelated reactions. [EU] Pachymeningitis: Inflammation of the dura mater of the brain, the spinal cord or the optic nerve. [NIH] Paclitaxel: Antineoplastic agent isolated from the bark of the Pacific yew tree, Taxus brevifolia. Paclitaxel stabilizes microtubules in their polymerized form and thus mimics the action of the proto-oncogene proteins c-mos. [NIH] Paediatric: Of or relating to the care and medical treatment of children; belonging to or concerned with paediatrics. [EU] Palate: The structure that forms the roof of the mouth. It consists of the anterior hard palate and the posterior soft palate. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU]
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Palsies: Disease of the peripheral nervous system occurring usually after many years of increased lead absorption. [NIH] Palsy: Disease of the peripheral nervous system occurring usually after many years of increased lead absorption. [NIH] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Pancreatitis: Acute or chronic inflammation of the pancreas, which may be asymptomatic or symptomatic, and which is due to autodigestion of a pancreatic tissue by its own enzymes. It is caused most often by alcoholism or biliary tract disease; less commonly it may be associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU] Pancytopenia: Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets. [NIH] Panniculitis: General term for inflammation of adipose tissue, usually of the skin, characterized by reddened subcutaneous nodules. [NIH] Papilloma: A benign epithelial neoplasm which may arise from the skin, mucous membranes or glandular ducts. [NIH] Papillomavirus: A genus of Papovaviridae causing proliferation of the epithelium, which may lead to malignancy. A wide range of animals are infected including humans, chimpanzees, cattle, rabbits, dogs, and horses. [NIH] Papovaviridae: A family of small, non-enveloped DNA viruses affecting mostly mammals. Most members can induce tumors in hosts. There are two genera: Papillomavirus and Polyomavirus. [NIH] Paraffin: A mixture of solid hydrocarbons obtained from petroleum. It has a wide range of uses including as a stiffening agent in ointments, as a lubricant, and as a topical antiinflammatory. It is also commonly used as an embedding material in histology. [NIH] Paranasal Sinuses: Air-filled extensions of the respiratory part of the nasal cavity into the frontal, ethmoid, sphenoid, and maxillary cranial bones. They vary in size and form in different individuals and are lined by the ciliated mucous membranes of the nasal cavity. [NIH]
Parietal: 1. Of or pertaining to the walls of a cavity. 2. Pertaining to or located near the parietal bone, as the parietal lobe. [EU] Parotid: The space that contains the parotid gland, the facial nerve, the external carotid artery, and the retromandibular vein. [NIH] Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Partial remission: The shrinking, but not complete disappearance, of a tumor in response to therapy. Also called partial response. [NIH] Particle: A tiny mass of material. [EU] Parvovirus: A genus of the family Parvoviridae, subfamily Parvovirinae, infecting a variety of vertebrates including humans. Parvoviruses are responsible for a number of important diseases but also can be non-pathogenic in certain hosts. The type species is mice minute virus. [NIH]
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Patch: A piece of material used to cover or protect a wound, an injured part, etc.: a patch over the eye. [NIH] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]
Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Education: The teaching or training of patients concerning their own health needs. [NIH]
PDQ: Physician Data Query. PDQ is an online database developed and maintained by the National Cancer Institute. Designed to make the most current, credible, and accurate cancer information available to health professionals and the public, PDQ contains peer-reviewed summaries on cancer treatment, screening, prevention, genetics, and supportive care; a registry of cancer clinical trials from around the world; and directories of physicians, professionals who provide genetics services, and organizations that provide cancer care. Most of this information is available on the CancerNet Web site, and more specific information about PDQ can be found at http://cancernet.nci.nih.gov/pdq.html. [NIH] Pelvic: Pertaining to the pelvis. [EU] Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [NIH] Pentamidine: Antiprotozoal agent effective in trypanosomiasis, leishmaniasis, and some fungal infections; used in treatment of Pneumocystis carinii pneumonia in HIV-infected patients. It may cause diabetes mellitus, central nervous system damage, and other toxic effects. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Pepsin A: Formed from pig pepsinogen by cleavage of one peptide bond. The enzyme is a single polypeptide chain and is inhibited by methyl 2-diaazoacetamidohexanoate. It cleaves peptides preferentially at the carbonyl linkages of phenylalanine or leucine and acts as the principal digestive enzyme of gastric juice. [NIH] Peptic: Pertaining to pepsin or to digestion; related to the action of gastric juices. [EU] Peptic Ulcer: Ulcer that occurs in those portions of the alimentary tract which come into contact with gastric juice containing pepsin and acid. It occurs when the amount of acid and pepsin is sufficient to overcome the gastric mucosal barrier. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Percutaneous: Performed through the skin, as injection of radiopacque material in radiological examination, or the removal of tissue for biopsy accomplished by a needle. [EU] Perennial: Lasting through the year of for several years. [EU] Performance status: A measure of how well a patient is able to perform ordinary tasks and carry out daily activities. [NIH]
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Pericardium: The fibroserous sac surrounding the heart and the roots of the great vessels. [NIH]
Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Periodontitis: Inflammation of the periodontal membrane; also called periodontitis simplex. [NIH]
Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral stem cell transplantation: A method of replacing blood-forming cells destroyed by cancer treatment. Immature blood cells (stem cells) in the circulating blood that are similar to those in the bone marrow are given after treatment to help the bone marrow recover and continue producing healthy blood cells. Transplantation may be autologous (an individual's own blood cells saved earlier), allogeneic (blood cells donated by someone else), or syngeneic (blood cells donated by an identical twin). Also called peripheral stem cell support. [NIH] Peripheral stem cells: Immature cells found circulating in the bloodstream. New blood cells develop from peripheral stem cells. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] Petroleum: Naturally occurring complex liquid hydrocarbons which, after distillation, yield combustible fuels, petrochemicals, and lubricants. [NIH] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Phallic: Pertaining to the phallus, or penis. [EU] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH]
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Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phorbol: Class of chemicals that promotes the development of tumors. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylating: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photochemotherapy: Therapy using oral or topical photosensitizing agents with subsequent exposure to light. [NIH] Photopheresis: A process in which peripheral blood is exposed in an extracorporeal flow system to photoactivated 8-methoxypsoralen (methoxsalen) and ultraviolet light - a procedure known as PUVA therapy. Photopheresis is at present a standard therapy for advanced cutaneous T-cell lymphoma; it shows promise in the treatment of autoimmune diseases. [NIH] Photosensitizing Agents: Drugs that are pharmacologically inactive but when exposed to ultraviolet radiation or sunlight are converted to their active metabolite to produce a beneficial reaction affecting the diseased tissue. These compounds can be administered topically or systemically and have been used therapeutically to treat psoriasis and various types of neoplasms. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physical Fitness: A state of well-being in which performance is optimal, often as a result of physical conditioning which may be prescribed for disease therapy. [NIH] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]
Phytohemagglutinins: Mucoproteins isolated from the kidney bean (Phaseolus vulgaris); some of them are mitogenic to lymphocytes, others agglutinate all or certain types of erythrocytes or lymphocytes. They are used mainly in the study of immune mechanisms and in cell culture. [NIH] Phytotoxin: A substance which is toxic for plants. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Pigmentation: Coloration or discoloration of a part by a pigment. [NIH] Pilocarpine: A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pineal gland: A tiny organ located in the cerebrum that produces melatonin. Also called pineal body or pineal organ. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of
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organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasmapheresis: Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use. [NIH] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [NIH] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelet Count: A count of the number of platelets per unit volume in a sample of venous blood. [NIH] Plateletpheresis: The preparation of platelet concentrates with the return of red cells and platelet-poor plasma to the donor. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]
Platinum Compounds: Inorganic compounds which contain platinum as the central atom. [NIH]
Pleura: The thin serous membrane enveloping the lungs and lining the thoracic cavity. [NIH] Pleural: A circumscribed area of hyaline whorled fibrous tissue which appears on the surface of the parietal pleura, on the fibrous part of the diaphragm or on the pleura in the interlobar fissures. [NIH] Pleural cavity: A space enclosed by the pleura (thin tissue covering the lungs and lining the interior wall of the chest cavity). It is bound by thin membranes. [NIH]
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Pleural Effusion: Presence of fluid in the pleural cavity resulting from excessive transudation or exudation from the pleural surfaces. It is a sign of disease and not a diagnosis in itself. [NIH] Pneumococcal Vaccines: Vaccines or candidate vaccines used to prevent infections with Streptococcus pneumoniae. [NIH] Podophyllotoxin: The main active constituent of the resin from the roots of may apple or mandrake (Podophyllum peltatum and P. emodi). It is a potent spindle poison, toxic if taken internally, and has been used as a cathartic. It is very irritating to skin and mucous membranes, has keratolytic actions, has been used to treat warts and keratoses, and may have antineoplastic properties, as do some of its congeners and derivatives. [NIH] Point Mutation: A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH] Polyethylene: A vinyl polymer made from ethylene. It can be branched or linear. Branched or low-density polyethylene is tough and pliable but not to the same degree as linear polyethylene. Linear or high-density polyethylene has a greater hardness and tensile strength. Polyethylene is used in a variety of products, including implants and prostheses. [NIH]
Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polyomavirus: A genus of the family papovaviridae consisting of potentially oncogenic viruses normally present in the host as a latent infection. The virus is oncogenic in hosts different from the species of origin. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Polyvalent: Having more than one valence. [EU]
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Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Potentiate: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiating: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH] Preclinical: Before a disease becomes clinically recognizable. [EU] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states. [NIH] Prednisone: A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [NIH] Preleukemia: Conditions in which the abnormalities in the peripheral blood or bone marrow represent the early manifestations of acute leukemia, but in which the changes are not of sufficient magnitude or specificity to permit a diagnosis of acute leukemia by the usual clinical criteria. [NIH] Premalignant: A term used to describe a condition that may (or is likely to) become cancer. Also called precancerous. [NIH] Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Prickle: Several layers of the epidermis where the individual cells are connected by cell bridges. [NIH] Primary central nervous system lymphoma: Cancer that arises in the lymphoid tissue found in the central nervous system (CNS). The CNS includes the brain and spinal cord.
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[NIH]
Primary tumor: The original tumor. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH] Procarbazine: An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease. [NIH] Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] Progeny: The offspring produced in any generation. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Prognostic factor: A situation or condition, or a characteristic of a patient, that can be used to estimate the chance of recovery from a disease, or the chance of the disease recurring (coming back). [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Progressive disease: Cancer that is increasing in scope or severity. [NIH] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Promyelocytic leukemia: A type of acute myeloid leukemia, a quickly progressing disease in which too many immature blood-forming cells are found in the blood and bone marrow. [NIH]
Prone: Having the front portion of the body downwards. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH]
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Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein Kinases: A family of enzymes that catalyze the conversion of ATP and a protein to ADP and a phosphoprotein. EC 2.7.1.37. [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Proton Pump: Integral membrane proteins that transport protons across a membrane against a concentration gradient. This transport is driven by hydrolysis of ATP by H(+)transporting ATP synthase. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity. [NIH] Proto-Oncogene Proteins c-mos: Cellular proteins encoded by the c-mos genes. They function in the cell cycle to maintain maturation promoting factor in the active state and have protein-serine/threonine kinase activity. Oncogenic transformation can take place when c-mos proteins are expressed at the wrong time. [NIH] Proto-Oncogenes: Normal cellular genes homologous to viral oncogenes. The products of proto-oncogenes are important regulators of biological processes and appear to be involved in the events that serve to maintain the ordered procession through the cell cycle. Protooncogenes have names of the form c-onc. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Provirus: Virus that is integrated into the chromosome of a host cell and is transmitted in that form from one host cell generation to another without leading to the lysis of the host cells. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Pruritic: Pertaining to or characterized by pruritus. [EU] Pruritus: An intense itching sensation that produces the urge to rub or scratch the skin to
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obtain relief. [NIH] Psoralen: A substance that binds to the DNA in cells and stops them from multiplying. It is being studied in the treatment of graft-versus-host disease and is used in the treatment of psoriasis and vitiligo. [NIH] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychological Tests: Standardized tests designed to measure abilities, as in intelligence, aptitude, and achievement tests, or to evaluate personality traits. [NIH] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]
Pulmonary: Relating to the lungs. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]
Purifying: Respiratory equipment whose function is to remove contaminants from otherwise wholesome air. [NIH] Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include adenine and guanine, constituents of nucleic acids, as well as many alkaloids such as caffeine and theophylline. Uric acid is the metabolic end product of purine metabolism. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Pustular: Pertaining to or of the nature of a pustule; consisting of pustules (= a visible collection of pus within or beneath the epidermis). [EU] Putrescine: A toxic diamine formed by putrefaction from the decarboxylation of arginine and ornithine. [NIH] Pyoderma: Any purulent skin disease (Dorland, 27th ed). [NIH] Pyoderma Gangrenosum: An idiopathic, rapidly evolving, and severely debilitating disease occurring most commonly in association with chronic ulcerative colitis. It is characterized by the presence of boggy, purplish ulcers with undermined borders, appearing mostly on the legs. The majority of cases are in people between 40 and 60 years old. Its etiology is
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unknown. [NIH] Pyridoxal: 3-Hydroxy-5-(hydroxymethyl)-2-methyl-4- pyridinecarboxaldehyde. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quiescent: Marked by a state of inactivity or repose. [EU] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation Oncology: A subspecialty of medical oncology and radiology concerned with the radiotherapy of cancer. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radioactivity: The quality of emitting or the emission of corpuscular or electromagnetic radiations consequent to nuclear disintegration, a natural property of all chemical elements of atomic number above 83, and possible of induction in all other known elements. [EU] Radioimmunotherapy: Radiotherapy where cytotoxic radionuclides are linked to antibodies in order to deliver toxins directly to tumor targets. Therapy with targeted radiation rather than antibody-targeted toxins (immunotoxins) has the advantage that adjacent tumor cells, which lack the appropriate antigenic determinants, can be destroyed by radiation cross-fire. Radioimmunotherapy is sometimes called targeted radiotherapy, but this latter term can also refer to radionuclides linked to non-immune molecules (radiotherapy). [NIH] Radioisotope: An unstable element that releases radiation as it breaks down. Radioisotopes can be used in imaging tests or as a treatment for cancer. [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Radiopharmaceuticals: Drugs containing a radioactive substance that are used in the diagnosis and treatment of cancer and in pain management of bone metastases. Also called radioactive drugs. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects
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are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Ras gene: A gene that has been found to cause cancer when it is altered (mutated). Agents that block its activity may stop the growth of cancer. A ras peptide is a protein fragment produced by the ras gene. [NIH] Reactivation: The restoration of activity to something that has been inactivated. [EU] Reactive Oxygen Species: Reactive intermediate oxygen species including both radicals and non-radicals. These substances are constantly formed in the human body and have been shown to kill bacteria and inactivate proteins, and have been implicated in a number of diseases. Scientific data exist that link the reactive oxygen species produced by inflammatory phagocytes to cancer development. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Antigen: Molecules on the surface of B- and T-lymphocytes that recognize and combine with specific antigens. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Reconstitution: 1. A type of regeneration in which a new organ forms by the rearrangement of tissues rather than from new formation at an injured surface. 2. The restoration to original form of a substance previously altered for preservation and storage, as the restoration to a liquid state of blood serum or plasma that has been dried and stored. [EU] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Refractory: Not readily yielding to treatment. [EU] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU]
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Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regional lymph node: In oncology, a lymph node that drains lymph from the region around a tumor. [NIH] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Remission Induction: Therapeutic act or process that initiates a response to a complete or partial remission level. [NIH] Repressor: Any of the specific allosteric protein molecules, products of regulator genes, which bind to the operator of operons and prevent RNA polymerase from proceeding into the operon to transcribe messenger RNA. [NIH] Reproductive cells: Egg and sperm cells. Each mature reproductive cell carries a single set of 23 chromosomes. [NIH] Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly. [NIH] Research Support: Financial support of research activities. [NIH] Resected: Surgical removal of part of an organ. [NIH] Resection: Removal of tissue or part or all of an organ by surgery. [NIH] Residual disease: Cancer cells that remain after attempts have been made to remove the cancer. [NIH] Resorption: The loss of substance through physiologic or pathologic means, such as loss of dentin and cementum of a tooth, or of the alveolar process of the mandible or maxilla. [EU] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Response rate: The percentage of patients whose cancer shrinks or disappears after treatment. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative
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enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinoblastoma: An eye cancer that most often occurs in children younger than 5 years. It occurs in hereditary and nonhereditary (sporadic) forms. [NIH] Retinoid: Vitamin A or a vitamin A-like compound. [NIH] Retrospective: Looking back at events that have already taken place. [NIH] Retrospective study: A study that looks backward in time, usually using medical records and interviews with patients who already have or had a disease. [NIH] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Retrovirus: A member of a group of RNA viruses, the RNA of which is copied during viral replication into DNA by reverse transcriptase. The viral DNA is then able to be integrated into the host chromosomal DNA. [NIH] Rheumatic Diseases: Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Ribavirin: 1-beta-D-Ribofuranosyl-1H-1,2,4-triazole-3-carboxamide. A nucleoside antimetabolite antiviral agent that blocks nucleic acid synthesis and is used against both RNA and DNA viruses. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Ribosome: A granule of protein and RNA, synthesized in the nucleolus and found in the cytoplasm of cells. Ribosomes are the main sites of protein synthesis. Messenger RNA attaches to them and there receives molecules of transfer RNA bearing amino acids. [NIH] Ricin: A protein phytotoxin from the seeds of Ricinus communis, the castor oil plant. It agglutinates cells, is proteolytic, and causes lethal inflammation and hemorrhage if taken internally. [NIH] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Risk patient: Patient who is at risk, because of his/her behaviour or because of the type of person he/she is. [EU] Rituximab: A type of monoclonal antibody used in cancer detection or therapy. Monoclonal antibodies are laboratory-produced substances that can locate and bind to cancer cells. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rodenticides: Substances used to destroy or inhibit the action of rats, mice, or other rodents. [NIH]
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Rosette Formation: The in vitro formation of clusters consisting of a cell (usually a lymphocyte) surrounded by antigenic cells or antigen-bearing particles (usually erythrocytes, which may or may not be coated with antibody or antibody and complement). The rosette-forming cell may be an antibody-forming cell, a memory cell, a T-cell, a cell bearing surface cytophilic antibodies, or a monocyte possessing Fc receptors. Rosette formation can be used to identify specific populations of these cells. [NIH] Rye: A hardy grain crop, Secale cereale, grown in northern climates. It is the most frequent host to ergot (claviceps), the toxic fungus. Its hybrid with wheat is triticale, another grain. [NIH]
S Phase: Phase of the cell cycle following G1 and preceding G2 when the entire DNA content of the nucleus is replicated. It is achieved by bidirectional replication at multiple sites along each chromosome. [NIH] Sagittal: The line of direction passing through the body from back to front, or any vertical plane parallel to the medial plane of the body and inclusive of that plane; often restricted to the medial plane, the plane of the sagittal suture. [NIH] Saimiri: A genus of the family Cebidae consisting of four species: S. boliviensis, S. orstedii (red-backed squirrel monkey), S. sciureus (common squirrel monkey), and S. ustus. They inhabit tropical rain forests in Central and South America. S. sciureus is used extensively in research studies. [NIH] Saliva: The clear, viscous fluid secreted by the salivary glands and mucous glands of the mouth. It contains mucins, water, organic salts, and ptylin. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Salvage Therapy: A therapeutic approach, involving chemotherapy, radiation therapy, or surgery, after initial regimens have failed to lead to improvement in a patient's condition. Salvage therapy is most often used for neoplastic diseases. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Sarcoidosis: An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands. [NIH] Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant. [NIH] Sargramostim: A colony-stimulating factor that stimulates the production of blood cells, especially platelets, during chemotherapy. It is a cytokine that belongs to the family of drugs called hematopoietic (blood-forming) agents. Also called GM-CSF. [NIH] Scans: Pictures of structures inside the body. Scans often used in diagnosing, staging, and monitoring disease include liver scans, bone scans, and computed tomography (CT) or computerized axial tomography (CAT) scans and magnetic resonance imaging (MRI) scans. In liver scanning and bone scanning, radioactive substances that are injected into the bloodstream collect in these organs. A scanner that detects the radiation is used to create pictures. In CT scanning, an x-ray machine linked to a computer is used to produce detailed pictures of organs inside the body. MRI scans use a large magnet connected to a computer to
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create pictures of areas inside the body. [NIH] Scatter: The extent to which relative success and failure are divergently manifested in qualitatively different tests. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Scleroderma: A chronic disorder marked by hardening and thickening of the skin. Scleroderma can be localized or it can affect the entire body (systemic). [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Secondary tumor: Cancer that has spread from the organ in which it first appeared to another organ. For example, breast cancer cells may spread (metastasize) to the lungs and cause the growth of a new tumor. When this happens, the disease is called metastatic breast cancer, and the tumor in the lungs is called a secondary tumor. Also called secondary cancer. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Selective estrogen receptor modulator: SERM. A drug that acts like estrogen on some tissues, but blocks the effect of estrogen on other tissues. Tamoxifen and raloxifene are SERMs. [NIH] Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase. [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Seminal vesicles: Glands that help produce semen. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senescence: The bodily and mental state associated with advancing age. [NIH] Sensitization: 1. Administration of antigen to induce a primary immune response; priming;
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immunization. 2. Exposure to allergen that results in the development of hypersensitivity. 3. The coating of erythrocytes with antibody so that they are subject to lysis by complement in the presence of homologous antigen, the first stage of a complement fixation test. [EU] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septal: An abscess occurring at the root of the tooth on the proximal surface. [NIH] Sequela: Any lesion or affection following or caused by an attack of disease. [EU] Sequencing: The determination of the order of nucleotides in a DNA or RNA chain. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines, pyrimidines, and other amino acids. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Serous: Having to do with serum, the clear liquid part of blood. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Sex Determination: The biological characteristics which distinguish human beings as female or male. [NIH] Shedding: Release of infectious particles (e. g., bacteria, viruses) into the environment, for example by sneezing, by fecal excretion, or from an open lesion. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]
Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH]
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Signs and Symptoms: Clinical manifestations that can be either objective when observed by a physician, or subjective when perceived by the patient. [NIH] Single-agent: The use of a single drug or other therapy. [NIH] Sister Chromatid Exchange: An exchange of segments between the sister chromatids of a chromosome, either between the sister chromatids of a meiotic tetrad or between the sister chromatids of a duplicated somatic chromosome. Its frequency is increased by ultraviolet and ionizing radiation and other mutagenic agents and is particularly high in Bloom syndrome. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skin Care: Maintenance of the hygienic state of the skin under optimal conditions of cleanliness and comfort. Effective in skin care are proper washing, bathing, cleansing, and the use of soaps, detergents, oils, etc. In various disease states, therapeutic and protective solutions and ointments are useful. The care of the skin is particularly important in various occupations, in exposure to sunlight, in neonates, and in decubitus ulcer. [NIH] Skin Manifestations: Dermatologic disorders attendant upon non-dermatologic disease or injury. [NIH] Sleep apnea: A serious, potentially life-threatening breathing disorder characterized by repeated cessation of breathing due to either collapse of the upper airway during sleep or absence of respiratory effort. [NIH] Small cell lung cancer: A type of lung cancer in which the cells appear small and round when viewed under the microscope. Also called oat cell lung cancer. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smoldering leukemia: Disease in which the bone marrow does not function normally. Also called preleukemia or myelodysplastic syndrome. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]
Sneezing: Sudden, forceful, involuntary expulsion of air from the nose and mouth caused by irritation to the mucous membranes of the upper respiratory tract. [NIH] Soaps: Sodium or potassium salts of long chain fatty acids. These detergent substances are obtained by boiling natural oils or fats with caustic alkali. Sodium soaps are harder and are used as topical anti-infectives and vehicles in pills and liniments; potassium soaps are soft, used as vehicles for ointments and also as topical antimicrobials. [NIH] Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH]
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Soft tissue sarcoma: A sarcoma that begins in the muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solid tumor: Cancer of body tissues other than blood, bone marrow, or the lymphatic system. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatic cells: All the body cells except the reproductive (germ) cells. [NIH] Somatic mutations: Alterations in DNA that occur after conception. Somatic mutations can occur in any of the cells of the body except the germ cells (sperm and egg) and therefore are not passed on to children. These alterations can (but do not always) cause cancer or other diseases. [NIH] Spastic: 1. Of the nature of or characterized by spasms. 2. Hypertonic, so that the muscles are stiff and the movements awkward. 3. A person exhibiting spasticity, such as occurs in spastic paralysis or in cerebral palsy. [EU] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Spermatic: A cord-like structure formed by the vas deferens and the blood vessels, nerves and lymphatics of the testis. [NIH] Spermidine: A polyamine formed from putrescine. It is found in almost all tissues in association with nucleic acids. It is found as a cation at all pH values, and is thought to help stabilize some membranes and nucleic acid structures. It is a precursor of spermine. [NIH] Sphincter: A ringlike band of muscle fibres that constricts a passage or closes a natural orifice; called also musculus sphincter. [EU] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spinal Nerves: The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included. [NIH] Spinous: Like a spine or thorn in shape; having spines. [NIH] Spirochete: Lyme disease. [NIH]
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Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Splenomegaly: Enlargement of the spleen. [NIH] Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Squamous: Scaly, or platelike. [EU] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cells: Flat cells that look like fish scales under a microscope. These cells cover internal and external surfaces of the body. [NIH] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]
Standard therapy: A currently accepted and widely used treatment for a certain type of cancer, based on the results of past research. [NIH] Status Epilepticus: Repeated and prolonged epileptic seizures without recovery of consciousness between attacks. [NIH] Stem cell transplantation: A method of replacing immature blood-forming cells that were destroyed by cancer treatment. The stem cells are given to the person after treatment to help the bone marrow recover and continue producing healthy blood cells. [NIH] Stem Cells: Relatively undifferentiated cells of the same lineage (family type) that retain the ability to divide and cycle throughout postnatal life to provide cells that can become specialized and take the place of those that die or are lost. [NIH] Sterile: Unable to produce children. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU]
Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stochastic Processes: Processes that incorporate some element of randomness, used particularly to refer to a time series of random variables. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between
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the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Streptavidin: A 60kD extracellular protein of Streptomyces avidinii with four high-affinity biotin binding sites. Unlike AVIDIN, streptavidin has a near neutral isoelectric point and is free of carbohydrate side chains. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subarachnoid: Situated or occurring between the arachnoid and the pia mater. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Sublingual: Located beneath the tongue. [EU] Submandibular: Four to six lymph glands, located between the lower jaw and the submandibular salivary gland. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]
Substrate: A substance upon which an enzyme acts. [EU] Suction: The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure. [NIH] Sunburn: An injury to the skin causing erythema, tenderness, and sometimes blistering and resulting from excessive exposure to the sun. The reaction is produced by the ultraviolet radiation in sunlight. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Supportive care: Treatment given to prevent, control, or relieve complications and side effects and to improve the comfort and quality of life of people who have cancer. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Supratentorial: Located in the upper part of the brain. [NIH]
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Survival Analysis: A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function. [NIH] Survival Rate: The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods. [NIH] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synapses: Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate through direct electrical connections which are sometimes called electrical synapses; these are not included here but rather in gap junctions. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Vesicles: Membrane-bound compartments which contain transmitter molecules. Synaptic vesicles are concentrated at presynaptic terminals. They actively sequester transmitter molecules from the cytoplasm. In at least some synapses, transmitter release occurs by fusion of these vesicles with the presynaptic membrane, followed by exocytosis of their contents. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Syphilis: A contagious venereal disease caused by the spirochete Treponema pallidum. [NIH]
Systemic: Affecting the entire body. [NIH] Systemic lupus erythematosus: SLE. A chronic inflammatory connective tissue disease marked by skin rashes, joint pain and swelling, inflammation of the kidneys, inflammation of the fibrous tissue surrounding the heart (i.e., the pericardium), as well as other problems. Not all affected individuals display all of these problems. May be referred to as lupus. [NIH] Systemic therapy: Treatment that uses substances that travel through the bloodstream, reaching and affecting cells all over the body. [NIH] Tachycardia: Excessive rapidity in the action of the heart, usually with a heart rate above 100 beats per minute. [NIH] Tachypnea: Rapid breathing. [NIH] Tamoxifen: A first generation selective estrogen receptor modulator (SERM). It acts as an agonist for bone tissue and cholesterol metabolism but is an estrogen antagonist in mammary and uterine. [NIH] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Teniposide: A semisynthetic derivative of podophyllotoxin that exhibits antitumor activity.
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Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle. [NIH] Teratogenic: Tending to produce anomalies of formation, or teratism (= anomaly of formation or development : condition of a monster). [EU] Teratoma: A type of germ cell tumor that may contain several different types of tissue, such as hair, muscle, and bone. Teratomas occur most often in the ovaries in women, the testicles in men, and the tailbone in children. Not all teratomas are malignant. [NIH] Testicular: Pertaining to a testis. [EU] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetravalent: Pertaining to a group of 4 homologous or partly homologous chromosomes during the zygotene stage of prophase to the first metaphase in meiosis. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Thalassemia: A group of hereditary hemolytic anemias in which there is decreased synthesis of one or more hemoglobin polypeptide chains. There are several genetic types with clinical pictures ranging from barely detectable hematologic abnormality to severe and fatal anemia. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Thoracic: Having to do with the chest. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Thorium Dioxide: Thorium oxide (ThO2). A radiographic contrast agent that was used in the early 1930s through about 1954. High rates of mortality have been linked to its use and it has been shown to cause liver cancer. [NIH] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytes: Blood cells that help prevent bleeding by causing blood clots to form. Also called platelets. [NIH] Thrombocytopenia: A decrease in the number of blood platelets. [NIH] Thromboembolism: Obstruction of a vessel by a blood clot that has been transported from a distant site by the blood stream. [NIH]
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Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]
Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thymidine: A chemical compound found in DNA. Also used as treatment for mucositis. [NIH]
Thymidine Kinase: An enzyme that catalyzes the conversion of ATP and thymidine to ADP and thymidine 5'-phosphate. Deoxyuridine can also act as an acceptor and dGTP as a donor. (From Enzyme Nomenclature, 1992) EC 2.7.1.21. [NIH] Thymus: An organ that is part of the lymphatic system, in which T lymphocytes grow and multiply. The thymus is in the chest behind the breastbone. [NIH] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyroid Gland: A highly vascular endocrine gland consisting of two lobes, one on either side of the trachea, joined by a narrow isthmus; it produces the thyroid hormones which are concerned in regulating the metabolic rate of the body. [NIH] Thyroid Hormones: Hormones secreted by the thyroid gland. [NIH] Thyroiditis: Inflammation of the thyroid gland. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Culture: Maintaining or growing of tissue, organ primordia, or the whole or part of an organ in vitro so as to preserve its architecture and/or function (Dorland, 28th ed). Tissue culture includes both organ culture and cell culture. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tome: A zone produced by a number of irregular spaces contained in the outermost layer of denture of the root of a tooth. [NIH] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tonsil: A round-to-oval mass of lymphoid tissue embedded in the lateral wall of the pharynx situated on each side of the fauces, between the anterior and posterior pillars of the soft palate. [NIH] Topical: On the surface of the body. [NIH] Topoisomerase inhibitors: A family of anticancer drugs. The topoisomerase enzymes are responsible for the arrangement and rearrangement of DNA in the cell and for cell growth and replication. Inhibiting these enzymes may kill cancer cells or stop their growth. [NIH] Topotecan: An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA topoisomerase. [NIH] Total-body irradiation: Radiation therapy to the entire body. Usually followed by bone marrow or peripheral stem cell transplantation. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic
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microbe or of a poison. [EU] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxins: Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals. [NIH] Toxoplasmosis: The acquired form of infection by Toxoplasma gondii in animals and man. [NIH]
Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Tracer: A substance (such as a radioisotope) used in imaging procedures. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Transcriptase: An enzyme which catalyses the synthesis of a complementary mRNA molecule from a DNA template in the presence of a mixture of the four ribonucleotides (ATP, UTP, GTP and CTP). [NIH] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle (pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfer Factor: Factor derived from leukocyte lysates of immune donors which can transfer both local and systemic cellular immunity to nonimmune recipients. [NIH] Transforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGFbeta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins. [NIH]
Translating: Conversion from one language to another language. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock,
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producing a disturbance. [NIH] Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, practicability, etc., of these interventions in individual cases or series. [NIH]
Trees: Woody, usually tall, perennial higher plants (Angiosperms, Gymnosperms, and some Pterophyta) having usually a main stem and numerous branches. [NIH] Triage: The sorting out and classification of patients or casualties to determine priority of need and proper place of treatment. [NIH] Tricuspid Valve: The valve consisting of three cusps situated between the right atrium and right ventricle of the heart. [NIH] Trigeminal: Cranial nerve V. It is sensory for the eyeball, the conjunctiva, the eyebrow, the skin of face and scalp, the teeth, the mucous membranes in the mouth and nose, and is motor to the muscles of mastication. [NIH] Tropism: Directed movements and orientations found in plants, such as the turning of the sunflower to face the sun. [NIH] Trypanosomiasis: Infection with protozoa of the genus Trypanosoma. [NIH] Trypsin: A serine endopeptidase that is formed from trypsinogen in the pancreas. It is converted into its active form by enteropeptidase in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberculosis: Any of the infectious diseases of man and other animals caused by species of Mycobacterium. [NIH] Tuberous Sclerosis: A rare congenital disease in which the essential pathology is the appearance of multiple tumors in the cerebrum and in other organs, such as the heart or kidneys. [NIH] Tumor Escape: The ability of tumors to evade destruction by the immune system. Theories concerning possible mechanisms by which this takes place involve both cellular and humoral immunity, and also costimulatory pathways related to CD28 antigens and CD80 antigens. [NIH] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tumor model: A type of animal model which can be used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumor suppressor gene: Genes in the body that can suppress or block the development of cancer. [NIH] Tumor-derived: Taken from an individual's own tumor tissue; may be used in the
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development of a vaccine that enhances the body's ability to build an immune response to the tumor. [NIH] Tumorigenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH]
Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] TYPHI: The bacterium that gives rise to typhoid fever. [NIH] Typhoid fever: The most important member of the enteric group of fevers which also includes the paratyphoids. [NIH] Typhoid fever: The most important member of the enteric group of fevers which also includes the paratyphoids. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Ulcerative colitis: Chronic inflammation of the colon that produces ulcers in its lining. This condition is marked by abdominal pain, cramps, and loose discharges of pus, blood, and mucus from the bowel. [NIH] Ultrasonography: The visualization of deep structures of the body by recording the reflections of echoes of pulses of ultrasonic waves directed into the tissues. Use of ultrasound for imaging or diagnostic purposes employs frequencies ranging from 1.6 to 10 megahertz. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Unresectable: Unable to be surgically removed. [NIH] Uraemia: 1. An excess in the blood of urea, creatinine, and other nitrogenous end products of protein and amino acids metabolism; more correctly referred to as azotemia. 2. In current usage the entire constellation of signs and symptoms of chronic renal failure, including nausea, vomiting anorexia, a metallic taste in the mouth, a uraemic odour of the breath, pruritus, uraemic frost on the skin, neuromuscular disorders, pain and twitching in the muscles, hypertension, edema, mental confusion, and acid-base and electrolyte imbalances. [EU]
Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]
Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] Urogenital System: All the organs involved in reproduction and the formation and release
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of urine. It includes the kidneys, ureters, bladder, urethra, and the organs of reproduction ovaries, uterus, fallopian tubes, vagina, and clitoris in women and the testes, seminal vesicles, prostate, seminal ducts, and penis in men. [NIH] Urokinase: A drug that dissolves blood clots or prevents them from forming. [NIH] Urticaria: A vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginitis: Inflammation of the vagina characterized by pain and a purulent discharge. [NIH] Valves: Flap-like structures that control the direction of blood flow through the heart. [NIH] Varicella: Chicken pox. [EU] Vas Deferens: The excretory duct of the testes that carries spermatozoa. It rises from the scrotum and joins the seminal vesicles to form the ejaculatory duct. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vascular endothelial growth factor: VEGF. A substance made by cells that stimulates new blood vessel formation. [NIH] Vasculitis: Inflammation of a blood vessel. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] VE: The total volume of gas either inspired or expired in one minute. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venereal: Pertaining or related to or transmitted by sexual contact. [EU] Venoms: Poisonous animal secretions forming fluid mixtures of many different enzymes, toxins, and other substances. These substances are produced in specialized glands and secreted through specialized delivery systems (nematocysts, spines, fangs, etc.) for disabling prey or predator. [NIH] Venous: Of or pertaining to the veins. [EU] Venous blood: Blood that has given up its oxygen to the tissues and carries carbon dioxide back for gas exchange. [NIH] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU]
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Ventricular Dysfunction: A condition in which the ventricles of the heart exhibit a decreased functionality. [NIH] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU] Veterinarians: Individuals with a degree in veterinary medicine that provides them with training and qualifications to treat diseases and injuries of animals. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Villi: The tiny, fingerlike projections on the surface of the small intestine. Villi help absorb nutrients. [NIH] Villous: Of a surface, covered with villi. [NIH] Vinblastine: An anticancer drug that belongs to the family of plant drugs called vinca alkaloids. It is a mitotic inhibitor. [NIH] Vinca Alkaloids: A class of alkaloids from the genus of apocyanaceous woody herbs including periwinkles. They are some of the most useful antineoplastic agents. [NIH] Vincristine: An anticancer drug that belongs to the family of plant drugs called vinca alkaloids. [NIH] Vinorelbine: An anticancer drug that belongs to the family of plant drugs called vinca alkaloids. [NIH] Vinyl Chloride: A gas that has been used as an aerosol propellant and is the starting material for polyvinyl resins. Toxicity studies have shown various adverse effects, particularly the occurrence of liver neoplasms. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral Hepatitis: Hepatitis caused by a virus. Five different viruses (A, B, C, D, and E) most commonly cause this form of hepatitis. Other rare viruses may also cause hepatitis. [NIH] Viral Load: The quantity of measurable virus in the blood. Change in viral load, measured in plasma, is used as a surrogate marker in HIV disease progression. [NIH] Viral vector: A type of virus used in cancer therapy. The virus is changed in the laboratory and cannot cause disease. Viral vectors produce tumor antigens (proteins found on a tumor cell) and can stimulate an antitumor immune response in the body. Viral vectors may also be used to carry genes that can change cancer cells back to normal cells. [NIH] Viremia: The presence of viruses in the blood. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Vitiligo: A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young
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adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] War: Hostile conflict between organized groups of people. [NIH] Warts: Benign epidermal proliferations or tumors; some are viral in origin. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]
Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Womb: A hollow, thick-walled, muscular organ in which the impregnated ovum is developed into a child. [NIH] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] Xerostomia: Decreased salivary flow. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] X-ray therapy: The use of high-energy radiation from x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. X-ray therapy is also called radiation therapy, radiotherapy, and irradiation. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Yttrium: An element of the rare earth family of metals. It has the atomic symbol Y, atomic number 39, and atomic weight 88.91. In conjunction with other rare earths, yttrium is used as a phosphor in television receivers and is a component of the yttrium-aluminum garnet (YAG) lasers. [NIH] Zoster: A virus infection of the Gasserian ganglion and its nerve branches, characterized by discrete areas of vesiculation of the epithelium of the forehead, the nose, the eyelids, and the cornea together with subepithelial infiltration. [NIH] Zygote: The fertilized ovum. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]
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INDEX 3 3-dimensional, 168, 337, 406 A Abdomen, 33, 198, 337, 347, 348, 365, 382, 385, 386, 388, 390, 398, 400, 417, 420, 426 Abdominal, 126, 146, 292, 337, 361, 382, 383, 398, 400, 424 Abdominal Pain, 126, 292, 337, 383, 424 Aberrant, 27, 30, 50, 61, 85, 238, 337 Ablation, 39, 337 Abscess, 4, 337, 414 Acceptor, 337, 386, 397, 421 Acitretin, 139, 337 Acquired Immunodeficiency Syndrome, 220, 237, 337 Actin, 337, 393 Acute leukemia, 36, 264, 337, 366, 404 Acute lymphoblastic leukemia, 8, 40, 98, 110, 205, 218, 219, 225, 231, 337, 395 Acute lymphocytic leukemia, 205, 225, 337, 388 Acute myelogenous leukemia, 144, 231, 337, 338 Acute myeloid leukemia, 64, 166, 225, 337, 338, 405 Acute nonlymphocytic leukemia, 337, 338 Acute renal, 97, 116, 338, 375 Adaptability, 338, 350, 351 Adenocarcinoma, 73, 221, 241, 244, 246, 338, 395 Adenosylmethionine Decarboxylase, 338, 391 Adenovirus, 229, 338 Adipose Tissue, 338, 398 Adjuvant, 214, 338, 371 Adnexa, 123, 338 Adolescence, 111, 162, 338 Adrenal Glands, 338, 340 Adrenal insufficiency, 92, 118, 167, 338 Adverse Effect, 338, 414, 426 Aerosol, 338, 426 Afferent, 338, 357, 367 Affinity, 35, 40, 42, 51, 58, 73, 232, 338, 339, 344, 415, 418 Agar, 338, 354, 402 Age-Adjusted, 168, 339 Agenesis, 6, 339 Aggressiveness, 24, 50, 339
Agonist, 228, 339, 362, 401, 419 Airway, 339, 415 Albumin, 339, 397 Algorithms, 339, 347 Alimentary, 339, 399 Alkaline, 339, 340, 348 Alkylating Agents, 100, 228, 231, 339 Alleles, 66, 224, 244, 339, 376 Allergen, 339, 414 Allium, 339 Allo, 231, 232, 339 Allogeneic, 31, 34, 47, 84, 128, 150, 159, 180, 202, 231, 232, 234, 268, 339, 373, 375, 400 Allogeneic bone marrow transplantation, 84, 232, 339 Allograft, 268, 339 Alopecia, 88, 227, 229, 339, 358 Alpha Particles, 340, 408 Alternative medicine, 291, 340 Aluminum, 340, 427 Alveolar Bone Loss, 5, 340 Alveolar Process, 340, 410 Ameliorating, 238, 340 Amine, 340, 376 Amino Acid Sequence, 226, 240, 249, 294, 340, 342, 355, 371, 379 Amino Acids, 232, 264, 340, 343, 371, 396, 399, 403, 406, 411, 414, 422, 424 Ammonia, 340, 373, 424 Amplification, 51, 68, 71, 86, 242, 243, 340 Ampulla, 340, 364, 367 Amyloidosis, 174, 183, 293, 340 Anabolic, 247, 340, 361 Anabolic Steroids, 247, 340 Anaesthesia, 341, 380 Anal, 9, 341, 365, 368 Analog, 9, 60, 222, 341, 369, 370 Analogous, 341, 422 Anaphylatoxins, 341, 355 Anaplastic, 39, 67, 77, 80, 85, 86, 88, 89, 92, 94, 98, 108, 118, 137, 139, 140, 172, 181, 187, 195, 197, 200, 204, 207, 208, 210, 215, 226, 250, 310, 341 Anatomical, 341, 344, 364, 380, 413 Anemia, 10, 148, 263, 308, 312, 322, 341, 368, 369, 393, 420 Anergy, 56, 341
430 Lymphoma
Angiogenesis, 14, 341, 364 Angiogenesis inhibitor, 341, 364 Animal model, 25, 40, 41, 51, 55, 61, 198, 265, 341, 423 Annealing, 341, 403 Anogenital, 8, 9, 43, 57, 341 Anoikis, 23, 341 Anomalies, 6, 246, 341, 420 Anorexia, 307, 341, 373, 424 Anterior chamber, 341, 378, 383 Anthracycline, 119, 341, 359, 365 Antiangiogenic, 255, 341 Antibacterial, 341, 416 Antibiotic, 106, 244, 341, 359, 362, 365, 416 Antibodies, 8, 35, 40, 44, 50, 51, 56, 60, 98, 114, 195, 196, 197, 203, 206, 207, 208, 210, 214, 216, 217, 223, 226, 229, 230, 235, 238, 241, 248, 249, 250, 251, 255, 258, 259, 262, 265, 266, 306, 325, 342, 343, 344, 374, 378, 379, 387, 392, 402, 408, 411, 412 Antibody therapy, 22, 39, 44, 115, 195, 196, 206, 208, 210, 255, 256, 258, 342 Antibody-Dependent Cell Cytotoxicity, 342, 384 Anticoagulant, 342, 405 Antidote, 342, 385 Antiemetic, 342, 374, 391 Antifungal, 244, 342, 384 Antigen-Antibody Complex, 342, 355 Antigen-presenting cell, 22, 342, 360 Anti-infective, 342, 383, 415 Anti-inflammatory, 342, 361, 372, 398, 404 Antimetabolite, 342, 360, 369, 411 Antineoplastic Agents, 259, 339, 342, 426 Antioxidant, 140, 342, 397 Antiproliferative, 136, 343 Antiserum, 343, 345 Antiviral, 125, 343, 360, 382, 411 Anus, 341, 343, 348 Apheresis, 198, 343 Aplasia, 174, 343 Apnea, 343 Aptitude, 343, 407 Aqueous, 293, 343, 345, 359, 364, 386 Arginine, 10, 132, 255, 341, 343, 396, 407, 423 Arginine butyrate, 10, 132, 343 Arsenic trioxide, 127, 264, 343 Arterial, 343, 348, 378, 406 Arteries, 343, 347, 357, 391 Arterioles, 343, 347
Asbestos, 343, 354, 388, 390 Asparaginase, 110, 165, 167, 343 Aspartate, 343 Aspartic, 255, 343 Aspartic Acid, 255, 343 Aspiration, 343 Assay, 26, 60, 123, 218, 343 Astringents, 344, 390 Astrocytes, 344, 382 Astrocytoma, 230, 231, 344, 372 Asymptomatic, 55, 111, 221, 241, 307, 344, 398 Ataxia, 166, 264, 312, 344, 420 Atopic, 227, 344 Atrial, 86, 118, 148, 344 Atrial Flutter, 86, 148, 344 Atrioventricular, 167, 344 Atrium, 344, 423, 425 Atrophy, 312, 344 Attenuated, 81, 265, 344 Attenuation, 33, 344 Atypical, 102, 344, 381, 388 Autoantibodies, 120, 344, 360 Autoantigens, 344 Autodigestion, 344, 398 Autoimmune disease, 48, 239, 243, 244, 258, 268, 344, 393, 401 Autologous bone marrow transplantation, 42, 209, 232, 344, 375 Autonomic, 345, 357, 400 Autonomic Nervous System, 345, 400 Autopsy, 57, 345 Avian, 14, 68, 73, 345 Avian Leukosis, 68, 73, 345 Avidity, 33, 51, 345 B Backcross, 29, 345 Bacteremia, 3, 345 Bacterial Infections, 307, 345, 351 Bacterial toxin, 219, 345 Bacteriophage, 345, 402, 422 Bacteriostatic, 339, 345 Bacterium, 221, 345, 362, 375, 424 Basal Ganglia, 344, 345, 348, 370, 372 Basal Ganglia Diseases, 344, 345 Base, 10, 15, 60, 119, 168, 345, 349, 358, 359, 360, 371, 376, 384, 403, 424 Base Pair Mismatch, 345, 376 Basophil, 230, 346, 376 BCL-1, 139, 218, 346 Benign, 26, 242, 243, 248, 346, 370, 371, 374, 388, 390, 394, 398, 408, 427
Index 431
Bewilderment, 346, 356 Bexarotene, 88, 136, 288, 296, 322, 346 Bile, 121, 346, 370, 377, 384, 386, 417 Bile Acids, 346, 417 Bile Acids and Salts, 346 Bile Ducts, 121, 346 Bile Pigments, 346, 384 Biliary, 346, 398 Biliary Tract, 346, 398 Binding Sites, 257, 346, 418 Biochemical, 8, 42, 51, 55, 103, 126, 158, 339, 342, 346, 369, 383, 385, 414 Biological response modifier, 346, 381 Biological therapy, 191, 346, 374 Biomarkers, 249, 346 Biopsy, 4, 5, 18, 58, 64, 107, 171, 181, 198, 291, 292, 346, 399 Biopsy specimen, 18, 58, 346 Biosynthesis, 346, 396, 414 Biotechnology, 66, 83, 280, 291, 305, 310, 311, 312, 313, 346 Biotin, 51, 347, 418 Bladder, 138, 172, 231, 242, 243, 253, 263, 264, 267, 347, 393, 405, 424, 425 Blastocyst, 347, 356 Bleomycin, 143, 144, 237, 271, 296, 347 Bloating, 292, 347, 383 Blood Coagulation, 347, 349, 421 Blood Platelets, 347, 389, 414, 420 Blood pressure, 347, 349, 378, 392, 415 Blot, 23, 347, 379 Blotting, Western, 347, 379 Body Fluids, 43, 346, 347, 348, 363, 415, 423 Bone marrow biopsy, 198, 347 Bone Marrow Cells, 347, 354, 374, 389, 393 Bone Marrow Transplantation, 4, 17, 83, 150, 153, 159, 180, 203, 204, 209, 235, 273, 318, 347 Bone metastases, 347, 370, 408 Bone scan, 348, 412 Boron, 348, 358 Bowel, 4, 156, 165, 240, 281, 292, 341, 348, 361, 381, 382, 400, 418, 424 Bowel Movement, 348, 361, 418 Brachytherapy, 348, 382, 383, 408, 427 Brain Hypoxia, 348, 420 Brain Infarction, 348 Brain Ischemia, 248, 348 Branch, 237, 333, 348, 358, 387, 389, 399, 407, 416, 420 Breakdown, 348, 351, 361, 370
Bronchi, 230, 348, 365, 389, 422 Bronchial, 348, 376 Buccal, 348, 387 Buffers, 244, 348 Bullous, 348, 360 Bypass, 54, 348 C Cachexia, 15, 348 Calcineurin, 69, 348 Calcium, 157, 237, 343, 348, 349, 355, 370, 378, 383, 385, 414 Calmodulin, 348, 349 Camptothecin, 149, 349, 383 Candidiasis, 293, 307, 349 Candidosis, 349 Canonical, 50, 349 Capsules, 322, 349, 371 Carbohydrate, 349, 403, 418 Carbon Dioxide, 349, 359, 368, 410, 425 Carboplatin, 119, 161, 168, 349 Carcinogen, 349, 389 Carcinogenesis, 28, 261, 280, 349 Carcinogenic, 214, 339, 349, 381, 396, 405, 417, 424 Carcinoma, 10, 24, 53, 55, 144, 222, 241, 244, 248, 254, 265, 349, 395 Cardiac, 3, 70, 78, 86, 91, 148, 171, 175, 349, 364, 365, 370, 393, 397, 417 Cardiotoxicity, 134, 155, 349, 366 Cardiovascular, 243, 349, 414 Cardiovascular disease, 243, 349 Case series, 350, 353 Case-Control Studies, 58, 135, 350, 365 Caspase, 12, 34, 60, 78, 94, 103, 126, 130, 150, 158, 350 Castor Oil, 350, 411 Cauda Equina, 164, 350 Caudal, 350, 404 Causal, 350, 365 Cause of Death, 32, 63, 247, 350 Cecum, 110, 350, 384 Celiac Disease, 96, 109, 183, 292, 294, 306, 350, 372 Cell Adhesion, 7, 350, 381 Cell Communication, 232, 350 Cell Count, 63, 350 Cell Differentiation, 52, 350, 414 Cell Division, 49, 247, 311, 345, 350, 351, 359, 366, 374, 382, 389, 390, 391, 401, 405, 413 Cell Extracts, 57, 350 Cell Lineage, 30, 49, 56, 61, 239, 350
432 Lymphoma
Cell membrane, 50, 63, 351, 360, 367, 370 Cell proliferation, 26, 50, 220, 228, 239, 242, 257, 351, 382, 414 Cell Size, 351, 369 Cell Survival, 53, 56, 61, 351, 374 Cellular metabolism, 54, 351 Cellulose, 351, 370, 401 Central Nervous System, 25, 26, 53, 70, 77, 87, 91, 94, 101, 104, 111, 121, 126, 132, 134, 137, 152, 177, 203, 223, 284, 322, 345, 348, 351, 370, 372, 373, 374, 393, 399, 404, 414 Central Nervous System Infections, 351, 374 Cerebellar, 344, 351, 409 Cerebral, 124, 344, 345, 348, 351, 365, 366, 372, 416 Cerebral hemispheres, 345, 348, 351, 372 Cerebrospinal, 70, 351 Cerebrospinal fluid, 70, 351 Cerebrovascular, 345, 349, 351, 420 Cerebrum, 351, 401, 423 Cervical, 5, 43, 106, 351 Cervix, 173, 351, 354 Character, 38, 351, 360, 373 Chemokines, 28, 32, 46, 352 Chemoprevention, 15, 352 Chemotactic Factors, 352, 355 Chloroform, 244, 352 Cholesterol, 69, 90, 183, 346, 352, 357, 386, 417, 419 Chondrosarcoma, 244, 352 Choriocarcinoma, 241, 352, 372, 377, 392 Chromatin, 343, 352 Chromosomal, 12, 18, 27, 56, 69, 71, 74, 77, 82, 87, 107, 218, 226, 246, 340, 352, 402, 411 Chromosome Aberrations, 24, 352 Chromosome Abnormalities, 35, 352 Chronic Disease, 265, 348, 352, 385 Chronic Fatigue Syndrome, 228, 352 Chronic granulocytic leukemia, 352 Chronic leukemia, 264, 352, 374 Chronic lymphocytic leukemia, 8, 40, 225, 227, 250, 251, 252, 269, 352 Chronic myelogenous leukemia, 64, 231, 268, 352, 387 Chronic renal, 352, 403, 424 Cicatricial, 227, 353 Ciliary, 353, 378 Ciliary Body, 353, 378 Circulatory system, 217, 240, 262, 353
CIS, 236, 244, 317, 318, 353, 411 Cisplatin, 60, 112, 166, 193, 353 Claviceps, 353, 412 Cleave, 225, 353 Clinical Medicine, 36, 153, 353, 404 Clinical Protocols, 10, 353 Clinical study, 163, 353 Clone, 30, 36, 45, 79, 124, 266, 353 Cloning, 29, 35, 186, 215, 217, 347, 353, 381 Codons, 353, 371, 396 Cofactor, 353, 406, 421 Cognition, 19, 353 Cohort Studies, 354, 365 Colitis, 281, 354, 383 Collagen, 293, 354, 371, 405 Collapse, 348, 354, 415 Colony-Stimulating Factors, 354, 374 Colorectal, 97, 144, 214, 242, 243, 246, 247, 253, 354 Colorectal Cancer, 247, 253, 354 Colorectal Neoplasms, 97, 354 Combination Therapy, 6, 10, 121, 137, 172, 235, 354 Combined Modality Therapy, 165, 354 Communication Barriers, 283, 354 Communis, 350, 354, 411 Comorbidity, 180, 354 Complement, 21, 26, 63, 258, 341, 342, 355, 371, 381, 384, 412, 414 Complementarity Determining Regions, 249, 355, 379 Complementary and alternative medicine, 143, 184, 355 Complementary medicine, 143, 355 Complementation, 48, 355 Complete remission, 41, 153, 235, 355, 410 Complete response, 21, 37, 176, 272, 355 Computational Biology, 305, 310, 355 Computed tomography, 118, 135, 355, 356, 412 Computerized axial tomography, 356, 412 Computerized tomography, 198, 356 Conception, 41, 352, 356, 368, 372, 391, 416, 417 Concomitant, 5, 107, 162, 356 Confounding, 19, 356 Confusion, 283, 356, 361, 424 Conjugated, 23, 214, 250, 258, 299, 346, 356, 358 Conjunctiva, 356, 423 Connective Tissue, 347, 354, 356, 368, 370, 371, 387, 390, 411, 412, 418, 419
Index 433
Consciousness, 356, 360, 362, 417 Consolidation, 151, 155, 176, 356 Constipation, 126, 356, 383 Consumption, 58, 356, 361, 410 Contact dermatitis, 227, 356 Continuous infusion, 139, 356 Contractility, 356, 363 Contraindications, ii, 356 Control group, 6, 356 Conventional therapy, 62, 105, 160, 258, 356 Conventional treatment, 39, 62, 356 Cooperative group, 14, 65, 137, 168, 356 Coordination, 357, 393 Core biopsy, 107, 357 Coreceptors, 232, 357 Cornea, 341, 357, 378, 427 Corneum, 357, 365 Coronary, 349, 357, 391 Coronary heart disease, 349, 357 Coronary Thrombosis, 357, 391 Cortex, 344, 357, 366, 405, 409 Cortical, 216, 357, 413, 420 Corticosteroids, 321, 357, 372, 404 Cortisone, 321, 357, 361, 404 Cranial, 107, 248, 357, 367, 374, 398, 400, 423 Cranial Nerves, 248, 357 Craniocerebral Trauma, 345, 357, 374, 420 Crossing-over, 357, 409 Cross-Sectional Studies, 357, 365 Croton Oil, 254, 357 Curative, 44, 235, 247, 253, 268, 358, 420 Curcumin, 132, 358 Cyclic, 349, 350, 358 Cyclin, 45, 52, 72, 75, 104, 218, 257, 346, 358 Cyclin-Dependent Kinases, 45, 358 Cyclosporine, 208, 358 Cysteine, 352, 358, 362, 383 Cystine, 358, 362 Cytarabine, 109, 163, 166, 177, 194, 237, 358 Cytidine, 98, 358 Cytidine Deaminase, 98, 358 Cytochrome, 70, 358, 397 Cytogenetic Analysis, 35, 117, 218, 261, 358 Cytogenetics, 15, 17, 86, 89, 95, 117, 120, 358 Cytokine, 8, 19, 21, 30, 42, 65, 101, 140, 154, 222, 230, 267, 359, 368, 412
Cytomegalovirus, 34, 83, 94, 123, 220, 233, 307, 359, 370 Cytomegalovirus Infections, 359, 370 Cytoplasm, 219, 247, 343, 351, 359, 365, 367, 374, 388, 411, 419 Cytosine, 345, 358, 359 Cytoskeleton, 359, 381, 391 Cytotoxic, 21, 22, 23, 42, 44, 60, 61, 63, 79, 104, 153, 191, 214, 215, 228, 238, 249, 250, 253, 255, 258, 359, 408, 414 Cytotoxicity, 21, 39, 44, 60, 132, 154, 176, 238, 258, 353, 359 Cytotoxins, 219, 359 D Dairy Products, 292, 359 Databases, Bibliographic, 305, 359 Daunorubicin, 359, 362 De novo, 27, 359 Deamination, 345, 358, 359, 424 Decarboxylation, 338, 359, 376, 396, 407 Decision Making, 151, 359 Decubitus, 359, 415 Decubitus Ulcer, 359, 415 Defense Mechanisms, 359, 381 Degenerative, 360, 376 Deletion, 45, 56, 86, 246, 343, 360, 371 Dementia, 248, 283, 337, 360 Denaturation, 266, 360, 376, 403 Dendrites, 360, 394 Dendritic, 26, 31, 35, 39, 44, 61, 129, 360, 389 Dendritic cell, 26, 31, 35, 39, 44, 61, 129, 360 Density, 37, 163, 360, 369, 386, 396, 403 Dental Care, 293, 308, 360 Dental Caries, 360, 369 Dentists, 307, 360 Deoxyglucose, 120, 171, 360 Depigmentation, 360, 426 Depolarization, 360, 414 Deprivation, 252, 360 Depsipeptide, 198, 360 Dermal, 186, 360, 386 Dermatitis, 5, 183, 227, 306, 360, 363 Dermatitis Herpetiformis, 5, 183, 306, 360 Detergents, 360, 415 Developing Countries, 247, 361 Dexamethasone, 134, 144, 152, 158, 159, 237, 361 Diabetes Mellitus, 361, 375, 399 Diagnostic Imaging, 23, 361 Diagnostic procedure, 213, 291, 361
434 Lymphoma
Diaphragm, 361, 402 Diarrhea, 233, 292, 361, 373, 383 Dietitian, 293, 294, 361 Diffusion, 361, 381 Digestion, 339, 346, 348, 361, 382, 386, 399, 417, 425 Digestive system, 211, 361, 392 Digestive tract, 361, 415, 417 Dihydrotestosterone, 361, 409 Dilatation, 361, 405 Dimerization, 252, 361 Dimethyl, 244, 361 Diploid, 355, 361, 402 Direct, iii, 21, 47, 55, 77, 222, 258, 268, 295, 350, 353, 361, 362, 409, 419 Disease Progression, 28, 39, 225, 361, 426 Disease-Free Survival, 232, 235, 361 Disorientation, 356, 361 Disparity, 268, 362 Dissociation, 28, 338, 362, 383 Dissociative Disorders, 362 Distal, 240, 244, 362, 406 Disulphide, 253, 362 Docetaxel, 169, 362 Dopamine, 362, 391, 401 Dormancy, 49, 68, 69, 362 Dorsal, 362, 404, 416 Dose-limiting, 255, 362 Dosimetry, 36, 168, 181, 217, 262, 362 Drive, ii, vi, 4, 5, 131, 325, 362 Drug Interactions, 297, 362 Drug Resistance, 221, 225, 252, 268, 274, 362, 363 Drug Tolerance, 362, 363, 421 Duct, 340, 363, 367, 412, 425 Duodenal Ulcer, 221, 233, 240, 363 Duodenum, 240, 346, 363, 364, 418 Dura mater, 363, 390, 397 Dysplasia, 43, 312, 363 Dystrophy, 312, 363 E Ectopic, 50, 71, 83, 363 Eczema, 6, 323, 363 Edema, 356, 363, 424 Effector, 19, 22, 26, 40, 63, 342, 355, 363, 384, 394 Effector cell, 19, 22, 40, 342, 363, 384, 394 Efficacy, 22, 39, 43, 51, 59, 60, 63, 135, 228, 246, 323, 363, 423 Effusion, 11, 31, 45, 67, 69, 70, 71, 73, 75, 82, 86, 91, 110, 148, 151, 186, 236, 363, 387
Ejection fraction, 134, 363 Elasticity, 294, 363 Elastin, 354, 363 Elective, 81, 363 Electrocardiogram, 198, 363 Electrolyte, 298, 363, 415, 424 Electrons, 342, 345, 363, 383, 388, 397, 408 Electrophoresis, 363, 376 Elementary Particles, 363, 364, 388, 394, 406 Emaciation, 337, 364 Embryo, 347, 350, 364, 380 Emetic, 357, 364 Emollient, 364, 395 Emulsion, 364, 368 Enamel, 6, 306, 360, 364, 384 Encapsulated, 364, 386 Encephalopathy, 364, 389 Endemic, 10, 71, 72, 220, 364, 417 Endocarditis, 3, 349, 364 Endocardium, 364 Endocytosis, 219, 364 Endogenous Retroviruses, 265, 364 Endometrial, 244, 364 Endometrium, 364 Endoscope, 364 Endoscopic, 281, 364 Endostatin, 289, 364 Endothelial cell, 230, 364, 421 Endotoxin, 365, 423 End-stage renal, 352, 365, 403 Enhancer, 25, 67, 68, 70, 74, 76, 80, 81, 108, 252, 365 Enteropeptidase, 365, 423 Environmental Exposure, 247, 365, 396 Environmental Health, 58, 304, 306, 365 Enzymatic, 216, 225, 238, 349, 355, 358, 360, 365, 376, 403, 411 Eosinophil, 230, 365, 374 Eosinophilia, 39, 365 Eosinophilic, 365 Epidemic, 237, 365, 417 Epidemiologic Studies, 18, 58, 237, 365 Epidemiological, 7, 57, 306, 365 Epidermal, 227, 365, 384, 386, 389, 427 Epidermis, 227, 357, 365, 377, 384, 386, 404, 407 Epidermoid carcinoma, 365, 417 Epigastric, 365, 398 Epinephrine, 362, 365, 424 Epirubicin, 161, 165, 178, 365
Index 435
Epithelial, 10, 53, 263, 264, 338, 353, 366, 376, 382, 398 Epithelial Cells, 10, 366, 376, 382 Epithelium, 352, 366, 370, 383, 398, 427 Epitope, 214, 366 Ergot, 366, 412 Erythema, 356, 366, 418, 425 Erythrocytes, 341, 347, 366, 398, 401, 409, 412, 414 Erythropoietin, 123, 229, 366 Escalation, 36, 366 Esophageal, 257, 366 Esophagus, 361, 366, 389, 400, 418 Essential Tremor, 312, 366 Estrogen, 366, 413, 419 Ether, 244, 366 Etretinate, 337, 366 Eukaryotic Cells, 366, 380, 395, 396 Evacuation, 356, 366 Evaluable patients, 46, 366 Evoke, 22, 366, 417 Excitation, 344, 367, 369 Exercise Therapy, 223, 367 Exfoliation, 248, 367 Exocrine, 367, 398 Exocytosis, 367, 376, 419 Exogenous, 14, 26, 225, 266, 363, 367 Exons, 257, 264, 367 Extensor, 367, 407, 426 External-beam radiation, 367, 383, 408, 427 Extracellular, 54, 230, 242, 243, 244, 247, 267, 341, 344, 356, 364, 367, 381, 415, 418 Extracellular Matrix, 341, 356, 367, 381 Extracorporeal, 6, 296, 367, 401 Extraction, 4, 33, 242, 243, 367 Extraocular, 338, 367 Eye Infections, 338, 367 F Facial, 133, 367, 389, 398 Facial Nerve, 367, 398 Fallopian Tubes, 367, 425 Familial polyposis, 354, 367 Family Planning, 305, 367 Farnesyl, 260, 367 Fat, 338, 346, 347, 357, 359, 367, 386, 393, 396, 411, 415, 416 Fatigue, 119, 292, 307, 308, 322, 325, 326, 352, 368, 375 Feces, 356, 368, 418 Fetal Hemoglobin, 10, 368 Fetus, 366, 368, 425
Fever of Unknown Origin, 181, 368 Fibrin, 3, 347, 368, 402, 420 Fibrinogen, 368, 402, 420 Fibrosarcoma, 242, 368 Fibrosis, 312, 368, 412, 413 Filgrastim, 151, 175, 194, 195, 199, 201, 368 Filtration, 253, 368 Fine-needle aspiration, 134, 368, 394 Fixation, 63, 97, 368, 414 Flatus, 368, 370 Flavodoxin, 221, 368 Flavopiridol, 100, 139, 158, 369 Flexor, 367, 369, 386 Flow Cytometry, 27, 161, 369, 379 Fludarabine, 100, 138, 158, 169, 174, 199, 231, 299, 369 Fluorescence, 18, 23, 36, 100, 101, 115, 369 Fluorescent Dyes, 369 Fluorine, 158, 173, 369 Fluorouracil, 242, 369, 385 Fold, 60, 223, 369 Folic Acid, 142, 369, 385 Follicles, 14, 369, 387 Follicular large cell lymphoma, 204, 206, 207, 369 Follow-Up Studies, 238, 369 Foramen, 354, 369, 389, 400 Fovea, 368, 369 Fractionation, 234, 238, 254, 369 Fungi, 240, 342, 353, 367, 369, 370, 374, 391, 427 Fungus, 349, 366, 370, 393, 412 G Gallbladder, 337, 346, 361, 370 Gallium, 33, 101, 135, 237, 370 Gallium nitrate, 101, 237, 370 Gamma Rays, 370, 408 Ganciclovir, 10, 25, 222, 370 Ganglia, 345, 370, 394, 400 Ganglion, 370, 427 Gap Junctions, 370, 419 Gas, 292, 340, 349, 361, 368, 369, 370, 377, 383, 389, 395, 418, 425, 426 Gastric Acid, 306, 370 Gastric Juices, 370, 399 Gastric Mucosa, 73, 74, 129, 221, 370, 399 Gastric Resection, 73, 370 Gastrin, 370, 377 Gastritis, 5, 103, 221, 233, 240, 371 Gastrointestinal, 16, 17, 102, 229, 240, 274, 285, 307, 343, 365, 371, 389, 414, 418, 423
436 Lymphoma
Gastrointestinal tract, 229, 240, 371, 414, 423 Gelatin, 371, 373, 420 Gels, 293, 371 Gemcitabine, 112, 125, 137, 176, 200, 371 Gene Deletion, 45, 371 Gene Fusion, 246, 371 Gene Rearrangement, 24, 27, 30, 114, 216, 371 Gene Silencing, 55, 69, 371 Genetic Code, 371, 395 Genetic Engineering, 347, 353, 371 Genetic Markers, 19, 371 Genetic testing, 371, 403 Genetics, 13, 31, 48, 65, 86, 89, 95, 117, 120, 125, 226, 230, 231, 247, 279, 358, 371, 399 Genital, 371, 424 Genitourinary, 371, 424 Genotype, 32, 36, 38, 371, 400 Germ cell tumors, 116, 371 Germ Cells, 372, 389, 397, 416, 420 Germinal Center, 27, 35, 38, 53, 78, 86, 93, 372, 387 Germline mutation, 231, 372, 376 Gestational, 140, 180, 372, 391 Gestational trophoblastic disease, 140, 180, 372, 392 Gestational trophoblastic neoplasia, 372, 392 Gestational trophoblastic tumor, 372, 392 Giant Cells, 372, 412 Ginger, 94, 154, 184, 372 Gland, 99, 291, 292, 293, 357, 372, 387, 398, 405, 413, 417, 418, 421 Gliadin, 294, 372 Glioblastoma, 230, 231, 372 Glioma, 94, 230, 231, 372 Glomerular, 253, 372 Glomerulus, 372 Glucocorticoid, 361, 372, 404 Glucose, 54, 144, 162, 312, 351, 360, 361, 372, 373, 375, 412 Glutamic Acid, 369, 373, 405 Glutamine, 294, 373 Glutathione Peroxidase, 373, 413 Gluten, 5, 292, 293, 294, 306, 350, 372, 373 Glycine, 255, 346, 373, 414 Glycolysis, 54, 373 Glycoprotein, 40, 186, 216, 240, 366, 368, 372, 373, 374, 421, 423 Goats, 359, 373 Gonadal, 373, 417
Gonadotropin, 352, 373 Governing Board, 373, 404 Grade, 4, 11, 21, 27, 30, 33, 46, 56, 62, 63, 64, 73, 74, 96, 100, 103, 119, 120, 122, 123, 127, 129, 133, 137, 138, 144, 146, 148, 149, 150, 154, 157, 169, 174, 186, 189, 190, 193, 195, 197, 201, 204, 206, 207, 210, 214, 235, 252, 256, 259, 261, 278, 284, 317, 318, 325, 373, 388 Grading, 292, 373 Graft, 31, 34, 202, 231, 232, 234, 243, 244, 268, 373, 374, 377, 380, 387, 407 Graft Rejection, 232, 373, 380, 387 Graft vs Host Disease, 243, 373 Graft vs Host Reaction, 373 Graft-versus-host disease, 374, 407 Gram-negative, 221, 374 Granisetron, 134, 152, 374 Granule, 374, 411 Granulocyte Colony-Stimulating Factor, 151, 354, 368, 374 Granulocyte-Macrophage ColonyStimulating Factor, 229, 354, 374 Granulocytes, 229, 346, 354, 374, 385, 393, 414, 427 Grasses, 294, 353, 369, 374 Growth factors, 215, 374 H Habitual, 352, 374 Hair follicles, 229, 374 Hairy cell leukemia, 135, 374 Half-Life, 244, 337, 374 Haploid, 374, 402 Haptens, 338, 374 Headache, 308, 374, 375 Headache Disorders, 375 Heart attack, 349, 375 Heart failure, 182, 375 Helix-loop-helix, 61, 375 Hematologic Diseases, 36, 47, 375 Hematologic malignancies, 17, 60, 65, 215, 231, 232, 252, 375 Hematopoiesis, 41, 52, 278, 375 Hematopoietic growth factors, 229, 375 Hematopoietic Stem Cell Transplantation, 128, 159, 180, 375 Hematopoietic Stem Cells, 34, 40, 42, 216, 231, 232, 234, 261, 375 Hemoglobin, 341, 366, 368, 375, 420 Hemoglobin H, 368, 375 Hemoglobin M, 375 Hemoglobinopathies, 263, 375
Index 437
Hemoglobinuria, 312, 375 Hemolytic, 375, 420 Hemorrhage, 357, 374, 375, 411, 418 Hemostasis, 273, 375, 381, 414 Hepatic, 134, 138, 220, 339, 376 Hepatitis, 72, 125, 177, 185, 267, 289, 376, 381, 426 Hepatocytes, 376 Hepatoma, 222, 246, 247, 376 Hepatomegaly, 376, 381 Hereditary, 178, 372, 376, 411, 420 Hereditary mutation, 372, 376 Heredity, 371, 376 Herpes, 10, 11, 25, 26, 31, 220, 222, 228, 229, 236, 307, 376 Herpes virus, 11, 26, 31, 220, 228, 229, 236, 376 Herpes Zoster, 376 Herpetiformis, 5, 360, 376 Heterodimers, 376, 381, 422 Heteroduplex Analysis, 93, 376 Heterogeneity, 62, 226, 338, 376 Heterotrophic, 369, 376 Heterozygotes, 38, 376 High-grade lymphomas, 235, 259, 376 Histamine, 230, 233, 341, 376, 377 Histamine Release, 230, 341, 376 Histidine, 376, 377 Histology, 36, 114, 284, 377, 398 Homeobox, 52, 127, 377 Homeostasis, 49, 109, 154, 186, 227, 377 Homodimer, 377, 422 Homologous, 14, 48, 246, 264, 339, 345, 357, 376, 377, 393, 406, 413, 414, 419, 420 Homotypic, 126, 377 Hormonal, 344, 377 Hormone, 228, 306, 339, 357, 365, 366, 370, 377, 383, 390, 405, 411, 414, 420, 421, 422 Horny layer, 365, 377 Humoral, 22, 217, 262, 373, 377, 379, 423 Humour, 377 Hybrid, 61, 181, 246, 345, 353, 377, 412 Hybridization, 18, 37, 85, 377 Hybridoma, 229, 377 Hydatidiform Mole, 352, 377 Hydrogen, 337, 340, 345, 348, 349, 360, 373, 377, 386, 392, 394, 395, 397, 400, 406 Hydrolysis, 343, 353, 377, 401, 403, 406, 423 Hydrophobic, 232, 361, 377, 386 Hydroxamic Acids, 242, 377 Hydroxylamine, 241, 242, 378
Hydroxylysine, 354, 378 Hydroxyproline, 354, 378 Hygienic, 378, 415 Hyperbilirubinemia, 378, 384 Hypercalcemia, 370, 378 Hyperplasia, 43, 273, 378, 386 Hypersensitivity, 34, 339, 365, 378, 411, 414 Hypertension, 349, 374, 378, 424 Hypertrophy, 378 Hypoglycemia, 106, 378 Hypoplasia, 6, 378 Hypopyon, 128, 378 I Ibritumomab tiuxetan, 129, 210, 378 Ibritumomab Tiuxetan, 298 Id, 22, 141, 182, 316, 317, 318, 320, 324, 332, 334, 378 Idiopathic, 378, 407, 412 Idiotype, 22, 61, 83, 161, 258, 266, 378 Ifosfamide, 109, 119, 137, 145, 152, 159, 161, 163, 166, 168, 177, 178, 206, 253, 296, 378 Ileum, 350, 378 Imaging procedures, 200, 378, 422 Imidazole, 347, 376, 378 Immortal, 45, 378 Immune function, 32, 50, 378, 422 Immune Sera, 378, 379 Immunity, 19, 21, 22, 26, 27, 32, 217, 250, 260, 262, 337, 359, 379, 396, 422, 423 Immunization, 22, 62, 68, 379, 414 Immunoblotting, 60, 64, 379 Immunocompromised, 25, 379 Immunoconjugates, 249, 250, 251, 379 Immunodeficiency syndrome, 6, 283, 379 Immunogenic, 75, 214, 220, 250, 266, 379 Immunoglobulin Variable Region, 27, 379 Immunohistochemistry, 56, 97, 379 Immunologic, 21, 98, 162, 265, 275, 352, 379, 408 Immunologic Diseases, 265, 379 Immunophenotyping, 113, 245, 379 Immunophilin, 348, 379 Immunosuppressant, 339, 369, 379 Immunosuppressive, 125, 220, 268, 348, 358, 372, 378, 379 Immunosuppressive therapy, 125, 220, 379 Immunotherapy, 36, 40, 44, 65, 214, 250, 251, 258, 346, 379 Immunotoxin, 62, 83, 132, 380
438 Lymphoma
Impairment, 344, 346, 367, 380, 390 Implant radiation, 380, 382, 383, 408, 427 Implantation, 356, 380 In situ, 36, 94, 100, 101, 115, 147, 380 In Situ Hybridization, 36, 94, 100, 101, 115, 380 In vivo, 11, 14, 19, 21, 22, 23, 24, 25, 27, 31, 35, 39, 40, 42, 44, 48, 49, 53, 62, 74, 77, 135, 166, 219, 222, 230, 239, 240, 244, 250, 267, 380, 387 Incision, 380, 383 Incubation, 11, 380, 385 Incubation period, 380, 385 Indicative, 269, 272, 380, 399, 425 Indolent lymphoma, 99, 105, 128, 158, 259, 380, 387 Induction therapy, 13, 380 Infarction, 348, 357, 380, 391 Infection Control, 307, 380 Infectious Mononucleosis, 10, 26, 53, 55, 90, 381, 392 Infiltration, 122, 136, 292, 381, 388, 427 Inflammatory bowel disease, 4, 97, 281, 381 Infusion, 11, 121, 128, 137, 180, 198, 234, 381 Initiation, 3, 8, 30, 53, 79, 80, 252, 381, 422 Inlay, 381, 410 Innervation, 367, 381, 396 Inorganic, 154, 353, 378, 381, 392, 402 Insecticides, 381, 400 Insertional, 74, 80, 381 Insight, 14, 22, 24, 37, 64, 215, 261, 381 Insulator, 381, 393 Integrins, 7, 79, 381 Intercalating Agents, 228, 381 Interferon, 6, 11, 21, 67, 71, 75, 109, 127, 135, 139, 179, 228, 267, 298, 322, 381, 382, 387 Interferon-alpha, 139, 381, 382 Interleukin-1, 105, 382 Interleukin-10, 105, 382 Interleukin-2, 19, 22, 198, 203, 219, 259, 322, 382 Interleukin-3, 230, 354, 382 Interleukins, 217, 262, 382, 387 Intermittent, 292, 382 Internal Medicine, 15, 16, 19, 21, 47, 57, 65, 132, 135, 382, 389 Internal radiation, 382, 383, 408, 427 Interphase, 76, 236, 382, 395 Interstitial, 348, 382, 383, 427
Intestinal, 100, 163, 281, 292, 350, 365, 382, 388 Intestine, 292, 346, 348, 354, 382, 384 Intoxication, 382, 427 Intracellular, 12, 23, 60, 71, 75, 219, 247, 267, 380, 381, 382, 383, 390, 413, 414 Intraepithelial, 109, 382 Intraperitoneal, 21, 382 Intrathecal, 298, 382 Intravascular, 97, 119, 136, 145, 147, 163, 164, 181, 382 Intravenous, 11, 198, 322, 381, 383 Intrinsic, 338, 383 Introns, 246, 383 Invasive, 21, 377, 379, 383, 388 Involuntary, 345, 366, 383, 393, 415 Iodine, 60, 139, 145, 298, 299, 383 Iodoacetic Acid, 267, 383 Ionization, 383 Ionizing, 24, 76, 340, 365, 383, 408, 415 Ionomycin, 42, 383 Ions, 345, 348, 349, 362, 363, 377, 383, 384 Irinotecan, 133, 136, 137, 164, 178, 383 Iris, 341, 357, 378, 383 Irradiation, 6, 24, 44, 84, 146, 354, 383, 390, 427 Irritable Bowel Syndrome, 292, 383 Ischemia, 344, 348, 359, 383 Isoelectric, 384, 418 Isoelectric Point, 384, 418 J Jaundice, 117, 118, 307, 378, 384 Joint, 369, 384, 419 K Karyotype, 36, 64, 261, 377, 384 Kb, 257, 264, 304, 384 Keratin, 384 Keratinocytes, 227, 384 Ketoconazole, 267, 384 Kidney Disease, 211, 304, 312, 384 Kidney Transplantation, 120, 384 Killer Cells, 116, 384 Kinetic, 383, 384 L Labile, 355, 384 Lacrimal, 110, 165, 338, 367, 384 Lacrimal Apparatus, 338, 384 Large Intestine, 350, 354, 361, 382, 384, 409, 415 Larynx, 147, 384, 422 Latency, 27, 46, 53, 71, 81, 236, 385 Latent, 10, 24, 70, 72, 75, 130, 385, 403, 404
Index 439
Lectin, 106, 145, 215, 294, 385, 390 Leiomyosarcoma, 242, 385 Leishmaniasis, 267, 385, 399 Lentivirus, 54, 385 Lesion, 4, 21, 148, 218, 385, 386, 414, 424 Lethal, 21, 24, 231, 232, 234, 385, 411 Leucocyte, 365, 385, 387 Leucovorin, 237, 296, 385 Leukaemia, 111, 281, 385 Leukapheresis, 201, 343, 385 Leukocytes, 21, 256, 347, 352, 374, 382, 385, 398, 423 Leukopenia, 263, 373, 385 Leukoplakia, 24, 307, 385 Levamisole, 267, 385 Levo, 385, 389 Library Services, 332, 385 Lichen Planus, 227, 366, 386 Life cycle, 370, 386 Ligament, 386, 405 Ligands, 11, 28, 51, 57, 81, 226, 381, 386 Ligation, 56, 386 Linkage, 29, 371, 386 Lipid, 50, 69, 386, 393, 397 Lipid Peroxidation, 386, 397 Lipopolysaccharide, 374, 386 Lipoprotein, 374, 386 Liposomal, 9, 115, 169, 204, 207, 251, 252, 386 Liposome, 219, 386 Liver cancer, 386, 420 Liver Neoplasms, 386, 426 Liver scan, 386, 412 Local therapy, 19, 386 Localization, 7, 22, 52, 76, 79, 379, 386 Locomotion, 386, 402 Loop, 224, 386 Low-grade lymphomas, 100, 158, 259, 261, 376, 387 Lubricants, 293, 387, 400 Lumbar, 350, 387 Lumen, 241, 387 Lupus, 96, 229, 244, 293, 387, 419 Lupus Nephritis, 96, 387 Lymphadenopathy, 5, 220, 307, 381, 387 Lymphatic, 220, 251, 256, 264, 320, 322, 325, 326, 341, 369, 380, 387, 390, 416, 417, 421 Lymphatic system, 256, 322, 325, 326, 341, 369, 387, 416, 417, 421
Lymphoblastic, 110, 112, 138, 165, 179, 190, 192, 202, 204, 205, 209, 216, 376, 387, 388 Lymphoblasts, 236, 337, 387, 388 Lymphocyte Count, 337, 387 Lymphocyte Transformation, 24, 34, 77, 387 Lymphocytic, 32, 78, 93, 199, 205, 207, 208, 209, 219, 238, 248, 256, 261, 269, 387, 388 Lymphocytosis, 147, 269, 387 Lymphoma, Follicular, 102, 387, 395 Lymphoma, Lymphoblastic, 388, 395 Lymphomatoid Papulosis, 103, 322, 388 Lymphoproliferative, 10, 11, 13, 18, 22, 24, 26, 31, 43, 53, 55, 179, 191, 214, 227, 263, 264, 388, 395 Lymphoproliferative Disorders, 11, 31, 55, 214, 388 Lysine, 378, 388, 423 Lysosome, 219, 388 Lytic, 25, 73, 75, 79, 81, 82, 223, 388 M Macrophage, 83, 267, 342, 354, 374, 382, 388 Magnetic Resonance Imaging, 388, 412 Magnetic Resonance Spectroscopy, 94, 388 Maintenance therapy, 156, 233, 388 Malabsorption, 312, 350, 388 Malignancy, 8, 9, 13, 21, 28, 34, 49, 50, 57, 64, 252, 263, 264, 269, 388, 398 Malignant mesothelioma, 388, 390 Malignant tumor, 49, 241, 352, 354, 388, 392, 397 Malnutrition, 339, 344, 348, 388, 393 Mammary, 29, 74, 388, 419 Mandible, 340, 388, 410 Mastication, 389, 423 Maxillary, 4, 389, 398 Maxillary Sinus, 4, 389 Meatus, 389 Mechlorethamine, 6, 389, 405 Medial, 389, 412 Mediastinum, 352, 389 Mediate, 28, 50, 73, 77, 236, 250, 362, 384, 389 Mediator, 12, 382, 389, 414 Medical Records, 389, 411 Medicament, 339, 389 MEDLINE, 305, 310, 312, 389 Megakaryocytes, 230, 347, 389 Meiosis, 389, 393, 419, 420
440 Lymphoma
Melanin, 307, 360, 383, 389, 401, 424 Melanocytes, 389 Melanoma, 222, 230, 231, 238, 242, 248, 254, 267, 311, 389 Melarsoprol, 264, 389 Melphalan, 84, 389 Membrane Proteins, 390, 406 Memory, 22, 26, 28, 31, 35, 48, 283, 341, 360, 372, 390, 412 Meningeal, 140, 181, 390 Meninges, 351, 357, 363, 390 Meningitis, 283, 307, 390 Mental Disorders, 211, 390, 407 Mental Health, iv, 7, 211, 304, 309, 390, 407 Mental Processes, 362, 390, 407 Mentors, 39, 390 Mercury, 154, 369, 390 Mesenchymal, 374, 377, 390 Mesothelioma, 66, 241, 388, 390 Metabolite, 337, 361, 385, 390, 401, 405 Metaphase, 390, 420 Metaplasia, 64, 390 Metastasis, 8, 23, 79, 264, 311, 390 Metastatic, 14, 59, 124, 166, 200, 222, 228, 243, 255, 390, 413 Methionine, 338, 361, 390 Methoxsalen, 296, 390, 401 Metoclopramide, 134, 152, 391 MI, 84, 96, 226, 235, 244, 335, 391 Mice Minute Virus, 391, 398 Microbe, 391, 422 Microbiology, 24, 26, 31, 37, 38, 52, 117, 123, 135, 276, 344, 391 Microorganism, 353, 391, 399, 427 Micro-organism, 240, 360, 391 Microscopy, 8, 23, 376, 391, 395 Microtubules, 391, 397 Migration, 7, 14, 46, 227, 391 Mineralization, 294, 391 Miotic, 391, 401 Mitochondrial Swelling, 391, 394 Mitoguazone, 299, 323, 391 Mitosis, 70, 236, 343, 391 Mitotic, 76, 93, 154, 228, 236, 362, 366, 391, 420, 426 Mitotic inhibitors, 228, 362, 391 Mitoxantrone, 140, 145, 158, 166, 180, 194, 391 Mobility, 35, 391 Mobilization, 145, 391 Modification, 47, 65, 371, 391, 408
Molar pregnancy, 372, 391 Molecular mass, 244, 266, 392 Molecule, 12, 22, 35, 39, 42, 51, 57, 83, 216, 217, 225, 230, 239, 247, 255, 261, 263, 266, 342, 345, 346, 355, 358, 362, 363, 366, 367, 369, 377, 379, 381, 385, 392, 395, 397, 402, 403, 408, 409, 414, 422, 425 Monitor, 33, 59, 241, 249, 392, 395 Monocyte, 239, 246, 342, 392, 412 Mononuclear, 43, 67, 381, 392, 423 Mononucleosis, 24, 288, 392 Monophosphate, 10, 392 Morphological, 7, 273, 364, 370, 389, 392 Morphology, 37, 110, 186, 269, 392 Motility, 7, 392, 414 Motion Sickness, 392, 393 Mucins, 392, 412 Mucocutaneous, 385, 392 Mucosa, 12, 68, 81, 101, 103, 110, 120, 123, 133, 149, 221, 261, 311, 350, 370, 387, 392, 418 Mucositis, 392, 421 Mucus, 392, 424 Multicenter study, 115, 159, 392 Multiple Myeloma, 12, 59, 99, 162, 231, 239, 260, 267, 273, 392 Multiple sclerosis, 228, 229, 265, 393 Multivalent, 345, 393 Muscle Fibers, 393 Muscular Atrophy, 312, 393 Muscular Dystrophies, 363, 393 Mutagenic, 247, 339, 393, 415 Mycosis, 6, 28, 113, 192, 198, 200, 227, 317, 321, 322, 323, 388, 393, 395 Mycosis Fungoides, 6, 113, 192, 198, 200, 227, 317, 321, 322, 388, 393, 395 Myelin, 393 Myelodysplasia, 41, 393 Myelodysplastic syndrome, 64, 144, 166, 225, 263, 393, 415 Myelofibrosis, 64, 393 Myelogenous, 391, 393 Myeloid Cells, 52, 393 Myeloma, 48, 59, 65, 136, 241, 290, 318, 323, 325, 377, 393 Myocardium, 391, 393 Myopathy, 308, 393 Myosin, 118, 348, 393 Myotonic Dystrophy, 312, 393 N Nadir, 272, 393 Naive, 48, 260, 393
Index 441
Nasopharynx, 118, 393 Nausea, 134, 152, 308, 342, 393, 424 Necrosis, 124, 228, 239, 248, 343, 348, 372, 380, 391, 394, 412 Needle biopsy, 368, 394 Neoplasia, 9, 43, 52, 242, 243, 265, 311, 366, 394 Neoplasm, 62, 220, 242, 243, 394, 398, 412, 424 Nephropathy, 384, 394 Nerve Growth Factor, 215, 394 Neural, 338, 377, 394 Neurologic, 293, 372, 394 Neuromuscular, 394, 396, 424 Neuromuscular Junction, 394, 396 Neuronal, 25, 394 Neurons, 248, 360, 370, 394, 419 Neuropathy, 178, 394 Neurotransmitters, 392, 394 Neutrons, 340, 383, 394, 408 Neutropenia, 167, 201, 202, 395 Neutrophil, 89, 172, 230, 395 Nitrogen, 237, 321, 340, 358, 368, 373, 389, 392, 395, 423 Non-Hodgkin's lymphoma, 40, 47, 52, 63, 118, 167, 245, 259, 278, 285, 395 Non-small cell lung cancer, 15, 254, 395 Nuclear Medicine, 33, 54, 96, 144, 156, 169, 171, 181, 285, 395 Nuclei, 79, 236, 340, 363, 367, 371, 383, 388, 391, 394, 395, 406 Nucleic Acid Hybridization, 377, 395 Nucleolus, 395, 411 O Occult, 78, 95, 395 Ocular, 123, 168, 227, 231, 307, 395, 396 Odds Ratio, 18, 395, 410 Ointments, 293, 395, 398, 415 Omega-3 fatty acid, 15, 396 Onchocerciasis, 267, 396 Oncogenic, 30, 42, 45, 53, 55, 78, 126, 129, 225, 226, 381, 385, 396, 403, 406 Oncogenic Viruses, 396, 403 Opacity, 360, 396 Open Reading Frames, 252, 385, 396 Operon, 396, 410 Ophthalmology, 93, 109, 110, 133, 165, 368, 396 Ophthalmoplegia, 138, 173, 396 Opportunistic Infections, 223, 307, 337, 396 Oral Health, 307, 396
Oral Hygiene, 293, 396 Orbit, 396 Orbital, 107, 118, 354, 396 Organ Culture, 396, 421 Organ Transplantation, 45, 179, 396 Organelles, 359, 389, 396 Ornithine, 238, 396, 407 Ornithine Decarboxylase, 238, 396 Osteogenic sarcoma, 397 Osteosarcoma, 46, 397 Outpatient, 9, 119, 168, 198, 397 Ovalbumin, 34, 397 Ovaries, 367, 397, 414, 420, 425 Ovary, 84, 230, 231, 397, 418 Overall survival, 32, 171, 397 Overexpress, 12, 269, 397 Oxaliplatin, 201, 397 Oxidation, 337, 342, 358, 362, 373, 375, 386, 397 Oxidative Phosphorylation, 136, 397 Oxidative Stress, 31, 140, 397 P P53 gene, 27, 397 Pacemaker, 118, 397 Pachymeningitis, 390, 397 Paclitaxel, 169, 176, 206, 208, 397 Paediatric, 125, 397 Palate, 113, 393, 397, 421 Palliative, 28, 59, 397, 420 Palsies, 98, 398 Palsy, 133, 398, 416 Pancreas, 230, 231, 247, 263, 264, 337, 346, 347, 361, 398, 423 Pancreatic, 85, 139, 214, 242, 243, 311, 366, 398 Pancreatic cancer, 311, 366, 398 Pancreatitis, 85, 139, 398 Pancytopenia, 263, 398 Panniculitis, 98, 153, 178, 398 Papilloma, 28, 222, 398 Papillomavirus, 307, 398 Papovaviridae, 398, 403 Paraffin, 18, 100, 135, 398 Paranasal Sinuses, 389, 398 Parietal, 398, 400, 402 Parotid, 99, 292, 398, 412 Paroxysmal, 312, 375, 398 Partial remission, 398, 410 Particle, 223, 386, 398, 422 Parvovirus, 79, 174, 391, 398 Patch, 6, 321, 385, 399 Pathogen, 10, 18, 55, 240, 380, 399
442 Lymphoma
Pathologic, 37, 63, 119, 259, 268, 343, 346, 349, 357, 378, 399, 407, 410 Pathologic Processes, 343, 399 Pathophysiology, 50, 399 Patient Education, 321, 322, 325, 330, 332, 335, 399 PDQ, 316, 317, 318, 399 Pelvic, 106, 119, 399, 405 Penis, 399, 400, 425 Pentamidine, 267, 399 Pepsin, 399 Pepsin A, 399 Peptic, 5, 103, 221, 233, 399 Peptic Ulcer, 5, 103, 221, 233, 399 Peptide, 23, 25, 81, 214, 223, 250, 365, 384, 399, 403, 405, 406, 409 Percutaneous, 107, 399 Perennial, 399, 423 Performance status, 32, 63, 399 Pericardium, 400, 419 Periodontal disease, 307, 340, 400 Periodontitis, 4, 400 Peripheral Nervous System, 136, 163, 398, 400, 418 Peripheral stem cell transplantation, 192, 193, 195, 198, 199, 202, 209, 400, 421 Peripheral stem cells, 201, 374, 400 Peritoneal, 46, 240, 382, 400 Peritoneal Cavity, 46, 240, 382, 400 Peritoneum, 400 Pesticides, 18, 109, 135, 381, 400 Petroleum, 398, 400 PH, 33, 68, 109, 169, 400 Phallic, 368, 400 Pharmacokinetic, 66, 400 Pharmacologic, 357, 374, 400, 422 Pharynx, 393, 400, 421 Phenotype, 21, 38, 46, 48, 56, 64, 68, 72, 98, 110, 116, 225, 250, 355, 371, 400 Phenylalanine, 399, 401, 424 Phorbol, 78, 254, 401 Phospholipases, 401, 414 Phosphorus, 349, 401 Phosphorylating, 257, 267, 401 Phosphorylation, 48, 54, 66, 257, 267, 358, 401 Photochemotherapy, 6, 401 Photopheresis, 6, 401 Photosensitizing Agents, 401 Physical Examination, 198, 323, 401 Physical Fitness, 367, 401
Physiologic, 26, 339, 346, 361, 374, 401, 409, 410 Phytohemagglutinins, 387, 401 Phytotoxin, 401, 411 Pigment, 360, 389, 401 Pigmentation, 307, 401 Pilocarpine, 293, 401 Pilot study, 10, 12, 15, 113, 125, 143, 176, 401 Pineal gland, 352, 401 Plants, 79, 238, 254, 266, 343, 349, 359, 373, 385, 390, 392, 401, 412, 422, 423 Plaque, 6, 321, 402 Plasma cells, 40, 48, 342, 392, 393, 402 Plasmapheresis, 343, 402 Plasmid, 22, 25, 80, 161, 402, 425 Plasmin, 402 Plasminogen, 149, 402 Plasminogen Activators, 402 Platelet Activation, 402, 414 Platelet Count, 272, 402 Plateletpheresis, 343, 402 Platelets, 198, 398, 402, 412, 420 Platinum, 353, 386, 397, 402 Platinum Compounds, 397, 402 Pleura, 402 Pleural, 45, 86, 121, 402, 403 Pleural cavity, 402, 403 Pleural Effusion, 86, 403 Pneumococcal Vaccines, 68, 403 Podophyllotoxin, 366, 403, 419 Point Mutation, 45, 264, 403 Poisoning, 366, 382, 390, 394, 403 Polycystic, 312, 403 Polyethylene, 219, 403 Polymerase, 18, 60, 93, 122, 124, 139, 403, 410 Polymerase Chain Reaction, 18, 93, 122, 124, 139, 403 Polymorphic, 244, 403 Polymorphism, 38, 120, 403 Polyomavirus, 71, 120, 398, 403 Polypeptide, 214, 215, 218, 226, 266, 340, 354, 368, 377, 399, 402, 403, 406, 420, 427 Polyposis, 354, 403 Polysaccharide, 342, 351, 403 Polyvalent, 68, 403 Posterior, 4, 341, 344, 362, 383, 397, 398, 404, 421 Postnatal, 216, 404, 417 Postsynaptic, 404, 414, 419 Potentiate, 11, 72, 404
Index 443
Potentiating, 50, 404 Potentiation, 404, 414 Practicability, 404, 423 Practice Guidelines, 308, 404 Precancerous, 404 Preclinical, 52, 63, 228, 404 Precursor, 86, 110, 127, 358, 362, 363, 365, 367, 374, 401, 402, 404, 405, 416, 422, 423, 424 Predisposition, 61, 78, 221, 230, 231, 263, 404 Prednisolone, 404 Prednisone, 96, 100, 138, 143, 154, 158, 165, 174, 180, 197, 204, 210, 237, 404, 405 Preleukemia, 393, 404, 415 Premalignant, 242, 243, 404 Presynaptic, 404, 419 Prevalence, 6, 9, 45, 58, 87, 120, 221, 395, 404 Prickle, 384, 404 Primary tumor, 45, 225, 243, 405 Probe, 58, 263, 405 Procarbazine, 143, 237, 405 Prodrug, 222, 405 Progeny, 27, 236, 405 Progesterone, 405, 417 Prognostic factor, 8, 27, 32, 160, 165, 177, 405, 419 Progressive, 138, 173, 203, 272, 350, 352, 360, 362, 363, 366, 374, 393, 394, 402, 405, 424 Progressive disease, 272, 405 Proline, 294, 354, 378, 405 Promoter, 20, 38, 67, 72, 77, 79, 82, 85, 129, 187, 218, 234, 405 Promyelocytic leukemia, 11, 140, 180, 405 Prone, 125, 322, 405 Prophase, 393, 405, 419, 420 Prophylaxis, 226, 233, 268, 271, 366, 405, 425 Prospective study, 146, 165, 405 Protease, 354, 405 Protein C, 57, 232, 264, 294, 339, 340, 345, 384, 386, 405, 406, 424 Protein Conformation, 340, 384, 406 Protein Kinases, 135, 406 Protein S, 58, 104, 267, 280, 312, 313, 347, 371, 406, 411 Proteins, 11, 12, 30, 32, 39, 47, 48, 50, 51, 53, 55, 57, 60, 61, 64, 67, 87, 126, 130, 186, 226, 228, 246, 247, 251, 252, 264, 266, 267, 292, 294, 340, 342, 343, 347,
350, 351, 352, 354, 355, 370, 375, 376, 377, 382, 384, 390, 392, 395, 399, 402, 406, 409, 414, 420, 422, 426 Proteinuria, 119, 393, 406 Proteolytic, 355, 365, 368, 402, 406, 411 Protocol, 13, 16, 19, 21, 36, 112, 133, 137, 144, 145, 156, 162, 165, 168, 405, 406 Proton Pump, 233, 406 Protons, 340, 377, 383, 388, 406, 408 Proto-Oncogene Proteins, 397, 406 Proto-Oncogene Proteins c-mos, 397, 406 Proto-Oncogenes, 218, 226, 406 Protozoa, 385, 391, 406, 423 Provirus, 52, 73, 74, 76, 406 Proximal, 362, 404, 406, 414 Pruritic, 360, 363, 386, 406 Pruritus, 128, 396, 406, 424 Psoralen, 6, 407 Psoriasis, 227, 287, 288, 319, 323, 337, 366, 401, 407 Psychiatry, 19, 368, 407 Psychic, 407, 413 Psychological Tests, 19, 407 Psychology, 362, 407 Public Health, 5, 17, 43, 58, 271, 309, 407 Public Policy, 305, 407 Publishing, 66, 261, 306, 307, 407 Pulmonary, 122, 153, 174, 307, 347, 356, 365, 407, 425 Pulse, 14, 392, 407 Purifying, 254, 360, 407 Purines, 407, 414 Purulent, 337, 407, 425 Pustular, 376, 407 Putrescine, 338, 396, 407, 416 Pyoderma, 227, 407 Pyoderma Gangrenosum, 227, 407 Pyridoxal, 396, 408 Q Quality of Life, 19, 43, 59, 63, 65, 66, 107, 187, 324, 325, 408, 418 Quiescent, 49, 246, 408, 427 R Race, 63, 384, 389, 391, 408 Radiation Oncology, 15, 66, 87, 99, 126, 139, 157, 408 Radioactive, 51, 210, 348, 374, 377, 380, 382, 383, 386, 392, 395, 396, 408, 412, 424, 427 Radioactivity, 235, 408 Radioimmunotherapy, 43, 50, 51, 60, 122, 129, 139, 159, 235, 255, 262, 354, 379, 408
444 Lymphoma
Radioisotope, 235, 378, 408, 422 Radiolabeled, 23, 40, 44, 51, 60, 208, 214, 217, 255, 262, 299, 347, 383, 408, 427 Radiological, 285, 399, 408 Radiology, 5, 17, 113, 118, 132, 136, 137, 148, 250, 273, 279, 395, 408 Radiopharmaceuticals, 23, 176, 408 Randomized clinical trial, 59, 133, 150, 409 Ras gene, 42, 225, 409 Reactivation, 67, 123, 177, 409 Reactive Oxygen Species, 88, 139, 149, 154, 409 Reagent, 214, 225, 250, 409 Receptor, 7, 11, 12, 21, 26, 30, 31, 44, 46, 50, 56, 60, 61, 66, 67, 75, 77, 81, 82, 104, 106, 128, 135, 187, 215, 216, 217, 219, 226, 227, 229, 230, 232, 238, 255, 262, 311, 342, 357, 362, 374, 409, 414 Receptors, Antigen, 355, 409 Recombinant, 27, 51, 70, 123, 219, 222, 229, 249, 298, 409, 425 Recombination, 14, 24, 27, 30, 48, 61, 264, 345, 371, 409 Reconstitution, 34, 161, 230, 409 Rectum, 230, 231, 343, 348, 354, 361, 367, 368, 370, 381, 384, 405, 409 Recurrence, 4, 124, 157, 159, 233, 352, 409 Red blood cells, 34, 366, 375, 409, 412 Red Nucleus, 344, 409 Reductase, 253, 409 Refer, 1, 43, 232, 348, 355, 368, 370, 376, 386, 392, 393, 395, 408, 409, 417 Refraction, 409, 416 Regeneration, 248, 409 Regional lymph node, 264, 410 Relapse, 31, 40, 41, 51, 62, 128, 221, 225, 232, 233, 234, 259, 268, 410 Relative risk, 4, 410 Remission, 5, 11, 87, 111, 124, 132, 133, 150, 173, 175, 225, 235, 288, 289, 388, 409, 410 Remission Induction, 133, 150, 410 Repressor, 52, 396, 410 Reproductive cells, 372, 376, 410 Research Design, 16, 18, 63, 410 Research Support, 47, 410 Resected, 282, 410 Resection, 5, 110, 112, 129, 247, 410 Residual disease, 41, 62, 410 Resorption, 5, 340, 410 Respiration, 167, 343, 349, 392, 410 Response rate, 21, 40, 52, 105, 271, 410
Restoration, 24, 56, 80, 409, 410, 427 Retina, 353, 410, 411 Retinal, 362, 410 Retinoblastoma, 75, 242, 311, 411 Retinoid, 264, 337, 366, 411 Retrospective, 4, 5, 37, 56, 123, 138, 152, 166, 175, 411 Retrospective study, 5, 56, 152, 166, 411 Retroviral vector, 14, 25, 411 Retrovirus, 52, 55, 69, 73, 74, 76, 81, 82, 222, 265, 411 Rheumatic Diseases, 265, 411 Rheumatism, 99, 106, 113, 123, 162, 411 Rheumatoid, 70, 123, 239, 411 Rheumatoid arthritis, 70, 123, 239, 411 Ribavirin, 127, 411 Ribose, 60, 358, 411 Ribosome, 214, 411, 422 Ricin, 132, 258, 299, 411 Rigidity, 401, 411 Risk factor, 7, 18, 38, 53, 58, 63, 109, 135, 247, 365, 405, 410, 411 Risk patient, 149, 411 Rod, 223, 345, 411 Rodenticides, 400, 411 Rosette Formation, 119, 412 Rye, 292, 353, 366, 372, 412 S S Phase, 65, 412 Sagittal, 124, 412 Saimiri, 81, 233, 412 Saliva, 293, 412 Salivary, 291, 292, 359, 361, 367, 398, 412, 418, 427 Salivary glands, 292, 359, 361, 367, 412 Salvage Therapy, 152, 156, 170, 178, 354, 412 Saponins, 412, 417 Sarcoidosis, 293, 412 Sargramostim, 203, 412 Scans, 169, 198, 200, 412 Scatter, 33, 413 Schizoid, 413, 427 Schizophrenia, 265, 413, 427 Schizotypal Personality Disorder, 413, 427 Scleroderma, 293, 413 Sclerosis, 5, 135, 172, 312, 393, 413 Screening, 38, 218, 223, 230, 231, 256, 265, 353, 399, 413 Secondary tumor, 390, 413 Secretion, 48, 306, 338, 352, 376, 377, 382, 392, 413, 422, 425
Index 445
Secretory, 48, 413, 419 Segregation, 236, 409, 413 Seizures, 283, 372, 398, 413, 417 Selective estrogen receptor modulator, 413, 419 Selenium, 171, 413 Semen, 405, 413 Seminal vesicles, 413, 425 Semisynthetic, 349, 366, 413, 419 Senescence, 45, 413 Sensitization, 125, 176, 413 Sepsis, 272, 414 Septal, 118, 414 Sequela, 3, 414 Sequencing, 18, 50, 403, 414 Serine, 23, 135, 406, 414, 423 Serotonin, 374, 414, 423 Serous, 133, 402, 414 Serum, 32, 63, 81, 171, 177, 242, 243, 252, 269, 339, 341, 343, 355, 373, 378, 409, 414, 423 Sex Characteristics, 338, 414, 420 Sex Determination, 312, 414 Shedding, 75, 414 Shock, 74, 252, 414, 422 Signal Transduction, 8, 42, 49, 67, 123, 228, 264, 348, 414 Signs and Symptoms, 410, 415, 424 Single-agent, 138, 173, 415 Sister Chromatid Exchange, 24, 415 Skeletal, 89, 247, 392, 393, 415 Skeleton, 337, 384, 415 Skin Care, 323, 415 Skin Manifestations, 323, 415 Sleep apnea, 167, 415 Small cell lung cancer, 149, 260, 415 Small intestine, 91, 281, 292, 346, 350, 363, 377, 378, 382, 415, 423, 426 Smoldering leukemia, 393, 415 Smooth muscle, 341, 376, 415, 418 Sneezing, 414, 415 Soaps, 415 Social Environment, 408, 415 Sodium, 253, 267, 298, 415 Soft tissue, 4, 6, 347, 368, 396, 415, 416 Soft tissue sarcoma, 368, 416 Solid tumor, 17, 65, 198, 200, 203, 222, 232, 243, 244, 252, 264, 341, 347, 362, 364, 416 Solvent, 254, 352, 416 Soma, 416 Somatic, 29, 30, 35, 72, 73, 78, 91, 108, 231, 269, 338, 357, 377, 389, 391, 400, 415, 416
Somatic cells, 389, 391, 416 Somatic mutations, 231, 269, 416 Spastic, 383, 416 Specialist, 318, 326, 416 Species, 254, 339, 351, 365, 377, 384, 385, 389, 390, 391, 392, 396, 398, 403, 408, 409, 412, 416, 418, 422, 423, 426, 427 Specificity, 23, 40, 42, 74, 239, 246, 260, 338, 379, 404, 416 Spectrum, 31, 37, 93, 228, 229, 358, 384, 416 Sperm, 352, 371, 372, 376, 410, 416 Spermatic, 159, 416 Spermidine, 338, 397, 416 Sphincter, 384, 416 Spinal cord, 344, 350, 351, 352, 363, 370, 382, 390, 394, 397, 400, 404, 416 Spinal Nerves, 400, 416 Spinous, 365, 384, 416 Spirochete, 416, 419 Spleen, 110, 114, 217, 247, 256, 262, 340, 359, 377, 387, 412, 417 Splenomegaly, 381, 417 Sporadic, 71, 72, 85, 220, 411, 417 Squamous, 8, 28, 147, 231, 365, 395, 417 Squamous cell carcinoma, 147, 231, 365, 395, 417 Squamous cells, 417 Staging, 6, 8, 33, 119, 144, 151, 162, 169, 170, 250, 251, 269, 285, 326, 412, 417 Standard therapy, 401, 417 Status Epilepticus, 248, 417 Stem Cells, 31, 63, 99, 122, 153, 201, 231, 232, 234, 339, 366, 375, 400, 417 Sterile, 3, 417 Sterility, 358, 417 Steroid, 177, 322, 346, 357, 412, 417 Stimulant, 293, 376, 417 Stimulus, 230, 252, 356, 362, 363, 367, 381, 385, 417 Stochastic Processes, 49, 417 Stool, 383, 384, 418 Strand, 24, 84, 403, 418 Streptavidin, 51, 79, 418 Stress, 93, 154, 292, 345, 383, 393, 397, 404, 411, 418, 425 Stroke, 211, 304, 349, 418 Stromal, 35, 347, 418 Stromal Cells, 35, 347, 418 Subacute, 118, 380, 418 Subarachnoid, 374, 418 Subclinical, 380, 413, 418
446 Lymphoma
Subcutaneous, 60, 98, 153, 178, 363, 396, 398, 418 Sublingual, 292, 418 Submandibular, 292, 418 Subspecies, 416, 418 Substance P, 390, 409, 413, 418 Substrate, 80, 187, 267, 418 Suction, 368, 418 Sunburn, 268, 418 Support group, 325, 418 Supportive care, 223, 399, 418 Suppression, 24, 30, 45, 61, 63, 229, 271, 371, 418 Supratentorial, 113, 418 Survival Analysis, 33, 419 Survival Rate, 23, 32, 44, 52, 159, 397, 419 Symphysis, 405, 419 Symptomatic, 398, 419 Synapses, 126, 394, 419 Synaptic, 414, 419 Synaptic Vesicles, 419 Synergistic, 11, 39, 56, 60, 126, 239, 240, 255, 419 Syphilis, 307, 419 Systemic lupus erythematosus, 239, 293, 387, 419 Systemic therapy, 322, 419 T Tachycardia, 345, 419 Tachypnea, 345, 419 Tamoxifen, 19, 413, 419 Telangiectasia, 166, 264, 312, 419 Teniposide, 206, 296, 419 Teratogenic, 339, 366, 420 Teratoma, 352, 420 Testicular, 116, 420 Testis, 172, 177, 230, 231, 280, 352, 416, 420 Testosterone, 340, 409, 420 Tetravalent, 51, 420 Thalamic, 344, 420 Thalamic Diseases, 344, 420 Thalassemia, 10, 375, 420 Therapeutics, 15, 16, 229, 256, 297, 420 Thermal, 343, 362, 395, 403, 420 Thoracic, 65, 96, 167, 361, 402, 420, 427 Thorax, 121, 178, 337, 387, 420 Thorium Dioxide, 247, 420 Threonine, 23, 135, 257, 406, 414, 420 Thrombin, 368, 405, 420, 421 Thrombocytes, 402, 420 Thrombocytopenia, 263, 373, 420 Thromboembolism, 104, 420
Thrombolytic, 402, 421 Thrombomodulin, 405, 421 Thrombosis, 381, 406, 418, 421 Thymidine, 10, 25, 222, 421 Thymidine Kinase, 10, 25, 222, 421 Thymus, 34, 61, 216, 217, 262, 379, 387, 421 Thyroid, 134, 140, 157, 176, 230, 231, 244, 306, 383, 421, 424 Thyroid Gland, 176, 421 Thyroid Hormones, 421, 424 Thyroiditis, 157, 421 Tissue Culture, 12, 421 Tolerance, 21, 35, 75, 233, 338, 421 Tome, 184, 421 Tonsil, 93, 421 Topical, 6, 288, 321, 322, 323, 344, 398, 401, 415, 421 Topoisomerase inhibitors, 60, 383, 421 Topotecan, 137, 169, 421 Total-body irradiation, 202, 421 Toxic, iv, 109, 164, 214, 222, 233, 235, 250, 251, 253, 294, 339, 345, 353, 359, 365, 372, 374, 379, 380, 389, 394, 399, 401, 403, 407, 412, 413, 421, 422 Toxicology, 60, 154, 306, 422 Toxins, 219, 342, 380, 392, 408, 422, 425 Toxoplasmosis, 77, 283, 307, 422 Trace element, 348, 369, 422 Tracer, 33, 422 Trachea, 348, 384, 389, 400, 421, 422 Transcriptase, 411, 422 Transcription Factors, 47, 61, 94, 127, 422 Transduction, 49, 83, 222, 414, 422 Transfection, 22, 347, 422 Transfer Factor, 379, 422 Transforming Growth Factor beta, 66, 422 Translating, 42, 422 Translation, 52, 55, 60, 252, 422 Translational, 15, 16, 19, 21, 33, 37, 39, 41, 55, 62, 65, 371, 422 Transmitter, 344, 362, 389, 419, 422 Trauma, 292, 394, 398, 422 Treatment Outcome, 23, 147, 245, 423 Trees, 254, 423 Triage, 59, 423 Tricuspid Valve, 167, 423 Trigeminal, 121, 423 Tropism, 46, 69, 423 Trypanosomiasis, 267, 399, 423 Trypsin, 145, 365, 423 Tryptophan, 354, 414, 423 Tuberculosis, 307, 356, 387, 423
Index 447
Tuberous Sclerosis, 312, 423 Tumor Escape, 259, 423 Tumor marker, 346, 423 Tumor model, 60, 423 Tumor Necrosis Factor, 113, 228, 238, 423 Tumor suppressor gene, 24, 32, 42, 45, 52, 56, 222, 224, 231, 397, 423 Tumor-derived, 79, 423 Tumorigenic, 55, 252, 424 Tumour, 86, 87, 124, 242, 370, 424 TYPHI, 84, 424 Typhoid fever, 424 Tyrosine, 34, 49, 64, 76, 77, 80, 226, 267, 362, 424 U Ulcer, 233, 240, 359, 363, 399, 424 Ulcerative colitis, 4, 240, 281, 354, 381, 407, 424 Ultrasonography, 114, 424 Unconscious, 359, 378, 424 Unresectable, 200, 424 Uraemia, 398, 424 Urea, 396, 424 Ureters, 424, 425 Urethra, 399, 405, 424, 425 Urinary, 240, 371, 424 Urinary tract, 240, 424 Urine, 77, 190, 253, 299, 347, 354, 375, 406, 424, 425 Urogenital, 240, 371, 424 Urogenital System, 240, 424 Urokinase, 149, 425 Urticaria, 227, 425 Uterus, 230, 231, 351, 364, 367, 372, 385, 391, 397, 405, 425 V Vaccination, 22, 61, 83, 129, 250, 425 Vaccine, 9, 48, 61, 161, 203, 266, 280, 338, 406, 424, 425 Vacuoles, 364, 396, 425 Vagina, 293, 349, 351, 425 Vaginitis, 349, 425 Valves, 3, 425 Varicella, 10, 307, 425 Vas Deferens, 416, 425 Vascular, 14, 73, 230, 243, 244, 253, 375, 380, 402, 421, 425 Vascular endothelial growth factor, 14, 425 Vasculitis, 125, 293, 398, 425 Vasodilator, 362, 376, 425 VE, 26, 112, 425
Vector, 25, 35, 218, 222, 234, 248, 381, 422, 425 Vein, 198, 383, 395, 398, 425 Venereal, 419, 425 Venoms, 359, 425 Venous, 348, 402, 406, 425 Venous blood, 348, 402, 425 Ventricle, 344, 407, 423, 425 Ventricular, 134, 363, 425, 426 Ventricular Dysfunction, 363, 426 Venules, 347, 426 Vesicular, 360, 376, 426 Veterinarians, 140, 426 Veterinary Medicine, 136, 153, 284, 305, 426 Villi, 377, 426 Villous, 122, 136, 350, 426 Vinblastine, 144, 165, 296, 426 Vinca Alkaloids, 426 Vincristine, 96, 100, 138, 143, 154, 158, 167, 174, 197, 204, 207, 210, 237, 271, 405, 426 Vinorelbine, 125, 137, 176, 426 Vinyl Chloride, 247, 426 Viral Hepatitis, 247, 426 Viral Load, 63, 426 Viral vector, 222, 426 Viremia, 107, 162, 426 Virulence, 25, 221, 344, 421, 426 Viscera, 220, 393, 416, 426 Visceral, 345, 357, 385, 400, 426 Vitiligo, 227, 407, 426 Vitro, 10, 11, 14, 21, 22, 23, 24, 25, 26, 31, 39, 40, 42, 44, 46, 48, 49, 50, 60, 61, 62, 63, 64, 72, 101, 135, 154, 219, 223, 225, 229, 230, 239, 244, 246, 250, 261, 265, 267, 289, 380, 403, 412, 421, 427 W War, 389, 427 Warts, 222, 254, 403, 427 White blood cell, 64, 191, 203, 217, 262, 321, 322, 325, 337, 342, 346, 352, 368, 374, 381, 385, 387, 388, 392, 393, 395, 402, 427 Windpipe, 400, 421, 427 Withdrawal, 52, 427 Womb, 425, 427 Wound Healing, 381, 427 X Xenograft, 51, 52, 60, 255, 341, 423, 427 Xerostomia, 292, 427 X-ray, 192, 193, 202, 204, 208, 210, 285, 356, 369, 370, 383, 395, 408, 412, 427
448 Lymphoma
X-ray therapy, 383, 427 Y Yeasts, 349, 370, 400, 427 Yttrium, 129, 210, 378, 427
Z Zoster, 10, 307, 427 Zygote, 356, 427 Zymogen, 405, 427
Index 449
450 Lymphoma
Index 451
452 Lymphoma