Volume I ABCD — Delta-9-tetrahydrocannabinol
Editor
Jeffrey A. Knight, Ph.D. Mount Holyoke College
Medical Consultan...
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Volume I ABCD — Delta-9-tetrahydrocannabinol
Editor
Jeffrey A. Knight, Ph.D. Mount Holyoke College
Medical Consultants
Laurie Jackson-Grusby, Ph.D. Children’s Hospital Boston, Harvard Medical School
Wendy White-Ryan, M.D., FAAP Golisano Children’s Hospital at Strong Memorial Hospital
SALEM PRESS, INC. Pasadena, California Hackensack, New Jersey
Editor in Chief: Dawn P. Dawson Editorial Director: Christina J. Moose Project Editors: Tracy Irons-Georges, Rowena Wildin Dehanke Editorial Assistant: Dana Garey
Production Editor: Joyce I. Buchea Acquisitions Editor: Mark Rehn Photo Editor: Cynthia Breslin Beres Design and Graphics: James Hutson Layout: William Zimmerman
Copyright © 2009, by Salem Press, Inc. All rights in this book are reserved. No part of this work may be used or reproduced in any manner whatsoever or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without written permission from the copyright owner except in the case of brief quotations embodied in critical articles and reviews or in the copying of images deemed to be freely licensed or in the public domain. For information address the publisher, Salem Press, Inc., P.O. Box 50062, Pasadena, California 91115. ∞ The paper used in these volumes conforms to the American National Standard for Permanence of Paper for Printed Library Materials, Z39.48-1992 (R1997). Note to Readers The material presented in Salem Health: Cancer is intended for broad informational and educational purposes. Readers who suspect that they or someone whom they know or provide caregiving for suffers from cancer or any other physical or psychological disorder, disease, or condition described in this set should contact a physician without delay; this work should not be used as a substitute for professional medical diagnosis or staging. Readers who are undergoing or about to undergo any treatment or procedure described in this set should refer to their physicians and other health care team members for guidance concerning preparation and possible effects. This set is not to be considered definitive on the covered topics, and readers should remember that the field of health care is characterized by a diversity of medical opinions and constant expansion in knowledge and understanding. Library of Congress Cataloging-in-Publication Data Salem health : cancer / Jeffrey A. Knight, Laurie Jackson-Grusby, Wendy White-Ryan. p. cm. Includes bibliographical references and index. ISBN 978-1-58765-505-0 (set : alk. paper) — ISBN 978-1-58765-506-7 (vol. 1 : alk. paper) — ISBN 978-1-58765-507-4 (vol. 2 : alk. paper) — ISBN 978-1-58765-508-1 (vol. 3 : alk. paper) — ISBN 978-1-58765-509-8 (vol. 4 : alk. paper) 1. Cancer. I. Knight, Jeffrey A., 1948- II. Jackson-Grusby, Laurie. III. White-Ryan, Wendy. RC265.S32 2008 616.99′4—dc22 2008030861
First Printing
printed in the united states of america
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Contents Alopecia . . . . . . . . . . . . . . . . . . . . . . . . 47 ALP. See Alkaline phosphatase test Alpha-fetoprotein (AFP) levels . . . . . . . . . . . . 48 Alternative therapies. See Complementary and alternative therapies Alveolar soft-part sarcomas . . . . . . . . . . . . . . 49 Amenorrhea . . . . . . . . . . . . . . . . . . . . . . 50 American Association for Cancer Research (AACR) . . . . . . . . . . . . . . . . . . . . . . . 52 American Cancer Society (ACS) . . . . . . . . . . . 53 American Institute for Cancer Research (AICR) . . . 54 4-Aminobiphenyl . . . . . . . . . . . . . . . . . . . 56 AML. See Acute myelocytic leukemia Amputation . . . . . . . . . . . . . . . . . . . . . . 56 Amyloidosis . . . . . . . . . . . . . . . . . . . . . . 58 Anal cancer . . . . . . . . . . . . . . . . . . . . . . 59 Androgen drugs . . . . . . . . . . . . . . . . . . . . 61 Anemia . . . . . . . . . . . . . . . . . . . . . . . . 62 Anemia, aplastic. See Aplastic anemia Anemia, hemolytic. See Hemolytic anemia Angiogenesis . . . . . . . . . . . . . . . . . . . . . 64 Angiogenesis inhibitors . . . . . . . . . . . . . . . . 66 Angiography. . . . . . . . . . . . . . . . . . . . . . 68 Angiosarcomas . . . . . . . . . . . . . . . . . . . . 69 Anoscopy . . . . . . . . . . . . . . . . . . . . . . . 70 Anthraquinones . . . . . . . . . . . . . . . . . . . . 71 Anthrax . . . . . . . . . . . . . . . . . . . . . . . . 71 Antiandrogens . . . . . . . . . . . . . . . . . . . . . 72 Antidiarrheal agents . . . . . . . . . . . . . . . . . . 73 Antiestrogens . . . . . . . . . . . . . . . . . . . . . 75 Antifungal therapies . . . . . . . . . . . . . . . . . . 76 Antimetabolites in chemotherapy . . . . . . . . . . . 78 Antinausea medications . . . . . . . . . . . . . . . . 81 Antineoplastics in chemotherapy . . . . . . . . . . . 83 Antioxidants . . . . . . . . . . . . . . . . . . . . . . 86 Antiperspirants and breast cancer . . . . . . . . . . . 88 Antiviral therapies. . . . . . . . . . . . . . . . . . . 90 Anxiety . . . . . . . . . . . . . . . . . . . . . . . . 93 APBI. See Accelerated partial breast irradiation APC gene testing . . . . . . . . . . . . . . . . . . . 94 Aplastic anemia . . . . . . . . . . . . . . . . . . . . 95 Appendix cancer . . . . . . . . . . . . . . . . . . . 97 Appetite loss. . . . . . . . . . . . . . . . . . . . . . 98 APR. See Abdominoperineal resection Arsenic compounds . . . . . . . . . . . . . . . . . 100 Arterial embolization . . . . . . . . . . . . . . . . 101 Artificial sweeteners . . . . . . . . . . . . . . . . . 102 Asbestos . . . . . . . . . . . . . . . . . . . . . . . 103
Publisher’s Note . . . . . . . . . . . . . . . . . . . . ix About the Editors . . . . . . . . . . . . . . . . . . . xi Contributors . . . . . . . . . . . . . . . . . . . . . xiii Complete List of Contents . . . . . . . . . . . . . . xv AACR. See American Association for Cancer Research ABCD. . . . . . . . . . . . . . . . . . . . . . . . . . 1 ACC. See Adenoid cystic carcinoma Abdominoperineal resection (APR) . . . . . . . . . . 1 Accelerated partial breast irradiation (APBI). . . . . . 3 Achlorhydria . . . . . . . . . . . . . . . . . . . . . . 4 Acoustic neuromas . . . . . . . . . . . . . . . . . . . 4 Acquired immunodeficiency disease-related cancers. See HIV/AIDS-related cancers Acrylamides . . . . . . . . . . . . . . . . . . . . . . 6 ACS. See American Cancer Society Acupuncture and acupressure for cancer patients . . . 8 Acute lymphocytic leukemia (ALL) . . . . . . . . . 11 Acute myelocytic leukemia (AML) . . . . . . . . . . 13 Adenocarcinomas . . . . . . . . . . . . . . . . . . . 16 Adenoid cystic carcinoma (ACC) . . . . . . . . . . . 17 Adenomatoid tumors . . . . . . . . . . . . . . . . . 18 Adenomatous polyps . . . . . . . . . . . . . . . . . 18 Adenoviruses . . . . . . . . . . . . . . . . . . . . . 19 Adjuvant therapy . . . . . . . . . . . . . . . . . . . 20 Adrenal gland cancers . . . . . . . . . . . . . . . . . 21 Adrenocortical cancer . . . . . . . . . . . . . . . . . 23 Advance directives . . . . . . . . . . . . . . . . . . 24 Aflatoxins . . . . . . . . . . . . . . . . . . . . . . . 26 AFP levels. See Alpha-fetoprotein levels African Americans and cancer . . . . . . . . . . . . 28 Africans and cancer . . . . . . . . . . . . . . . . . . 31 Afterloading radiation therapy . . . . . . . . . . . . 32 Agent Orange . . . . . . . . . . . . . . . . . . . . . 34 Aging and cancer . . . . . . . . . . . . . . . . . . . 34 AICR. See American Institute for Cancer Research Aids and devices for cancer patients . . . . . . . . . 38 AIDS-related cancers. See HIV/AIDS-related cancers Air pollution . . . . . . . . . . . . . . . . . . . . . . 39 Alcohol, alcoholism, and cancer . . . . . . . . . . . 42 Aleukemia . . . . . . . . . . . . . . . . . . . . . . . 43 Alkaline phosphatase test (ALP) . . . . . . . . . . . 44 Alkylating agents in chemotherapy . . . . . . . . . . 45 ALL. See Acute lymphocytic leukemia Allicin, garlic and. See Garlic and allicin v
Salem Health: Cancer Ascites . . . . . . . . . . . . Ashkenazi Jews and cancer . Asian Americans and cancer. Astrocytomas. . . . . . . . . Ataxia telangiectasia (AT) . . Autologous blood transfusion Axillary dissection . . . . . . Azathioprine . . . . . . . . .
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105 107 109 112 114 115 116 117
Bacillus Calmette Guérin (BCG) . . . . . . . . Bacteria as causes of cancer . . . . . . . . . . . Barium enema . . . . . . . . . . . . . . . . . . Barium swallow . . . . . . . . . . . . . . . . . Barrett esophagus . . . . . . . . . . . . . . . . Basal cell carcinomas . . . . . . . . . . . . . . BCG. See Bacillus Calmette Guérin Beckwith-Wiedemann syndrome (BWS) . . . . Benign prostatic hyperplasia (BPH) . . . . . . . Benign tumors . . . . . . . . . . . . . . . . . . Benzene . . . . . . . . . . . . . . . . . . . . . Benzidine and dyes metabolized to benzidine . . Benzodiazepines . . . . . . . . . . . . . . . . . Bereavement, grief and. See Grief and bereavement Beryllium and beryllium compounds . . . . . . Beta-carotene . . . . . . . . . . . . . . . . . . Bethesda criteria . . . . . . . . . . . . . . . . . BHDS. See Birt-Hogg-Dubé syndrome Bile duct cancer . . . . . . . . . . . . . . . . . Bilobectomy . . . . . . . . . . . . . . . . . . . Bioflavonoids . . . . . . . . . . . . . . . . . . Biological therapy . . . . . . . . . . . . . . . . Biopsy. See also Computed tomography-guided biopsy; Core needle biopsy; Liver biopsy; Needle biopsies; Pleural biopsy; Stereotactic needle biopsy; Surgical biopsies . . . . . . . Birt-Hogg-Dubé syndrome (BHDS) . . . . . . . Birth control pills and cancer . . . . . . . . . . Bis(chloromethyl) ether and technical-grade chloromethyl methyl ether . . . . . . . . . . Bisphenol A (BPA) . . . . . . . . . . . . . . . Bisphosphonates . . . . . . . . . . . . . . . . . Bladder cancer . . . . . . . . . . . . . . . . . . Blood cancers . . . . . . . . . . . . . . . . . . BMT. See Bone marrow transplantation BNCT. See Boron neutron capture therapy Body image. See Self-image and body image Bone cancers . . . . . . . . . . . . . . . . . . . Bone marrow aspiration and biopsy . . . . . . . Bone marrow transplantation (BMT) . . . . . . Bone pain . . . . . . . . . . . . . . . . . . . .
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118 118 120 121 123 124
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126 128 128 130 131 132
Bone scan . . . . . . . . . . . . . . . . . . . . Boron neutron capture therapy (BNCT) . . . . . Bowen disease . . . . . . . . . . . . . . . . . . BPA. See Bisphenol A BPH. See Benign prostatic hyperplasia BPI. See Brief Pain Inventory Brachytherapy . . . . . . . . . . . . . . . . . . BRAF gene . . . . . . . . . . . . . . . . . . . . Brain and central nervous system cancers . . . . Brain scan . . . . . . . . . . . . . . . . . . . . BRCA1 and BRCA2 genes . . . . . . . . . . . . Breakthrough pain . . . . . . . . . . . . . . . . Breast, calcifications of. See Calcifications of the breast Breast, medullary carcinoma of. See Medullary carcinoma of the breast Breast cancer, cutaneous. See Cutaneous breast cancer Breast cancer, estrogen-receptor-sensitive. See Estrogen-receptor-sensitive breast cancer Breast cancer in children and adolescents . . . . Breast cancer in men . . . . . . . . . . . . . . . Breast cancer in pregnant women . . . . . . . . Breast cancers . . . . . . . . . . . . . . . . . . Breast implants. . . . . . . . . . . . . . . . . . Breast reconstruction. . . . . . . . . . . . . . . Breast self-examination (BSE). . . . . . . . . . Breast ultrasound. . . . . . . . . . . . . . . . . Breslow’s staging . . . . . . . . . . . . . . . . Brief Pain Inventory (BPI) . . . . . . . . . . . . Brompton cocktail . . . . . . . . . . . . . . . . Bronchial adenomas . . . . . . . . . . . . . . . Bronchoalveolar lung cancer . . . . . . . . . . Bronchography. . . . . . . . . . . . . . . . . . Bronchoscopy . . . . . . . . . . . . . . . . . . BSE. See Breast self-examination Burkitt lymphoma . . . . . . . . . . . . . . . . 1,3-Butadiene . . . . . . . . . . . . . . . . . . 1,4-Butanediol dimethanesulfonate . . . . . . . BWS. See Beckwith-Wiedemann syndrome
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CA 15-3 test . . . . . . . . . . . . . CA 19-9 test . . . . . . . . . . . . . CA 27-29 test . . . . . . . . . . . . CA 125 test. . . . . . . . . . . . . . Cachexia . . . . . . . . . . . . . . . Cadmium and cadmium compounds. Caffeine . . . . . . . . . . . . . . . Calcifications of the breast. . . . . . Calcium . . . . . . . . . . . . . . . Cancell . . . . . . . . . . . . . . . . vi
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205 205 206 206 207 208 209 211 212 212
Contents Cancer biology . . . . . . . . . . . . . . . . . . . Cancer care team . . . . . . . . . . . . . . . . . . Cancer clusters . . . . . . . . . . . . . . . . . . . Cancer education. . . . . . . . . . . . . . . . . . Candidiasis . . . . . . . . . . . . . . . . . . . . . Carcinoembryonic antigen antibody (CEA) test . . . . . . . . . . . . . . . . . . . . . . . . Carcinogens, known . . . . . . . . . . . . . . . . Carcinogens, reasonably anticipated. . . . . . . . Carcinoid tumors and carcinoid syndrome . . . . Carcinoma of unknown primary origin (CUP) . . . . . . . . . . . . . . . . . . . . . . Carcinomas. . . . . . . . . . . . . . . . . . . . . Carcinomas, invasive ductal. See Invasive ductal carcinomas Carcinomas, invasive lobular. See Invasive lobular carcinomas Carcinomas, leptomeningeal. See Leptomeningeal carcinomas Carcinomatosis. . . . . . . . . . . . . . . . . . . Carcinomatous meningitis . . . . . . . . . . . . . Carcinosarcomas . . . . . . . . . . . . . . . . . . Cardiomyopathy in cancer patients . . . . . . . . Cardiopulmonary resuscitation (CPR) . . . . . . . Caregivers and caregiving . . . . . . . . . . . . . Caregiving, long-distance. See Long-distance caregiving Carney complex . . . . . . . . . . . . . . . . . . Carotenoids . . . . . . . . . . . . . . . . . . . . Cartilage supplements . . . . . . . . . . . . . . . Case management . . . . . . . . . . . . . . . . . Castleman disease . . . . . . . . . . . . . . . . . CBC. See Complete blood count CBE. See Clinical breast exam CDKN2A. See Cyclin-dependent kinase inhibitor-2A CEA test. See Carcinoembryonic antigen antibody test Cell phones. . . . . . . . . . . . . . . . . . . . . Cervical cancer. . . . . . . . . . . . . . . . . . . Chemoembolization . . . . . . . . . . . . . . . . Chemoprevention . . . . . . . . . . . . . . . . . Chemotherapy . . . . . . . . . . . . . . . . . . . Chemotherapy, cognitive effects of. See Cognitive effects of cancer and chemotherapy Chewing tobacco. . . . . . . . . . . . . . . . . . Childbirth and cancer . . . . . . . . . . . . . . . Childhood cancers . . . . . . . . . . . . . . . . . Chlorambucil. . . . . . . . . . . . . . . . . . . . 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)1-nitrosourea (MeCCNU) . . . . . . . . . . . .
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213 216 218 220 221
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223 224 227 230
Cholecystectomy . . . . . . . . . . . . . . . . . Chordomas . . . . . . . . . . . . . . . . . . . . Choriocarcinomas . . . . . . . . . . . . . . . . CHPP. See Continuous hyperthermic peritoneal perfusion Chromium hexavalent compounds. . . . . . . . Chromosomes and cancer . . . . . . . . . . . . Chronic lymphocytic leukemia (CLL) . . . . . . Chronic myeloid leukemia (CML). . . . . . . . Cigarettes and cigars . . . . . . . . . . . . . . . Clinical breast exam (CBE) . . . . . . . . . . . Clinical trials . . . . . . . . . . . . . . . . . . . CLL. See Chronic lymphocytic leukemia CML. See Chronic myeloid leukemia Coal tars and coal tar pitches . . . . . . . . . . Cobalt 60 radiation. . . . . . . . . . . . . . . . Coenzyme Q10. . . . . . . . . . . . . . . . . . Cognitive effects of cancer and chemotherapy . Coke oven emissions. . . . . . . . . . . . . . . Cold nodule . . . . . . . . . . . . . . . . . . . Colectomy . . . . . . . . . . . . . . . . . . . . Coloanal anastomosis . . . . . . . . . . . . . . Colon polyps . . . . . . . . . . . . . . . . . . . Colonoscopy and virtual colonoscopy . . . . . . Colony-stimulating factors (CSFs) . . . . . . . Colorectal cancer. . . . . . . . . . . . . . . . . Colorectal cancer screening . . . . . . . . . . . Colostomy . . . . . . . . . . . . . . . . . . . . Colposcopy. . . . . . . . . . . . . . . . . . . . Comedo carcinomas . . . . . . . . . . . . . . . Complementary and alternative therapies . . . . Complete blood count (CBC) . . . . . . . . . . Computed tomography (CT)-guided biopsy . . . . . . . . . . . . . . . . . . . . . Computed tomography (CT) scan . . . . . . . . Conization . . . . . . . . . . . . . . . . . . . . Continuous hyperthermic peritoneal perfusion (CHPP) . . . . . . . . . . . . . . . . . . . . Cordectomy . . . . . . . . . . . . . . . . . . . Cordotomy . . . . . . . . . . . . . . . . . . . . Core needle biopsy. . . . . . . . . . . . . . . . Corticosteroids . . . . . . . . . . . . . . . . . . Coughing . . . . . . . . . . . . . . . . . . . . . Counseling for cancer patients and survivors . . Cowden syndrome . . . . . . . . . . . . . . . . COX-2 inhibitors. See Cyclooxygenase 2 inhibitors CPR. See Cardiopulmonary resuscitation Craniopharyngiomas . . . . . . . . . . . . . . . Craniosynostosis . . . . . . . . . . . . . . . . . Craniotomy. . . . . . . . . . . . . . . . . . . .
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288 289 289 290 292 292 293 294 296 297 299 300 304 306 308 309 309 312
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Salem Health: Cancer Crohn disease . . . . . . . . . . . . . . . Cruciferous vegetables . . . . . . . . . . . Cryoablation . . . . . . . . . . . . . . . . Cryptorchidism. . . . . . . . . . . . . . . CSFs. See Colony-stimulating factors CT scan. See Computed tomography scan CTCL. See Cutaneous T-cell lymphoma Culdoscopy. . . . . . . . . . . . . . . . . CUP. See Carcinoma of unknown primary origin Curcumin. . . . . . . . . . . . . . . . . . Cushing syndrome and cancer . . . . . . . Cutaneous breast cancer . . . . . . . . . . Cutaneous T-cell lymphoma (CTCL) . . . Cyclin-dependent kinase inhibitor-2A (CDKN2A). . . . . . . . . . . . . . . .
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332 335 336 338
Cyclooxygenase 2 (COX-2) inhibitors . Cyclophosphamide. . . . . . . . . . . . Cyclosporin A . . . . . . . . . . . . . . Cystography . . . . . . . . . . . . . . . Cystoscopy . . . . . . . . . . . . . . . . Cytogenetics . . . . . . . . . . . . . . . Cytokines . . . . . . . . . . . . . . . . Cytology . . . . . . . . . . . . . . . . . Cytology, sputum. See Sputum cytology
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344 345 346 347 347 348 350 350
D&C. See Dilation and curettage Dana-Farber Cancer Institute . . . . . . . . . . . . 354 DCIS. See Ductal carcinoma in situ DEA. See Diethanolamine DEHP. See Di(2-ethylhexyl) phthalate Delta-9-tetrahydrocannabinol . . . . . . . . . . . . 355
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Publisher’s Note not only the names of the specializations but also related subspecialists, the cancers they treat, how they are trained and certified, and the range of services and procedures they perform. Finally, a group of topics addressing social and personal issues, lifestyle choices, nutritional supplements, and complementary or alternative therapies are similarly formatted into subsections that call out key areas of interest for readers. Special features of the set include tables throughout identifying the most important chemotherapeutic and other drugs and the symptoms and conditions they address, population statistics, survival rates, and other core information. Every essay includes a section of “See also” cross-references to other essays in the set that will be of interest to those consulting the topic at hand. A fully crossreferenced “Complete List of Contents” at the beginning of every volume also assists readers in locating related topics of interest. Photographs display for readers typical instances of lesions, tumors, procedures, and anatomical cross-sections to locate areas of the body affected. In addition, 8 appendixes at the end of volume 4 provide information on the following:
Salem Health: Cancer alphabetically arranges 835 essays on all aspects of cancer for all nonspecialist interest groups—from those who have been diagnosed to caregivers, family members, students, and readers with a general interest in health. The essays in this 4-volume set address diseases, conditions, symptoms, cancer-related syndromes, chemotherapy and other drugs, cancer centers, genetics, the biology of cancer, medical specialties, tests, procedures, complementary and alternative therapies, lifestyles, healthy and preventive strategies, and the many social and personal issues surrounding cancer, from cancer’s impact on minority populations to finances, insurance, relationships, and emotional coping. Written by physicians, nurses, and professional medical writers whose credentials and degrees are clearly listed in the byline to every essay, this comprehensive reference publication will be of interest not only to public library patrons but also to premedical students and those building collections for the patient population. Essays vary in length from 400 to 2,000 words, ranging from one to five pages. The information is presented in one of six standard essay formats by type of topic covered: carcinogen, disease or condition, drug or drug class, medical specialty, procedure, or “overview” (of an aspect of cancer biology, a personal or lifestyle issue, or an area of social concern). All essays present a capsule definition of the topic, and all but the briefest essays list sources of further information from both print and online resources. The essay formats are designed for the reader for whom the information is compelling or urgent, fostering quick identification and retrieval of essential facts: Essays on diseases and conditions, for example, list “also known as” names and describe related conditions, risk factors, the disease process, incidence, symptoms, screening and diagnosis, treatment, and prognosis. Essays on carcinogens list “also known as” names for the chemical or substance, cancers related to the carcinogen, exposure routes, principal places where the substance is found, populations at risk, symptoms to watch for, and a brief history of how we came to identify the substance as a carcinogen. Essays on drugs list the Anatomical Therapeutic Chemical (ATC) classification system code if one exists; the types of cancer, side effect, or other condition for which the drug is indicated; the delivery routes (such as pill form or injection); the way the drug works; and side effects. Essays on procedures apprise patients and their caregivers of why the procedure is performed, how to prepare, aftercare, risks, and the range of results. Essays on medical specialties identify
• • • • • • • •
Drugs by Generic Name Drugs by Trade Name Associations and Agencies Cancer Centers and Hospitals Cancer Support Groups Carcinogens Glossary Bibliography
A Category List and a complete subject index round out the set. Salem Health: Cancer has been the beneficiary of many expert contributors—physicians, nurses, pharmacists, and professional medical writers—whose names and academic or professional affiliations appear in the list of contributors that follows. Finally, this publication was made possible above all by our three consulting editors: Jeffrey A. Knight, Chair of the Department of Biological Sciences at Mount Holyoke College; Laurie JacksonGrusby, Ph.D., Assistant Professor in Pathology at Harvard Medical School, Children’s Hospital Boston; and Wendy White-Ryan, M.D., FAAP, is a board-certified pediatrician and member of the American Academy of Pediatrics. ix
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About the Editors from the Sontag Foundation for her work on pediatric brain tumors.
Jeffrey A. Knight, Ph.D., is Chair of the Department of Biological Sciences at Mount Holyoke College, where he teaches courses in genetics, molecular biology, and microbiology. He has held Visiting Professor appointments at the medical schools of the Universities of Massachusetts, Florida, and Vermont. Author of several research papers on the mitochondrial genetics of baker’s yeast, he has also been a frequent contributor to Salem Press publications. He edited the first edition of the Encyclopedia of Genetics (Salem Press, 1999), winner of the American Library Association, Reference and User Services Association’s “Outstanding Reference Source,” 2000.
Wendy White-Ryan, M.D., FAAP, is a board-certified pediatrician and member of the American Academy of Pediatrics as well as Alpha Omega Alpha. She completed her B.A. at Mount Holyoke College, her M.D. at New York Medical College, and her residency training in pediatrics at Strong Memorial Hospital in Rochester, New York. She worked in toxicology research at the University of Rochester for two years between earning her bachelor’s degree and entering medical school. She practiced pediatrics full-time for nine years in the inner city of Rochester until being diagnosed with Stage IV breast cancer in 2005. She became medically stable after undergoing both conventional and integrative treatments, including changes in diet and exercise, while remaining affiliated with Golisano Children’s Hospital at Strong Memorial Hospital in Rochester. She supports mind-body work, nutritional support through nutriceuticals, and other health-promoting lifestyle changes in the prevention or treatment of cancer.
Laurie Jackson-Grusby, Ph.D., is an Assistant Professor in Pathology at Harvard Medical School, Children’s Hospital Boston, and a faculty member of the Harvard Stem Cell Institute and Kirby Center for Neuroscience. She is a visiting instructor at the Harvard Extension school, where she teaches genetics. Her laboratory investigates the role of epigenetics in development of disease. She was awarded the Distinguished Scientist Award
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Contributors
Abbie L. Abboud, M.S., C.G.C.
Kerry L. Cheesman, Ph.D.
H. Bradford Hawley, M.D.
Richard Adler, Ph.D.
Wanda E. Clark, M.T. (ASCP)
Peter B. Heller, Ph.D.
Jane Adrian, M.P.H., Ed.M., M.T. (ASCP)
Lisa M. Cockrell, B.S.
Collette Bishop Hendler, R.N., M.S.
Pam Conboy, B.S.
Michelle L. Herdman, Ph.D.
Pamela S. Cooper, Ph.D.
Jennifer M. Hickin, B.S.
Angela M. Costello, B.S.
Carl W. Hoagstrom, Ph.D.
Charlotte Crowder, M.P.H., ELS
Christine G. Holzmueller, B.L.A.
Reyniel Cruz-Aguado, Ph.D.
Mary Hurd, M.A.
D. Scott Cunningham, M.D., Ph.D.
Bernard Jacobson, Ph.D.
Arun S. Dabholkar, Ph.D.
Clair Kaplan, R.N., M.S.N., A.P.R.N. (WHNP), M.H.S., M.T. (ASCP)
Robert J. Amato, D.O. Cathy Anderson, R.N., B.A. Terry A. Anderson, B.S. Wendell Anderson, B.A. Michele Arduengo, Ph.D., ELS Bryan C. Auday, Ph.D. Tanja Bekhuis, Ph.D. Paul F. Bell, Ph.D. Alvin K. Benson, Ph.D. Anna Binda, Ph.D. Robert Bockstiegel, B.S. Scott A. Boerner, M.S. Patricia Boone, Ph.D. Andrea Bradford, M.A. Wanda Todd Bradshaw, R.N.C., M.S.N. Thomas L. Brown, Ph.D. Suzette Buhr, R.T.R., C.D.A. Amy Bull, D.S.N., A.P.N. Michael A. Buratovich, Ph.D. Bharat Burman, B.A. Jaime Stockslager Buss, M.S.P.H., ELS Alex B. Cantrell, B.A. Richard P. Capriccioso, M.D. Mary Car-Blanchard, O.T.D., B.S.O.T. Christine M. Carroll, R.N., B.S.N., M.B.A.
Helen Davidson, B.A. Martiscia Davidson, A.M. Cynthia L. De Vine, B.A. Jackie Dial, Ph.D. Jeremy W. Dugosh, Ph.D. Aldo C. Dumlao, M.D Patricia Stanfill Edens, R.N., Ph.D., FACHE Renée Euchner, R.N. Jill Ferguson, Ph.D.
Susan J. Karcher, Ph.D. Sarah Kasprowicz, M.D. Michelle Kasprzak, R.N., B.S.N., O.C.N. Keller Kaufman-Fox, B.A. Debra B. Kessler, M.D., Ph.D. A. K. Khan, M.D., M.R.C.P. M. A. Q. Khan, M.D., Ph.D. Samreen F. Khan, M.A. Ing-Wei Khor, Ph.D.
Adi Ferrara, B.S. Amber L. Fields, M.S. K. Thomas Finley, Ph.D. MaryAnn Foote, M.S., Ph.D. Jo Gambosi, M.A., B.S.N. James S. Godde, Ph.D. Janet R. Green, M.S.P.H. Katrina Green, R.N., B.S.N., O.C.N. Silke Haidekker, Ph.D. Linda Hart, M.S., M.A. Melanie Hawkins, B.S.N., R.N., O.C.N. xiii
Michael R. King, Ph.D. Samuel V. A. Kisseadoo, Ph.D. Jeffrey A. Knight, Ph.D. Marylane Wade Koch, M.S.N., R.N. Robert W. Koch, D.N.S., R.N. Lalitha Krishnan, Ph.D. Anita P. Kuan, Ph.D. Steven A. Kuhl, Ph.D. Jeffrey P. Larson, P.T., B.S., A.T.C. Lindsay Lewellyn, B.S. Lisa M. Lines, M.P.H.
Salem Health: Cancer Martha O. Loustaunau, Ph.D.
Marcia Pinneau, R.N.
Amanda McQuade, Ph.D.
Nancy A. Piotrowski, Ph.D.
Kyle J. McQuade, Ph.D.
Victoria Price, Ph.D.
Marianne M. Madsen, M.S.
Christopher Pung, B.S., C.L.Sp. (CG)
Judy Majewski, M.S.
Cynthia Racer, M.A., M.P.H.
Elizabeth A. Manning, Ph.D.
Bagirathy Ravishankar, Ph.D.
Vicki Miskovsky, B.S., R.D.
Pamela Richardson, M.S.
Paul Moglia, Ph.D.
Alice C. Richer, R.D., M.B.A., L.D.
Christina J. Moose, M.A.
Elizabeth D. Schafer, Ph.D.
Linda August Vrooman, R.N., B.S.N., O.C.N.
Karen M. Nagel, Ph.D.
Jason J. Schwartz, Ph.D., J.D.
C. J. Walsh, Ph.D.
Anita Nagypál, Ph.D.
Miriam E. Schwartz, M.D., M.A., Ph.D.
Stephanie Watson, B.S.
Amy J. Neil, M.S., M.A.P. David A. Olle, M.S. Colm A. Ó’Moráin, M.A., M.D., M.Sc., D.Sc.
Banalata Sen, Ph.D. Terry J. Shackleford, Ph.D. Lisa J. Shientag, V.M.D.
Carol Ann Suda, B.S., M.T. (ASCP), S.M. Rena C. Tabata, M.Sc. Dorothy P. Terry, R.N. Susan E. Ullmann, M.T. (ASCP), M.A. Nicole M. Van Hoey, Pharm.D. Charles L. Vigue, Ph.D.
Marcia J. Weiss, J.D. John B. Welsh, M.D., Ph.D. Bradley R. A. Wilson, Ph.D.
Ophelia Panganiban, B.S.
R. Baird Shuman, Ph.D.
Nicola E. Wittekindt, Dr.Sc. (ETH Zürich)
Jeannie V. Pasacreta, Ph.D., A.P.R.N.
Vonne Sieve, M.A.
Geetha Yadav, Ph.D.
Anna Perez, M.Sc.
Dwight G. Smith, Ph.D.
John L. Zeller, M.D., Ph.D.
Susan H. Peterman, M.P.H.
Richard S. Spira, D.V.M.
Diego Pineda, M.S.
Kelli Miller Stacy, ELS
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Complete List of Contents Volume 1 Alkylating agents in chemotherapy . . . . . . . ALL. See Acute lymphocytic leukemia Allicin, garlic and. See Garlic and allicin Alopecia . . . . . . . . . . . . . . . . . . . . . ALP. See Alkaline phosphatase test Alpha-fetoprotein (AFP) levels . . . . . . . . . Alternative therapies. See Complementary and alternative therapies Alveolar soft-part sarcomas . . . . . . . . . . . Amenorrhea . . . . . . . . . . . . . . . . . . . American Association for Cancer Research (AACR) . . . . . . . . . . . . . . . . . . . . American Cancer Society (ACS) . . . . . . . . American Institute for Cancer Research (AICR) 4-Aminobiphenyl . . . . . . . . . . . . . . . . AML. See Acute myelocytic leukemia Amputation . . . . . . . . . . . . . . . . . . . Amyloidosis . . . . . . . . . . . . . . . . . . . Anal cancer . . . . . . . . . . . . . . . . . . . Androgen drugs . . . . . . . . . . . . . . . . . Anemia . . . . . . . . . . . . . . . . . . . . . Anemia, aplastic. See Aplastic anemia Anemia, hemolytic. See Hemolytic anemia Angiogenesis . . . . . . . . . . . . . . . . . . Angiogenesis inhibitors . . . . . . . . . . . . . Angiography. . . . . . . . . . . . . . . . . . . Angiosarcomas . . . . . . . . . . . . . . . . . Anoscopy . . . . . . . . . . . . . . . . . . . . Anthraquinones . . . . . . . . . . . . . . . . . Anthrax . . . . . . . . . . . . . . . . . . . . . Antiandrogens . . . . . . . . . . . . . . . . . . Antidiarrheal agents . . . . . . . . . . . . . . . Antiestrogens . . . . . . . . . . . . . . . . . . Antifungal therapies . . . . . . . . . . . . . . . Antimetabolites in chemotherapy . . . . . . . . Antinausea medications . . . . . . . . . . . . . Antineoplastics in chemotherapy . . . . . . . . Antioxidants . . . . . . . . . . . . . . . . . . . Antiperspirants and breast cancer . . . . . . . . Antiviral therapies. . . . . . . . . . . . . . . . Anxiety . . . . . . . . . . . . . . . . . . . . . APBI. See Accelerated partial breast irradiation APC gene testing . . . . . . . . . . . . . . . . Aplastic anemia . . . . . . . . . . . . . . . . . Appendix cancer . . . . . . . . . . . . . . . . Appetite loss. . . . . . . . . . . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . . . v Publisher’s Note . . . . . . . . . . . . . . . . . . . . ix About the Editors . . . . . . . . . . . . . . . . . . . xi Contributors . . . . . . . . . . . . . . . . . . . . . xiii Complete List of Contents . . . . . . . . . . . . . . xv AACR. See American Association for Cancer Research ABCD. . . . . . . . . . . . . . . . . . . . . . . . . . 1 ACC. See Adenoid cystic carcinoma Abdominoperineal resection (APR) . . . . . . . . . . 1 Accelerated partial breast irradiation (APBI). . . . . . 3 Achlorhydria . . . . . . . . . . . . . . . . . . . . . . 4 Acoustic neuromas . . . . . . . . . . . . . . . . . . . 4 Acquired immunodeficiency disease-related cancers. See HIV/AIDS-related cancers Acrylamides . . . . . . . . . . . . . . . . . . . . . . 6 ACS. See American Cancer Society Acupuncture and acupressure for cancer patients . . . 8 Acute lymphocytic leukemia (ALL) . . . . . . . . . 11 Acute myelocytic leukemia (AML) . . . . . . . . . . 13 Adenocarcinomas . . . . . . . . . . . . . . . . . . . 16 Adenoid cystic carcinoma (ACC) . . . . . . . . . . . 17 Adenomatoid tumors . . . . . . . . . . . . . . . . . 18 Adenomatous polyps . . . . . . . . . . . . . . . . . 18 Adenoviruses . . . . . . . . . . . . . . . . . . . . . 19 Adjuvant therapy . . . . . . . . . . . . . . . . . . . 20 Adrenal gland cancers . . . . . . . . . . . . . . . . . 21 Adrenocortical cancer . . . . . . . . . . . . . . . . . 23 Advance directives . . . . . . . . . . . . . . . . . . 24 Aflatoxins . . . . . . . . . . . . . . . . . . . . . . . 26 AFP levels. See Alpha-fetoprotein levels African Americans and cancer . . . . . . . . . . . . 28 Africans and cancer . . . . . . . . . . . . . . . . . . 31 Afterloading radiation therapy . . . . . . . . . . . . 32 Agent Orange . . . . . . . . . . . . . . . . . . . . . 34 Aging and cancer . . . . . . . . . . . . . . . . . . . 34 AICR. See American Institute for Cancer Research Aids and devices for cancer patients . . . . . . . . . 38 AIDS-related cancers. See HIV/AIDS-related cancers Air pollution . . . . . . . . . . . . . . . . . . . . . . 39 Alcohol, alcoholism, and cancer . . . . . . . . . . . 42 Aleukemia . . . . . . . . . . . . . . . . . . . . . . . 43 Alkaline phosphatase test (ALP) . . . . . . . . . . . 44 xv
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Salem Health: Cancer APR. See Abdominoperineal resection Arsenic compounds . . . . . . . . . . Arterial embolization . . . . . . . . . Artificial sweeteners . . . . . . . . . . Asbestos . . . . . . . . . . . . . . . . Ascites . . . . . . . . . . . . . . . . . Ashkenazi Jews and cancer . . . . . . Asian Americans and cancer. . . . . . Astrocytomas. . . . . . . . . . . . . . Ataxia telangiectasia (AT) . . . . . . . Autologous blood transfusion . . . . . Axillary dissection . . . . . . . . . . . Azathioprine . . . . . . . . . . . . . .
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Bacillus Calmette Guérin (BCG) . . . . . . . . Bacteria as causes of cancer . . . . . . . . . . . Barium enema . . . . . . . . . . . . . . . . . . Barium swallow . . . . . . . . . . . . . . . . . Barrett esophagus . . . . . . . . . . . . . . . . Basal cell carcinomas . . . . . . . . . . . . . . BCG. See Bacillus Calmette Guérin Beckwith-Wiedemann syndrome (BWS) . . . . Benign prostatic hyperplasia (BPH) . . . . . . . Benign tumors . . . . . . . . . . . . . . . . . . Benzene . . . . . . . . . . . . . . . . . . . . . Benzidine and dyes metabolized to benzidine . . Benzodiazepines . . . . . . . . . . . . . . . . . Bereavement, grief and. See Grief and bereavement Beryllium and beryllium compounds . . . . . . Beta-carotene . . . . . . . . . . . . . . . . . . Bethesda criteria . . . . . . . . . . . . . . . . . BHDS. See Birt-Hogg-Dubé syndrome Bile duct cancer . . . . . . . . . . . . . . . . . Bilobectomy . . . . . . . . . . . . . . . . . . . Bioflavonoids . . . . . . . . . . . . . . . . . . Biological therapy . . . . . . . . . . . . . . . . Biopsy. See also Computed tomography-guided biopsy; Core needle biopsy; Liver biopsy; Needle biopsies; Pleural biopsy; Stereotactic needle biopsy; Surgical biopsies . . . . . . . Birt-Hogg-Dubé syndrome (BHDS) . . . . . . . Birth control pills and cancer . . . . . . . . . . Bis(chloromethyl) ether and technical-grade chloromethyl methyl ether . . . . . . . . . . Bisphenol A (BPA) . . . . . . . . . . . . . . . Bisphosphonates . . . . . . . . . . . . . . . . . Bladder cancer . . . . . . . . . . . . . . . . . . Blood cancers . . . . . . . . . . . . . . . . . . BMT. See Bone marrow transplantation BNCT. See Boron neutron capture therapy
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Body image. See Self-image and body image Bone cancers . . . . . . . . . . . . . . . . . . . Bone marrow aspiration and biopsy . . . . . . . Bone marrow transplantation (BMT) . . . . . . Bone pain . . . . . . . . . . . . . . . . . . . . Bone scan . . . . . . . . . . . . . . . . . . . . Boron neutron capture therapy (BNCT) . . . . . Bowen disease . . . . . . . . . . . . . . . . . . BPA. See Bisphenol A BPH. See Benign prostatic hyperplasia BPI. See Brief Pain Inventory Brachytherapy . . . . . . . . . . . . . . . . . . BRAF gene . . . . . . . . . . . . . . . . . . . . Brain and central nervous system cancers . . . . Brain scan . . . . . . . . . . . . . . . . . . . . BRCA1 and BRCA2 genes . . . . . . . . . . . . Breakthrough pain . . . . . . . . . . . . . . . . Breast, calcifications of. See Calcifications of the breast Breast, medullary carcinoma of. See Medullary carcinoma of the breast Breast cancer, cutaneous. See Cutaneous breast cancer Breast cancer, estrogen-receptor-sensitive. See Estrogen-receptor-sensitive breast cancer Breast cancer in children and adolescents . . . . Breast cancer in men . . . . . . . . . . . . . . . Breast cancer in pregnant women . . . . . . . . Breast cancers . . . . . . . . . . . . . . . . . . Breast implants. . . . . . . . . . . . . . . . . . Breast reconstruction. . . . . . . . . . . . . . . Breast self-examination (BSE). . . . . . . . . . Breast ultrasound. . . . . . . . . . . . . . . . . Breslow’s staging . . . . . . . . . . . . . . . . Brief Pain Inventory (BPI) . . . . . . . . . . . . Brompton cocktail . . . . . . . . . . . . . . . . Bronchial adenomas . . . . . . . . . . . . . . . Bronchoalveolar lung cancer . . . . . . . . . . Bronchography. . . . . . . . . . . . . . . . . . Bronchoscopy . . . . . . . . . . . . . . . . . . BSE. See Breast self-examination Burkitt lymphoma . . . . . . . . . . . . . . . . 1,3-Butadiene . . . . . . . . . . . . . . . . . . 1,4-Butanediol dimethanesulfonate . . . . . . . BWS. See Beckwith-Wiedemann syndrome
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CA 15-3 test . CA 19-9 test . CA 27-29 test CA 125 test. . Cachexia . . . xvi
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Complete List of Contents Cadmium and cadmium compounds. . . . . . . . Caffeine . . . . . . . . . . . . . . . . . . . . . . Calcifications of the breast. . . . . . . . . . . . . Calcium . . . . . . . . . . . . . . . . . . . . . . Cancell . . . . . . . . . . . . . . . . . . . . . . . Cancer biology . . . . . . . . . . . . . . . . . . . Cancer care team . . . . . . . . . . . . . . . . . . Cancer clusters . . . . . . . . . . . . . . . . . . . Cancer education. . . . . . . . . . . . . . . . . . Candidiasis . . . . . . . . . . . . . . . . . . . . . Carcinoembryonic antigen antibody (CEA) test . . . . . . . . . . . . . . . . . . . . . . . . Carcinogens, known . . . . . . . . . . . . . . . . Carcinogens, reasonably anticipated. . . . . . . . Carcinoid tumors and carcinoid syndrome . . . . Carcinoma of unknown primary origin (CUP) . . Carcinomas. . . . . . . . . . . . . . . . . . . . . Carcinomas, invasive ductal. See Invasive ductal carcinomas Carcinomas, invasive lobular. See Invasive lobular carcinomas Carcinomas, leptomeningeal. See Leptomeningeal carcinomas Carcinomatosis. . . . . . . . . . . . . . . . . . . Carcinomatous meningitis . . . . . . . . . . . . . Carcinosarcomas . . . . . . . . . . . . . . . . . . Cardiomyopathy in cancer patients . . . . . . . . Cardiopulmonary resuscitation (CPR) . . . . . . . Caregivers and caregiving . . . . . . . . . . . . . Caregiving, long-distance. See Long-distance caregiving Carney complex . . . . . . . . . . . . . . . . . . Carotenoids . . . . . . . . . . . . . . . . . . . . Cartilage supplements . . . . . . . . . . . . . . . Case management . . . . . . . . . . . . . . . . . Castleman disease . . . . . . . . . . . . . . . . . CBC. See Complete blood count CBE. See Clinical breast exam CDKN2A. See Cyclin-dependent kinase inhibitor-2A CEA test. See Carcinoembryonic antigen antibody test Cell phones. . . . . . . . . . . . . . . . . . . . . Cervical cancer. . . . . . . . . . . . . . . . . . . Chemoembolization . . . . . . . . . . . . . . . . Chemoprevention . . . . . . . . . . . . . . . . . Chemotherapy . . . . . . . . . . . . . . . . . . . Chemotherapy, cognitive effects of. See Cognitive effects of cancer and chemotherapy Chewing tobacco. . . . . . . . . . . . . . . . . . Childbirth and cancer . . . . . . . . . . . . . . .
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Childhood cancers . . . . . . . . . . . . . . . . Chlorambucil. . . . . . . . . . . . . . . . . . . 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)1-nitrosourea (MeCCNU) . . . . . . . . . . . Cholecystectomy . . . . . . . . . . . . . . . . . Chordomas . . . . . . . . . . . . . . . . . . . . Choriocarcinomas . . . . . . . . . . . . . . . . CHPP. See Continuous hyperthermic peritoneal perfusion Chromium hexavalent compounds. . . . . . . . Chromosomes and cancer . . . . . . . . . . . . Chronic lymphocytic leukemia (CLL) . . . . . . Chronic myeloid leukemia (CML). . . . . . . . Cigarettes and cigars . . . . . . . . . . . . . . . Clinical breast exam (CBE) . . . . . . . . . . . Clinical trials . . . . . . . . . . . . . . . . . . . CLL. See Chronic lymphocytic leukemia CML. See Chronic myeloid leukemia Coal tars and coal tar pitches . . . . . . . . . . Cobalt 60 radiation. . . . . . . . . . . . . . . . Coenzyme Q10. . . . . . . . . . . . . . . . . . Cognitive effects of cancer and chemotherapy . Coke oven emissions. . . . . . . . . . . . . . . Cold nodule . . . . . . . . . . . . . . . . . . . Colectomy . . . . . . . . . . . . . . . . . . . . Coloanal anastomosis . . . . . . . . . . . . . . Colon polyps . . . . . . . . . . . . . . . . . . . Colonoscopy and virtual colonoscopy . . . . . . Colony-stimulating factors (CSFs) . . . . . . . Colorectal cancer. . . . . . . . . . . . . . . . . Colorectal cancer screening . . . . . . . . . . . Colostomy . . . . . . . . . . . . . . . . . . . . Colposcopy. . . . . . . . . . . . . . . . . . . . Comedo carcinomas . . . . . . . . . . . . . . . Complementary and alternative therapies . . . . Complete blood count (CBC) . . . . . . . . . . Computed tomography (CT)-guided biopsy . . . . . . . . . . . . . . . . . . . . . Computed tomography (CT) scan . . . . . . . . Conization . . . . . . . . . . . . . . . . . . . . Continuous hyperthermic peritoneal perfusion (CHPP) . . . . . . . . . . . . . . . . . . . . Cordectomy . . . . . . . . . . . . . . . . . . . Cordotomy . . . . . . . . . . . . . . . . . . . . Core needle biopsy. . . . . . . . . . . . . . . . Corticosteroids . . . . . . . . . . . . . . . . . . Coughing . . . . . . . . . . . . . . . . . . . . . Counseling for cancer patients and survivors . . Cowden syndrome . . . . . . . . . . . . . . . . COX-2 inhibitors. See Cyclooxygenase 2 inhibitors
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269 269 271 272
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274 274 276 279 281 283 285
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288 289 289 290 292 292 293 294 296 297 299 300 304 306 308 309 309 312
. . 313 . . 315 . . 317 . . . . . . . .
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318 318 319 321 321 322 324 326
Salem Health: Cancer CPR. See Cardiopulmonary resuscitation Craniopharyngiomas . . . . . . . . . . . . Craniosynostosis . . . . . . . . . . . . . . Craniotomy. . . . . . . . . . . . . . . . . Crohn disease . . . . . . . . . . . . . . . Cruciferous vegetables . . . . . . . . . . . Cryoablation . . . . . . . . . . . . . . . . Cryptorchidism. . . . . . . . . . . . . . . CSFs. See Colony-stimulating factors CT scan. See Computed tomography scan CTCL. See Cutaneous T-cell lymphoma Culdoscopy. . . . . . . . . . . . . . . . . CUP. See Carcinoma of unknown primary origin Curcumin. . . . . . . . . . . . . . . . . . Cushing syndrome and cancer . . . . . . . Cutaneous breast cancer . . . . . . . . . . Cutaneous T-cell lymphoma (CTCL) . . .
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Cyclin-dependent kinase inhibitor-2A (CDKN2A). . . . . . . . . . . . . . . Cyclooxygenase 2 (COX-2) inhibitors . Cyclophosphamide. . . . . . . . . . . . Cyclosporin A . . . . . . . . . . . . . . Cystography . . . . . . . . . . . . . . . Cystoscopy . . . . . . . . . . . . . . . . Cytogenetics . . . . . . . . . . . . . . . Cytokines . . . . . . . . . . . . . . . . Cytology . . . . . . . . . . . . . . . . . Cytology, sputum. See Sputum cytology
327 329 331 332 335 336 338
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344 344 345 346 347 347 348 350 350
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D&C. See Dilation and curettage Dana-Farber Cancer Institute . . . . . . . . . . . . 354 DCIS. See Ductal carcinoma in situ DEA. See Diethanolamine DEHP. See Di(2-ethylhexyl) phthalate Delta-9-tetrahydrocannabinol . . . . . . . . . . . . 355
339 340 341 342
Volume 2 Down syndrome and leukemia. . . . . . . . DPC4 gene testing . . . . . . . . . . . . . . DRE. See Digital rectal exam Drug resistance and multidrug resistance (MDR) . . . . . . . . . . . . . . . . . . . Dry mouth . . . . . . . . . . . . . . . . . . DSRCT. See Desmoplastic small round cell tumor Duct ectasia . . . . . . . . . . . . . . . . . Ductal carcinoma in situ (DCIS). . . . . . . Ductal lavage. . . . . . . . . . . . . . . . . Ductogram . . . . . . . . . . . . . . . . . . Duke Comprehensive Cancer Center . . . . Dukes’ classification . . . . . . . . . . . . . Duodenal carcinomas . . . . . . . . . . . . Dye, hair. See Hair dye Dysplastic nevus syndrome . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . xxxiii Complete List of Contents . . . . . . . . . . . . xxxvii Denys-Drash syndrome and cancer . . . . . . Depression . . . . . . . . . . . . . . . . . . . Dermatofibrosarcoma protuberans (DFSP) . . Dermatology oncology. . . . . . . . . . . . . DES. See Diethylstilbestrol Desmoid tumors . . . . . . . . . . . . . . . . Desmoplastic small round cell tumor (DSRCT) . . . . . . . . . . . . . . . . . . Developing nations and cancer . . . . . . . . DFSP. See Dermatofibrosarcoma protuberans Di(2-ethylhexyl) phthalate (DEHP) . . . . . . Diarrhea . . . . . . . . . . . . . . . . . . . . DIC. See Disseminated intravascular coagulation Dietary supplements . . . . . . . . . . . . . . Diethanolamine (DEA) . . . . . . . . . . . . Diethylstilbestrol (DES) . . . . . . . . . . . . Digital rectal exam (DRE) . . . . . . . . . . . Dilation and curettage (D&C) . . . . . . . . . Dioxins . . . . . . . . . . . . . . . . . . . . . Disseminated intravascular coagulation (DIC) . . . . . . . . . . . . . . . . . . . . Diverticulosis and diverticulitis . . . . . . . . DNR. See Do-not-resuscitate order Do-not-resuscitate (DNR) order . . . . . . . .
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357 357 360 362
. . . 365 . . . 365 . . . 366 . . . 368 . . . 369
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370 373 373 374 375 376
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. . . 380 xviii
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386 387 389 389 390 392 393
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Eaton-Lambert syndrome. See Lambert-Eaton myasthenic syndrome EBRT. See External beam radiation therapy Edema . . . . . . . . . . . . . . . . . . . . . Education, cancer. See Cancer education Elderly and cancer . . . . . . . . . . . . . . . Electrolarynx . . . . . . . . . . . . . . . . . . Electromagnetic radiation . . . . . . . . . . . Electroporation therapy . . . . . . . . . . . . Electrosurgery . . . . . . . . . . . . . . . . .
. . . 378 . . . 378
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396 399 399 400 401
Complete List of Contents Embolization . . . . . . . . . . . . . . . . . . . . Embryonal cell cancer . . . . . . . . . . . . . . . End-of-life care . . . . . . . . . . . . . . . . . . Endocrine cancers . . . . . . . . . . . . . . . . . Endocrinology oncology . . . . . . . . . . . . . . Endometrial cancer . . . . . . . . . . . . . . . . Endometrial hyperplasia . . . . . . . . . . . . . . Endorectal ultrasound . . . . . . . . . . . . . . . Endoscopic retrograde cholangiopancreatography (ERCP) . . . . . . . . . . . . . . . . . . . . . Endoscopy . . . . . . . . . . . . . . . . . . . . . Endoscopy, upper gastrointestinal. See Upper gastrointestinal endoscopy Endotheliomas . . . . . . . . . . . . . . . . . . . Enteritis . . . . . . . . . . . . . . . . . . . . . . Enterostomal therapy . . . . . . . . . . . . . . . Eosinophilic leukemia . . . . . . . . . . . . . . . Ependymomas . . . . . . . . . . . . . . . . . . . Epidemiology of cancer . . . . . . . . . . . . . . Epidermoid cancers of mucous membranes . . . . Epstein-Barr virus . . . . . . . . . . . . . . . . . ERCP. See Endoscopic retrograde cholangiopancreatography ERD. See Estrogen receptor downregulator Erionite. . . . . . . . . . . . . . . . . . . . . . . Erythroplakia. . . . . . . . . . . . . . . . . . . . Esophageal cancer . . . . . . . . . . . . . . . . . Esophageal speech . . . . . . . . . . . . . . . . . Esophagectomy . . . . . . . . . . . . . . . . . . Esophagitis . . . . . . . . . . . . . . . . . . . . . Essiac . . . . . . . . . . . . . . . . . . . . . . . Estrogen receptor downregulator (ERD) . . . . . Estrogen-receptor-sensitive breast cancer . . . . . Ethnicity and cancer . . . . . . . . . . . . . . . . Ethylene oxide . . . . . . . . . . . . . . . . . . . Ewing sarcoma . . . . . . . . . . . . . . . . . . . Exenteration . . . . . . . . . . . . . . . . . . . . Exercise and cancer . . . . . . . . . . . . . . . . External beam radiation therapy (EBRT) . . . . . Eye cancers . . . . . . . . . . . . . . . . . . . . Eyelid cancer. . . . . . . . . . . . . . . . . . . .
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Fallopian tube cancer . . . . . . . Family history and risk assessment Fanconi anemia . . . . . . . . . . Fatigue . . . . . . . . . . . . . . . Fecal occult blood test (FOBT) . . Fertility drugs and cancer . . . . . Fertility issues . . . . . . . . . . . Fever . . . . . . . . . . . . . . . . Fiber . . . . . . . . . . . . . . . .
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402 403 404 406 409 412 414 416
. 417 . 417
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420 421 422 424 425 426 429 431
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433 433 434 436 438 439 441 441 442 444 447 447 450 451 454 455 458
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460 461 464 466 467 469 471 472 474 xix
Fibroadenomas . . . . . . . . . . . . . . . . Fibrocystic breast changes . . . . . . . . . . Fibrosarcomas, soft-tissue . . . . . . . . . . Financial issues . . . . . . . . . . . . . . . 5HIAA test. See 5-Hydroxyindoleacetic acid test 5Q minus syndrome . . . . . . . . . . . . . Flow cytometry . . . . . . . . . . . . . . . FOBT. See Fecal occult blood test Folic acid. . . . . . . . . . . . . . . . . . . Formaldehyde . . . . . . . . . . . . . . . . Fox Chase Cancer Center . . . . . . . . . . Fred Hutchinson Cancer Research Center . . Free radicals . . . . . . . . . . . . . . . . . Fruits . . . . . . . . . . . . . . . . . . . . .
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475 476 478 481
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486 486 487 488 490 491
Gallbladder cancer . . . . . . . . . . . . . . Gallium scan . . . . . . . . . . . . . . . . . Gamma Knife . . . . . . . . . . . . . . . . Gardner syndrome . . . . . . . . . . . . . . Garlic and allicin . . . . . . . . . . . . . . . Gastric polyps . . . . . . . . . . . . . . . . Gastrinomas . . . . . . . . . . . . . . . . . Gastrointestinal cancers . . . . . . . . . . . Gastrointestinal complications of cancer treatment. . . . . . . . . . . . . . . . . . Gastrointestinal oncology . . . . . . . . . . Gastrointestinal stromal tumors (GISTs) . . GCTs. See Giant cell tumors Gene therapy . . . . . . . . . . . . . . . . . Genetic counseling . . . . . . . . . . . . . . Genetic testing . . . . . . . . . . . . . . . . Genetics of cancer . . . . . . . . . . . . . . Geography and cancer . . . . . . . . . . . . Germ-cell tumors . . . . . . . . . . . . . . Gerson therapy . . . . . . . . . . . . . . . . Gestational trophoblastic tumors (GTTs) . . Giant cell tumors (GCTs) . . . . . . . . . . Ginseng, panax. . . . . . . . . . . . . . . . GISTs. See Gastrointestinal stromal tumors Gleason grading system . . . . . . . . . . . Gliomas . . . . . . . . . . . . . . . . . . . Glomus tumors . . . . . . . . . . . . . . . . Glossectomy . . . . . . . . . . . . . . . . . Glutamine . . . . . . . . . . . . . . . . . . Gonioscopy . . . . . . . . . . . . . . . . . Grading of tumors . . . . . . . . . . . . . . Graft-versus-host disease (GVHD) . . . . . Granulosa cell tumors . . . . . . . . . . . . Green tea . . . . . . . . . . . . . . . . . . . Grief and bereavement . . . . . . . . . . . .
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493 495 497 498 499 500 501 502
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512 515 517 519 522 525 527 527 530 531
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532 533 534 535 536 536 537 538 540 540 541
Salem Health: Cancer GTTs. See Gestational trophoblastic tumors GVHD. See Graft-versus-host disease Gynecologic cancers . . . . . . . . . . . . . . . . . 543 Gynecologic oncology . . . . . . . . . . . . . . . . 547 H. pylori. See Helicobacter pylori HAI. See Hepatic arterial infusion Hair dye . . . . . . . . . . . . . . . . . . . . . . Hairy cell leukemia . . . . . . . . . . . . . . . . Hand-foot syndrome (HFS) . . . . . . . . . . . . HBV. See Hepatitis B virus HCG. See Human chorionic gonadotropin HCV. See Hepatitis C virus Head and neck cancers . . . . . . . . . . . . . . . Health maintenance organizations (HMOs) . . . . Helicobacter pylori. . . . . . . . . . . . . . . . . Hemangioblastomas . . . . . . . . . . . . . . . . Hemangiopericytomas . . . . . . . . . . . . . . . Hemangiosarcomas . . . . . . . . . . . . . . . . Hematemesis . . . . . . . . . . . . . . . . . . . . Hematologic oncology . . . . . . . . . . . . . . . Hematuria . . . . . . . . . . . . . . . . . . . . . Hemochromatosis . . . . . . . . . . . . . . . . . Hemolytic anemia . . . . . . . . . . . . . . . . . Hemoptysis. . . . . . . . . . . . . . . . . . . . . Hemorrhoids . . . . . . . . . . . . . . . . . . . . Hepatic arterial infusion (HAI) . . . . . . . . . . Hepatitis B virus (HBV) . . . . . . . . . . . . . . Hepatitis C virus (HCV) . . . . . . . . . . . . . . Hepatomegaly . . . . . . . . . . . . . . . . . . . HER2/neu protein . . . . . . . . . . . . . . . . . Herbs as antioxidants . . . . . . . . . . . . . . . Hereditary cancer syndromes . . . . . . . . . . . Hereditary diffuse gastric cancer . . . . . . . . . Hereditary leiomyomatosis and renal cell cancer (HLRCC) . . . . . . . . . . . . . . . . Hereditary mixed polyposis syndrome . . . . . . Hereditary non-VHL clear cell renal cell carcinomas . . . . . . . . . . . . . . . . . . . Hereditary pancreatitis . . . . . . . . . . . . . . . Hereditary papillary renal cell carcinomas . . . . Hereditary polyposis syndromes . . . . . . . . . . Herpes simplex virus. . . . . . . . . . . . . . . . Herpes zoster virus. . . . . . . . . . . . . . . . . HFS. See Hand-foot syndrome Hispanics and cancer. See Latinos/Hispanics and cancer Histamine 2 antagonists . . . . . . . . . . . . . . Histiocytosis X . . . . . . . . . . . . . . . . . . . HIV/AIDS-related cancers . . . . . . . . . . . . .
HLRCC. See Hereditary leiomyomatosis and renal cell cancer HMOs. See Health maintenance organizations Hodgkin disease . . . . . . . . . . . . . . . . . Home health services . . . . . . . . . . . . . . Hormonal therapies . . . . . . . . . . . . . . . Hormone receptor tests . . . . . . . . . . . . . Hormone replacement therapy (HRT) . . . . . . Horner syndrome. . . . . . . . . . . . . . . . . Hospice care . . . . . . . . . . . . . . . . . . . Hot flashes . . . . . . . . . . . . . . . . . . . . HPV. See Human papillomavirus HRAS gene testing . . . . . . . . . . . . . . . . HRT. See Hormone replacement therapy HTLV. See Human T-cell leukemia virus Human chorionic gonadotropin (HCG) . . . . . Human growth factors and tumor growth . . . . Human immunodeficiency virus-related cancers. See HIV/AIDS-related cancers Human papillomavirus (HPV) . . . . . . . . . . Human T-cell leukemia virus (HTLV) . . . . . Hydatidiform mole . . . . . . . . . . . . . . . . 5-Hydroxyindoleacetic acid (5HIAA) test . . . . Hypercalcemia . . . . . . . . . . . . . . . . . . Hypercoagulation disorders . . . . . . . . . . . Hyperthermia therapy . . . . . . . . . . . . . . Hyperthermic perfusion . . . . . . . . . . . . . Hypopharyngeal cancer . . . . . . . . . . . . . Hysterectomy . . . . . . . . . . . . . . . . . . Hysterography . . . . . . . . . . . . . . . . . . Hystero-oophorectomy. . . . . . . . . . . . . . Hysteroscopy. . . . . . . . . . . . . . . . . . .
. 550 . 550 . 552
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554 557 558 559 559 560 561 562 564 565 566 566 567 568 569 570 571 573 573 574 576
IEP. See Immunoelectrophoresis iFOBT. See Immunochemical fecal occult blood test Ileostomy. . . . . . . . . . . . . . . . . . . . . Imaging tests . . . . . . . . . . . . . . . . . . . Immune response to cancer . . . . . . . . . . . Immunochemical fecal occult blood test (iFOBT) . . . . . . . . . . . . . . . . . . . . Immunocytochemistry and immunohistochemistry . . . . . . . . . . . . Immunoelectrophoresis (IEP) . . . . . . . . . . Immunotherapy . . . . . . . . . . . . . . . . . IMRT. See Intensity-modulated radiation therapy Indoles . . . . . . . . . . . . . . . . . . . . . . Infection and sepsis . . . . . . . . . . . . . . . Infectious cancers . . . . . . . . . . . . . . . . Infertility and cancer . . . . . . . . . . . . . . .
. 577 . 579 . . . . . .
580 580 581 582 584 586
. 587 . 588 . 590 xx
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593 597 599 601 603 605 606 608
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611 612 612 613 614 615 617 618 619 620 621 622 623
. . 625 . . 626 . . 629 . . 632 . . 633 . . 634 . . 635
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638 638 641 643
Complete List of Contents Inflammatory bowel disease . . . . . . . . . . Informed consent. . . . . . . . . . . . . . . . Infusion therapies . . . . . . . . . . . . . . . Insurance . . . . . . . . . . . . . . . . . . . . Integrative oncology . . . . . . . . . . . . . . Intensity-modulated radiation therapy (IMRT) Interferon. . . . . . . . . . . . . . . . . . . . Interleukins. . . . . . . . . . . . . . . . . . . Invasive cancer. . . . . . . . . . . . . . . . . Invasive ductal carcinomas . . . . . . . . . . Invasive lobular carcinomas . . . . . . . . . . Ionizing radiation . . . . . . . . . . . . . . . Iridium seeds . . . . . . . . . . . . . . . . . . Islet cell tumors . . . . . . . . . . . . . . . . Isoflavones . . . . . . . . . . . . . . . . . . . Itching . . . . . . . . . . . . . . . . . . . . .
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645 646 647 648 651 652 653 654 655 656 657 657 658 659 661 661
Lambert-Eaton myasthenic syndrome (LEMS) Laparoscopy and laparoscopic surgery . . . . Laryngeal cancer . . . . . . . . . . . . . . . . Laryngeal nerve palsy . . . . . . . . . . . . . Laryngectomy . . . . . . . . . . . . . . . . . Laryngoscopy . . . . . . . . . . . . . . . . . Laser therapies . . . . . . . . . . . . . . . . . Latinos/Hispanics and cancer . . . . . . . . . Laxatives . . . . . . . . . . . . . . . . . . . . LCIS. See Lobular carcinoma in situ LDH test. See Lactate dehydrogenase test Leiomyomas . . . . . . . . . . . . . . . . . . Leiomyosarcomas . . . . . . . . . . . . . . . LEMS. See Lambert-Eaton myasthenic syndrome Leptomeningeal carcinomas . . . . . . . . . . Leukapharesis . . . . . . . . . . . . . . . . . Leukemia, Down syndrome and. See Down syndrome and leukemia Leukemia, eosinophilic. See Eosinophilic leukemia Leukemia, hairy cell. See Hairy cell leukemia Leukemias . . . . . . . . . . . . . . . . . . . Leukoencephalopathy . . . . . . . . . . . . . Leukopenia. . . . . . . . . . . . . . . . . . . Leukoplakia . . . . . . . . . . . . . . . . . . Leydig cell tumors . . . . . . . . . . . . . . . Li-Fraumeni syndrome (LFS) . . . . . . . . . Limb salvage . . . . . . . . . . . . . . . . . . Linear accelerator . . . . . . . . . . . . . . . Lip cancers . . . . . . . . . . . . . . . . . . . Liposarcomas . . . . . . . . . . . . . . . . . Liver biopsy . . . . . . . . . . . . . . . . . . Liver cancers . . . . . . . . . . . . . . . . . .
Jonsson Comprehensive Cancer Center (JCCC) . . . . . . . . . . . . . . . . . . . . . . 664 Journaling . . . . . . . . . . . . . . . . . . . . . . 665 Juvenile polyposis syndrome . . . . . . . . . . . . 665 Kaposi sarcoma . . . . . . . . . . . . . Karnofsky performance status (KPS) . . Keratosis . . . . . . . . . . . . . . . . . Ki67 test . . . . . . . . . . . . . . . . . Kidney cancer . . . . . . . . . . . . . . Klinefelter syndrome and cancer . . . . KPS. See Karnofsky performance status Krukenberg tumors . . . . . . . . . . .
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667 669 670 670 671 674
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Lacrimal gland tumors . . . . . . . . . . . . . . . . 677 Lactate dehydrogenase (LDH) test . . . . . . . . . 678 Laetrile . . . . . . . . . . . . . . . . . . . . . . . . 679
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679 681 682 685 686 687 688 690 692
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. . . 696 . . . 698
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698 702 704 704 706 706 708 709 710 712 714 715
Volume 3 Lumps . . . . . . . . . . . . . . Lung cancer, brochoalveolar. See Bronchoalveolar lung cancer Lung cancers . . . . . . . . . . . Lutein . . . . . . . . . . . . . . Lycopene . . . . . . . . . . . . . Lymphadenectomy. . . . . . . . Lymphangiography . . . . . . . Lymphangiosarcomas . . . . . . Lymphedema. . . . . . . . . . . Lymphocytosis . . . . . . . . . . Lymphomas . . . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . . . lv Complete List of Contents . . . . . . . . . . . . . . lix Living will . . . . . . . . . . . . . . . . . Living with cancer . . . . . . . . . . . . . Lobectomy . . . . . . . . . . . . . . . . . Lobular carcinoma in situ (LCIS) . . . . . Long-distance caregiving . . . . . . . . . Loop electrosurgical excisional procedure (LEEP) . . . . . . . . . . . . . . . . . Lumbar puncture . . . . . . . . . . . . . . Lumpectomy . . . . . . . . . . . . . . . .
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719 720 723 725 726
. . . . . 727 . . . . . 728 . . . . . 730 xxi
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733 737 737 738 740 741 742 743 744
Salem Health: Cancer M. D. Anderson Cancer Center . . . . . . . . . Macrobiotic diet . . . . . . . . . . . . . . . . . Magnetic resonance imaging (MRI) . . . . . . . Malignant fibrous histiocytoma (MFH) . . . . . Malignant rhabdoid tumor of the kidney . . . . Malignant tumors . . . . . . . . . . . . . . . . MALT lymphomas. See Mucosa-associated lymphoid tissue lymphomas Mammography . . . . . . . . . . . . . . . . . . Managed care . . . . . . . . . . . . . . . . . . Mantle cell lymphoma (MCL) . . . . . . . . . . Mastectomy . . . . . . . . . . . . . . . . . . . Mastocytomas . . . . . . . . . . . . . . . . . . Matrix metalloproteinase inhibitors . . . . . . . Mayo Clinic Cancer Center . . . . . . . . . . . MCC. See Merkel cell carcinomas MCL. See Mantle cell lymphoma MDR. See Drug resistance and multidrug resistance Mediastinal tumors. . . . . . . . . . . . . . . . Mediastinoscopy . . . . . . . . . . . . . . . . . Medical marijuana . . . . . . . . . . . . . . . . Medical oncology . . . . . . . . . . . . . . . . Medicare and cancer . . . . . . . . . . . . . . . Medullary carcinoma of the breast. . . . . . . . Medulloblastomas . . . . . . . . . . . . . . . . Melanomas . . . . . . . . . . . . . . . . . . . . Melphalan . . . . . . . . . . . . . . . . . . . . Memorial Sloan-Kettering Cancer Center . . . . MEN 1. See Multiple endocrine neoplasia type 1 MEN 2. See Multiple endocrine neoplasia type 2 Meningeal carcinomatosis . . . . . . . . . . . . Meningiomas. . . . . . . . . . . . . . . . . . . Merkel cell carcinomas (MCC) . . . . . . . . . Mesenchymomas, malignant. . . . . . . . . . . Mesothelioma . . . . . . . . . . . . . . . . . . Metastasis . . . . . . . . . . . . . . . . . . . . Metastatic squamous neck cancer with occult primary . . . . . . . . . . . . . . . . . . . . MFH. See Malignant fibrous histiocytoma Microcalcifications. . . . . . . . . . . . . . . . Microwave hyperthermia therapy . . . . . . . . Mineral oils . . . . . . . . . . . . . . . . . . . Mistletoe . . . . . . . . . . . . . . . . . . . . . Mitochondrial DNA mutations. . . . . . . . . . MLH1 gene. . . . . . . . . . . . . . . . . . . . Mohs surgery. . . . . . . . . . . . . . . . . . . Molecular oncology . . . . . . . . . . . . . . . Moles. . . . . . . . . . . . . . . . . . . . . . . Monoclonal antibodies . . . . . . . . . . . . . . Motion sickness devices . . . . . . . . . . . . .
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748 750 750 752 753 754
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754 757 759 761 763 764 765
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766 768 768 770 772 774 775 776 779 780
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MRI. See Magnetic resonance imaging MSH genes . . . . . . . . . . . . . . . . . . . . Mucinous carcinomas . . . . . . . . . . . . . . Mucosa-associated lymphoid tissue (MALT) lymphomas . . . . . . . . . . . . . . . . . . Mucositis . . . . . . . . . . . . . . . . . . . . . Mucous membranes, epidermoid cancers of. See Epidermoid cancers of mucous membranes Multiple endocrine neoplasia type 1 (MEN 1). . Multiple endocrine neoplasia type 2 (MEN 2). . Multiple myeloma . . . . . . . . . . . . . . . . Mustard gas . . . . . . . . . . . . . . . . . . . Mutagenesis and cancer . . . . . . . . . . . . . Myasthenia gravis . . . . . . . . . . . . . . . . MYC oncogene . . . . . . . . . . . . . . . . . . Mycosis fungoides . . . . . . . . . . . . . . . . Myelodysplastic syndromes . . . . . . . . . . . Myelofibrosis . . . . . . . . . . . . . . . . . . Myeloma . . . . . . . . . . . . . . . . . . . . . Myeloproliferative disorders. . . . . . . . . . . Myelosuppression . . . . . . . . . . . . . . . . 2-Naphthylamine. . . . . . . . . . . . . . . . Nasal cavity and paranasal sinus cancers . . . National Cancer Institute (NCI) . . . . . . . . National Science Foundation (NSF) . . . . . . Native North Americans and cancer . . . . . . Nausea and vomiting. . . . . . . . . . . . . . NCI. See National Cancer Institute Needle biopsies . . . . . . . . . . . . . . . . Needle localization. . . . . . . . . . . . . . . Nephroblastomas. . . . . . . . . . . . . . . . Nephrostomy . . . . . . . . . . . . . . . . . . Neuroblastomas . . . . . . . . . . . . . . . . Neuroectodermal tumors. . . . . . . . . . . . Neuroendocrine tumors . . . . . . . . . . . . Neurofibromatosis type 1 (NF1) . . . . . . . . Neurologic oncology. . . . . . . . . . . . . . Neutropenia . . . . . . . . . . . . . . . . . . NF1. See Neurofibromatosis type 1 Nickel compounds and metallic nickel . . . . Night sweats . . . . . . . . . . . . . . . . . . Nijmegen breakage syndrome . . . . . . . . . Nipple discharge . . . . . . . . . . . . . . . . Non-Hodgkin lymphoma . . . . . . . . . . . Nonsteroidal anti-inflammatory drugs (NSAIDs) . . . . . . . . . . . . . . . . . . NSAIDs. See Nonsteroidal anti-inflammatory drugs NSF. See National Science Foundation Nuclear medicine scan . . . . . . . . . . . . .
781 782 783 785 786 788
. . 790 . . . . . . . . . . .
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790 791 792 793 794 795 796 796 798 800 802 xxii
. . 803 . . 803 . . 804 . . 806
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807 808 809 812 813 815 817 817 819 820 822 823 825
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826 826 829 830 832 834
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836 838 839 839 841 842 844 845 847 849
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851 852 853 854 855
. . . 858
. . . 859
Complete List of Contents Pediatric oncology and hematology . . . . . . . . . 938 Pelvic examination . . . . . . . . . . . . . . . . . . 940 Penile cancer . . . . . . . . . . . . . . . . . . . . . 941 Percutaneous transhepatic cholangiography (PTHC) . . . . . . . . . . . . . . . . . . . . . . 943 Pericardial effusion . . . . . . . . . . . . . . . . . 944 Pericardiocentesis . . . . . . . . . . . . . . . . . . 946 Peritoneovenous shunts . . . . . . . . . . . . . . . 946 Personality and cancer . . . . . . . . . . . . . . . . 947 Pesticides and the food chain . . . . . . . . . . . . 948 PET. See Positron emission tomography Peutz-Jeghers syndrome (PJS) . . . . . . . . . . . . 951 Pharmacy oncology . . . . . . . . . . . . . . . . . 952 Phenacetin . . . . . . . . . . . . . . . . . . . . . . 955 Phenolics . . . . . . . . . . . . . . . . . . . . . . . 955 Pheochromocytomas . . . . . . . . . . . . . . . . . 956 Pheresis . . . . . . . . . . . . . . . . . . . . . . . 958 Photodynamic therapy (PDT) . . . . . . . . . . . . 959 Phyllodes tumors. . . . . . . . . . . . . . . . . . . 960 Phytoestrogens . . . . . . . . . . . . . . . . . . . . 962 Pineoblastomas. . . . . . . . . . . . . . . . . . . . 963 Pituitary tumors . . . . . . . . . . . . . . . . . . . 965 PJS. See Peutz-Jeghers syndrome Placental alkaline phosphatase (PALP) . . . . . . . 968 Plant alkaloids and terpenoids in chemotherapy . . . . . . . . . . . . . . . . . . . 968 Plasticizers . . . . . . . . . . . . . . . . . . . . . . 971 Pleural biopsy . . . . . . . . . . . . . . . . . . . . 972 Pleural effusion . . . . . . . . . . . . . . . . . . . 973 Pleurodesis . . . . . . . . . . . . . . . . . . . . . . 975 Pleuropulmonary blastomas . . . . . . . . . . . . . 975 PMS genes . . . . . . . . . . . . . . . . . . . . . . 976 Pneumonectomy . . . . . . . . . . . . . . . . . . . 977 Pneumonia . . . . . . . . . . . . . . . . . . . . . . 979 Polycyclic aromatic hydrocarbons . . . . . . . . . . 981 Polycythemia vera . . . . . . . . . . . . . . . . . . 981 Polypectomy . . . . . . . . . . . . . . . . . . . . . 982 Polyps . . . . . . . . . . . . . . . . . . . . . . . . 983 Polyps, colon. See Colon polyps Polyps, gastric. See Gastric polyps Positron emission tomography (PET) . . . . . . . . 984 Poverty and cancer . . . . . . . . . . . . . . . . . . 987 PPOs. See Preferred provider organizations Prayer and cancer support . . . . . . . . . . . . . . 989 Preferred provider organizations (PPOs) . . . . . . 990 Pregnancy and cancer . . . . . . . . . . . . . . . . 992 Premalignancies . . . . . . . . . . . . . . . . . . . 994 Prevent Cancer Foundation . . . . . . . . . . . . . 997 Prevention . . . . . . . . . . . . . . . . . . . . . . 999 Primary care physician . . . . . . . . . . . . . . . 1001
Nutrition and cancer prevention . . . . . . . . . . . 861 Nutrition and cancer treatment. . . . . . . . . . . . 864 Obesity-associated cancers . . . . . Occupational exposures and cancer . Occupational therapy . . . . . . . . OCs. See Organochlorines Oligodendrogliomas . . . . . . . . . Omega-3 fatty acids . . . . . . . . . Ommaya reservoir . . . . . . . . . . Oncogenes . . . . . . . . . . . . . . Oncogenic viruses . . . . . . . . . . Oncology . . . . . . . . . . . . . . . Oncology clinical nurse specialist . . Oncology social worker . . . . . . . Oophorectomy . . . . . . . . . . . . Ophthalmic oncology . . . . . . . . Opioids . . . . . . . . . . . . . . . . Oral and maxillofacial surgery. . . . Oral and oropharyngeal cancers . . . Orbit tumors . . . . . . . . . . . . . Orchiectomy . . . . . . . . . . . . . Organ transplantation and cancer . . Organochlorines (OCs) . . . . . . . Oropharyngeal cancers. See Oral and oropharyngeal cancers Orthopedic surgery. . . . . . . . . . Otolaryngology . . . . . . . . . . . Ovarian cancers . . . . . . . . . . . Ovarian cysts. . . . . . . . . . . . . Ovarian epithelial cancer . . . . . . Overtreatment . . . . . . . . . . . .
. . . . . . . . 868 . . . . . . . . 871 . . . . . . . . 873 . . . . . . . . . . . . . . . . .
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875 877 878 878 881 882 885 887 888 889 892 893 894 897 898 899 901
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902 903 905 908 909 911
Paget disease of bone . . . . . . . . . . . . . Pain management medications. . . . . . . . . Palliative treatment . . . . . . . . . . . . . . PALP. See Placental alkaline phosphatase Palpation . . . . . . . . . . . . . . . . . . . . Pancolitis . . . . . . . . . . . . . . . . . . . . Pancreatectomy . . . . . . . . . . . . . . . . Pancreatic cancers . . . . . . . . . . . . . . . Pancreatitis . . . . . . . . . . . . . . . . . . . Pap test . . . . . . . . . . . . . . . . . . . . . Paracentesis . . . . . . . . . . . . . . . . . . Paranasal sinus cancers. See Nasal cavity and paranasal sinus cancers Paraneoplastic syndromes . . . . . . . . . . . Parathyroid cancer . . . . . . . . . . . . . . . Pathology . . . . . . . . . . . . . . . . . . . PC-SPES . . . . . . . . . . . . . . . . . . . . PDT. See Photodynamic therapy
. . . 912 . . . 914 . . . 917 . . . . . . .
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920 920 921 923 927 928 929
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931 932 934 937 xxiii
Salem Health: Cancer Primary central nervous system lymphomas . . . . . . . . . . . . . . . . Progesterone receptor assay . . . . . . . . Prostate cancer . . . . . . . . . . . . . . . Prostate-specific antigen (PSA) test . . . . Prostatectomy. . . . . . . . . . . . . . . . Prostatitis . . . . . . . . . . . . . . . . . . Proteasome inhibitors. . . . . . . . . . . . Protein electrophoresis . . . . . . . . . . . Proteomics and cancer research . . . . . . Proton beam therapy . . . . . . . . . . . . Proto-oncogenes and carcinogenesis . . . . PSA test. See Prostate-specific antigen test Psycho-oncology . . . . . . . . . . . . . . Psychosocial aspects of cancer . . . . . . . PTHC. See Percutaneous transhepatic cholangiography Radiation, ionizing. See Ionizing radiation Radiation oncology . . . . . . . . . . . . . Radiation therapies . . . . . . . . . . . . . Radiation therapy, afterloading. See Afterloading radiation therapy Radical neck dissection . . . . . . . . . . . Radiofrequency ablation . . . . . . . . . . Radionuclide scan . . . . . . . . . . . . . Radiopharmaceuticals . . . . . . . . . . . Radon . . . . . . . . . . . . . . . . . . . . RB1 gene . . . . . . . . . . . . . . . . . . Receptor analysis . . . . . . . . . . . . . .
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1003 1003 1004 1006 1008 1009 1010 1010 1012 1014 1015
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. . . . 1021 . . . . 1023
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1027 1027 1030 1030 1032 1032 1033
Reconstructive surgery . . . . . . . . . . . . . . Rectal cancer . . . . . . . . . . . . . . . . . . . Recurrence . . . . . . . . . . . . . . . . . . . . Rehabilitation . . . . . . . . . . . . . . . . . . . Relationships . . . . . . . . . . . . . . . . . . . Renal pelvis tumors. . . . . . . . . . . . . . . . Report on Carcinogens (RoC) . . . . . . . . . . Resveratrol . . . . . . . . . . . . . . . . . . . . Retinoblastomas . . . . . . . . . . . . . . . . . Rhabdomyosarcomas . . . . . . . . . . . . . . . RhoGD12 gene . . . . . . . . . . . . . . . . . . Richter syndrome . . . . . . . . . . . . . . . . . Risk assessment, family history and. See Family history and risk assessment Risks for cancer. . . . . . . . . . . . . . . . . . Robert H. Lurie Cancer Center . . . . . . . . . . RoC. See Report on Carcinogens Rothmund-Thomson syndrome . . . . . . . . . .
. . . . . . . . . . . .
Salivary gland cancer . . . . . . . . . . . . . Salpingectomy and salpingo-oophorectomy . Sarcomas, soft-tissue . . . . . . . . . . . . . Saw palmetto . . . . . . . . . . . . . . . . . Schwannoma tumors . . . . . . . . . . . . . SCLC1 gene. . . . . . . . . . . . . . . . . . Screening, colorectal cancer. See Colorectal cancer screening Screening for cancer . . . . . . . . . . . . . Second opinions . . . . . . . . . . . . . . . Self-image and body image. . . . . . . . . .
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1034 1036 1038 1038 1041 1043 1044 1045 1046 1048 1050 1050
. 1052 . 1054 . 1056 1058 1060 1062 1065 1066 1067
. . . 1067 . . . 1070 . . . 1071
Volume 4 Sjögren syndrome. . . . . . . . . . . . . . . . Skin cancers . . . . . . . . . . . . . . . . . . SLN biopsy and mapping. See Sentinel lymph node biopsy and mapping Small intestine cancer . . . . . . . . . . . . . Smoking cessation . . . . . . . . . . . . . . . Social Security Disability Insurance (SSDI) . . Soft-tissue fibrosarcomas. See Fibrosarcomas, soft-tissue Soots . . . . . . . . . . . . . . . . . . . . . . Soy foods . . . . . . . . . . . . . . . . . . . . Spermatocytomas . . . . . . . . . . . . . . . . Spinal axis tumors . . . . . . . . . . . . . . . Spinal cord compression . . . . . . . . . . . . Splenectomy . . . . . . . . . . . . . . . . . . Sputum cytology . . . . . . . . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . lxxvii Complete List of Contents . . . . . . . . . . . . . lxxix Sentinel lymph node (SLN) biopsy and mapping . . . . . . . . . . . . . . . Sepsis. See Infection and sepsis Sertoli cell tumors . . . . . . . . . . . Sexuality and cancer . . . . . . . . . . Sézary syndrome . . . . . . . . . . . . SIADH. See Syndrome of inappropriate antidiuretic hormone production Side effects . . . . . . . . . . . . . . . Sigmoidoscopy . . . . . . . . . . . . . Silica, crystalline . . . . . . . . . . . . Simian virus 40 . . . . . . . . . . . . . Singlehood and cancer . . . . . . . . .
. . . . . . 1073 . . . . . . 1073 . . . . . . 1074 . . . . . . 1076
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1078 1082 1083 1084 1084 xxiv
. . 1086 . . 1088
. . 1091 . . 1093 . . 1096
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1097 1098 1099 1100 1102 1103 1105
Complete List of Contents Squamous cell carcinomas . . . . . . . . . . . SRS. See Stereotactic radiosurgery SSDI. See Social Security Disability Insurance Staging of cancer . . . . . . . . . . . . . . . . Statistics of cancer . . . . . . . . . . . . . . . Stem cell transplantation . . . . . . . . . . . . Stent therapy . . . . . . . . . . . . . . . . . . Stereotactic needle biopsy . . . . . . . . . . . Stereotactic radiosurgery (SRS) . . . . . . . . Sterility . . . . . . . . . . . . . . . . . . . . . Stomach cancers . . . . . . . . . . . . . . . . Stomatitis . . . . . . . . . . . . . . . . . . . . Stress management . . . . . . . . . . . . . . . Sunlamps . . . . . . . . . . . . . . . . . . . . Sun’s soup . . . . . . . . . . . . . . . . . . . Sunscreens . . . . . . . . . . . . . . . . . . . Superior vena cava syndrome . . . . . . . . . Support groups . . . . . . . . . . . . . . . . . Surgical biopsies . . . . . . . . . . . . . . . . Surgical oncology. . . . . . . . . . . . . . . . Survival rates . . . . . . . . . . . . . . . . . . Survivorship issues . . . . . . . . . . . . . . . Symptoms and cancer. . . . . . . . . . . . . . Syndrome of inappropriate antidiuretic hormone production (SIADH) . . . . . . . . Synovial sarcomas . . . . . . . . . . . . . . . Taste alteration . . . . . . . . . . . . . . Teratocarcinomas . . . . . . . . . . . . . Teratomas . . . . . . . . . . . . . . . . . Testicular cancer . . . . . . . . . . . . . Testicular self-examination (TSE) . . . . Thermal imaging . . . . . . . . . . . . . Thiotepa. . . . . . . . . . . . . . . . . . Thoracentesis . . . . . . . . . . . . . . . Thoracoscopy . . . . . . . . . . . . . . . Thoracotomy . . . . . . . . . . . . . . . Throat cancer . . . . . . . . . . . . . . . Thrombocytopenia . . . . . . . . . . . . Thymomas . . . . . . . . . . . . . . . . Thymus cancer . . . . . . . . . . . . . . Thyroid cancer . . . . . . . . . . . . . . Thyroid nuclear medicine scan . . . . . . TNF. See Tumor necrosis factor TNM staging . . . . . . . . . . . . . . . Tobacco, chewing. See Chewing tobacco Tobacco-related cancers . . . . . . . . . Topoisomerase inhibitors . . . . . . . . . TP53 protein . . . . . . . . . . . . . . . Tracheostomy . . . . . . . . . . . . . . . Transfusion therapy. . . . . . . . . . . .
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Transitional care . . . . . . . . . . . Transitional cell carcinomas . . . . . Transrectal ultrasound . . . . . . . . Transvaginal ultrasound . . . . . . . Trichilemmal carcinomas. . . . . . . TSE. See Testicular self-examination Tuberous sclerosis . . . . . . . . . . Tubular carcinomas . . . . . . . . . . Tumor flare . . . . . . . . . . . . . . Tumor lysis syndrome . . . . . . . . Tumor markers . . . . . . . . . . . . Tumor necrosis factor (TNF) . . . . . Tumor-suppressor genes . . . . . . . Turcot syndrome . . . . . . . . . . . Tyrosine kinase inhibitors . . . . . .
. . 1106
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1108 1111 1114 1116 1118 1119 1120 1121 1124 1125 1127 1128 1129 1130 1132 1135 1138 1140 1143 1144
. . 1147 . . 1149 . . . . . . . . . . . . . . . .
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1151 1152 1153 1154 1156 1157 1158 1158 1160 1161 1162 1164 1166 1167 1169 1172
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1182 1183 1185 1186 1187
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1187 1188 1189 1189 1191 1193 1194 1195 1196
Ultrasound, breast. See Breast ultrasound Ultrasound, endorectal. See Endorectal ultrasound Ultrasound, transrectal. See Transrectal ultrasound Ultrasound, transvaginal. See Transvaginal ultrasound Ultrasound tests . . . . . . . . . . . . . . . Ultraviolet radiation and related exposures Umbilical cord blood transplantation. . . . Upper gastrointestinal (GI) endoscopy . . . Upper gastrointestinal (GI) series . . . . . Urethral cancer . . . . . . . . . . . . . . . Urinalysis . . . . . . . . . . . . . . . . . . Urinary system cancers . . . . . . . . . . . Urography . . . . . . . . . . . . . . . . . Urologic oncology . . . . . . . . . . . . . Urostomy . . . . . . . . . . . . . . . . . . Uterine cancer . . . . . . . . . . . . . . .
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1199 1200 1201 1202 1203 1205 1207 1209 1213 1214 1216 1217
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1220 1221 1223 1225 1226
Vaccines, preventive . . . . . . . . . . . Vaccines, therapeutic . . . . . . . . . . . Vaginal cancer . . . . . . . . . . . . . . Vascular access tubes. . . . . . . . . . . Vasectomy and cancer . . . . . . . . . . Vegetables, cruciferous. See Cruciferous vegetables Veterinary oncology . . . . . . . . . . . VHL disease. See Von Hippel-Lindau disease Vinyl chloride . . . . . . . . . . . . . . Viral oncology . . . . . . . . . . . . . . Virus-related cancers . . . . . . . . . . . Von Hippel-Lindau (VHL) disease. . . . Vulvar cancer . . . . . . . . . . . . . . .
. . . . . 1173 . . . . .
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1174 1175 1177 1179 1180 xxv
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1230 1230 1232 1235 1237
Salem Health: Cancer WAGR syndrome. See Wilms’ tumor aniridiagenitourinary anomalies-mental retardation syndrome and cancer Waldenström macroglobulinemia (WM) . . . . . . 1240 Watchful waiting . . . . . . . . . . . . . . . . . . 1242 Weight loss . . . . . . . . . . . . . . . . . . . . . 1243 Wilms’ tumor . . . . . . . . . . . . . . . . . . . . 1245 Wilms’ tumor aniridia-genitourinary anomaliesmental retardation (WAGR) syndrome and cancer . . . . . . . . . . . . . . . . . . . . . . 1248 Wine and cancer . . . . . . . . . . . . . . . . . . 1250 Wire localization . . . . . . . . . . . . . . . . . . 1250 WM. See Waldenström macroglobulinemia Wood dust . . . . . . . . . . . . . . . . . . . . . 1251
Yolk sac carcinomas . . . . . . . . . . . . . . . . 1256 Young adult cancers . . . . . . . . . . . . . . . . 1256 Zollinger-Ellison syndrome . . . . . . . . . . . . 1260 Drugs by Generic Name . . . Drugs by Trade Name . . . . Associations and Agencies . . Cancer Centers and Hospitals Cancer Support Groups . . . . Carcinogens. . . . . . . . . . Glossary . . . . . . . . . . . Bibliography . . . . . . . . .
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1265 1309 1348 1352 1357 1362 1383 1400
Category List . . . . . . . . . . . . . . . . . . . . 1409 Index . . . . . . . . . . . . . . . . . . . . . . . . 1419
X-ray tests . . . . . . . . . . . . . . . . . . . . . 1252 Xeroderma pigmentosa . . . . . . . . . . . . . . . 1254
xxvi
Volume II Denys-Drash syndrome and cancer — Liver cancers
Editor
Jeffrey A. Knight, Ph.D. Mount Holyoke College
Medical Consultants
Laurie Jackson-Grusby, Ph.D. Children’s Hospital Boston, Harvard Medical School
Wendy White-Ryan, M.D., FAAP Golisano Children’s Hospital at Strong Memorial Hospital
SALEM PRESS, INC. Pasadena, California Hackensack, New Jersey
Editor in Chief: Dawn P. Dawson Editorial Director: Christina J. Moose Project Editors: Tracy Irons-Georges, Rowena Wildin Dehanke Editorial Assistant: Dana Garey
Production Editor: Joyce I. Buchea Acquisitions Editor: Mark Rehn Photo Editor: Cynthia Breslin Beres Design and Graphics: James Hutson Layout: William Zimmerman
Copyright © 2009, by Salem Press, Inc. All rights in this book are reserved. No part of this work may be used or reproduced in any manner whatsoever or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without written permission from the copyright owner except in the case of brief quotations embodied in critical articles and reviews or in the copying of images deemed to be freely licensed or in the public domain. For information address the publisher, Salem Press, Inc., P.O. Box 50062, Pasadena, California 91115. ∞ The paper used in these volumes conforms to the American National Standard for Permanence of Paper for Printed Library Materials, Z39.48-1992 (R1997). Note to Readers The material presented in Salem Health: Cancer is intended for broad informational and educational purposes. Readers who suspect that they or someone whom they know or provide caregiving for suffers from cancer or any other physical or psychological disorder, disease, or condition described in this set should contact a physician without delay; this work should not be used as a substitute for professional medical diagnosis or staging. Readers who are undergoing or about to undergo any treatment or procedure described in this set should refer to their physicians and other health care team members for guidance concerning preparation and possible effects. This set is not to be considered definitive on the covered topics, and readers should remember that the field of health care is characterized by a diversity of medical opinions and constant expansion in knowledge and understanding. Library of Congress Cataloging-in-Publication Data Salem health : cancer / Jeffrey A. Knight, Laurie Jackson-Grusby, Wendy White-Ryan. p. cm. Includes bibliographical references and index. ISBN 978-1-58765-505-0 (set : alk. paper) — ISBN 978-1-58765-506-7 (vol. 1 : alk. paper) — ISBN 978-1-58765-507-4 (vol. 2 : alk. paper) — ISBN 978-1-58765-508-1 (vol. 3 : alk. paper) — ISBN 978-1-58765-509-8 (vol. 4 : alk. paper) 1. Cancer. I. Knight, Jeffrey A., 1948- II. Jackson-Grusby, Laurie. III. White-Ryan, Wendy. RC265.S32 2008 616.99′4—dc22 2008030861
First Printing
printed in the united states of america
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Contents
Complete List of Contents . . . . . . . . . . . . xxxvii Denys-Drash syndrome and cancer . . . . . . Depression . . . . . . . . . . . . . . . . . . . Dermatofibrosarcoma protuberans (DFSP) . . Dermatology oncology. . . . . . . . . . . . . DES. See Diethylstilbestrol Desmoid tumors . . . . . . . . . . . . . . . . Desmoplastic small round cell tumor (DSRCT) . . . . . . . . . . . . . . . . . . Developing nations and cancer . . . . . . . . DFSP. See Dermatofibrosarcoma protuberans Di(2-ethylhexyl) phthalate (DEHP) . . . . . . Diarrhea . . . . . . . . . . . . . . . . . . . . DIC. See Disseminated intravascular coagulation Dietary supplements . . . . . . . . . . . . . . Diethanolamine (DEA) . . . . . . . . . . . . Diethylstilbestrol (DES) . . . . . . . . . . . . Digital rectal exam (DRE) . . . . . . . . . . . Dilation and curettage (D&C) . . . . . . . . . Dioxins . . . . . . . . . . . . . . . . . . . . . Disseminated intravascular coagulation (DIC) . . . . . . . . . . . . . . . . . . . . Diverticulosis and diverticulitis . . . . . . . . DNR. See Do-not-resuscitate order Do-not-resuscitate (DNR) order . . . . . . . . Down syndrome and leukemia. . . . . . . . . DPC4 gene testing . . . . . . . . . . . . . . . DRE. See Digital rectal exam Drug resistance and multidrug resistance (MDR) . . . . . . . . . . . . . . . . . . . . Dry mouth . . . . . . . . . . . . . . . . . . . DSRCT. See Desmoplastic small round cell tumor Duct ectasia . . . . . . . . . . . . . . . . . . Ductal carcinoma in situ (DCIS). . . . . . . . Ductal lavage. . . . . . . . . . . . . . . . . . Ductogram . . . . . . . . . . . . . . . . . . . Duke Comprehensive Cancer Center . . . . . Dukes’ classification . . . . . . . . . . . . . . Duodenal carcinomas . . . . . . . . . . . . . Dye, hair. See Hair dye Dysplastic nevus syndrome . . . . . . . . . .
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Edema . . . . . . . . . . . . . . . . . . . . . . . Education, cancer. See Cancer education Elderly and cancer . . . . . . . . . . . . . . . . . Electrolarynx . . . . . . . . . . . . . . . . . . . . Electromagnetic radiation . . . . . . . . . . . . . Electroporation therapy . . . . . . . . . . . . . . Electrosurgery . . . . . . . . . . . . . . . . . . . Embolization . . . . . . . . . . . . . . . . . . . . Embryonal cell cancer . . . . . . . . . . . . . . . End-of-life care . . . . . . . . . . . . . . . . . . Endocrine cancers . . . . . . . . . . . . . . . . . Endocrinology oncology . . . . . . . . . . . . . . Endometrial cancer . . . . . . . . . . . . . . . . Endometrial hyperplasia . . . . . . . . . . . . . . Endorectal ultrasound . . . . . . . . . . . . . . . Endoscopic retrograde cholangiopancreatography (ERCP) . . . . . . . . . . . . . . . . . . . . . Endoscopy . . . . . . . . . . . . . . . . . . . . . Endoscopy, upper gastrointestinal. See Upper gastrointestinal endoscopy Endotheliomas . . . . . . . . . . . . . . . . . . . Enteritis . . . . . . . . . . . . . . . . . . . . . . Enterostomal therapy . . . . . . . . . . . . . . . Eosinophilic leukemia . . . . . . . . . . . . . . . Ependymomas . . . . . . . . . . . . . . . . . . . Epidemiology of cancer . . . . . . . . . . . . . . Epidermoid cancers of mucous membranes . . . . Epstein-Barr virus . . . . . . . . . . . . . . . . . ERCP. See Endoscopic retrograde cholangiopancreatography ERD. See Estrogen receptor downregulator Erionite. . . . . . . . . . . . . . . . . . . . . . . Erythroplakia. . . . . . . . . . . . . . . . . . . . Esophageal cancer . . . . . . . . . . . . . . . . . Esophageal speech . . . . . . . . . . . . . . . . . Esophagectomy . . . . . . . . . . . . . . . . . . Esophagitis . . . . . . . . . . . . . . . . . . . . . Essiac . . . . . . . . . . . . . . . . . . . . . . . Estrogen receptor downregulator (ERD) . . . . . Estrogen-receptor-sensitive breast cancer . . . . . Ethnicity and cancer . . . . . . . . . . . . . . . . Ethylene oxide . . . . . . . . . . . . . . . . . . . Ewing sarcoma . . . . . . . . . . . . . . . . . . . Exenteration . . . . . . . . . . . . . . . . . . . . Exercise and cancer . . . . . . . . . . . . . . . . External beam radiation therapy (EBRT) . . . . . Eye cancers . . . . . . . . . . . . . . . . . . . . Eyelid cancer. . . . . . . . . . . . . . . . . . . .
357 357 360 362
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370 373 373 374 375 376
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386 387 389 389 390 392 393
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Eaton-Lambert syndrome. See Lambert-Eaton myasthenic syndrome EBRT. See External beam radiation therapy xxxiii
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396 399 399 400 401 402 403 404 406 409 412 414 416
. 417 . 417
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420 421 422 424 425 426 429 431
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433 433 434 436 438 439 441 441 442 444 447 447 450 451 454 455 458
Salem Health: Cancer Fallopian tube cancer . . . . . . . . . . . . Family history and risk assessment . . . . . Fanconi anemia . . . . . . . . . . . . . . . Fatigue . . . . . . . . . . . . . . . . . . . . Fecal occult blood test (FOBT) . . . . . . . Fertility drugs and cancer . . . . . . . . . . Fertility issues . . . . . . . . . . . . . . . . Fever . . . . . . . . . . . . . . . . . . . . . Fiber . . . . . . . . . . . . . . . . . . . . . Fibroadenomas . . . . . . . . . . . . . . . . Fibrocystic breast changes . . . . . . . . . . Fibrosarcomas, soft-tissue . . . . . . . . . . Financial issues . . . . . . . . . . . . . . . 5HIAA test. See 5-Hydroxyindoleacetic acid test 5Q minus syndrome . . . . . . . . . . . . . Flow cytometry . . . . . . . . . . . . . . . FOBT. See Fecal occult blood test Folic acid. . . . . . . . . . . . . . . . . . . Formaldehyde . . . . . . . . . . . . . . . . Fox Chase Cancer Center . . . . . . . . . . Fred Hutchinson Cancer Research Center . . Free radicals . . . . . . . . . . . . . . . . . Fruits . . . . . . . . . . . . . . . . . . . . .
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486 486 487 488 490 491
Gallbladder cancer . . . . . . . . . . . . . . Gallium scan . . . . . . . . . . . . . . . . . Gamma Knife . . . . . . . . . . . . . . . . Gardner syndrome . . . . . . . . . . . . . . Garlic and allicin . . . . . . . . . . . . . . . Gastric polyps . . . . . . . . . . . . . . . . Gastrinomas . . . . . . . . . . . . . . . . . Gastrointestinal cancers . . . . . . . . . . . Gastrointestinal complications of cancer treatment. . . . . . . . . . . . . . . . . . Gastrointestinal oncology . . . . . . . . . . Gastrointestinal stromal tumors (GISTs) . . GCTs. See Giant cell tumors Gene therapy . . . . . . . . . . . . . . . . . Genetic counseling . . . . . . . . . . . . . . Genetic testing . . . . . . . . . . . . . . . . Genetics of cancer . . . . . . . . . . . . . . Geography and cancer . . . . . . . . . . . . Germ-cell tumors . . . . . . . . . . . . . . Gerson therapy . . . . . . . . . . . . . . . . Gestational trophoblastic tumors (GTTs) . . Giant cell tumors (GCTs) . . . . . . . . . . Ginseng, panax. . . . . . . . . . . . . . . . GISTs. See Gastrointestinal stromal tumors Gleason grading system . . . . . . . . . . . Gliomas . . . . . . . . . . . . . . . . . . .
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493 495 497 498 499 500 501 502
Glomus tumors . . . . . . . . . . . . . . . . Glossectomy . . . . . . . . . . . . . . . . . Glutamine . . . . . . . . . . . . . . . . . . Gonioscopy . . . . . . . . . . . . . . . . . Grading of tumors . . . . . . . . . . . . . . Graft-versus-host disease (GVHD) . . . . . Granulosa cell tumors . . . . . . . . . . . . Green tea . . . . . . . . . . . . . . . . . . . Grief and bereavement . . . . . . . . . . . . GTTs. See Gestational trophoblastic tumors GVHD. See Graft-versus-host disease Gynecologic cancers . . . . . . . . . . . . . Gynecologic oncology . . . . . . . . . . . .
460 461 464 466 467 469 471 472 474 475 476 478 481
H. pylori. See Helicobacter pylori HAI. See Hepatic arterial infusion Hair dye . . . . . . . . . . . . . . . . . . Hairy cell leukemia . . . . . . . . . . . . Hand-foot syndrome (HFS) . . . . . . . . HBV. See Hepatitis B virus HCG. See Human chorionic gonadotropin HCV. See Hepatitis C virus Head and neck cancers . . . . . . . . . . . Health maintenance organizations (HMOs) Helicobacter pylori. . . . . . . . . . . . . Hemangioblastomas . . . . . . . . . . . . Hemangiopericytomas . . . . . . . . . . . Hemangiosarcomas . . . . . . . . . . . . Hematemesis . . . . . . . . . . . . . . . . Hematologic oncology . . . . . . . . . . . Hematuria . . . . . . . . . . . . . . . . . Hemochromatosis . . . . . . . . . . . . . Hemolytic anemia . . . . . . . . . . . . . Hemoptysis. . . . . . . . . . . . . . . . . Hemorrhoids . . . . . . . . . . . . . . . . Hepatic arterial infusion (HAI) . . . . . . Hepatitis B virus (HBV) . . . . . . . . . . Hepatitis C virus (HCV) . . . . . . . . . . Hepatomegaly . . . . . . . . . . . . . . . HER2/neu protein . . . . . . . . . . . . . Herbs as antioxidants . . . . . . . . . . . Hereditary cancer syndromes . . . . . . . Hereditary diffuse gastric cancer . . . . . Hereditary leiomyomatosis and renal cell cancer (HLRCC) . . . . . . . . . . . . Hereditary mixed polyposis syndrome . . Hereditary non-VHL clear cell renal cell carcinomas . . . . . . . . . . . . . . . Hereditary pancreatitis . . . . . . . . . . . Hereditary papillary renal cell carcinomas Hereditary polyposis syndromes . . . . . .
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512 515 517 519 522 525 527 527 530 531
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534 535 536 536 537 538 540 540 541
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554 557 558 559 559 560 561 562 564 565 566 566 567 568 569 570 571 573 573 574 576
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580 580 581 582
Contents Herpes simplex virus. . . . . . . . . . . . . . . . Herpes zoster virus. . . . . . . . . . . . . . . . . HFS. See Hand-foot syndrome Hispanics and cancer. See Latinos/Hispanics and cancer Histamine 2 antagonists . . . . . . . . . . . . . . Histiocytosis X . . . . . . . . . . . . . . . . . . . HIV/AIDS-related cancers . . . . . . . . . . . . . HLRCC. See Hereditary leiomyomatosis and renal cell cancer HMOs. See Health maintenance organizations Hodgkin disease . . . . . . . . . . . . . . . . . . Home health services . . . . . . . . . . . . . . . Hormonal therapies . . . . . . . . . . . . . . . . Hormone receptor tests . . . . . . . . . . . . . . Hormone replacement therapy (HRT) . . . . . . . Horner syndrome. . . . . . . . . . . . . . . . . . Hospice care . . . . . . . . . . . . . . . . . . . . Hot flashes . . . . . . . . . . . . . . . . . . . . . HPV. See Human papillomavirus HRAS gene testing . . . . . . . . . . . . . . . . . HRT. See Hormone replacement therapy HTLV. See Human T-cell leukemia virus Human chorionic gonadotropin (HCG) . . . . . . Human growth factors and tumor growth . . . . . Human immunodeficiency virus-related cancers. See HIV/AIDS-related cancers Human papillomavirus (HPV) . . . . . . . . . . . Human T-cell leukemia virus (HTLV) . . . . . . Hydatidiform mole . . . . . . . . . . . . . . . . . 5-Hydroxyindoleacetic acid (5HIAA) test . . . . . Hypercalcemia . . . . . . . . . . . . . . . . . . . Hypercoagulation disorders . . . . . . . . . . . . Hyperthermia therapy . . . . . . . . . . . . . . . Hyperthermic perfusion . . . . . . . . . . . . . . Hypopharyngeal cancer . . . . . . . . . . . . . . Hysterectomy . . . . . . . . . . . . . . . . . . . Hysterography . . . . . . . . . . . . . . . . . . . Hystero-oophorectomy. . . . . . . . . . . . . . . Hysteroscopy. . . . . . . . . . . . . . . . . . . . IEP. See Immunoelectrophoresis iFOBT. See Immunochemical fecal occult blood test Ileostomy. . . . . . . . . . . . . . . . . . . . . Imaging tests . . . . . . . . . . . . . . . . . . . Immune response to cancer . . . . . . . . . . . Immunochemical fecal occult blood test (iFOBT) . . . . . . . . . . . . . . . . . . . . Immunocytochemistry and immunohistochemistry . . . . . . . . . . . .
Immunoelectrophoresis (IEP) . . . . . . Immunotherapy . . . . . . . . . . . . . IMRT. See Intensity-modulated radiation therapy Indoles . . . . . . . . . . . . . . . . . . Infection and sepsis . . . . . . . . . . . Infectious cancers . . . . . . . . . . . . Infertility and cancer . . . . . . . . . . . Inflammatory bowel disease . . . . . . . Informed consent. . . . . . . . . . . . . Infusion therapies . . . . . . . . . . . . Insurance . . . . . . . . . . . . . . . . . Integrative oncology . . . . . . . . . . . Intensity-modulated radiation therapy (IMRT) . . . . . . . . . . . . . . . . Interferon. . . . . . . . . . . . . . . . . Interleukins. . . . . . . . . . . . . . . . Invasive cancer. . . . . . . . . . . . . . Invasive ductal carcinomas . . . . . . . Invasive lobular carcinomas . . . . . . . Ionizing radiation . . . . . . . . . . . . Iridium seeds . . . . . . . . . . . . . . . Islet cell tumors . . . . . . . . . . . . . Isoflavones . . . . . . . . . . . . . . . . Itching . . . . . . . . . . . . . . . . . .
. 584 . 586
. 587 . 588 . 590
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593 597 599 601 603 605 606 608
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. 609 . 610
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638 638 641 643 645 646 647 648 651
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652 653 654 655 656 657 657 658 659 661 661
Jonsson Comprehensive Cancer Center (JCCC) . . . . . . . . . . . . . . . . . . . . . . 664 Journaling . . . . . . . . . . . . . . . . . . . . . . 665 Juvenile polyposis syndrome . . . . . . . . . . . . 665
611 612 612 613 614 615 617 618 619 620 621 622 623
Kaposi sarcoma . . . . . . . . . . . . . Karnofsky performance status (KPS) . . Keratosis . . . . . . . . . . . . . . . . . Ki67 test . . . . . . . . . . . . . . . . . Kidney cancer . . . . . . . . . . . . . . Klinefelter syndrome and cancer . . . . KPS. See Karnofsky performance status Krukenberg tumors . . . . . . . . . . . Lacrimal gland tumors . . . . . . . . . Lactate dehydrogenase (LDH) test . . Laetrile . . . . . . . . . . . . . . . . . Lambert-Eaton myasthenic syndrome (LEMS) . . . . . . . . . . . . . . . Laparoscopy and laparoscopic surgery Laryngeal cancer . . . . . . . . . . . . Laryngeal nerve palsy . . . . . . . . . Laryngectomy . . . . . . . . . . . . . Laryngoscopy . . . . . . . . . . . . . Laser therapies . . . . . . . . . . . . .
. . 625 . . 626 . . 629 . . 632 . . 633 xxxv
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667 669 670 670 671 674
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679 681 682 685 686 687 688
Salem Health: Cancer Latinos/Hispanics and cancer . . . . . . . . . . . Laxatives . . . . . . . . . . . . . . . . . . . . . . LCIS. See Lobular carcinoma in situ LDH test. See Lactate dehydrogenase test Leiomyomas . . . . . . . . . . . . . . . . . . . . Leiomyosarcomas . . . . . . . . . . . . . . . . . LEMS. See Lambert-Eaton myasthenic syndrome Leptomeningeal carcinomas . . . . . . . . . . . . Leukapharesis . . . . . . . . . . . . . . . . . . . Leukemia, Down syndrome and. See Down syndrome and leukemia Leukemia, eosinophilic. See Eosinophilic leukemia
. 690 . 692
Leukemia, hairy cell. See Hairy cell leukemia Leukemias . . . . . . . . . . . . . . . . . . . Leukoencephalopathy . . . . . . . . . . . . . Leukopenia. . . . . . . . . . . . . . . . . . . Leukoplakia . . . . . . . . . . . . . . . . . . Leydig cell tumors . . . . . . . . . . . . . . . Li-Fraumeni syndrome (LFS) . . . . . . . . . Limb salvage . . . . . . . . . . . . . . . . . . Linear accelerator . . . . . . . . . . . . . . . Lip cancers . . . . . . . . . . . . . . . . . . . Liposarcomas . . . . . . . . . . . . . . . . . Liver biopsy . . . . . . . . . . . . . . . . . . Liver cancers . . . . . . . . . . . . . . . . . .
. 693 . 694 . 696 . 698
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698 702 704 704 706 706 708 709 710 712 714 715
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Complete List of Contents Volume 1
Contents . . . . . . . . . . . . . . . . . . . . . . . . v Publisher’s Note . . . . . . . . . . . . . . . . . . . . ix About the Editors . . . . . . . . . . . . . . . . . . . xi Contributors . . . . . . . . . . . . . . . . . . . . . xiii Complete List of Contents . . . . . . . . . . . . . . xv AACR. See American Association for Cancer Research ABCD. . . . . . . . . . . . . . . . . . . . . . . . . . 1 ACC. See Adenoid cystic carcinoma Abdominoperineal resection (APR) . . . . . . . . . . 1 Accelerated partial breast irradiation (APBI). . . . . . 3 Achlorhydria . . . . . . . . . . . . . . . . . . . . . . 4 Acoustic neuromas . . . . . . . . . . . . . . . . . . . 4 Acquired immunodeficiency disease-related cancers. See HIV/AIDS-related cancers Acrylamides . . . . . . . . . . . . . . . . . . . . . . 6 ACS. See American Cancer Society Acupuncture and acupressure for cancer patients . . . 8 Acute lymphocytic leukemia (ALL) . . . . . . . . . 11 Acute myelocytic leukemia (AML) . . . . . . . . . . 13 Adenocarcinomas . . . . . . . . . . . . . . . . . . . 16 Adenoid cystic carcinoma (ACC) . . . . . . . . . . . 17 Adenomatoid tumors . . . . . . . . . . . . . . . . . 18 Adenomatous polyps . . . . . . . . . . . . . . . . . 18 Adenoviruses . . . . . . . . . . . . . . . . . . . . . 19 Adjuvant therapy . . . . . . . . . . . . . . . . . . . 20 Adrenal gland cancers . . . . . . . . . . . . . . . . . 21 Adrenocortical cancer . . . . . . . . . . . . . . . . . 23 Advance directives . . . . . . . . . . . . . . . . . . 24 Aflatoxins . . . . . . . . . . . . . . . . . . . . . . . 26 AFP levels. See Alpha-fetoprotein levels African Americans and cancer . . . . . . . . . . . . 28 Africans and cancer . . . . . . . . . . . . . . . . . . 31 Afterloading radiation therapy . . . . . . . . . . . . 32 Agent Orange . . . . . . . . . . . . . . . . . . . . . 34 Aging and cancer . . . . . . . . . . . . . . . . . . . 34 AICR. See American Institute for Cancer Research Aids and devices for cancer patients . . . . . . . . . 38 AIDS-related cancers. See HIV/AIDS-related cancers Air pollution . . . . . . . . . . . . . . . . . . . . . . 39 Alcohol, alcoholism, and cancer . . . . . . . . . . . 42 Aleukemia . . . . . . . . . . . . . . . . . . . . . . . 43 Alkaline phosphatase test (ALP) . . . . . . . . . . . 44
Alkylating agents in chemotherapy . . . . . . . ALL. See Acute lymphocytic leukemia Allicin, garlic and. See Garlic and allicin Alopecia . . . . . . . . . . . . . . . . . . . . . ALP. See Alkaline phosphatase test Alpha-fetoprotein (AFP) levels . . . . . . . . . Alternative therapies. See Complementary and alternative therapies Alveolar soft-part sarcomas . . . . . . . . . . . Amenorrhea . . . . . . . . . . . . . . . . . . . American Association for Cancer Research (AACR) . . . . . . . . . . . . . . . . . . . . American Cancer Society (ACS) . . . . . . . . American Institute for Cancer Research (AICR) 4-Aminobiphenyl . . . . . . . . . . . . . . . . AML. See Acute myelocytic leukemia Amputation . . . . . . . . . . . . . . . . . . . Amyloidosis . . . . . . . . . . . . . . . . . . . Anal cancer . . . . . . . . . . . . . . . . . . . Androgen drugs . . . . . . . . . . . . . . . . . Anemia . . . . . . . . . . . . . . . . . . . . . Anemia, aplastic. See Aplastic anemia Anemia, hemolytic. See Hemolytic anemia Angiogenesis . . . . . . . . . . . . . . . . . . Angiogenesis inhibitors . . . . . . . . . . . . . Angiography. . . . . . . . . . . . . . . . . . . Angiosarcomas . . . . . . . . . . . . . . . . . Anoscopy . . . . . . . . . . . . . . . . . . . . Anthraquinones . . . . . . . . . . . . . . . . . Anthrax . . . . . . . . . . . . . . . . . . . . . Antiandrogens . . . . . . . . . . . . . . . . . . Antidiarrheal agents . . . . . . . . . . . . . . . Antiestrogens . . . . . . . . . . . . . . . . . . Antifungal therapies . . . . . . . . . . . . . . . Antimetabolites in chemotherapy . . . . . . . . Antinausea medications . . . . . . . . . . . . . Antineoplastics in chemotherapy . . . . . . . . Antioxidants . . . . . . . . . . . . . . . . . . . Antiperspirants and breast cancer . . . . . . . . Antiviral therapies. . . . . . . . . . . . . . . . Anxiety . . . . . . . . . . . . . . . . . . . . . APBI. See Accelerated partial breast irradiation APC gene testing . . . . . . . . . . . . . . . . Aplastic anemia . . . . . . . . . . . . . . . . . Appendix cancer . . . . . . . . . . . . . . . . Appetite loss. . . . . . . . . . . . . . . . . . .
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64 66 68 69 70 71 71 72 73 75 76 78 81 83 86 88 90 93
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Salem Health: Cancer APR. See Abdominoperineal resection Arsenic compounds . . . . . . . . . . Arterial embolization . . . . . . . . . Artificial sweeteners . . . . . . . . . . Asbestos . . . . . . . . . . . . . . . . Ascites . . . . . . . . . . . . . . . . . Ashkenazi Jews and cancer . . . . . . Asian Americans and cancer. . . . . . Astrocytomas. . . . . . . . . . . . . . Ataxia telangiectasia (AT) . . . . . . . Autologous blood transfusion . . . . . Axillary dissection . . . . . . . . . . . Azathioprine . . . . . . . . . . . . . .
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Bacillus Calmette Guérin (BCG) . . . . . . . . Bacteria as causes of cancer . . . . . . . . . . . Barium enema . . . . . . . . . . . . . . . . . . Barium swallow . . . . . . . . . . . . . . . . . Barrett esophagus . . . . . . . . . . . . . . . . Basal cell carcinomas . . . . . . . . . . . . . . BCG. See Bacillus Calmette Guérin Beckwith-Wiedemann syndrome (BWS) . . . . Benign prostatic hyperplasia (BPH) . . . . . . . Benign tumors . . . . . . . . . . . . . . . . . . Benzene . . . . . . . . . . . . . . . . . . . . . Benzidine and dyes metabolized to benzidine . . Benzodiazepines . . . . . . . . . . . . . . . . . Bereavement, grief and. See Grief and bereavement Beryllium and beryllium compounds . . . . . . Beta-carotene . . . . . . . . . . . . . . . . . . Bethesda criteria . . . . . . . . . . . . . . . . . BHDS. See Birt-Hogg-Dubé syndrome Bile duct cancer . . . . . . . . . . . . . . . . . Bilobectomy . . . . . . . . . . . . . . . . . . . Bioflavonoids . . . . . . . . . . . . . . . . . . Biological therapy . . . . . . . . . . . . . . . . Biopsy. See also Computed tomography-guided biopsy; Core needle biopsy; Liver biopsy; Needle biopsies; Pleural biopsy; Stereotactic needle biopsy; Surgical biopsies . . . . . . . Birt-Hogg-Dubé syndrome (BHDS) . . . . . . . Birth control pills and cancer . . . . . . . . . . Bis(chloromethyl) ether and technical-grade chloromethyl methyl ether . . . . . . . . . . Bisphenol A (BPA) . . . . . . . . . . . . . . . Bisphosphonates . . . . . . . . . . . . . . . . . Bladder cancer . . . . . . . . . . . . . . . . . . Blood cancers . . . . . . . . . . . . . . . . . . BMT. See Bone marrow transplantation BNCT. See Boron neutron capture therapy
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148 149 151 151 154
Body image. See Self-image and body image Bone cancers . . . . . . . . . . . . . . . . . . . Bone marrow aspiration and biopsy . . . . . . . Bone marrow transplantation (BMT) . . . . . . Bone pain . . . . . . . . . . . . . . . . . . . . Bone scan . . . . . . . . . . . . . . . . . . . . Boron neutron capture therapy (BNCT) . . . . . Bowen disease . . . . . . . . . . . . . . . . . . BPA. See Bisphenol A BPH. See Benign prostatic hyperplasia BPI. See Brief Pain Inventory Brachytherapy . . . . . . . . . . . . . . . . . . BRAF gene . . . . . . . . . . . . . . . . . . . . Brain and central nervous system cancers . . . . Brain scan . . . . . . . . . . . . . . . . . . . . BRCA1 and BRCA2 genes . . . . . . . . . . . . Breakthrough pain . . . . . . . . . . . . . . . . Breast, calcifications of. See Calcifications of the breast Breast, medullary carcinoma of. See Medullary carcinoma of the breast Breast cancer, cutaneous. See Cutaneous breast cancer Breast cancer, estrogen-receptor-sensitive. See Estrogen-receptor-sensitive breast cancer Breast cancer in children and adolescents . . . . Breast cancer in men . . . . . . . . . . . . . . . Breast cancer in pregnant women . . . . . . . . Breast cancers . . . . . . . . . . . . . . . . . . Breast implants. . . . . . . . . . . . . . . . . . Breast reconstruction. . . . . . . . . . . . . . . Breast self-examination (BSE). . . . . . . . . . Breast ultrasound. . . . . . . . . . . . . . . . . Breslow’s staging . . . . . . . . . . . . . . . . Brief Pain Inventory (BPI) . . . . . . . . . . . . Brompton cocktail . . . . . . . . . . . . . . . . Bronchial adenomas . . . . . . . . . . . . . . . Bronchoalveolar lung cancer . . . . . . . . . . Bronchography. . . . . . . . . . . . . . . . . . Bronchoscopy . . . . . . . . . . . . . . . . . . BSE. See Breast self-examination Burkitt lymphoma . . . . . . . . . . . . . . . . 1,3-Butadiene . . . . . . . . . . . . . . . . . . 1,4-Butanediol dimethanesulfonate . . . . . . . BWS. See Beckwith-Wiedemann syndrome CA 15-3 test . CA 19-9 test . CA 27-29 test CA 125 test. . Cachexia . . .
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158 161 163 165 166 167 168
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180 182 184 185 188 190 193 194 195 196 196 197 197 199 199
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205 205 206 206 207
Complete List of Contents Cadmium and cadmium compounds. . . . . . . . Caffeine . . . . . . . . . . . . . . . . . . . . . . Calcifications of the breast. . . . . . . . . . . . . Calcium . . . . . . . . . . . . . . . . . . . . . . Cancell . . . . . . . . . . . . . . . . . . . . . . . Cancer biology . . . . . . . . . . . . . . . . . . . Cancer care team . . . . . . . . . . . . . . . . . . Cancer clusters . . . . . . . . . . . . . . . . . . . Cancer education. . . . . . . . . . . . . . . . . . Candidiasis . . . . . . . . . . . . . . . . . . . . . Carcinoembryonic antigen antibody (CEA) test . . . . . . . . . . . . . . . . . . . . . . . . Carcinogens, known . . . . . . . . . . . . . . . . Carcinogens, reasonably anticipated. . . . . . . . Carcinoid tumors and carcinoid syndrome . . . . Carcinoma of unknown primary origin (CUP) . . Carcinomas. . . . . . . . . . . . . . . . . . . . . Carcinomas, invasive ductal. See Invasive ductal carcinomas Carcinomas, invasive lobular. See Invasive lobular carcinomas Carcinomas, leptomeningeal. See Leptomeningeal carcinomas Carcinomatosis. . . . . . . . . . . . . . . . . . . Carcinomatous meningitis . . . . . . . . . . . . . Carcinosarcomas . . . . . . . . . . . . . . . . . . Cardiomyopathy in cancer patients . . . . . . . . Cardiopulmonary resuscitation (CPR) . . . . . . . Caregivers and caregiving . . . . . . . . . . . . . Caregiving, long-distance. See Long-distance caregiving Carney complex . . . . . . . . . . . . . . . . . . Carotenoids . . . . . . . . . . . . . . . . . . . . Cartilage supplements . . . . . . . . . . . . . . . Case management . . . . . . . . . . . . . . . . . Castleman disease . . . . . . . . . . . . . . . . . CBC. See Complete blood count CBE. See Clinical breast exam CDKN2A. See Cyclin-dependent kinase inhibitor-2A CEA test. See Carcinoembryonic antigen antibody test Cell phones. . . . . . . . . . . . . . . . . . . . . Cervical cancer. . . . . . . . . . . . . . . . . . . Chemoembolization . . . . . . . . . . . . . . . . Chemoprevention . . . . . . . . . . . . . . . . . Chemotherapy . . . . . . . . . . . . . . . . . . . Chemotherapy, cognitive effects of. See Cognitive effects of cancer and chemotherapy Chewing tobacco. . . . . . . . . . . . . . . . . . Childbirth and cancer . . . . . . . . . . . . . . .
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Childhood cancers . . . . . . . . . . . . . . . . Chlorambucil. . . . . . . . . . . . . . . . . . . 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)1-nitrosourea (MeCCNU) . . . . . . . . . . . Cholecystectomy . . . . . . . . . . . . . . . . . Chordomas . . . . . . . . . . . . . . . . . . . . Choriocarcinomas . . . . . . . . . . . . . . . . CHPP. See Continuous hyperthermic peritoneal perfusion Chromium hexavalent compounds. . . . . . . . Chromosomes and cancer . . . . . . . . . . . . Chronic lymphocytic leukemia (CLL) . . . . . . Chronic myeloid leukemia (CML). . . . . . . . Cigarettes and cigars . . . . . . . . . . . . . . . Clinical breast exam (CBE) . . . . . . . . . . . Clinical trials . . . . . . . . . . . . . . . . . . . CLL. See Chronic lymphocytic leukemia CML. See Chronic myeloid leukemia Coal tars and coal tar pitches . . . . . . . . . . Cobalt 60 radiation. . . . . . . . . . . . . . . . Coenzyme Q10. . . . . . . . . . . . . . . . . . Cognitive effects of cancer and chemotherapy . Coke oven emissions. . . . . . . . . . . . . . . Cold nodule . . . . . . . . . . . . . . . . . . . Colectomy . . . . . . . . . . . . . . . . . . . . Coloanal anastomosis . . . . . . . . . . . . . . Colon polyps . . . . . . . . . . . . . . . . . . . Colonoscopy and virtual colonoscopy . . . . . . Colony-stimulating factors (CSFs) . . . . . . . Colorectal cancer. . . . . . . . . . . . . . . . . Colorectal cancer screening . . . . . . . . . . . Colostomy . . . . . . . . . . . . . . . . . . . . Colposcopy. . . . . . . . . . . . . . . . . . . . Comedo carcinomas . . . . . . . . . . . . . . . Complementary and alternative therapies . . . . Complete blood count (CBC) . . . . . . . . . . Computed tomography (CT)-guided biopsy . . . . . . . . . . . . . . . . . . . . . Computed tomography (CT) scan . . . . . . . . Conization . . . . . . . . . . . . . . . . . . . . Continuous hyperthermic peritoneal perfusion (CHPP) . . . . . . . . . . . . . . . . . . . . Cordectomy . . . . . . . . . . . . . . . . . . . Cordotomy . . . . . . . . . . . . . . . . . . . . Core needle biopsy. . . . . . . . . . . . . . . . Corticosteroids . . . . . . . . . . . . . . . . . . Coughing . . . . . . . . . . . . . . . . . . . . . Counseling for cancer patients and survivors . . Cowden syndrome . . . . . . . . . . . . . . . . COX-2 inhibitors. See Cyclooxygenase 2 inhibitors
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288 289 289 290 292 292 293 294 296 297 299 300 304 306 308 309 309 312
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318 318 319 321 321 322 324 326
Salem Health: Cancer CPR. See Cardiopulmonary resuscitation Craniopharyngiomas . . . . . . . . . . . . Craniosynostosis . . . . . . . . . . . . . . Craniotomy. . . . . . . . . . . . . . . . . Crohn disease . . . . . . . . . . . . . . . Cruciferous vegetables . . . . . . . . . . . Cryoablation . . . . . . . . . . . . . . . . Cryptorchidism. . . . . . . . . . . . . . . CSFs. See Colony-stimulating factors CT scan. See Computed tomography scan CTCL. See Cutaneous T-cell lymphoma Culdoscopy. . . . . . . . . . . . . . . . . CUP. See Carcinoma of unknown primary origin Curcumin. . . . . . . . . . . . . . . . . . Cushing syndrome and cancer . . . . . . . Cutaneous breast cancer . . . . . . . . . . Cutaneous T-cell lymphoma (CTCL) . . .
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Cyclin-dependent kinase inhibitor-2A (CDKN2A). . . . . . . . . . . . . . . Cyclooxygenase 2 (COX-2) inhibitors . Cyclophosphamide. . . . . . . . . . . . Cyclosporin A . . . . . . . . . . . . . . Cystography . . . . . . . . . . . . . . . Cystoscopy . . . . . . . . . . . . . . . . Cytogenetics . . . . . . . . . . . . . . . Cytokines . . . . . . . . . . . . . . . . Cytology . . . . . . . . . . . . . . . . . Cytology, sputum. See Sputum cytology
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344 344 345 346 347 347 348 350 350
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D&C. See Dilation and curettage Dana-Farber Cancer Institute . . . . . . . . . . . . 354 DCIS. See Ductal carcinoma in situ DEA. See Diethanolamine DEHP. See Di(2-ethylhexyl) phthalate Delta-9-tetrahydrocannabinol . . . . . . . . . . . . 355
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Volume 2 Down syndrome and leukemia. . . . . . . . DPC4 gene testing . . . . . . . . . . . . . . DRE. See Digital rectal exam Drug resistance and multidrug resistance (MDR) . . . . . . . . . . . . . . . . . . . Dry mouth . . . . . . . . . . . . . . . . . . DSRCT. See Desmoplastic small round cell tumor Duct ectasia . . . . . . . . . . . . . . . . . Ductal carcinoma in situ (DCIS). . . . . . . Ductal lavage. . . . . . . . . . . . . . . . . Ductogram . . . . . . . . . . . . . . . . . . Duke Comprehensive Cancer Center . . . . Dukes’ classification . . . . . . . . . . . . . Duodenal carcinomas . . . . . . . . . . . . Dye, hair. See Hair dye Dysplastic nevus syndrome . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . xxxiii Complete List of Contents . . . . . . . . . . . . xxxvii Denys-Drash syndrome and cancer . . . . . . Depression . . . . . . . . . . . . . . . . . . . Dermatofibrosarcoma protuberans (DFSP) . . Dermatology oncology. . . . . . . . . . . . . DES. See Diethylstilbestrol Desmoid tumors . . . . . . . . . . . . . . . . Desmoplastic small round cell tumor (DSRCT) . . . . . . . . . . . . . . . . . . Developing nations and cancer . . . . . . . . DFSP. See Dermatofibrosarcoma protuberans Di(2-ethylhexyl) phthalate (DEHP) . . . . . . Diarrhea . . . . . . . . . . . . . . . . . . . . DIC. See Disseminated intravascular coagulation Dietary supplements . . . . . . . . . . . . . . Diethanolamine (DEA) . . . . . . . . . . . . Diethylstilbestrol (DES) . . . . . . . . . . . . Digital rectal exam (DRE) . . . . . . . . . . . Dilation and curettage (D&C) . . . . . . . . . Dioxins . . . . . . . . . . . . . . . . . . . . . Disseminated intravascular coagulation (DIC) . . . . . . . . . . . . . . . . . . . . Diverticulosis and diverticulitis . . . . . . . . DNR. See Do-not-resuscitate order Do-not-resuscitate (DNR) order . . . . . . . .
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Eaton-Lambert syndrome. See Lambert-Eaton myasthenic syndrome EBRT. See External beam radiation therapy Edema . . . . . . . . . . . . . . . . . . . . . Education, cancer. See Cancer education Elderly and cancer . . . . . . . . . . . . . . . Electrolarynx . . . . . . . . . . . . . . . . . . Electromagnetic radiation . . . . . . . . . . . Electroporation therapy . . . . . . . . . . . . Electrosurgery . . . . . . . . . . . . . . . . .
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396 399 399 400 401
Complete List of Contents Embolization . . . . . . . . . . . . . . . . . . . . Embryonal cell cancer . . . . . . . . . . . . . . . End-of-life care . . . . . . . . . . . . . . . . . . Endocrine cancers . . . . . . . . . . . . . . . . . Endocrinology oncology . . . . . . . . . . . . . . Endometrial cancer . . . . . . . . . . . . . . . . Endometrial hyperplasia . . . . . . . . . . . . . . Endorectal ultrasound . . . . . . . . . . . . . . . Endoscopic retrograde cholangiopancreatography (ERCP) . . . . . . . . . . . . . . . . . . . . . Endoscopy . . . . . . . . . . . . . . . . . . . . . Endoscopy, upper gastrointestinal. See Upper gastrointestinal endoscopy Endotheliomas . . . . . . . . . . . . . . . . . . . Enteritis . . . . . . . . . . . . . . . . . . . . . . Enterostomal therapy . . . . . . . . . . . . . . . Eosinophilic leukemia . . . . . . . . . . . . . . . Ependymomas . . . . . . . . . . . . . . . . . . . Epidemiology of cancer . . . . . . . . . . . . . . Epidermoid cancers of mucous membranes . . . . Epstein-Barr virus . . . . . . . . . . . . . . . . . ERCP. See Endoscopic retrograde cholangiopancreatography ERD. See Estrogen receptor downregulator Erionite. . . . . . . . . . . . . . . . . . . . . . . Erythroplakia. . . . . . . . . . . . . . . . . . . . Esophageal cancer . . . . . . . . . . . . . . . . . Esophageal speech . . . . . . . . . . . . . . . . . Esophagectomy . . . . . . . . . . . . . . . . . . Esophagitis . . . . . . . . . . . . . . . . . . . . . Essiac . . . . . . . . . . . . . . . . . . . . . . . Estrogen receptor downregulator (ERD) . . . . . Estrogen-receptor-sensitive breast cancer . . . . . Ethnicity and cancer . . . . . . . . . . . . . . . . Ethylene oxide . . . . . . . . . . . . . . . . . . . Ewing sarcoma . . . . . . . . . . . . . . . . . . . Exenteration . . . . . . . . . . . . . . . . . . . . Exercise and cancer . . . . . . . . . . . . . . . . External beam radiation therapy (EBRT) . . . . . Eye cancers . . . . . . . . . . . . . . . . . . . . Eyelid cancer. . . . . . . . . . . . . . . . . . . .
. . . . . . . .
Fallopian tube cancer . . . . . . . Family history and risk assessment Fanconi anemia . . . . . . . . . . Fatigue . . . . . . . . . . . . . . . Fecal occult blood test (FOBT) . . Fertility drugs and cancer . . . . . Fertility issues . . . . . . . . . . . Fever . . . . . . . . . . . . . . . . Fiber . . . . . . . . . . . . . . . .
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402 403 404 406 409 412 414 416
. 417 . 417
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420 421 422 424 425 426 429 431
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433 433 434 436 438 439 441 441 442 444 447 447 450 451 454 455 458
. . . . . . . . .
460 461 464 466 467 469 471 472 474 xli
Fibroadenomas . . . . . . . . . . . . . . . . Fibrocystic breast changes . . . . . . . . . . Fibrosarcomas, soft-tissue . . . . . . . . . . Financial issues . . . . . . . . . . . . . . . 5HIAA test. See 5-Hydroxyindoleacetic acid test 5Q minus syndrome . . . . . . . . . . . . . Flow cytometry . . . . . . . . . . . . . . . FOBT. See Fecal occult blood test Folic acid. . . . . . . . . . . . . . . . . . . Formaldehyde . . . . . . . . . . . . . . . . Fox Chase Cancer Center . . . . . . . . . . Fred Hutchinson Cancer Research Center . . Free radicals . . . . . . . . . . . . . . . . . Fruits . . . . . . . . . . . . . . . . . . . . .
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475 476 478 481
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486 486 487 488 490 491
Gallbladder cancer . . . . . . . . . . . . . . Gallium scan . . . . . . . . . . . . . . . . . Gamma Knife . . . . . . . . . . . . . . . . Gardner syndrome . . . . . . . . . . . . . . Garlic and allicin . . . . . . . . . . . . . . . Gastric polyps . . . . . . . . . . . . . . . . Gastrinomas . . . . . . . . . . . . . . . . . Gastrointestinal cancers . . . . . . . . . . . Gastrointestinal complications of cancer treatment. . . . . . . . . . . . . . . . . . Gastrointestinal oncology . . . . . . . . . . Gastrointestinal stromal tumors (GISTs) . . GCTs. See Giant cell tumors Gene therapy . . . . . . . . . . . . . . . . . Genetic counseling . . . . . . . . . . . . . . Genetic testing . . . . . . . . . . . . . . . . Genetics of cancer . . . . . . . . . . . . . . Geography and cancer . . . . . . . . . . . . Germ-cell tumors . . . . . . . . . . . . . . Gerson therapy . . . . . . . . . . . . . . . . Gestational trophoblastic tumors (GTTs) . . Giant cell tumors (GCTs) . . . . . . . . . . Ginseng, panax. . . . . . . . . . . . . . . . GISTs. See Gastrointestinal stromal tumors Gleason grading system . . . . . . . . . . . Gliomas . . . . . . . . . . . . . . . . . . . Glomus tumors . . . . . . . . . . . . . . . . Glossectomy . . . . . . . . . . . . . . . . . Glutamine . . . . . . . . . . . . . . . . . . Gonioscopy . . . . . . . . . . . . . . . . . Grading of tumors . . . . . . . . . . . . . . Graft-versus-host disease (GVHD) . . . . . Granulosa cell tumors . . . . . . . . . . . . Green tea . . . . . . . . . . . . . . . . . . . Grief and bereavement . . . . . . . . . . . .
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493 495 497 498 499 500 501 502
. . . . 484 . . . . 484
. . . . 506 . . . . 508 . . . . 511 . . . . . . . . . .
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512 515 517 519 522 525 527 527 530 531
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532 533 534 535 536 536 537 538 540 540 541
Salem Health: Cancer GTTs. See Gestational trophoblastic tumors GVHD. See Graft-versus-host disease Gynecologic cancers . . . . . . . . . . . . . . . . . 543 Gynecologic oncology . . . . . . . . . . . . . . . . 547 H. pylori. See Helicobacter pylori HAI. See Hepatic arterial infusion Hair dye . . . . . . . . . . . . . . . . . . . . . . Hairy cell leukemia . . . . . . . . . . . . . . . . Hand-foot syndrome (HFS) . . . . . . . . . . . . HBV. See Hepatitis B virus HCG. See Human chorionic gonadotropin HCV. See Hepatitis C virus Head and neck cancers . . . . . . . . . . . . . . . Health maintenance organizations (HMOs) . . . . Helicobacter pylori. . . . . . . . . . . . . . . . . Hemangioblastomas . . . . . . . . . . . . . . . . Hemangiopericytomas . . . . . . . . . . . . . . . Hemangiosarcomas . . . . . . . . . . . . . . . . Hematemesis . . . . . . . . . . . . . . . . . . . . Hematologic oncology . . . . . . . . . . . . . . . Hematuria . . . . . . . . . . . . . . . . . . . . . Hemochromatosis . . . . . . . . . . . . . . . . . Hemolytic anemia . . . . . . . . . . . . . . . . . Hemoptysis. . . . . . . . . . . . . . . . . . . . . Hemorrhoids . . . . . . . . . . . . . . . . . . . . Hepatic arterial infusion (HAI) . . . . . . . . . . Hepatitis B virus (HBV) . . . . . . . . . . . . . . Hepatitis C virus (HCV) . . . . . . . . . . . . . . Hepatomegaly . . . . . . . . . . . . . . . . . . . HER2/neu protein . . . . . . . . . . . . . . . . . Herbs as antioxidants . . . . . . . . . . . . . . . Hereditary cancer syndromes . . . . . . . . . . . Hereditary diffuse gastric cancer . . . . . . . . . Hereditary leiomyomatosis and renal cell cancer (HLRCC) . . . . . . . . . . . . . . . . Hereditary mixed polyposis syndrome . . . . . . Hereditary non-VHL clear cell renal cell carcinomas . . . . . . . . . . . . . . . . . . . Hereditary pancreatitis . . . . . . . . . . . . . . . Hereditary papillary renal cell carcinomas . . . . Hereditary polyposis syndromes . . . . . . . . . . Herpes simplex virus. . . . . . . . . . . . . . . . Herpes zoster virus. . . . . . . . . . . . . . . . . HFS. See Hand-foot syndrome Hispanics and cancer. See Latinos/Hispanics and cancer Histamine 2 antagonists . . . . . . . . . . . . . . Histiocytosis X . . . . . . . . . . . . . . . . . . . HIV/AIDS-related cancers . . . . . . . . . . . . .
HLRCC. See Hereditary leiomyomatosis and renal cell cancer HMOs. See Health maintenance organizations Hodgkin disease . . . . . . . . . . . . . . . . . Home health services . . . . . . . . . . . . . . Hormonal therapies . . . . . . . . . . . . . . . Hormone receptor tests . . . . . . . . . . . . . Hormone replacement therapy (HRT) . . . . . . Horner syndrome. . . . . . . . . . . . . . . . . Hospice care . . . . . . . . . . . . . . . . . . . Hot flashes . . . . . . . . . . . . . . . . . . . . HPV. See Human papillomavirus HRAS gene testing . . . . . . . . . . . . . . . . HRT. See Hormone replacement therapy HTLV. See Human T-cell leukemia virus Human chorionic gonadotropin (HCG) . . . . . Human growth factors and tumor growth . . . . Human immunodeficiency virus-related cancers. See HIV/AIDS-related cancers Human papillomavirus (HPV) . . . . . . . . . . Human T-cell leukemia virus (HTLV) . . . . . Hydatidiform mole . . . . . . . . . . . . . . . . 5-Hydroxyindoleacetic acid (5HIAA) test . . . . Hypercalcemia . . . . . . . . . . . . . . . . . . Hypercoagulation disorders . . . . . . . . . . . Hyperthermia therapy . . . . . . . . . . . . . . Hyperthermic perfusion . . . . . . . . . . . . . Hypopharyngeal cancer . . . . . . . . . . . . . Hysterectomy . . . . . . . . . . . . . . . . . . Hysterography . . . . . . . . . . . . . . . . . . Hystero-oophorectomy. . . . . . . . . . . . . . Hysteroscopy. . . . . . . . . . . . . . . . . . .
. 550 . 550 . 552
. . . . . . . . . . . . . . . . . . . . .
554 557 558 559 559 560 561 562 564 565 566 566 567 568 569 570 571 573 573 574 576
IEP. See Immunoelectrophoresis iFOBT. See Immunochemical fecal occult blood test Ileostomy. . . . . . . . . . . . . . . . . . . . . Imaging tests . . . . . . . . . . . . . . . . . . . Immune response to cancer . . . . . . . . . . . Immunochemical fecal occult blood test (iFOBT) . . . . . . . . . . . . . . . . . . . . Immunocytochemistry and immunohistochemistry . . . . . . . . . . . . Immunoelectrophoresis (IEP) . . . . . . . . . . Immunotherapy . . . . . . . . . . . . . . . . . IMRT. See Intensity-modulated radiation therapy Indoles . . . . . . . . . . . . . . . . . . . . . . Infection and sepsis . . . . . . . . . . . . . . . Infectious cancers . . . . . . . . . . . . . . . . Infertility and cancer . . . . . . . . . . . . . . .
. 577 . 579 . . . . . .
580 580 581 582 584 586
. 587 . 588 . 590 xlii
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593 597 599 601 603 605 606 608
. . 609
. . 609 . . 610
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611 612 612 613 614 615 617 618 619 620 621 622 623
. . 625 . . 626 . . 629 . . 632 . . 633 . . 634 . . 635
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638 638 641 643
Complete List of Contents Inflammatory bowel disease . . . . . . . . . . Informed consent. . . . . . . . . . . . . . . . Infusion therapies . . . . . . . . . . . . . . . Insurance . . . . . . . . . . . . . . . . . . . . Integrative oncology . . . . . . . . . . . . . . Intensity-modulated radiation therapy (IMRT) Interferon. . . . . . . . . . . . . . . . . . . . Interleukins. . . . . . . . . . . . . . . . . . . Invasive cancer. . . . . . . . . . . . . . . . . Invasive ductal carcinomas . . . . . . . . . . Invasive lobular carcinomas . . . . . . . . . . Ionizing radiation . . . . . . . . . . . . . . . Iridium seeds . . . . . . . . . . . . . . . . . . Islet cell tumors . . . . . . . . . . . . . . . . Isoflavones . . . . . . . . . . . . . . . . . . . Itching . . . . . . . . . . . . . . . . . . . . .
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645 646 647 648 651 652 653 654 655 656 657 657 658 659 661 661
Lambert-Eaton myasthenic syndrome (LEMS) Laparoscopy and laparoscopic surgery . . . . Laryngeal cancer . . . . . . . . . . . . . . . . Laryngeal nerve palsy . . . . . . . . . . . . . Laryngectomy . . . . . . . . . . . . . . . . . Laryngoscopy . . . . . . . . . . . . . . . . . Laser therapies . . . . . . . . . . . . . . . . . Latinos/Hispanics and cancer . . . . . . . . . Laxatives . . . . . . . . . . . . . . . . . . . . LCIS. See Lobular carcinoma in situ LDH test. See Lactate dehydrogenase test Leiomyomas . . . . . . . . . . . . . . . . . . Leiomyosarcomas . . . . . . . . . . . . . . . LEMS. See Lambert-Eaton myasthenic syndrome Leptomeningeal carcinomas . . . . . . . . . . Leukapharesis . . . . . . . . . . . . . . . . . Leukemia, Down syndrome and. See Down syndrome and leukemia Leukemia, eosinophilic. See Eosinophilic leukemia Leukemia, hairy cell. See Hairy cell leukemia Leukemias . . . . . . . . . . . . . . . . . . . Leukoencephalopathy . . . . . . . . . . . . . Leukopenia. . . . . . . . . . . . . . . . . . . Leukoplakia . . . . . . . . . . . . . . . . . . Leydig cell tumors . . . . . . . . . . . . . . . Li-Fraumeni syndrome (LFS) . . . . . . . . . Limb salvage . . . . . . . . . . . . . . . . . . Linear accelerator . . . . . . . . . . . . . . . Lip cancers . . . . . . . . . . . . . . . . . . . Liposarcomas . . . . . . . . . . . . . . . . . Liver biopsy . . . . . . . . . . . . . . . . . . Liver cancers . . . . . . . . . . . . . . . . . .
Jonsson Comprehensive Cancer Center (JCCC) . . . . . . . . . . . . . . . . . . . . . . 664 Journaling . . . . . . . . . . . . . . . . . . . . . . 665 Juvenile polyposis syndrome . . . . . . . . . . . . 665 Kaposi sarcoma . . . . . . . . . . . . . Karnofsky performance status (KPS) . . Keratosis . . . . . . . . . . . . . . . . . Ki67 test . . . . . . . . . . . . . . . . . Kidney cancer . . . . . . . . . . . . . . Klinefelter syndrome and cancer . . . . KPS. See Karnofsky performance status Krukenberg tumors . . . . . . . . . . .
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667 669 670 670 671 674
. . . . . . 675
Lacrimal gland tumors . . . . . . . . . . . . . . . . 677 Lactate dehydrogenase (LDH) test . . . . . . . . . 678 Laetrile . . . . . . . . . . . . . . . . . . . . . . . . 679
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679 681 682 685 686 687 688 690 692
. . . 693 . . . 694
. . . 696 . . . 698
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698 702 704 704 706 706 708 709 710 712 714 715
Volume 3 Lumps . . . . . . . . . . . . . . Lung cancer, brochoalveolar. See Bronchoalveolar lung cancer Lung cancers . . . . . . . . . . . Lutein . . . . . . . . . . . . . . Lycopene . . . . . . . . . . . . . Lymphadenectomy. . . . . . . . Lymphangiography . . . . . . . Lymphangiosarcomas . . . . . . Lymphedema. . . . . . . . . . . Lymphocytosis . . . . . . . . . . Lymphomas . . . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . . . lv Complete List of Contents . . . . . . . . . . . . . . lix Living will . . . . . . . . . . . . . . . . . Living with cancer . . . . . . . . . . . . . Lobectomy . . . . . . . . . . . . . . . . . Lobular carcinoma in situ (LCIS) . . . . . Long-distance caregiving . . . . . . . . . Loop electrosurgical excisional procedure (LEEP) . . . . . . . . . . . . . . . . . Lumbar puncture . . . . . . . . . . . . . . Lumpectomy . . . . . . . . . . . . . . . .
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719 720 723 725 726
. . . . . 727 . . . . . 728 . . . . . 730 xliii
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733 737 737 738 740 741 742 743 744
Salem Health: Cancer M. D. Anderson Cancer Center . . . . . . . . . Macrobiotic diet . . . . . . . . . . . . . . . . . Magnetic resonance imaging (MRI) . . . . . . . Malignant fibrous histiocytoma (MFH) . . . . . Malignant rhabdoid tumor of the kidney . . . . Malignant tumors . . . . . . . . . . . . . . . . MALT lymphomas. See Mucosa-associated lymphoid tissue lymphomas Mammography . . . . . . . . . . . . . . . . . . Managed care . . . . . . . . . . . . . . . . . . Mantle cell lymphoma (MCL) . . . . . . . . . . Mastectomy . . . . . . . . . . . . . . . . . . . Mastocytomas . . . . . . . . . . . . . . . . . . Matrix metalloproteinase inhibitors . . . . . . . Mayo Clinic Cancer Center . . . . . . . . . . . MCC. See Merkel cell carcinomas MCL. See Mantle cell lymphoma MDR. See Drug resistance and multidrug resistance Mediastinal tumors. . . . . . . . . . . . . . . . Mediastinoscopy . . . . . . . . . . . . . . . . . Medical marijuana . . . . . . . . . . . . . . . . Medical oncology . . . . . . . . . . . . . . . . Medicare and cancer . . . . . . . . . . . . . . . Medullary carcinoma of the breast. . . . . . . . Medulloblastomas . . . . . . . . . . . . . . . . Melanomas . . . . . . . . . . . . . . . . . . . . Melphalan . . . . . . . . . . . . . . . . . . . . Memorial Sloan-Kettering Cancer Center . . . . MEN 1. See Multiple endocrine neoplasia type 1 MEN 2. See Multiple endocrine neoplasia type 2 Meningeal carcinomatosis . . . . . . . . . . . . Meningiomas. . . . . . . . . . . . . . . . . . . Merkel cell carcinomas (MCC) . . . . . . . . . Mesenchymomas, malignant. . . . . . . . . . . Mesothelioma . . . . . . . . . . . . . . . . . . Metastasis . . . . . . . . . . . . . . . . . . . . Metastatic squamous neck cancer with occult primary . . . . . . . . . . . . . . . . . . . . MFH. See Malignant fibrous histiocytoma Microcalcifications. . . . . . . . . . . . . . . . Microwave hyperthermia therapy . . . . . . . . Mineral oils . . . . . . . . . . . . . . . . . . . Mistletoe . . . . . . . . . . . . . . . . . . . . . Mitochondrial DNA mutations. . . . . . . . . . MLH1 gene. . . . . . . . . . . . . . . . . . . . Mohs surgery. . . . . . . . . . . . . . . . . . . Molecular oncology . . . . . . . . . . . . . . . Moles. . . . . . . . . . . . . . . . . . . . . . . Monoclonal antibodies . . . . . . . . . . . . . . Motion sickness devices . . . . . . . . . . . . .
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748 750 750 752 753 754
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754 757 759 761 763 764 765
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766 768 768 770 772 774 775 776 779 780
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MRI. See Magnetic resonance imaging MSH genes . . . . . . . . . . . . . . . . . . . . Mucinous carcinomas . . . . . . . . . . . . . . Mucosa-associated lymphoid tissue (MALT) lymphomas . . . . . . . . . . . . . . . . . . Mucositis . . . . . . . . . . . . . . . . . . . . . Mucous membranes, epidermoid cancers of. See Epidermoid cancers of mucous membranes Multiple endocrine neoplasia type 1 (MEN 1). . Multiple endocrine neoplasia type 2 (MEN 2). . Multiple myeloma . . . . . . . . . . . . . . . . Mustard gas . . . . . . . . . . . . . . . . . . . Mutagenesis and cancer . . . . . . . . . . . . . Myasthenia gravis . . . . . . . . . . . . . . . . MYC oncogene . . . . . . . . . . . . . . . . . . Mycosis fungoides . . . . . . . . . . . . . . . . Myelodysplastic syndromes . . . . . . . . . . . Myelofibrosis . . . . . . . . . . . . . . . . . . Myeloma . . . . . . . . . . . . . . . . . . . . . Myeloproliferative disorders. . . . . . . . . . . Myelosuppression . . . . . . . . . . . . . . . . 2-Naphthylamine. . . . . . . . . . . . . . . . Nasal cavity and paranasal sinus cancers . . . National Cancer Institute (NCI) . . . . . . . . National Science Foundation (NSF) . . . . . . Native North Americans and cancer . . . . . . Nausea and vomiting. . . . . . . . . . . . . . NCI. See National Cancer Institute Needle biopsies . . . . . . . . . . . . . . . . Needle localization. . . . . . . . . . . . . . . Nephroblastomas. . . . . . . . . . . . . . . . Nephrostomy . . . . . . . . . . . . . . . . . . Neuroblastomas . . . . . . . . . . . . . . . . Neuroectodermal tumors. . . . . . . . . . . . Neuroendocrine tumors . . . . . . . . . . . . Neurofibromatosis type 1 (NF1) . . . . . . . . Neurologic oncology. . . . . . . . . . . . . . Neutropenia . . . . . . . . . . . . . . . . . . NF1. See Neurofibromatosis type 1 Nickel compounds and metallic nickel . . . . Night sweats . . . . . . . . . . . . . . . . . . Nijmegen breakage syndrome . . . . . . . . . Nipple discharge . . . . . . . . . . . . . . . . Non-Hodgkin lymphoma . . . . . . . . . . . Nonsteroidal anti-inflammatory drugs (NSAIDs) . . . . . . . . . . . . . . . . . . NSAIDs. See Nonsteroidal anti-inflammatory drugs NSF. See National Science Foundation Nuclear medicine scan . . . . . . . . . . . . .
781 782 783 785 786 788
. . 790 . . . . . . . . . . .
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790 791 792 793 794 795 796 796 798 800 802 xliv
. . 803 . . 803 . . 804 . . 806
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807 808 809 812 813 815 817 817 819 820 822 823 825
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826 826 829 830 832 834
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836 838 839 839 841 842 844 845 847 849
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851 852 853 854 855
. . . 858
. . . 859
Complete List of Contents Pediatric oncology and hematology . . . . . . . . . 938 Pelvic examination . . . . . . . . . . . . . . . . . . 940 Penile cancer . . . . . . . . . . . . . . . . . . . . . 941 Percutaneous transhepatic cholangiography (PTHC) . . . . . . . . . . . . . . . . . . . . . . 943 Pericardial effusion . . . . . . . . . . . . . . . . . 944 Pericardiocentesis . . . . . . . . . . . . . . . . . . 946 Peritoneovenous shunts . . . . . . . . . . . . . . . 946 Personality and cancer . . . . . . . . . . . . . . . . 947 Pesticides and the food chain . . . . . . . . . . . . 948 PET. See Positron emission tomography Peutz-Jeghers syndrome (PJS) . . . . . . . . . . . . 951 Pharmacy oncology . . . . . . . . . . . . . . . . . 952 Phenacetin . . . . . . . . . . . . . . . . . . . . . . 955 Phenolics . . . . . . . . . . . . . . . . . . . . . . . 955 Pheochromocytomas . . . . . . . . . . . . . . . . . 956 Pheresis . . . . . . . . . . . . . . . . . . . . . . . 958 Photodynamic therapy (PDT) . . . . . . . . . . . . 959 Phyllodes tumors. . . . . . . . . . . . . . . . . . . 960 Phytoestrogens . . . . . . . . . . . . . . . . . . . . 962 Pineoblastomas. . . . . . . . . . . . . . . . . . . . 963 Pituitary tumors . . . . . . . . . . . . . . . . . . . 965 PJS. See Peutz-Jeghers syndrome Placental alkaline phosphatase (PALP) . . . . . . . 968 Plant alkaloids and terpenoids in chemotherapy . . . . . . . . . . . . . . . . . . . 968 Plasticizers . . . . . . . . . . . . . . . . . . . . . . 971 Pleural biopsy . . . . . . . . . . . . . . . . . . . . 972 Pleural effusion . . . . . . . . . . . . . . . . . . . 973 Pleurodesis . . . . . . . . . . . . . . . . . . . . . . 975 Pleuropulmonary blastomas . . . . . . . . . . . . . 975 PMS genes . . . . . . . . . . . . . . . . . . . . . . 976 Pneumonectomy . . . . . . . . . . . . . . . . . . . 977 Pneumonia . . . . . . . . . . . . . . . . . . . . . . 979 Polycyclic aromatic hydrocarbons . . . . . . . . . . 981 Polycythemia vera . . . . . . . . . . . . . . . . . . 981 Polypectomy . . . . . . . . . . . . . . . . . . . . . 982 Polyps . . . . . . . . . . . . . . . . . . . . . . . . 983 Polyps, colon. See Colon polyps Polyps, gastric. See Gastric polyps Positron emission tomography (PET) . . . . . . . . 984 Poverty and cancer . . . . . . . . . . . . . . . . . . 987 PPOs. See Preferred provider organizations Prayer and cancer support . . . . . . . . . . . . . . 989 Preferred provider organizations (PPOs) . . . . . . 990 Pregnancy and cancer . . . . . . . . . . . . . . . . 992 Premalignancies . . . . . . . . . . . . . . . . . . . 994 Prevent Cancer Foundation . . . . . . . . . . . . . 997 Prevention . . . . . . . . . . . . . . . . . . . . . . 999 Primary care physician . . . . . . . . . . . . . . . 1001
Nutrition and cancer prevention . . . . . . . . . . . 861 Nutrition and cancer treatment. . . . . . . . . . . . 864 Obesity-associated cancers . . . . . Occupational exposures and cancer . Occupational therapy . . . . . . . . OCs. See Organochlorines Oligodendrogliomas . . . . . . . . . Omega-3 fatty acids . . . . . . . . . Ommaya reservoir . . . . . . . . . . Oncogenes . . . . . . . . . . . . . . Oncogenic viruses . . . . . . . . . . Oncology . . . . . . . . . . . . . . . Oncology clinical nurse specialist . . Oncology social worker . . . . . . . Oophorectomy . . . . . . . . . . . . Ophthalmic oncology . . . . . . . . Opioids . . . . . . . . . . . . . . . . Oral and maxillofacial surgery. . . . Oral and oropharyngeal cancers . . . Orbit tumors . . . . . . . . . . . . . Orchiectomy . . . . . . . . . . . . . Organ transplantation and cancer . . Organochlorines (OCs) . . . . . . . Oropharyngeal cancers. See Oral and oropharyngeal cancers Orthopedic surgery. . . . . . . . . . Otolaryngology . . . . . . . . . . . Ovarian cancers . . . . . . . . . . . Ovarian cysts. . . . . . . . . . . . . Ovarian epithelial cancer . . . . . . Overtreatment . . . . . . . . . . . .
. . . . . . . . 868 . . . . . . . . 871 . . . . . . . . 873 . . . . . . . . . . . . . . . . .
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875 877 878 878 881 882 885 887 888 889 892 893 894 897 898 899 901
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902 903 905 908 909 911
Paget disease of bone . . . . . . . . . . . . . Pain management medications. . . . . . . . . Palliative treatment . . . . . . . . . . . . . . PALP. See Placental alkaline phosphatase Palpation . . . . . . . . . . . . . . . . . . . . Pancolitis . . . . . . . . . . . . . . . . . . . . Pancreatectomy . . . . . . . . . . . . . . . . Pancreatic cancers . . . . . . . . . . . . . . . Pancreatitis . . . . . . . . . . . . . . . . . . . Pap test . . . . . . . . . . . . . . . . . . . . . Paracentesis . . . . . . . . . . . . . . . . . . Paranasal sinus cancers. See Nasal cavity and paranasal sinus cancers Paraneoplastic syndromes . . . . . . . . . . . Parathyroid cancer . . . . . . . . . . . . . . . Pathology . . . . . . . . . . . . . . . . . . . PC-SPES . . . . . . . . . . . . . . . . . . . . PDT. See Photodynamic therapy
. . . 912 . . . 914 . . . 917 . . . . . . .
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920 920 921 923 927 928 929
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931 932 934 937 xlv
Salem Health: Cancer Primary central nervous system lymphomas . . . . . . . . . . . . . . . . Progesterone receptor assay . . . . . . . . Prostate cancer . . . . . . . . . . . . . . . Prostate-specific antigen (PSA) test . . . . Prostatectomy. . . . . . . . . . . . . . . . Prostatitis . . . . . . . . . . . . . . . . . . Proteasome inhibitors. . . . . . . . . . . . Protein electrophoresis . . . . . . . . . . . Proteomics and cancer research . . . . . . Proton beam therapy . . . . . . . . . . . . Proto-oncogenes and carcinogenesis . . . . PSA test. See Prostate-specific antigen test Psycho-oncology . . . . . . . . . . . . . . Psychosocial aspects of cancer . . . . . . . PTHC. See Percutaneous transhepatic cholangiography Radiation, ionizing. See Ionizing radiation Radiation oncology . . . . . . . . . . . . . Radiation therapies . . . . . . . . . . . . . Radiation therapy, afterloading. See Afterloading radiation therapy Radical neck dissection . . . . . . . . . . . Radiofrequency ablation . . . . . . . . . . Radionuclide scan . . . . . . . . . . . . . Radiopharmaceuticals . . . . . . . . . . . Radon . . . . . . . . . . . . . . . . . . . . RB1 gene . . . . . . . . . . . . . . . . . . Receptor analysis . . . . . . . . . . . . . .
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1003 1003 1004 1006 1008 1009 1010 1010 1012 1014 1015
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1027 1027 1030 1030 1032 1032 1033
Reconstructive surgery . . . . . . . . . . . . . . Rectal cancer . . . . . . . . . . . . . . . . . . . Recurrence . . . . . . . . . . . . . . . . . . . . Rehabilitation . . . . . . . . . . . . . . . . . . . Relationships . . . . . . . . . . . . . . . . . . . Renal pelvis tumors. . . . . . . . . . . . . . . . Report on Carcinogens (RoC) . . . . . . . . . . Resveratrol . . . . . . . . . . . . . . . . . . . . Retinoblastomas . . . . . . . . . . . . . . . . . Rhabdomyosarcomas . . . . . . . . . . . . . . . RhoGD12 gene . . . . . . . . . . . . . . . . . . Richter syndrome . . . . . . . . . . . . . . . . . Risk assessment, family history and. See Family history and risk assessment Risks for cancer. . . . . . . . . . . . . . . . . . Robert H. Lurie Cancer Center . . . . . . . . . . RoC. See Report on Carcinogens Rothmund-Thomson syndrome . . . . . . . . . .
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Salivary gland cancer . . . . . . . . . . . . . Salpingectomy and salpingo-oophorectomy . Sarcomas, soft-tissue . . . . . . . . . . . . . Saw palmetto . . . . . . . . . . . . . . . . . Schwannoma tumors . . . . . . . . . . . . . SCLC1 gene. . . . . . . . . . . . . . . . . . Screening, colorectal cancer. See Colorectal cancer screening Screening for cancer . . . . . . . . . . . . . Second opinions . . . . . . . . . . . . . . . Self-image and body image. . . . . . . . . .
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1034 1036 1038 1038 1041 1043 1044 1045 1046 1048 1050 1050
. 1052 . 1054 . 1056 1058 1060 1062 1065 1066 1067
. . . 1067 . . . 1070 . . . 1071
Volume 4 Sjögren syndrome. . . . . . . . . . . . . . . . Skin cancers . . . . . . . . . . . . . . . . . . SLN biopsy and mapping. See Sentinel lymph node biopsy and mapping Small intestine cancer . . . . . . . . . . . . . Smoking cessation . . . . . . . . . . . . . . . Social Security Disability Insurance (SSDI) . . Soft-tissue fibrosarcomas. See Fibrosarcomas, soft-tissue Soots . . . . . . . . . . . . . . . . . . . . . . Soy foods . . . . . . . . . . . . . . . . . . . . Spermatocytomas . . . . . . . . . . . . . . . . Spinal axis tumors . . . . . . . . . . . . . . . Spinal cord compression . . . . . . . . . . . . Splenectomy . . . . . . . . . . . . . . . . . . Sputum cytology . . . . . . . . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . lxxvii Complete List of Contents . . . . . . . . . . . . . lxxix Sentinel lymph node (SLN) biopsy and mapping . . . . . . . . . . . . . . . Sepsis. See Infection and sepsis Sertoli cell tumors . . . . . . . . . . . Sexuality and cancer . . . . . . . . . . Sézary syndrome . . . . . . . . . . . . SIADH. See Syndrome of inappropriate antidiuretic hormone production Side effects . . . . . . . . . . . . . . . Sigmoidoscopy . . . . . . . . . . . . . Silica, crystalline . . . . . . . . . . . . Simian virus 40 . . . . . . . . . . . . . Singlehood and cancer . . . . . . . . .
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1078 1082 1083 1084 1084 xlvi
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1097 1098 1099 1100 1102 1103 1105
Complete List of Contents Squamous cell carcinomas . . . . . . . . . . . SRS. See Stereotactic radiosurgery SSDI. See Social Security Disability Insurance Staging of cancer . . . . . . . . . . . . . . . . Statistics of cancer . . . . . . . . . . . . . . . Stem cell transplantation . . . . . . . . . . . . Stent therapy . . . . . . . . . . . . . . . . . . Stereotactic needle biopsy . . . . . . . . . . . Stereotactic radiosurgery (SRS) . . . . . . . . Sterility . . . . . . . . . . . . . . . . . . . . . Stomach cancers . . . . . . . . . . . . . . . . Stomatitis . . . . . . . . . . . . . . . . . . . . Stress management . . . . . . . . . . . . . . . Sunlamps . . . . . . . . . . . . . . . . . . . . Sun’s soup . . . . . . . . . . . . . . . . . . . Sunscreens . . . . . . . . . . . . . . . . . . . Superior vena cava syndrome . . . . . . . . . Support groups . . . . . . . . . . . . . . . . . Surgical biopsies . . . . . . . . . . . . . . . . Surgical oncology. . . . . . . . . . . . . . . . Survival rates . . . . . . . . . . . . . . . . . . Survivorship issues . . . . . . . . . . . . . . . Symptoms and cancer. . . . . . . . . . . . . . Syndrome of inappropriate antidiuretic hormone production (SIADH) . . . . . . . . Synovial sarcomas . . . . . . . . . . . . . . . Taste alteration . . . . . . . . . . . . . . Teratocarcinomas . . . . . . . . . . . . . Teratomas . . . . . . . . . . . . . . . . . Testicular cancer . . . . . . . . . . . . . Testicular self-examination (TSE) . . . . Thermal imaging . . . . . . . . . . . . . Thiotepa. . . . . . . . . . . . . . . . . . Thoracentesis . . . . . . . . . . . . . . . Thoracoscopy . . . . . . . . . . . . . . . Thoracotomy . . . . . . . . . . . . . . . Throat cancer . . . . . . . . . . . . . . . Thrombocytopenia . . . . . . . . . . . . Thymomas . . . . . . . . . . . . . . . . Thymus cancer . . . . . . . . . . . . . . Thyroid cancer . . . . . . . . . . . . . . Thyroid nuclear medicine scan . . . . . . TNF. See Tumor necrosis factor TNM staging . . . . . . . . . . . . . . . Tobacco, chewing. See Chewing tobacco Tobacco-related cancers . . . . . . . . . Topoisomerase inhibitors . . . . . . . . . TP53 protein . . . . . . . . . . . . . . . Tracheostomy . . . . . . . . . . . . . . . Transfusion therapy. . . . . . . . . . . .
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Transitional care . . . . . . . . . . . Transitional cell carcinomas . . . . . Transrectal ultrasound . . . . . . . . Transvaginal ultrasound . . . . . . . Trichilemmal carcinomas. . . . . . . TSE. See Testicular self-examination Tuberous sclerosis . . . . . . . . . . Tubular carcinomas . . . . . . . . . . Tumor flare . . . . . . . . . . . . . . Tumor lysis syndrome . . . . . . . . Tumor markers . . . . . . . . . . . . Tumor necrosis factor (TNF) . . . . . Tumor-suppressor genes . . . . . . . Turcot syndrome . . . . . . . . . . . Tyrosine kinase inhibitors . . . . . .
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1108 1111 1114 1116 1118 1119 1120 1121 1124 1125 1127 1128 1129 1130 1132 1135 1138 1140 1143 1144
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1151 1152 1153 1154 1156 1157 1158 1158 1160 1161 1162 1164 1166 1167 1169 1172
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1182 1183 1185 1186 1187
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1187 1188 1189 1189 1191 1193 1194 1195 1196
Ultrasound, breast. See Breast ultrasound Ultrasound, endorectal. See Endorectal ultrasound Ultrasound, transrectal. See Transrectal ultrasound Ultrasound, transvaginal. See Transvaginal ultrasound Ultrasound tests . . . . . . . . . . . . . . . Ultraviolet radiation and related exposures Umbilical cord blood transplantation. . . . Upper gastrointestinal (GI) endoscopy . . . Upper gastrointestinal (GI) series . . . . . Urethral cancer . . . . . . . . . . . . . . . Urinalysis . . . . . . . . . . . . . . . . . . Urinary system cancers . . . . . . . . . . . Urography . . . . . . . . . . . . . . . . . Urologic oncology . . . . . . . . . . . . . Urostomy . . . . . . . . . . . . . . . . . . Uterine cancer . . . . . . . . . . . . . . .
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1199 1200 1201 1202 1203 1205 1207 1209 1213 1214 1216 1217
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1220 1221 1223 1225 1226
Vaccines, preventive . . . . . . . . . . . Vaccines, therapeutic . . . . . . . . . . . Vaginal cancer . . . . . . . . . . . . . . Vascular access tubes. . . . . . . . . . . Vasectomy and cancer . . . . . . . . . . Vegetables, cruciferous. See Cruciferous vegetables Veterinary oncology . . . . . . . . . . . VHL disease. See Von Hippel-Lindau disease Vinyl chloride . . . . . . . . . . . . . . Viral oncology . . . . . . . . . . . . . . Virus-related cancers . . . . . . . . . . . Von Hippel-Lindau (VHL) disease. . . . Vulvar cancer . . . . . . . . . . . . . . .
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1174 1175 1177 1179 1180 xlvii
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1230 1230 1232 1235 1237
Salem Health: Cancer WAGR syndrome. See Wilms’ tumor aniridiagenitourinary anomalies-mental retardation syndrome and cancer Waldenström macroglobulinemia (WM) . . . . . . 1240 Watchful waiting . . . . . . . . . . . . . . . . . . 1242 Weight loss . . . . . . . . . . . . . . . . . . . . . 1243 Wilms’ tumor . . . . . . . . . . . . . . . . . . . . 1245 Wilms’ tumor aniridia-genitourinary anomaliesmental retardation (WAGR) syndrome and cancer . . . . . . . . . . . . . . . . . . . . . . 1248 Wine and cancer . . . . . . . . . . . . . . . . . . 1250 Wire localization . . . . . . . . . . . . . . . . . . 1250 WM. See Waldenström macroglobulinemia Wood dust . . . . . . . . . . . . . . . . . . . . . 1251
Yolk sac carcinomas . . . . . . . . . . . . . . . . 1256 Young adult cancers . . . . . . . . . . . . . . . . 1256 Zollinger-Ellison syndrome . . . . . . . . . . . . 1260 Drugs by Generic Name . . . Drugs by Trade Name . . . . Associations and Agencies . . Cancer Centers and Hospitals Cancer Support Groups . . . . Carcinogens. . . . . . . . . . Glossary . . . . . . . . . . . Bibliography . . . . . . . . .
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1265 1309 1348 1352 1357 1362 1383 1400
Category List . . . . . . . . . . . . . . . . . . . . 1409 Index . . . . . . . . . . . . . . . . . . . . . . . . 1419
X-ray tests . . . . . . . . . . . . . . . . . . . . . 1252 Xeroderma pigmentosa . . . . . . . . . . . . . . . 1254
xlviii
Volume III Living will — Self-image and body image
Editor
Jeffrey A. Knight, Ph.D. Mount Holyoke College
Medical Consultants
Laurie Jackson-Grusby, Ph.D. Children’s Hospital Boston, Harvard Medical School
Wendy White-Ryan, M.D., FAAP Golisano Children’s Hospital at Strong Memorial Hospital
SALEM PRESS, INC. Pasadena, California Hackensack, New Jersey
Editor in Chief: Dawn P. Dawson Editorial Director: Christina J. Moose Project Editors: Tracy Irons-Georges, Rowena Wildin Dehanke Editorial Assistant: Dana Garey
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Copyright © 2009, by Salem Press, Inc. All rights in this book are reserved. No part of this work may be used or reproduced in any manner whatsoever or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without written permission from the copyright owner except in the case of brief quotations embodied in critical articles and reviews or in the copying of images deemed to be freely licensed or in the public domain. For information address the publisher, Salem Press, Inc., P.O. Box 50062, Pasadena, California 91115. ∞ The paper used in these volumes conforms to the American National Standard for Permanence of Paper for Printed Library Materials, Z39.48-1992 (R1997). Note to Readers The material presented in Salem Health: Cancer is intended for broad informational and educational purposes. Readers who suspect that they or someone whom they know or provide caregiving for suffers from cancer or any other physical or psychological disorder, disease, or condition described in this set should contact a physician without delay; this work should not be used as a substitute for professional medical diagnosis or staging. Readers who are undergoing or about to undergo any treatment or procedure described in this set should refer to their physicians and other health care team members for guidance concerning preparation and possible effects. This set is not to be considered definitive on the covered topics, and readers should remember that the field of health care is characterized by a diversity of medical opinions and constant expansion in knowledge and understanding. Library of Congress Cataloging-in-Publication Data Salem health : cancer / Jeffrey A. Knight, Laurie Jackson-Grusby, Wendy White-Ryan. p. cm. Includes bibliographical references and index. ISBN 978-1-58765-505-0 (set : alk. paper) — ISBN 978-1-58765-506-7 (vol. 1 : alk. paper) — ISBN 978-1-58765-507-4 (vol. 2 : alk. paper) — ISBN 978-1-58765-508-1 (vol. 3 : alk. paper) — ISBN 978-1-58765-509-8 (vol. 4 : alk. paper) 1. Cancer. I. Knight, Jeffrey A., 1948- II. Jackson-Grusby, Laurie. III. White-Ryan, Wendy. RC265.S32 2008 616.99′4—dc22 2008030861
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printed in the united states of america
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Contents Medullary carcinoma of the breast. . . . . . . . Medulloblastomas . . . . . . . . . . . . . . . . Melanomas . . . . . . . . . . . . . . . . . . . . Melphalan . . . . . . . . . . . . . . . . . . . . Memorial Sloan-Kettering Cancer Center . . . . MEN 1. See Multiple endocrine neoplasia type 1 MEN 2. See Multiple endocrine neoplasia type 2 Meningeal carcinomatosis . . . . . . . . . . . . Meningiomas. . . . . . . . . . . . . . . . . . . Merkel cell carcinomas (MCC) . . . . . . . . . Mesenchymomas, malignant. . . . . . . . . . . Mesothelioma . . . . . . . . . . . . . . . . . . Metastasis . . . . . . . . . . . . . . . . . . . . Metastatic squamous neck cancer with occult primary . . . . . . . . . . . . . . . . . . . . MFH. See Malignant fibrous histiocytoma Microcalcifications. . . . . . . . . . . . . . . . Microwave hyperthermia therapy . . . . . . . . Mineral oils . . . . . . . . . . . . . . . . . . . Mistletoe . . . . . . . . . . . . . . . . . . . . . Mitochondrial DNA mutations. . . . . . . . . . MLH1 gene. . . . . . . . . . . . . . . . . . . . Mohs surgery. . . . . . . . . . . . . . . . . . . Molecular oncology . . . . . . . . . . . . . . . Moles. . . . . . . . . . . . . . . . . . . . . . . Monoclonal antibodies . . . . . . . . . . . . . . Motion sickness devices . . . . . . . . . . . . . MRI. See Magnetic resonance imaging MSH genes . . . . . . . . . . . . . . . . . . . . Mucinous carcinomas . . . . . . . . . . . . . . Mucosa-associated lymphoid tissue (MALT) lymphomas . . . . . . . . . . . . . . . . . . Mucositis . . . . . . . . . . . . . . . . . . . . . Mucous membranes, epidermoid cancers of. See Epidermoid cancers of mucous membranes Multiple endocrine neoplasia type 1 (MEN 1). . Multiple endocrine neoplasia type 2 (MEN 2). . Multiple myeloma . . . . . . . . . . . . . . . . Mustard gas . . . . . . . . . . . . . . . . . . . Mutagenesis and cancer . . . . . . . . . . . . . Myasthenia gravis . . . . . . . . . . . . . . . . MYC oncogene . . . . . . . . . . . . . . . . . . Mycosis fungoides . . . . . . . . . . . . . . . . Myelodysplastic syndromes . . . . . . . . . . . Myelofibrosis . . . . . . . . . . . . . . . . . . Myeloma . . . . . . . . . . . . . . . . . . . . . Myeloproliferative disorders. . . . . . . . . . . Myelosuppression . . . . . . . . . . . . . . . .
Complete List of Contents . . . . . . . . . . . . . . lix Living will . . . . . . . . . . . . . . . . . Living with cancer . . . . . . . . . . . . . Lobectomy . . . . . . . . . . . . . . . . . Lobular carcinoma in situ (LCIS) . . . . . Long-distance caregiving . . . . . . . . . Loop electrosurgical excisional procedure (LEEP) . . . . . . . . . . . . . . . . . Lumbar puncture . . . . . . . . . . . . . . Lumpectomy . . . . . . . . . . . . . . . . Lumps . . . . . . . . . . . . . . . . . . . Lung cancer, brochoalveolar. See Bronchoalveolar lung cancer Lung cancers . . . . . . . . . . . . . . . . Lutein . . . . . . . . . . . . . . . . . . . Lycopene . . . . . . . . . . . . . . . . . . Lymphadenectomy. . . . . . . . . . . . . Lymphangiography . . . . . . . . . . . . Lymphangiosarcomas . . . . . . . . . . . Lymphedema. . . . . . . . . . . . . . . . Lymphocytosis . . . . . . . . . . . . . . . Lymphomas . . . . . . . . . . . . . . . .
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719 720 723 725 726
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733 737 737 738 740 741 742 743 744
M. D. Anderson Cancer Center . . . . . . . Macrobiotic diet . . . . . . . . . . . . . . . Magnetic resonance imaging (MRI) . . . . . Malignant fibrous histiocytoma (MFH) . . . Malignant rhabdoid tumor of the kidney . . Malignant tumors . . . . . . . . . . . . . . MALT lymphomas. See Mucosa-associated lymphoid tissue lymphomas Mammography . . . . . . . . . . . . . . . . Managed care . . . . . . . . . . . . . . . . Mantle cell lymphoma (MCL) . . . . . . . . Mastectomy . . . . . . . . . . . . . . . . . Mastocytomas . . . . . . . . . . . . . . . . Matrix metalloproteinase inhibitors . . . . . Mayo Clinic Cancer Center . . . . . . . . . MCC. See Merkel cell carcinomas MCL. See Mantle cell lymphoma MDR. See Drug resistance and multidrug resistance Mediastinal tumors. . . . . . . . . . . . . . Mediastinoscopy . . . . . . . . . . . . . . . Medical marijuana . . . . . . . . . . . . . . Medical oncology . . . . . . . . . . . . . . Medicare and cancer . . . . . . . . . . . . .
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766 768 768 770 772 lv
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774 775 776 779 780
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781 782 783 785 786 788
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790 791 792 793 794 795 796 796 798 800 802
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807 808 809 812 813 815 817 817 819 820 822 823 825
Salem Health: Cancer 2-Naphthylamine. . . . . . . . . . . . . . . . Nasal cavity and paranasal sinus cancers . . . National Cancer Institute (NCI) . . . . . . . . National Science Foundation (NSF) . . . . . . Native North Americans and cancer . . . . . . Nausea and vomiting. . . . . . . . . . . . . . NCI. See National Cancer Institute Needle biopsies . . . . . . . . . . . . . . . . Needle localization. . . . . . . . . . . . . . . Nephroblastomas. . . . . . . . . . . . . . . . Nephrostomy . . . . . . . . . . . . . . . . . . Neuroblastomas . . . . . . . . . . . . . . . . Neuroectodermal tumors. . . . . . . . . . . . Neuroendocrine tumors . . . . . . . . . . . . Neurofibromatosis type 1 (NF1) . . . . . . . . Neurologic oncology. . . . . . . . . . . . . . Neutropenia . . . . . . . . . . . . . . . . . . NF1. See Neurofibromatosis type 1 Nickel compounds and metallic nickel . . . . Night sweats . . . . . . . . . . . . . . . . . . Nijmegen breakage syndrome . . . . . . . . . Nipple discharge . . . . . . . . . . . . . . . . Non-Hodgkin lymphoma . . . . . . . . . . . Nonsteroidal anti-inflammatory drugs (NSAIDs) . . . . . . . . . . . . . . . . . . NSAIDs. See Nonsteroidal anti-inflammatory drugs NSF. See National Science Foundation Nuclear medicine scan . . . . . . . . . . . . . Nutrition and cancer prevention . . . . . . . . Nutrition and cancer treatment. . . . . . . . . Obesity-associated cancers . . . . Occupational exposures and cancer Occupational therapy . . . . . . . OCs. See Organochlorines Oligodendrogliomas . . . . . . . . Omega-3 fatty acids . . . . . . . . Ommaya reservoir . . . . . . . . . Oncogenes . . . . . . . . . . . . . Oncogenic viruses . . . . . . . . . Oncology . . . . . . . . . . . . . . Oncology clinical nurse specialist . Oncology social worker . . . . . . Oophorectomy . . . . . . . . . . . Ophthalmic oncology . . . . . . . Opioids . . . . . . . . . . . . . . . Oral and maxillofacial surgery. . . Oral and oropharyngeal cancers . . Orbit tumors . . . . . . . . . . . . Orchiectomy . . . . . . . . . . . .
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836 838 839 839 841 842 844 845 847 849
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851 852 853 854 855
Organ transplantation and cancer . . Organochlorines (OCs) . . . . . . . Oropharyngeal cancers. See Oral and oropharyngeal cancers Orthopedic surgery. . . . . . . . . . Otolaryngology . . . . . . . . . . . Ovarian cancers . . . . . . . . . . . Ovarian cysts. . . . . . . . . . . . . Ovarian epithelial cancer . . . . . . Overtreatment . . . . . . . . . . . .
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Paget disease of bone . . . . . . . . . . . . . Pain management medications. . . . . . . . . Palliative treatment . . . . . . . . . . . . . . PALP. See Placental alkaline phosphatase Palpation . . . . . . . . . . . . . . . . . . . . Pancolitis . . . . . . . . . . . . . . . . . . . . Pancreatectomy . . . . . . . . . . . . . . . . Pancreatic cancers . . . . . . . . . . . . . . . Pancreatitis . . . . . . . . . . . . . . . . . . . Pap test . . . . . . . . . . . . . . . . . . . . . Paracentesis . . . . . . . . . . . . . . . . . . Paranasal sinus cancers. See Nasal cavity and paranasal sinus cancers Paraneoplastic syndromes . . . . . . . . . . . Parathyroid cancer . . . . . . . . . . . . . . . Pathology . . . . . . . . . . . . . . . . . . . PC-SPES . . . . . . . . . . . . . . . . . . . . PDT. See Photodynamic therapy Pediatric oncology and hematology . . . . . . Pelvic examination . . . . . . . . . . . . . . . Penile cancer . . . . . . . . . . . . . . . . . . Percutaneous transhepatic cholangiography (PTHC) . . . . . . . . . . . . . . . . . . . Pericardial effusion . . . . . . . . . . . . . . Pericardiocentesis . . . . . . . . . . . . . . . Peritoneovenous shunts . . . . . . . . . . . . Personality and cancer . . . . . . . . . . . . . Pesticides and the food chain . . . . . . . . . PET. See Positron emission tomography Peutz-Jeghers syndrome (PJS) . . . . . . . . . Pharmacy oncology . . . . . . . . . . . . . . Phenacetin . . . . . . . . . . . . . . . . . . . Phenolics . . . . . . . . . . . . . . . . . . . . Pheochromocytomas . . . . . . . . . . . . . . Pheresis . . . . . . . . . . . . . . . . . . . . Photodynamic therapy (PDT) . . . . . . . . . Phyllodes tumors. . . . . . . . . . . . . . . . Phytoestrogens . . . . . . . . . . . . . . . . . Pineoblastomas. . . . . . . . . . . . . . . . . Pituitary tumors . . . . . . . . . . . . . . . .
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875 877 878 878 881 882 885 887 888 889 892 893 894 897 898 lvi
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902 903 905 908 909 911
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951 952 955 955 956 958 959 960 962 963 965
Contents PJS. See Peutz-Jeghers syndrome Placental alkaline phosphatase (PALP) . . . . . . . 968 Plant alkaloids and terpenoids in chemotherapy . . . . . . . . . . . . . . . . . . . 968 Plasticizers . . . . . . . . . . . . . . . . . . . . . . 971 Pleural biopsy . . . . . . . . . . . . . . . . . . . . 972 Pleural effusion . . . . . . . . . . . . . . . . . . . 973 Pleurodesis . . . . . . . . . . . . . . . . . . . . . . 975 Pleuropulmonary blastomas . . . . . . . . . . . . . 975 PMS genes . . . . . . . . . . . . . . . . . . . . . . 976 Pneumonectomy . . . . . . . . . . . . . . . . . . . 977 Pneumonia . . . . . . . . . . . . . . . . . . . . . . 979 Polycyclic aromatic hydrocarbons . . . . . . . . . . 981 Polycythemia vera . . . . . . . . . . . . . . . . . . 981 Polypectomy . . . . . . . . . . . . . . . . . . . . . 982 Polyps . . . . . . . . . . . . . . . . . . . . . . . . 983 Polyps, colon. See Colon polyps Polyps, gastric. See Gastric polyps Positron emission tomography (PET) . . . . . . . . 984 Poverty and cancer . . . . . . . . . . . . . . . . . . 987 PPOs. See Preferred provider organizations Prayer and cancer support . . . . . . . . . . . . . . 989 Preferred provider organizations (PPOs) . . . . . . 990 Pregnancy and cancer . . . . . . . . . . . . . . . . 992 Premalignancies . . . . . . . . . . . . . . . . . . . 994 Prevent Cancer Foundation . . . . . . . . . . . . . 997 Prevention . . . . . . . . . . . . . . . . . . . . . . 999 Primary care physician . . . . . . . . . . . . . . . 1001 Primary central nervous system lymphomas . . . . 1003 Progesterone receptor assay . . . . . . . . . . . . 1003 Prostate cancer . . . . . . . . . . . . . . . . . . . 1004 Prostate-specific antigen (PSA) test . . . . . . . . 1006 Prostatectomy. . . . . . . . . . . . . . . . . . . . 1008 Prostatitis . . . . . . . . . . . . . . . . . . . . . . 1009 Proteasome inhibitors. . . . . . . . . . . . . . . . 1010 Protein electrophoresis . . . . . . . . . . . . . . . 1010 Proteomics and cancer research . . . . . . . . . . 1012 Proton beam therapy . . . . . . . . . . . . . . . . 1014 Proto-oncogenes and carcinogenesis . . . . . . . . 1015 PSA test. See Prostate-specific antigen test Psycho-oncology . . . . . . . . . . . . . . . . . . 1016 Psychosocial aspects of cancer . . . . . . . . . . . 1018 PTHC. See Percutaneous transhepatic cholangiography
Radiation, ionizing. See Ionizing radiation Radiation oncology . . . . . . . . . . . . . . . . Radiation therapies . . . . . . . . . . . . . . . . Radiation therapy, afterloading. See Afterloading radiation therapy Radical neck dissection . . . . . . . . . . . . . . Radiofrequency ablation . . . . . . . . . . . . . Radionuclide scan . . . . . . . . . . . . . . . . Radiopharmaceuticals . . . . . . . . . . . . . . Radon . . . . . . . . . . . . . . . . . . . . . . . RB1 gene . . . . . . . . . . . . . . . . . . . . . Receptor analysis . . . . . . . . . . . . . . . . . Reconstructive surgery . . . . . . . . . . . . . . Rectal cancer . . . . . . . . . . . . . . . . . . . Recurrence . . . . . . . . . . . . . . . . . . . . Rehabilitation . . . . . . . . . . . . . . . . . . . Relationships . . . . . . . . . . . . . . . . . . . Renal pelvis tumors. . . . . . . . . . . . . . . . Report on Carcinogens (RoC) . . . . . . . . . . Resveratrol . . . . . . . . . . . . . . . . . . . . Retinoblastomas . . . . . . . . . . . . . . . . . Rhabdomyosarcomas . . . . . . . . . . . . . . . RhoGD12 gene . . . . . . . . . . . . . . . . . . Richter syndrome . . . . . . . . . . . . . . . . . Risk assessment, family history and. See Family history and risk assessment Risks for cancer. . . . . . . . . . . . . . . . . . Robert H. Lurie Cancer Center . . . . . . . . . . RoC. See Report on Carcinogens Rothmund-Thomson syndrome . . . . . . . . . . Salivary gland cancer . . . . . . . . . . . . . Salpingectomy and salpingo-oophorectomy . Sarcomas, soft-tissue . . . . . . . . . . . . . Saw palmetto . . . . . . . . . . . . . . . . . Schwannoma tumors . . . . . . . . . . . . . SCLC1 gene. . . . . . . . . . . . . . . . . . Screening, colorectal cancer. See Colorectal cancer screening Screening for cancer . . . . . . . . . . . . . Second opinions . . . . . . . . . . . . . . . Self-image and body image. . . . . . . . . .
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Complete List of Contents Volume 1 Alkylating agents in chemotherapy . . . . . . . ALL. See Acute lymphocytic leukemia Allicin, garlic and. See Garlic and allicin Alopecia . . . . . . . . . . . . . . . . . . . . . ALP. See Alkaline phosphatase test Alpha-fetoprotein (AFP) levels . . . . . . . . . Alternative therapies. See Complementary and alternative therapies Alveolar soft-part sarcomas . . . . . . . . . . . Amenorrhea . . . . . . . . . . . . . . . . . . . American Association for Cancer Research (AACR) . . . . . . . . . . . . . . . . . . . . American Cancer Society (ACS) . . . . . . . . American Institute for Cancer Research (AICR) 4-Aminobiphenyl . . . . . . . . . . . . . . . . AML. See Acute myelocytic leukemia Amputation . . . . . . . . . . . . . . . . . . . Amyloidosis . . . . . . . . . . . . . . . . . . . Anal cancer . . . . . . . . . . . . . . . . . . . Androgen drugs . . . . . . . . . . . . . . . . . Anemia . . . . . . . . . . . . . . . . . . . . . Anemia, aplastic. See Aplastic anemia Anemia, hemolytic. See Hemolytic anemia Angiogenesis . . . . . . . . . . . . . . . . . . Angiogenesis inhibitors . . . . . . . . . . . . . Angiography. . . . . . . . . . . . . . . . . . . Angiosarcomas . . . . . . . . . . . . . . . . . Anoscopy . . . . . . . . . . . . . . . . . . . . Anthraquinones . . . . . . . . . . . . . . . . . Anthrax . . . . . . . . . . . . . . . . . . . . . Antiandrogens . . . . . . . . . . . . . . . . . . Antidiarrheal agents . . . . . . . . . . . . . . . Antiestrogens . . . . . . . . . . . . . . . . . . Antifungal therapies . . . . . . . . . . . . . . . Antimetabolites in chemotherapy . . . . . . . . Antinausea medications . . . . . . . . . . . . . Antineoplastics in chemotherapy . . . . . . . . Antioxidants . . . . . . . . . . . . . . . . . . . Antiperspirants and breast cancer . . . . . . . . Antiviral therapies. . . . . . . . . . . . . . . . Anxiety . . . . . . . . . . . . . . . . . . . . . APBI. See Accelerated partial breast irradiation APC gene testing . . . . . . . . . . . . . . . . Aplastic anemia . . . . . . . . . . . . . . . . . Appendix cancer . . . . . . . . . . . . . . . . Appetite loss. . . . . . . . . . . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . . . v Publisher’s Note . . . . . . . . . . . . . . . . . . . . ix About the Editors . . . . . . . . . . . . . . . . . . . xi Contributors . . . . . . . . . . . . . . . . . . . . . xiii Complete List of Contents . . . . . . . . . . . . . . xv AACR. See American Association for Cancer Research ABCD. . . . . . . . . . . . . . . . . . . . . . . . . . 1 ACC. See Adenoid cystic carcinoma Abdominoperineal resection (APR) . . . . . . . . . . 1 Accelerated partial breast irradiation (APBI). . . . . . 3 Achlorhydria . . . . . . . . . . . . . . . . . . . . . . 4 Acoustic neuromas . . . . . . . . . . . . . . . . . . . 4 Acquired immunodeficiency disease-related cancers. See HIV/AIDS-related cancers Acrylamides . . . . . . . . . . . . . . . . . . . . . . 6 ACS. See American Cancer Society Acupuncture and acupressure for cancer patients . . . 8 Acute lymphocytic leukemia (ALL) . . . . . . . . . 11 Acute myelocytic leukemia (AML) . . . . . . . . . . 13 Adenocarcinomas . . . . . . . . . . . . . . . . . . . 16 Adenoid cystic carcinoma (ACC) . . . . . . . . . . . 17 Adenomatoid tumors . . . . . . . . . . . . . . . . . 18 Adenomatous polyps . . . . . . . . . . . . . . . . . 18 Adenoviruses . . . . . . . . . . . . . . . . . . . . . 19 Adjuvant therapy . . . . . . . . . . . . . . . . . . . 20 Adrenal gland cancers . . . . . . . . . . . . . . . . . 21 Adrenocortical cancer . . . . . . . . . . . . . . . . . 23 Advance directives . . . . . . . . . . . . . . . . . . 24 Aflatoxins . . . . . . . . . . . . . . . . . . . . . . . 26 AFP levels. See Alpha-fetoprotein levels African Americans and cancer . . . . . . . . . . . . 28 Africans and cancer . . . . . . . . . . . . . . . . . . 31 Afterloading radiation therapy . . . . . . . . . . . . 32 Agent Orange . . . . . . . . . . . . . . . . . . . . . 34 Aging and cancer . . . . . . . . . . . . . . . . . . . 34 AICR. See American Institute for Cancer Research Aids and devices for cancer patients . . . . . . . . . 38 AIDS-related cancers. See HIV/AIDS-related cancers Air pollution . . . . . . . . . . . . . . . . . . . . . . 39 Alcohol, alcoholism, and cancer . . . . . . . . . . . 42 Aleukemia . . . . . . . . . . . . . . . . . . . . . . . 43 Alkaline phosphatase test (ALP) . . . . . . . . . . . 44 lix
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64 66 68 69 70 71 71 72 73 75 76 78 81 83 86 88 90 93
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Salem Health: Cancer APR. See Abdominoperineal resection Arsenic compounds . . . . . . . . . . Arterial embolization . . . . . . . . . Artificial sweeteners . . . . . . . . . . Asbestos . . . . . . . . . . . . . . . . Ascites . . . . . . . . . . . . . . . . . Ashkenazi Jews and cancer . . . . . . Asian Americans and cancer. . . . . . Astrocytomas. . . . . . . . . . . . . . Ataxia telangiectasia (AT) . . . . . . . Autologous blood transfusion . . . . . Axillary dissection . . . . . . . . . . . Azathioprine . . . . . . . . . . . . . .
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100 101 102 103 105 107 109 112 114 115 116 117
Bacillus Calmette Guérin (BCG) . . . . . . . . Bacteria as causes of cancer . . . . . . . . . . . Barium enema . . . . . . . . . . . . . . . . . . Barium swallow . . . . . . . . . . . . . . . . . Barrett esophagus . . . . . . . . . . . . . . . . Basal cell carcinomas . . . . . . . . . . . . . . BCG. See Bacillus Calmette Guérin Beckwith-Wiedemann syndrome (BWS) . . . . Benign prostatic hyperplasia (BPH) . . . . . . . Benign tumors . . . . . . . . . . . . . . . . . . Benzene . . . . . . . . . . . . . . . . . . . . . Benzidine and dyes metabolized to benzidine . . Benzodiazepines . . . . . . . . . . . . . . . . . Bereavement, grief and. See Grief and bereavement Beryllium and beryllium compounds . . . . . . Beta-carotene . . . . . . . . . . . . . . . . . . Bethesda criteria . . . . . . . . . . . . . . . . . BHDS. See Birt-Hogg-Dubé syndrome Bile duct cancer . . . . . . . . . . . . . . . . . Bilobectomy . . . . . . . . . . . . . . . . . . . Bioflavonoids . . . . . . . . . . . . . . . . . . Biological therapy . . . . . . . . . . . . . . . . Biopsy. See also Computed tomography-guided biopsy; Core needle biopsy; Liver biopsy; Needle biopsies; Pleural biopsy; Stereotactic needle biopsy; Surgical biopsies . . . . . . . Birt-Hogg-Dubé syndrome (BHDS) . . . . . . . Birth control pills and cancer . . . . . . . . . . Bis(chloromethyl) ether and technical-grade chloromethyl methyl ether . . . . . . . . . . Bisphenol A (BPA) . . . . . . . . . . . . . . . Bisphosphonates . . . . . . . . . . . . . . . . . Bladder cancer . . . . . . . . . . . . . . . . . . Blood cancers . . . . . . . . . . . . . . . . . . BMT. See Bone marrow transplantation BNCT. See Boron neutron capture therapy
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118 118 120 121 123 124
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126 128 128 130 131 132
Body image. See Self-image and body image Bone cancers . . . . . . . . . . . . . . . . . . . Bone marrow aspiration and biopsy . . . . . . . Bone marrow transplantation (BMT) . . . . . . Bone pain . . . . . . . . . . . . . . . . . . . . Bone scan . . . . . . . . . . . . . . . . . . . . Boron neutron capture therapy (BNCT) . . . . . Bowen disease . . . . . . . . . . . . . . . . . . BPA. See Bisphenol A BPH. See Benign prostatic hyperplasia BPI. See Brief Pain Inventory Brachytherapy . . . . . . . . . . . . . . . . . . BRAF gene . . . . . . . . . . . . . . . . . . . . Brain and central nervous system cancers . . . . Brain scan . . . . . . . . . . . . . . . . . . . . BRCA1 and BRCA2 genes . . . . . . . . . . . . Breakthrough pain . . . . . . . . . . . . . . . . Breast, calcifications of. See Calcifications of the breast Breast, medullary carcinoma of. See Medullary carcinoma of the breast Breast cancer, cutaneous. See Cutaneous breast cancer Breast cancer, estrogen-receptor-sensitive. See Estrogen-receptor-sensitive breast cancer Breast cancer in children and adolescents . . . . Breast cancer in men . . . . . . . . . . . . . . . Breast cancer in pregnant women . . . . . . . . Breast cancers . . . . . . . . . . . . . . . . . . Breast implants. . . . . . . . . . . . . . . . . . Breast reconstruction. . . . . . . . . . . . . . . Breast self-examination (BSE). . . . . . . . . . Breast ultrasound. . . . . . . . . . . . . . . . . Breslow’s staging . . . . . . . . . . . . . . . . Brief Pain Inventory (BPI) . . . . . . . . . . . . Brompton cocktail . . . . . . . . . . . . . . . . Bronchial adenomas . . . . . . . . . . . . . . . Bronchoalveolar lung cancer . . . . . . . . . . Bronchography. . . . . . . . . . . . . . . . . . Bronchoscopy . . . . . . . . . . . . . . . . . . BSE. See Breast self-examination Burkitt lymphoma . . . . . . . . . . . . . . . . 1,3-Butadiene . . . . . . . . . . . . . . . . . . 1,4-Butanediol dimethanesulfonate . . . . . . . BWS. See Beckwith-Wiedemann syndrome
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136 138 138 139
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148 149 151 151 154
CA 15-3 test . CA 19-9 test . CA 27-29 test CA 125 test. . Cachexia . . . lx
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158 161 163 165 166 167 168
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180 182 184 185 188 190 193 194 195 196 196 197 197 199 199
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205 205 206 206 207
Complete List of Contents Cadmium and cadmium compounds. . . . . . . . Caffeine . . . . . . . . . . . . . . . . . . . . . . Calcifications of the breast. . . . . . . . . . . . . Calcium . . . . . . . . . . . . . . . . . . . . . . Cancell . . . . . . . . . . . . . . . . . . . . . . . Cancer biology . . . . . . . . . . . . . . . . . . . Cancer care team . . . . . . . . . . . . . . . . . . Cancer clusters . . . . . . . . . . . . . . . . . . . Cancer education. . . . . . . . . . . . . . . . . . Candidiasis . . . . . . . . . . . . . . . . . . . . . Carcinoembryonic antigen antibody (CEA) test . . . . . . . . . . . . . . . . . . . . . . . . Carcinogens, known . . . . . . . . . . . . . . . . Carcinogens, reasonably anticipated. . . . . . . . Carcinoid tumors and carcinoid syndrome . . . . Carcinoma of unknown primary origin (CUP) . . Carcinomas. . . . . . . . . . . . . . . . . . . . . Carcinomas, invasive ductal. See Invasive ductal carcinomas Carcinomas, invasive lobular. See Invasive lobular carcinomas Carcinomas, leptomeningeal. See Leptomeningeal carcinomas Carcinomatosis. . . . . . . . . . . . . . . . . . . Carcinomatous meningitis . . . . . . . . . . . . . Carcinosarcomas . . . . . . . . . . . . . . . . . . Cardiomyopathy in cancer patients . . . . . . . . Cardiopulmonary resuscitation (CPR) . . . . . . . Caregivers and caregiving . . . . . . . . . . . . . Caregiving, long-distance. See Long-distance caregiving Carney complex . . . . . . . . . . . . . . . . . . Carotenoids . . . . . . . . . . . . . . . . . . . . Cartilage supplements . . . . . . . . . . . . . . . Case management . . . . . . . . . . . . . . . . . Castleman disease . . . . . . . . . . . . . . . . . CBC. See Complete blood count CBE. See Clinical breast exam CDKN2A. See Cyclin-dependent kinase inhibitor-2A CEA test. See Carcinoembryonic antigen antibody test Cell phones. . . . . . . . . . . . . . . . . . . . . Cervical cancer. . . . . . . . . . . . . . . . . . . Chemoembolization . . . . . . . . . . . . . . . . Chemoprevention . . . . . . . . . . . . . . . . . Chemotherapy . . . . . . . . . . . . . . . . . . . Chemotherapy, cognitive effects of. See Cognitive effects of cancer and chemotherapy Chewing tobacco. . . . . . . . . . . . . . . . . . Childbirth and cancer . . . . . . . . . . . . . . .
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208 209 211 212 212 213 216 218 220 221
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223 224 227 230 232 233
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235 237 238 239 240 242
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245 245 246 247 248
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Childhood cancers . . . . . . . . . . . . . . . . Chlorambucil. . . . . . . . . . . . . . . . . . . 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)1-nitrosourea (MeCCNU) . . . . . . . . . . . Cholecystectomy . . . . . . . . . . . . . . . . . Chordomas . . . . . . . . . . . . . . . . . . . . Choriocarcinomas . . . . . . . . . . . . . . . . CHPP. See Continuous hyperthermic peritoneal perfusion Chromium hexavalent compounds. . . . . . . . Chromosomes and cancer . . . . . . . . . . . . Chronic lymphocytic leukemia (CLL) . . . . . . Chronic myeloid leukemia (CML). . . . . . . . Cigarettes and cigars . . . . . . . . . . . . . . . Clinical breast exam (CBE) . . . . . . . . . . . Clinical trials . . . . . . . . . . . . . . . . . . . CLL. See Chronic lymphocytic leukemia CML. See Chronic myeloid leukemia Coal tars and coal tar pitches . . . . . . . . . . Cobalt 60 radiation. . . . . . . . . . . . . . . . Coenzyme Q10. . . . . . . . . . . . . . . . . . Cognitive effects of cancer and chemotherapy . Coke oven emissions. . . . . . . . . . . . . . . Cold nodule . . . . . . . . . . . . . . . . . . . Colectomy . . . . . . . . . . . . . . . . . . . . Coloanal anastomosis . . . . . . . . . . . . . . Colon polyps . . . . . . . . . . . . . . . . . . . Colonoscopy and virtual colonoscopy . . . . . . Colony-stimulating factors (CSFs) . . . . . . . Colorectal cancer. . . . . . . . . . . . . . . . . Colorectal cancer screening . . . . . . . . . . . Colostomy . . . . . . . . . . . . . . . . . . . . Colposcopy. . . . . . . . . . . . . . . . . . . . Comedo carcinomas . . . . . . . . . . . . . . . Complementary and alternative therapies . . . . Complete blood count (CBC) . . . . . . . . . . Computed tomography (CT)-guided biopsy . . . . . . . . . . . . . . . . . . . . . Computed tomography (CT) scan . . . . . . . . Conization . . . . . . . . . . . . . . . . . . . . Continuous hyperthermic peritoneal perfusion (CHPP) . . . . . . . . . . . . . . . . . . . . Cordectomy . . . . . . . . . . . . . . . . . . . Cordotomy . . . . . . . . . . . . . . . . . . . . Core needle biopsy. . . . . . . . . . . . . . . . Corticosteroids . . . . . . . . . . . . . . . . . . Coughing . . . . . . . . . . . . . . . . . . . . . Counseling for cancer patients and survivors . . Cowden syndrome . . . . . . . . . . . . . . . . COX-2 inhibitors. See Cyclooxygenase 2 inhibitors
249 251 253 254 257
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274 274 276 279 281 283 285
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288 289 289 290 292 292 293 294 296 297 299 300 304 306 308 309 309 312
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318 318 319 321 321 322 324 326
Salem Health: Cancer CPR. See Cardiopulmonary resuscitation Craniopharyngiomas . . . . . . . . . . . . Craniosynostosis . . . . . . . . . . . . . . Craniotomy. . . . . . . . . . . . . . . . . Crohn disease . . . . . . . . . . . . . . . Cruciferous vegetables . . . . . . . . . . . Cryoablation . . . . . . . . . . . . . . . . Cryptorchidism. . . . . . . . . . . . . . . CSFs. See Colony-stimulating factors CT scan. See Computed tomography scan CTCL. See Cutaneous T-cell lymphoma Culdoscopy. . . . . . . . . . . . . . . . . CUP. See Carcinoma of unknown primary origin Curcumin. . . . . . . . . . . . . . . . . . Cushing syndrome and cancer . . . . . . . Cutaneous breast cancer . . . . . . . . . . Cutaneous T-cell lymphoma (CTCL) . . .
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Cyclin-dependent kinase inhibitor-2A (CDKN2A). . . . . . . . . . . . . . . Cyclooxygenase 2 (COX-2) inhibitors . Cyclophosphamide. . . . . . . . . . . . Cyclosporin A . . . . . . . . . . . . . . Cystography . . . . . . . . . . . . . . . Cystoscopy . . . . . . . . . . . . . . . . Cytogenetics . . . . . . . . . . . . . . . Cytokines . . . . . . . . . . . . . . . . Cytology . . . . . . . . . . . . . . . . . Cytology, sputum. See Sputum cytology
327 329 331 332 335 336 338
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344 344 345 346 347 347 348 350 350
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D&C. See Dilation and curettage Dana-Farber Cancer Institute . . . . . . . . . . . . 354 DCIS. See Ductal carcinoma in situ DEA. See Diethanolamine DEHP. See Di(2-ethylhexyl) phthalate Delta-9-tetrahydrocannabinol . . . . . . . . . . . . 355
339 340 341 342
Volume 2 Down syndrome and leukemia. . . . . . . . DPC4 gene testing . . . . . . . . . . . . . . DRE. See Digital rectal exam Drug resistance and multidrug resistance (MDR) . . . . . . . . . . . . . . . . . . . Dry mouth . . . . . . . . . . . . . . . . . . DSRCT. See Desmoplastic small round cell tumor Duct ectasia . . . . . . . . . . . . . . . . . Ductal carcinoma in situ (DCIS). . . . . . . Ductal lavage. . . . . . . . . . . . . . . . . Ductogram . . . . . . . . . . . . . . . . . . Duke Comprehensive Cancer Center . . . . Dukes’ classification . . . . . . . . . . . . . Duodenal carcinomas . . . . . . . . . . . . Dye, hair. See Hair dye Dysplastic nevus syndrome . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . xxxiii Complete List of Contents . . . . . . . . . . . . xxxvii Denys-Drash syndrome and cancer . . . . . . Depression . . . . . . . . . . . . . . . . . . . Dermatofibrosarcoma protuberans (DFSP) . . Dermatology oncology. . . . . . . . . . . . . DES. See Diethylstilbestrol Desmoid tumors . . . . . . . . . . . . . . . . Desmoplastic small round cell tumor (DSRCT) . . . . . . . . . . . . . . . . . . Developing nations and cancer . . . . . . . . DFSP. See Dermatofibrosarcoma protuberans Di(2-ethylhexyl) phthalate (DEHP) . . . . . . Diarrhea . . . . . . . . . . . . . . . . . . . . DIC. See Disseminated intravascular coagulation Dietary supplements . . . . . . . . . . . . . . Diethanolamine (DEA) . . . . . . . . . . . . Diethylstilbestrol (DES) . . . . . . . . . . . . Digital rectal exam (DRE) . . . . . . . . . . . Dilation and curettage (D&C) . . . . . . . . . Dioxins . . . . . . . . . . . . . . . . . . . . . Disseminated intravascular coagulation (DIC) . . . . . . . . . . . . . . . . . . . . Diverticulosis and diverticulitis . . . . . . . . DNR. See Do-not-resuscitate order Do-not-resuscitate (DNR) order . . . . . . . .
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357 357 360 362
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370 373 373 374 375 376
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386 387 389 389 390 392 393
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Eaton-Lambert syndrome. See Lambert-Eaton myasthenic syndrome EBRT. See External beam radiation therapy Edema . . . . . . . . . . . . . . . . . . . . . Education, cancer. See Cancer education Elderly and cancer . . . . . . . . . . . . . . . Electrolarynx . . . . . . . . . . . . . . . . . . Electromagnetic radiation . . . . . . . . . . . Electroporation therapy . . . . . . . . . . . . Electrosurgery . . . . . . . . . . . . . . . . .
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396 399 399 400 401
Complete List of Contents Embolization . . . . . . . . . . . . . . . . . . . . Embryonal cell cancer . . . . . . . . . . . . . . . End-of-life care . . . . . . . . . . . . . . . . . . Endocrine cancers . . . . . . . . . . . . . . . . . Endocrinology oncology . . . . . . . . . . . . . . Endometrial cancer . . . . . . . . . . . . . . . . Endometrial hyperplasia . . . . . . . . . . . . . . Endorectal ultrasound . . . . . . . . . . . . . . . Endoscopic retrograde cholangiopancreatography (ERCP) . . . . . . . . . . . . . . . . . . . . . Endoscopy . . . . . . . . . . . . . . . . . . . . . Endoscopy, upper gastrointestinal. See Upper gastrointestinal endoscopy Endotheliomas . . . . . . . . . . . . . . . . . . . Enteritis . . . . . . . . . . . . . . . . . . . . . . Enterostomal therapy . . . . . . . . . . . . . . . Eosinophilic leukemia . . . . . . . . . . . . . . . Ependymomas . . . . . . . . . . . . . . . . . . . Epidemiology of cancer . . . . . . . . . . . . . . Epidermoid cancers of mucous membranes . . . . Epstein-Barr virus . . . . . . . . . . . . . . . . . ERCP. See Endoscopic retrograde cholangiopancreatography ERD. See Estrogen receptor downregulator Erionite. . . . . . . . . . . . . . . . . . . . . . . Erythroplakia. . . . . . . . . . . . . . . . . . . . Esophageal cancer . . . . . . . . . . . . . . . . . Esophageal speech . . . . . . . . . . . . . . . . . Esophagectomy . . . . . . . . . . . . . . . . . . Esophagitis . . . . . . . . . . . . . . . . . . . . . Essiac . . . . . . . . . . . . . . . . . . . . . . . Estrogen receptor downregulator (ERD) . . . . . Estrogen-receptor-sensitive breast cancer . . . . . Ethnicity and cancer . . . . . . . . . . . . . . . . Ethylene oxide . . . . . . . . . . . . . . . . . . . Ewing sarcoma . . . . . . . . . . . . . . . . . . . Exenteration . . . . . . . . . . . . . . . . . . . . Exercise and cancer . . . . . . . . . . . . . . . . External beam radiation therapy (EBRT) . . . . . Eye cancers . . . . . . . . . . . . . . . . . . . . Eyelid cancer. . . . . . . . . . . . . . . . . . . .
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Fallopian tube cancer . . . . . . . Family history and risk assessment Fanconi anemia . . . . . . . . . . Fatigue . . . . . . . . . . . . . . . Fecal occult blood test (FOBT) . . Fertility drugs and cancer . . . . . Fertility issues . . . . . . . . . . . Fever . . . . . . . . . . . . . . . . Fiber . . . . . . . . . . . . . . . .
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402 403 404 406 409 412 414 416
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433 433 434 436 438 439 441 441 442 444 447 447 450 451 454 455 458
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460 461 464 466 467 469 471 472 474 lxiii
Fibroadenomas . . . . . . . . . . . . . . . . Fibrocystic breast changes . . . . . . . . . . Fibrosarcomas, soft-tissue . . . . . . . . . . Financial issues . . . . . . . . . . . . . . . 5HIAA test. See 5-Hydroxyindoleacetic acid test 5Q minus syndrome . . . . . . . . . . . . . Flow cytometry . . . . . . . . . . . . . . . FOBT. See Fecal occult blood test Folic acid. . . . . . . . . . . . . . . . . . . Formaldehyde . . . . . . . . . . . . . . . . Fox Chase Cancer Center . . . . . . . . . . Fred Hutchinson Cancer Research Center . . Free radicals . . . . . . . . . . . . . . . . . Fruits . . . . . . . . . . . . . . . . . . . . .
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475 476 478 481
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486 486 487 488 490 491
Gallbladder cancer . . . . . . . . . . . . . . Gallium scan . . . . . . . . . . . . . . . . . Gamma Knife . . . . . . . . . . . . . . . . Gardner syndrome . . . . . . . . . . . . . . Garlic and allicin . . . . . . . . . . . . . . . Gastric polyps . . . . . . . . . . . . . . . . Gastrinomas . . . . . . . . . . . . . . . . . Gastrointestinal cancers . . . . . . . . . . . Gastrointestinal complications of cancer treatment. . . . . . . . . . . . . . . . . . Gastrointestinal oncology . . . . . . . . . . Gastrointestinal stromal tumors (GISTs) . . GCTs. See Giant cell tumors Gene therapy . . . . . . . . . . . . . . . . . Genetic counseling . . . . . . . . . . . . . . Genetic testing . . . . . . . . . . . . . . . . Genetics of cancer . . . . . . . . . . . . . . Geography and cancer . . . . . . . . . . . . Germ-cell tumors . . . . . . . . . . . . . . Gerson therapy . . . . . . . . . . . . . . . . Gestational trophoblastic tumors (GTTs) . . Giant cell tumors (GCTs) . . . . . . . . . . Ginseng, panax. . . . . . . . . . . . . . . . GISTs. See Gastrointestinal stromal tumors Gleason grading system . . . . . . . . . . . Gliomas . . . . . . . . . . . . . . . . . . . Glomus tumors . . . . . . . . . . . . . . . . Glossectomy . . . . . . . . . . . . . . . . . Glutamine . . . . . . . . . . . . . . . . . . Gonioscopy . . . . . . . . . . . . . . . . . Grading of tumors . . . . . . . . . . . . . . Graft-versus-host disease (GVHD) . . . . . Granulosa cell tumors . . . . . . . . . . . . Green tea . . . . . . . . . . . . . . . . . . . Grief and bereavement . . . . . . . . . . . .
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493 495 497 498 499 500 501 502
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512 515 517 519 522 525 527 527 530 531
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532 533 534 535 536 536 537 538 540 540 541
Salem Health: Cancer GTTs. See Gestational trophoblastic tumors GVHD. See Graft-versus-host disease Gynecologic cancers . . . . . . . . . . . . . . . . . 543 Gynecologic oncology . . . . . . . . . . . . . . . . 547 H. pylori. See Helicobacter pylori HAI. See Hepatic arterial infusion Hair dye . . . . . . . . . . . . . . . . . . . . . . Hairy cell leukemia . . . . . . . . . . . . . . . . Hand-foot syndrome (HFS) . . . . . . . . . . . . HBV. See Hepatitis B virus HCG. See Human chorionic gonadotropin HCV. See Hepatitis C virus Head and neck cancers . . . . . . . . . . . . . . . Health maintenance organizations (HMOs) . . . . Helicobacter pylori. . . . . . . . . . . . . . . . . Hemangioblastomas . . . . . . . . . . . . . . . . Hemangiopericytomas . . . . . . . . . . . . . . . Hemangiosarcomas . . . . . . . . . . . . . . . . Hematemesis . . . . . . . . . . . . . . . . . . . . Hematologic oncology . . . . . . . . . . . . . . . Hematuria . . . . . . . . . . . . . . . . . . . . . Hemochromatosis . . . . . . . . . . . . . . . . . Hemolytic anemia . . . . . . . . . . . . . . . . . Hemoptysis. . . . . . . . . . . . . . . . . . . . . Hemorrhoids . . . . . . . . . . . . . . . . . . . . Hepatic arterial infusion (HAI) . . . . . . . . . . Hepatitis B virus (HBV) . . . . . . . . . . . . . . Hepatitis C virus (HCV) . . . . . . . . . . . . . . Hepatomegaly . . . . . . . . . . . . . . . . . . . HER2/neu protein . . . . . . . . . . . . . . . . . Herbs as antioxidants . . . . . . . . . . . . . . . Hereditary cancer syndromes . . . . . . . . . . . Hereditary diffuse gastric cancer . . . . . . . . . Hereditary leiomyomatosis and renal cell cancer (HLRCC) . . . . . . . . . . . . . . . . Hereditary mixed polyposis syndrome . . . . . . Hereditary non-VHL clear cell renal cell carcinomas . . . . . . . . . . . . . . . . . . . Hereditary pancreatitis . . . . . . . . . . . . . . . Hereditary papillary renal cell carcinomas . . . . Hereditary polyposis syndromes . . . . . . . . . . Herpes simplex virus. . . . . . . . . . . . . . . . Herpes zoster virus. . . . . . . . . . . . . . . . . HFS. See Hand-foot syndrome Hispanics and cancer. See Latinos/Hispanics and cancer Histamine 2 antagonists . . . . . . . . . . . . . . Histiocytosis X . . . . . . . . . . . . . . . . . . . HIV/AIDS-related cancers . . . . . . . . . . . . .
HLRCC. See Hereditary leiomyomatosis and renal cell cancer HMOs. See Health maintenance organizations Hodgkin disease . . . . . . . . . . . . . . . . . Home health services . . . . . . . . . . . . . . Hormonal therapies . . . . . . . . . . . . . . . Hormone receptor tests . . . . . . . . . . . . . Hormone replacement therapy (HRT) . . . . . . Horner syndrome. . . . . . . . . . . . . . . . . Hospice care . . . . . . . . . . . . . . . . . . . Hot flashes . . . . . . . . . . . . . . . . . . . . HPV. See Human papillomavirus HRAS gene testing . . . . . . . . . . . . . . . . HRT. See Hormone replacement therapy HTLV. See Human T-cell leukemia virus Human chorionic gonadotropin (HCG) . . . . . Human growth factors and tumor growth . . . . Human immunodeficiency virus-related cancers. See HIV/AIDS-related cancers Human papillomavirus (HPV) . . . . . . . . . . Human T-cell leukemia virus (HTLV) . . . . . Hydatidiform mole . . . . . . . . . . . . . . . . 5-Hydroxyindoleacetic acid (5HIAA) test . . . . Hypercalcemia . . . . . . . . . . . . . . . . . . Hypercoagulation disorders . . . . . . . . . . . Hyperthermia therapy . . . . . . . . . . . . . . Hyperthermic perfusion . . . . . . . . . . . . . Hypopharyngeal cancer . . . . . . . . . . . . . Hysterectomy . . . . . . . . . . . . . . . . . . Hysterography . . . . . . . . . . . . . . . . . . Hystero-oophorectomy. . . . . . . . . . . . . . Hysteroscopy. . . . . . . . . . . . . . . . . . .
. 550 . 550 . 552
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554 557 558 559 559 560 561 562 564 565 566 566 567 568 569 570 571 573 573 574 576
IEP. See Immunoelectrophoresis iFOBT. See Immunochemical fecal occult blood test Ileostomy. . . . . . . . . . . . . . . . . . . . . Imaging tests . . . . . . . . . . . . . . . . . . . Immune response to cancer . . . . . . . . . . . Immunochemical fecal occult blood test (iFOBT) . . . . . . . . . . . . . . . . . . . . Immunocytochemistry and immunohistochemistry . . . . . . . . . . . . Immunoelectrophoresis (IEP) . . . . . . . . . . Immunotherapy . . . . . . . . . . . . . . . . . IMRT. See Intensity-modulated radiation therapy Indoles . . . . . . . . . . . . . . . . . . . . . . Infection and sepsis . . . . . . . . . . . . . . . Infectious cancers . . . . . . . . . . . . . . . . Infertility and cancer . . . . . . . . . . . . . . .
. 577 . 579 . . . . . .
580 580 581 582 584 586
. 587 . 588 . 590 lxiv
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593 597 599 601 603 605 606 608
. . 609
. . 609 . . 610
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611 612 612 613 614 615 617 618 619 620 621 622 623
. . 625 . . 626 . . 629 . . 632 . . 633 . . 634 . . 635
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638 638 641 643
Complete List of Contents Inflammatory bowel disease . . . . . . . . . . Informed consent. . . . . . . . . . . . . . . . Infusion therapies . . . . . . . . . . . . . . . Insurance . . . . . . . . . . . . . . . . . . . . Integrative oncology . . . . . . . . . . . . . . Intensity-modulated radiation therapy (IMRT) Interferon. . . . . . . . . . . . . . . . . . . . Interleukins. . . . . . . . . . . . . . . . . . . Invasive cancer. . . . . . . . . . . . . . . . . Invasive ductal carcinomas . . . . . . . . . . Invasive lobular carcinomas . . . . . . . . . . Ionizing radiation . . . . . . . . . . . . . . . Iridium seeds . . . . . . . . . . . . . . . . . . Islet cell tumors . . . . . . . . . . . . . . . . Isoflavones . . . . . . . . . . . . . . . . . . . Itching . . . . . . . . . . . . . . . . . . . . .
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645 646 647 648 651 652 653 654 655 656 657 657 658 659 661 661
Lambert-Eaton myasthenic syndrome (LEMS) Laparoscopy and laparoscopic surgery . . . . Laryngeal cancer . . . . . . . . . . . . . . . . Laryngeal nerve palsy . . . . . . . . . . . . . Laryngectomy . . . . . . . . . . . . . . . . . Laryngoscopy . . . . . . . . . . . . . . . . . Laser therapies . . . . . . . . . . . . . . . . . Latinos/Hispanics and cancer . . . . . . . . . Laxatives . . . . . . . . . . . . . . . . . . . . LCIS. See Lobular carcinoma in situ LDH test. See Lactate dehydrogenase test Leiomyomas . . . . . . . . . . . . . . . . . . Leiomyosarcomas . . . . . . . . . . . . . . . LEMS. See Lambert-Eaton myasthenic syndrome Leptomeningeal carcinomas . . . . . . . . . . Leukapharesis . . . . . . . . . . . . . . . . . Leukemia, Down syndrome and. See Down syndrome and leukemia Leukemia, eosinophilic. See Eosinophilic leukemia Leukemia, hairy cell. See Hairy cell leukemia Leukemias . . . . . . . . . . . . . . . . . . . Leukoencephalopathy . . . . . . . . . . . . . Leukopenia. . . . . . . . . . . . . . . . . . . Leukoplakia . . . . . . . . . . . . . . . . . . Leydig cell tumors . . . . . . . . . . . . . . . Li-Fraumeni syndrome (LFS) . . . . . . . . . Limb salvage . . . . . . . . . . . . . . . . . . Linear accelerator . . . . . . . . . . . . . . . Lip cancers . . . . . . . . . . . . . . . . . . . Liposarcomas . . . . . . . . . . . . . . . . . Liver biopsy . . . . . . . . . . . . . . . . . . Liver cancers . . . . . . . . . . . . . . . . . .
Jonsson Comprehensive Cancer Center (JCCC) . . . . . . . . . . . . . . . . . . . . . . 664 Journaling . . . . . . . . . . . . . . . . . . . . . . 665 Juvenile polyposis syndrome . . . . . . . . . . . . 665 Kaposi sarcoma . . . . . . . . . . . . . Karnofsky performance status (KPS) . . Keratosis . . . . . . . . . . . . . . . . . Ki67 test . . . . . . . . . . . . . . . . . Kidney cancer . . . . . . . . . . . . . . Klinefelter syndrome and cancer . . . . KPS. See Karnofsky performance status Krukenberg tumors . . . . . . . . . . .
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667 669 670 670 671 674
. . . . . . 675
Lacrimal gland tumors . . . . . . . . . . . . . . . . 677 Lactate dehydrogenase (LDH) test . . . . . . . . . 678 Laetrile . . . . . . . . . . . . . . . . . . . . . . . . 679
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679 681 682 685 686 687 688 690 692
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. . . 696 . . . 698
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698 702 704 704 706 706 708 709 710 712 714 715
Volume 3 Lumps . . . . . . . . . . . . . . Lung cancer, brochoalveolar. See Bronchoalveolar lung cancer Lung cancers . . . . . . . . . . . Lutein . . . . . . . . . . . . . . Lycopene . . . . . . . . . . . . . Lymphadenectomy. . . . . . . . Lymphangiography . . . . . . . Lymphangiosarcomas . . . . . . Lymphedema. . . . . . . . . . . Lymphocytosis . . . . . . . . . . Lymphomas . . . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . . . lv Complete List of Contents . . . . . . . . . . . . . . lix Living will . . . . . . . . . . . . . . . . . Living with cancer . . . . . . . . . . . . . Lobectomy . . . . . . . . . . . . . . . . . Lobular carcinoma in situ (LCIS) . . . . . Long-distance caregiving . . . . . . . . . Loop electrosurgical excisional procedure (LEEP) . . . . . . . . . . . . . . . . . Lumbar puncture . . . . . . . . . . . . . . Lumpectomy . . . . . . . . . . . . . . . .
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719 720 723 725 726
. . . . . 727 . . . . . 728 . . . . . 730 lxv
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733 737 737 738 740 741 742 743 744
Salem Health: Cancer M. D. Anderson Cancer Center . . . . . . . . . Macrobiotic diet . . . . . . . . . . . . . . . . . Magnetic resonance imaging (MRI) . . . . . . . Malignant fibrous histiocytoma (MFH) . . . . . Malignant rhabdoid tumor of the kidney . . . . Malignant tumors . . . . . . . . . . . . . . . . MALT lymphomas. See Mucosa-associated lymphoid tissue lymphomas Mammography . . . . . . . . . . . . . . . . . . Managed care . . . . . . . . . . . . . . . . . . Mantle cell lymphoma (MCL) . . . . . . . . . . Mastectomy . . . . . . . . . . . . . . . . . . . Mastocytomas . . . . . . . . . . . . . . . . . . Matrix metalloproteinase inhibitors . . . . . . . Mayo Clinic Cancer Center . . . . . . . . . . . MCC. See Merkel cell carcinomas MCL. See Mantle cell lymphoma MDR. See Drug resistance and multidrug resistance Mediastinal tumors. . . . . . . . . . . . . . . . Mediastinoscopy . . . . . . . . . . . . . . . . . Medical marijuana . . . . . . . . . . . . . . . . Medical oncology . . . . . . . . . . . . . . . . Medicare and cancer . . . . . . . . . . . . . . . Medullary carcinoma of the breast. . . . . . . . Medulloblastomas . . . . . . . . . . . . . . . . Melanomas . . . . . . . . . . . . . . . . . . . . Melphalan . . . . . . . . . . . . . . . . . . . . Memorial Sloan-Kettering Cancer Center . . . . MEN 1. See Multiple endocrine neoplasia type 1 MEN 2. See Multiple endocrine neoplasia type 2 Meningeal carcinomatosis . . . . . . . . . . . . Meningiomas. . . . . . . . . . . . . . . . . . . Merkel cell carcinomas (MCC) . . . . . . . . . Mesenchymomas, malignant. . . . . . . . . . . Mesothelioma . . . . . . . . . . . . . . . . . . Metastasis . . . . . . . . . . . . . . . . . . . . Metastatic squamous neck cancer with occult primary . . . . . . . . . . . . . . . . . . . . MFH. See Malignant fibrous histiocytoma Microcalcifications. . . . . . . . . . . . . . . . Microwave hyperthermia therapy . . . . . . . . Mineral oils . . . . . . . . . . . . . . . . . . . Mistletoe . . . . . . . . . . . . . . . . . . . . . Mitochondrial DNA mutations. . . . . . . . . . MLH1 gene. . . . . . . . . . . . . . . . . . . . Mohs surgery. . . . . . . . . . . . . . . . . . . Molecular oncology . . . . . . . . . . . . . . . Moles. . . . . . . . . . . . . . . . . . . . . . . Monoclonal antibodies . . . . . . . . . . . . . . Motion sickness devices . . . . . . . . . . . . .
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748 750 750 752 753 754
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754 757 759 761 763 764 765
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766 768 768 770 772 774 775 776 779 780
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MRI. See Magnetic resonance imaging MSH genes . . . . . . . . . . . . . . . . . . . . Mucinous carcinomas . . . . . . . . . . . . . . Mucosa-associated lymphoid tissue (MALT) lymphomas . . . . . . . . . . . . . . . . . . Mucositis . . . . . . . . . . . . . . . . . . . . . Mucous membranes, epidermoid cancers of. See Epidermoid cancers of mucous membranes Multiple endocrine neoplasia type 1 (MEN 1). . Multiple endocrine neoplasia type 2 (MEN 2). . Multiple myeloma . . . . . . . . . . . . . . . . Mustard gas . . . . . . . . . . . . . . . . . . . Mutagenesis and cancer . . . . . . . . . . . . . Myasthenia gravis . . . . . . . . . . . . . . . . MYC oncogene . . . . . . . . . . . . . . . . . . Mycosis fungoides . . . . . . . . . . . . . . . . Myelodysplastic syndromes . . . . . . . . . . . Myelofibrosis . . . . . . . . . . . . . . . . . . Myeloma . . . . . . . . . . . . . . . . . . . . . Myeloproliferative disorders. . . . . . . . . . . Myelosuppression . . . . . . . . . . . . . . . . 2-Naphthylamine. . . . . . . . . . . . . . . . Nasal cavity and paranasal sinus cancers . . . National Cancer Institute (NCI) . . . . . . . . National Science Foundation (NSF) . . . . . . Native North Americans and cancer . . . . . . Nausea and vomiting. . . . . . . . . . . . . . NCI. See National Cancer Institute Needle biopsies . . . . . . . . . . . . . . . . Needle localization. . . . . . . . . . . . . . . Nephroblastomas. . . . . . . . . . . . . . . . Nephrostomy . . . . . . . . . . . . . . . . . . Neuroblastomas . . . . . . . . . . . . . . . . Neuroectodermal tumors. . . . . . . . . . . . Neuroendocrine tumors . . . . . . . . . . . . Neurofibromatosis type 1 (NF1) . . . . . . . . Neurologic oncology. . . . . . . . . . . . . . Neutropenia . . . . . . . . . . . . . . . . . . NF1. See Neurofibromatosis type 1 Nickel compounds and metallic nickel . . . . Night sweats . . . . . . . . . . . . . . . . . . Nijmegen breakage syndrome . . . . . . . . . Nipple discharge . . . . . . . . . . . . . . . . Non-Hodgkin lymphoma . . . . . . . . . . . Nonsteroidal anti-inflammatory drugs (NSAIDs) . . . . . . . . . . . . . . . . . . NSAIDs. See Nonsteroidal anti-inflammatory drugs NSF. See National Science Foundation Nuclear medicine scan . . . . . . . . . . . . .
781 782 783 785 786 788
. . 790 . . . . . . . . . . .
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790 791 792 793 794 795 796 796 798 800 802 lxvi
. . 803 . . 803 . . 804 . . 806
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807 808 809 812 813 815 817 817 819 820 822 823 825
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826 826 829 830 832 834
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836 838 839 839 841 842 844 845 847 849
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851 852 853 854 855
. . . 858
. . . 859
Complete List of Contents Pediatric oncology and hematology . . . . . . . . . 938 Pelvic examination . . . . . . . . . . . . . . . . . . 940 Penile cancer . . . . . . . . . . . . . . . . . . . . . 941 Percutaneous transhepatic cholangiography (PTHC) . . . . . . . . . . . . . . . . . . . . . . 943 Pericardial effusion . . . . . . . . . . . . . . . . . 944 Pericardiocentesis . . . . . . . . . . . . . . . . . . 946 Peritoneovenous shunts . . . . . . . . . . . . . . . 946 Personality and cancer . . . . . . . . . . . . . . . . 947 Pesticides and the food chain . . . . . . . . . . . . 948 PET. See Positron emission tomography Peutz-Jeghers syndrome (PJS) . . . . . . . . . . . . 951 Pharmacy oncology . . . . . . . . . . . . . . . . . 952 Phenacetin . . . . . . . . . . . . . . . . . . . . . . 955 Phenolics . . . . . . . . . . . . . . . . . . . . . . . 955 Pheochromocytomas . . . . . . . . . . . . . . . . . 956 Pheresis . . . . . . . . . . . . . . . . . . . . . . . 958 Photodynamic therapy (PDT) . . . . . . . . . . . . 959 Phyllodes tumors. . . . . . . . . . . . . . . . . . . 960 Phytoestrogens . . . . . . . . . . . . . . . . . . . . 962 Pineoblastomas. . . . . . . . . . . . . . . . . . . . 963 Pituitary tumors . . . . . . . . . . . . . . . . . . . 965 PJS. See Peutz-Jeghers syndrome Placental alkaline phosphatase (PALP) . . . . . . . 968 Plant alkaloids and terpenoids in chemotherapy . . . . . . . . . . . . . . . . . . . 968 Plasticizers . . . . . . . . . . . . . . . . . . . . . . 971 Pleural biopsy . . . . . . . . . . . . . . . . . . . . 972 Pleural effusion . . . . . . . . . . . . . . . . . . . 973 Pleurodesis . . . . . . . . . . . . . . . . . . . . . . 975 Pleuropulmonary blastomas . . . . . . . . . . . . . 975 PMS genes . . . . . . . . . . . . . . . . . . . . . . 976 Pneumonectomy . . . . . . . . . . . . . . . . . . . 977 Pneumonia . . . . . . . . . . . . . . . . . . . . . . 979 Polycyclic aromatic hydrocarbons . . . . . . . . . . 981 Polycythemia vera . . . . . . . . . . . . . . . . . . 981 Polypectomy . . . . . . . . . . . . . . . . . . . . . 982 Polyps . . . . . . . . . . . . . . . . . . . . . . . . 983 Polyps, colon. See Colon polyps Polyps, gastric. See Gastric polyps Positron emission tomography (PET) . . . . . . . . 984 Poverty and cancer . . . . . . . . . . . . . . . . . . 987 PPOs. See Preferred provider organizations Prayer and cancer support . . . . . . . . . . . . . . 989 Preferred provider organizations (PPOs) . . . . . . 990 Pregnancy and cancer . . . . . . . . . . . . . . . . 992 Premalignancies . . . . . . . . . . . . . . . . . . . 994 Prevent Cancer Foundation . . . . . . . . . . . . . 997 Prevention . . . . . . . . . . . . . . . . . . . . . . 999 Primary care physician . . . . . . . . . . . . . . . 1001
Nutrition and cancer prevention . . . . . . . . . . . 861 Nutrition and cancer treatment. . . . . . . . . . . . 864 Obesity-associated cancers . . . . . Occupational exposures and cancer . Occupational therapy . . . . . . . . OCs. See Organochlorines Oligodendrogliomas . . . . . . . . . Omega-3 fatty acids . . . . . . . . . Ommaya reservoir . . . . . . . . . . Oncogenes . . . . . . . . . . . . . . Oncogenic viruses . . . . . . . . . . Oncology . . . . . . . . . . . . . . . Oncology clinical nurse specialist . . Oncology social worker . . . . . . . Oophorectomy . . . . . . . . . . . . Ophthalmic oncology . . . . . . . . Opioids . . . . . . . . . . . . . . . . Oral and maxillofacial surgery. . . . Oral and oropharyngeal cancers . . . Orbit tumors . . . . . . . . . . . . . Orchiectomy . . . . . . . . . . . . . Organ transplantation and cancer . . Organochlorines (OCs) . . . . . . . Oropharyngeal cancers. See Oral and oropharyngeal cancers Orthopedic surgery. . . . . . . . . . Otolaryngology . . . . . . . . . . . Ovarian cancers . . . . . . . . . . . Ovarian cysts. . . . . . . . . . . . . Ovarian epithelial cancer . . . . . . Overtreatment . . . . . . . . . . . .
. . . . . . . . 868 . . . . . . . . 871 . . . . . . . . 873 . . . . . . . . . . . . . . . . .
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875 877 878 878 881 882 885 887 888 889 892 893 894 897 898 899 901
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902 903 905 908 909 911
Paget disease of bone . . . . . . . . . . . . . Pain management medications. . . . . . . . . Palliative treatment . . . . . . . . . . . . . . PALP. See Placental alkaline phosphatase Palpation . . . . . . . . . . . . . . . . . . . . Pancolitis . . . . . . . . . . . . . . . . . . . . Pancreatectomy . . . . . . . . . . . . . . . . Pancreatic cancers . . . . . . . . . . . . . . . Pancreatitis . . . . . . . . . . . . . . . . . . . Pap test . . . . . . . . . . . . . . . . . . . . . Paracentesis . . . . . . . . . . . . . . . . . . Paranasal sinus cancers. See Nasal cavity and paranasal sinus cancers Paraneoplastic syndromes . . . . . . . . . . . Parathyroid cancer . . . . . . . . . . . . . . . Pathology . . . . . . . . . . . . . . . . . . . PC-SPES . . . . . . . . . . . . . . . . . . . . PDT. See Photodynamic therapy
. . . 912 . . . 914 . . . 917 . . . . . . .
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920 920 921 923 927 928 929
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931 932 934 937 lxvii
Salem Health: Cancer Primary central nervous system lymphomas . . . . . . . . . . . . . . . . Progesterone receptor assay . . . . . . . . Prostate cancer . . . . . . . . . . . . . . . Prostate-specific antigen (PSA) test . . . . Prostatectomy. . . . . . . . . . . . . . . . Prostatitis . . . . . . . . . . . . . . . . . . Proteasome inhibitors. . . . . . . . . . . . Protein electrophoresis . . . . . . . . . . . Proteomics and cancer research . . . . . . Proton beam therapy . . . . . . . . . . . . Proto-oncogenes and carcinogenesis . . . . PSA test. See Prostate-specific antigen test Psycho-oncology . . . . . . . . . . . . . . Psychosocial aspects of cancer . . . . . . . PTHC. See Percutaneous transhepatic cholangiography Radiation, ionizing. See Ionizing radiation Radiation oncology . . . . . . . . . . . . . Radiation therapies . . . . . . . . . . . . . Radiation therapy, afterloading. See Afterloading radiation therapy Radical neck dissection . . . . . . . . . . . Radiofrequency ablation . . . . . . . . . . Radionuclide scan . . . . . . . . . . . . . Radiopharmaceuticals . . . . . . . . . . . Radon . . . . . . . . . . . . . . . . . . . . RB1 gene . . . . . . . . . . . . . . . . . . Receptor analysis . . . . . . . . . . . . . .
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1003 1003 1004 1006 1008 1009 1010 1010 1012 1014 1015
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. . . . 1021 . . . . 1023
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1027 1027 1030 1030 1032 1032 1033
Reconstructive surgery . . . . . . . . . . . . . . Rectal cancer . . . . . . . . . . . . . . . . . . . Recurrence . . . . . . . . . . . . . . . . . . . . Rehabilitation . . . . . . . . . . . . . . . . . . . Relationships . . . . . . . . . . . . . . . . . . . Renal pelvis tumors. . . . . . . . . . . . . . . . Report on Carcinogens (RoC) . . . . . . . . . . Resveratrol . . . . . . . . . . . . . . . . . . . . Retinoblastomas . . . . . . . . . . . . . . . . . Rhabdomyosarcomas . . . . . . . . . . . . . . . RhoGD12 gene . . . . . . . . . . . . . . . . . . Richter syndrome . . . . . . . . . . . . . . . . . Risk assessment, family history and. See Family history and risk assessment Risks for cancer. . . . . . . . . . . . . . . . . . Robert H. Lurie Cancer Center . . . . . . . . . . RoC. See Report on Carcinogens Rothmund-Thomson syndrome . . . . . . . . . .
. . . . . . . . . . . .
Salivary gland cancer . . . . . . . . . . . . . Salpingectomy and salpingo-oophorectomy . Sarcomas, soft-tissue . . . . . . . . . . . . . Saw palmetto . . . . . . . . . . . . . . . . . Schwannoma tumors . . . . . . . . . . . . . SCLC1 gene. . . . . . . . . . . . . . . . . . Screening, colorectal cancer. See Colorectal cancer screening Screening for cancer . . . . . . . . . . . . . Second opinions . . . . . . . . . . . . . . . Self-image and body image. . . . . . . . . .
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1034 1036 1038 1038 1041 1043 1044 1045 1046 1048 1050 1050
. 1052 . 1054 . 1056 1058 1060 1062 1065 1066 1067
. . . 1067 . . . 1070 . . . 1071
Volume 4 Sjögren syndrome. . . . . . . . . . . . . . . . Skin cancers . . . . . . . . . . . . . . . . . . SLN biopsy and mapping. See Sentinel lymph node biopsy and mapping Small intestine cancer . . . . . . . . . . . . . Smoking cessation . . . . . . . . . . . . . . . Social Security Disability Insurance (SSDI) . . Soft-tissue fibrosarcomas. See Fibrosarcomas, soft-tissue Soots . . . . . . . . . . . . . . . . . . . . . . Soy foods . . . . . . . . . . . . . . . . . . . . Spermatocytomas . . . . . . . . . . . . . . . . Spinal axis tumors . . . . . . . . . . . . . . . Spinal cord compression . . . . . . . . . . . . Splenectomy . . . . . . . . . . . . . . . . . . Sputum cytology . . . . . . . . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . lxxvii Complete List of Contents . . . . . . . . . . . . . lxxix Sentinel lymph node (SLN) biopsy and mapping . . . . . . . . . . . . . . . Sepsis. See Infection and sepsis Sertoli cell tumors . . . . . . . . . . . Sexuality and cancer . . . . . . . . . . Sézary syndrome . . . . . . . . . . . . SIADH. See Syndrome of inappropriate antidiuretic hormone production Side effects . . . . . . . . . . . . . . . Sigmoidoscopy . . . . . . . . . . . . . Silica, crystalline . . . . . . . . . . . . Simian virus 40 . . . . . . . . . . . . . Singlehood and cancer . . . . . . . . .
. . . . . . 1073 . . . . . . 1073 . . . . . . 1074 . . . . . . 1076
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1078 1082 1083 1084 1084 lxviii
. . 1086 . . 1088
. . 1091 . . 1093 . . 1096
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1097 1098 1099 1100 1102 1103 1105
Complete List of Contents Squamous cell carcinomas . . . . . . . . . . . SRS. See Stereotactic radiosurgery SSDI. See Social Security Disability Insurance Staging of cancer . . . . . . . . . . . . . . . . Statistics of cancer . . . . . . . . . . . . . . . Stem cell transplantation . . . . . . . . . . . . Stent therapy . . . . . . . . . . . . . . . . . . Stereotactic needle biopsy . . . . . . . . . . . Stereotactic radiosurgery (SRS) . . . . . . . . Sterility . . . . . . . . . . . . . . . . . . . . . Stomach cancers . . . . . . . . . . . . . . . . Stomatitis . . . . . . . . . . . . . . . . . . . . Stress management . . . . . . . . . . . . . . . Sunlamps . . . . . . . . . . . . . . . . . . . . Sun’s soup . . . . . . . . . . . . . . . . . . . Sunscreens . . . . . . . . . . . . . . . . . . . Superior vena cava syndrome . . . . . . . . . Support groups . . . . . . . . . . . . . . . . . Surgical biopsies . . . . . . . . . . . . . . . . Surgical oncology. . . . . . . . . . . . . . . . Survival rates . . . . . . . . . . . . . . . . . . Survivorship issues . . . . . . . . . . . . . . . Symptoms and cancer. . . . . . . . . . . . . . Syndrome of inappropriate antidiuretic hormone production (SIADH) . . . . . . . . Synovial sarcomas . . . . . . . . . . . . . . . Taste alteration . . . . . . . . . . . . . . Teratocarcinomas . . . . . . . . . . . . . Teratomas . . . . . . . . . . . . . . . . . Testicular cancer . . . . . . . . . . . . . Testicular self-examination (TSE) . . . . Thermal imaging . . . . . . . . . . . . . Thiotepa. . . . . . . . . . . . . . . . . . Thoracentesis . . . . . . . . . . . . . . . Thoracoscopy . . . . . . . . . . . . . . . Thoracotomy . . . . . . . . . . . . . . . Throat cancer . . . . . . . . . . . . . . . Thrombocytopenia . . . . . . . . . . . . Thymomas . . . . . . . . . . . . . . . . Thymus cancer . . . . . . . . . . . . . . Thyroid cancer . . . . . . . . . . . . . . Thyroid nuclear medicine scan . . . . . . TNF. See Tumor necrosis factor TNM staging . . . . . . . . . . . . . . . Tobacco, chewing. See Chewing tobacco Tobacco-related cancers . . . . . . . . . Topoisomerase inhibitors . . . . . . . . . TP53 protein . . . . . . . . . . . . . . . Tracheostomy . . . . . . . . . . . . . . . Transfusion therapy. . . . . . . . . . . .
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Transitional care . . . . . . . . . . . Transitional cell carcinomas . . . . . Transrectal ultrasound . . . . . . . . Transvaginal ultrasound . . . . . . . Trichilemmal carcinomas. . . . . . . TSE. See Testicular self-examination Tuberous sclerosis . . . . . . . . . . Tubular carcinomas . . . . . . . . . . Tumor flare . . . . . . . . . . . . . . Tumor lysis syndrome . . . . . . . . Tumor markers . . . . . . . . . . . . Tumor necrosis factor (TNF) . . . . . Tumor-suppressor genes . . . . . . . Turcot syndrome . . . . . . . . . . . Tyrosine kinase inhibitors . . . . . .
. . 1106
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1108 1111 1114 1116 1118 1119 1120 1121 1124 1125 1127 1128 1129 1130 1132 1135 1138 1140 1143 1144
. . 1147 . . 1149 . . . . . . . . . . . . . . . .
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1151 1152 1153 1154 1156 1157 1158 1158 1160 1161 1162 1164 1166 1167 1169 1172
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1182 1183 1185 1186 1187
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1187 1188 1189 1189 1191 1193 1194 1195 1196
Ultrasound, breast. See Breast ultrasound Ultrasound, endorectal. See Endorectal ultrasound Ultrasound, transrectal. See Transrectal ultrasound Ultrasound, transvaginal. See Transvaginal ultrasound Ultrasound tests . . . . . . . . . . . . . . . Ultraviolet radiation and related exposures Umbilical cord blood transplantation. . . . Upper gastrointestinal (GI) endoscopy . . . Upper gastrointestinal (GI) series . . . . . Urethral cancer . . . . . . . . . . . . . . . Urinalysis . . . . . . . . . . . . . . . . . . Urinary system cancers . . . . . . . . . . . Urography . . . . . . . . . . . . . . . . . Urologic oncology . . . . . . . . . . . . . Urostomy . . . . . . . . . . . . . . . . . . Uterine cancer . . . . . . . . . . . . . . .
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1199 1200 1201 1202 1203 1205 1207 1209 1213 1214 1216 1217
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1220 1221 1223 1225 1226
Vaccines, preventive . . . . . . . . . . . Vaccines, therapeutic . . . . . . . . . . . Vaginal cancer . . . . . . . . . . . . . . Vascular access tubes. . . . . . . . . . . Vasectomy and cancer . . . . . . . . . . Vegetables, cruciferous. See Cruciferous vegetables Veterinary oncology . . . . . . . . . . . VHL disease. See Von Hippel-Lindau disease Vinyl chloride . . . . . . . . . . . . . . Viral oncology . . . . . . . . . . . . . . Virus-related cancers . . . . . . . . . . . Von Hippel-Lindau (VHL) disease. . . . Vulvar cancer . . . . . . . . . . . . . . .
. . . . . 1173 . . . . .
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1174 1175 1177 1179 1180 lxix
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1230 1230 1232 1235 1237
Salem Health: Cancer WAGR syndrome. See Wilms’ tumor aniridiagenitourinary anomalies-mental retardation syndrome and cancer Waldenström macroglobulinemia (WM) . . . . . . 1240 Watchful waiting . . . . . . . . . . . . . . . . . . 1242 Weight loss . . . . . . . . . . . . . . . . . . . . . 1243 Wilms’ tumor . . . . . . . . . . . . . . . . . . . . 1245 Wilms’ tumor aniridia-genitourinary anomaliesmental retardation (WAGR) syndrome and cancer . . . . . . . . . . . . . . . . . . . . . . 1248 Wine and cancer . . . . . . . . . . . . . . . . . . 1250 Wire localization . . . . . . . . . . . . . . . . . . 1250 WM. See Waldenström macroglobulinemia Wood dust . . . . . . . . . . . . . . . . . . . . . 1251
Yolk sac carcinomas . . . . . . . . . . . . . . . . 1256 Young adult cancers . . . . . . . . . . . . . . . . 1256 Zollinger-Ellison syndrome . . . . . . . . . . . . 1260 Drugs by Generic Name . . . Drugs by Trade Name . . . . Associations and Agencies . . Cancer Centers and Hospitals Cancer Support Groups . . . . Carcinogens. . . . . . . . . . Glossary . . . . . . . . . . . Bibliography . . . . . . . . .
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1265 1309 1348 1352 1357 1362 1383 1400
Category List . . . . . . . . . . . . . . . . . . . . 1409 Index . . . . . . . . . . . . . . . . . . . . . . . . 1419
X-ray tests . . . . . . . . . . . . . . . . . . . . . 1252 Xeroderma pigmentosa . . . . . . . . . . . . . . . 1254
lxx
Volume IV Sentinel lymph node (SLN) biopsy and mapping — Zollinger-Ellison syndrome Appendixes Indexes Editor
Jeffrey A. Knight, Ph.D. Mount Holyoke College Medical Consultants
Laurie Jackson-Grusby, Ph.D. Children’s Hospital Boston, Harvard Medical School
Wendy White-Ryan, M.D., FAAP Golisano Children’s Hospital at Strong Memorial Hospital
SALEM PRESS, INC. Pasadena, California Hackensack, New Jersey
Editor in Chief: Dawn P. Dawson Editorial Director: Christina J. Moose Project Editors: Tracy Irons-Georges, Rowena Wildin Dehanke Editorial Assistant: Dana Garey
Production Editor: Joyce I. Buchea Acquisitions Editor: Mark Rehn Photo Editor: Cynthia Breslin Beres Design and Graphics: James Hutson Layout: William Zimmerman
Copyright © 2009, by Salem Press, Inc. All rights in this book are reserved. No part of this work may be used or reproduced in any manner whatsoever or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without written permission from the copyright owner except in the case of brief quotations embodied in critical articles and reviews or in the copying of images deemed to be freely licensed or in the public domain. For information address the publisher, Salem Press, Inc., P.O. Box 50062, Pasadena, California 91115. ∞ The paper used in these volumes conforms to the American National Standard for Permanence of Paper for Printed Library Materials, Z39.48-1992 (R1997). Note to Readers The material presented in Salem Health: Cancer is intended for broad informational and educational purposes. Readers who suspect that they or someone whom they know or provide caregiving for suffers from cancer or any other physical or psychological disorder, disease, or condition described in this set should contact a physician without delay; this work should not be used as a substitute for professional medical diagnosis or staging. Readers who are undergoing or about to undergo any treatment or procedure described in this set should refer to their physicians and other health care team members for guidance concerning preparation and possible effects. This set is not to be considered definitive on the covered topics, and readers should remember that the field of health care is characterized by a diversity of medical opinions and constant expansion in knowledge and understanding. Library of Congress Cataloging-in-Publication Data Salem health : cancer / Jeffrey A. Knight, Laurie Jackson-Grusby, Wendy White-Ryan. p. cm. Includes bibliographical references and index. ISBN 978-1-58765-505-0 (set : alk. paper) — ISBN 978-1-58765-506-7 (vol. 1 : alk. paper) — ISBN 978-1-58765-507-4 (vol. 2 : alk. paper) — ISBN 978-1-58765-508-1 (vol. 3 : alk. paper) — ISBN 978-1-58765-509-8 (vol. 4 : alk. paper) 1. Cancer. I. Knight, Jeffrey A., 1948- II. Jackson-Grusby, Laurie. III. White-Ryan, Wendy. RC265.S32 2008 616.99′4—dc22 2008030861
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Contents Superior vena cava syndrome . . . . . Support groups . . . . . . . . . . . . . Surgical biopsies . . . . . . . . . . . . Surgical oncology. . . . . . . . . . . . Survival rates . . . . . . . . . . . . . . Survivorship issues . . . . . . . . . . . Symptoms and cancer. . . . . . . . . . Syndrome of inappropriate antidiuretic hormone production (SIADH) . . . . Synovial sarcomas . . . . . . . . . . .
Complete List of Contents . . . . . . . . . . . . . lxxix Sentinel lymph node (SLN) biopsy and mapping . . . . . . . . . . . . . . . . . . . Sepsis. See Infection and sepsis Sertoli cell tumors . . . . . . . . . . . . . . . Sexuality and cancer . . . . . . . . . . . . . . Sézary syndrome . . . . . . . . . . . . . . . . SIADH. See Syndrome of inappropriate antidiuretic hormone production Side effects . . . . . . . . . . . . . . . . . . . Sigmoidoscopy . . . . . . . . . . . . . . . . . Silica, crystalline . . . . . . . . . . . . . . . . Simian virus 40 . . . . . . . . . . . . . . . . . Singlehood and cancer . . . . . . . . . . . . . Sjögren syndrome. . . . . . . . . . . . . . . . Skin cancers . . . . . . . . . . . . . . . . . . SLN biopsy and mapping. See Sentinel lymph node biopsy and mapping Small intestine cancer . . . . . . . . . . . . . Smoking cessation . . . . . . . . . . . . . . . Social Security Disability Insurance (SSDI) . . Soft-tissue fibrosarcomas. See Fibrosarcomas, soft-tissue Soots . . . . . . . . . . . . . . . . . . . . . . Soy foods . . . . . . . . . . . . . . . . . . . . Spermatocytomas . . . . . . . . . . . . . . . . Spinal axis tumors . . . . . . . . . . . . . . . Spinal cord compression . . . . . . . . . . . . Splenectomy . . . . . . . . . . . . . . . . . . Sputum cytology . . . . . . . . . . . . . . . . Squamous cell carcinomas . . . . . . . . . . . SRS. See Stereotactic radiosurgery SSDI. See Social Security Disability Insurance Staging of cancer . . . . . . . . . . . . . . . . Statistics of cancer . . . . . . . . . . . . . . . Stem cell transplantation . . . . . . . . . . . . Stent therapy . . . . . . . . . . . . . . . . . . Stereotactic needle biopsy . . . . . . . . . . . Stereotactic radiosurgery (SRS) . . . . . . . . Sterility . . . . . . . . . . . . . . . . . . . . . Stomach cancers . . . . . . . . . . . . . . . . Stomatitis . . . . . . . . . . . . . . . . . . . . Stress management . . . . . . . . . . . . . . . Sunlamps . . . . . . . . . . . . . . . . . . . . Sun’s soup . . . . . . . . . . . . . . . . . . . Sunscreens . . . . . . . . . . . . . . . . . . .
. . 1073 . . 1073 . . 1074 . . 1076
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1078 1082 1083 1084 1084 1086 1088
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1097 1098 1099 1100 1102 1103 1105 1106
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1108 1111 1114 1116 1118 1119 1120 1121 1124 1125 1127 1128 1129 lxxvii
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1130 1132 1135 1138 1140 1143 1144
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Taste alteration . . . . . . . . . . . . . . Teratocarcinomas . . . . . . . . . . . . . Teratomas . . . . . . . . . . . . . . . . . Testicular cancer . . . . . . . . . . . . . Testicular self-examination (TSE) . . . . Thermal imaging . . . . . . . . . . . . . Thiotepa. . . . . . . . . . . . . . . . . . Thoracentesis . . . . . . . . . . . . . . . Thoracoscopy . . . . . . . . . . . . . . . Thoracotomy . . . . . . . . . . . . . . . Throat cancer . . . . . . . . . . . . . . . Thrombocytopenia . . . . . . . . . . . . Thymomas . . . . . . . . . . . . . . . . Thymus cancer . . . . . . . . . . . . . . Thyroid cancer . . . . . . . . . . . . . . Thyroid nuclear medicine scan . . . . . . TNF. See Tumor necrosis factor TNM staging . . . . . . . . . . . . . . . Tobacco, chewing. See Chewing tobacco Tobacco-related cancers . . . . . . . . . Topoisomerase inhibitors . . . . . . . . . TP53 protein . . . . . . . . . . . . . . . Tracheostomy . . . . . . . . . . . . . . . Transfusion therapy. . . . . . . . . . . . Transitional care . . . . . . . . . . . . . Transitional cell carcinomas . . . . . . . Transrectal ultrasound . . . . . . . . . . Transvaginal ultrasound . . . . . . . . . Trichilemmal carcinomas. . . . . . . . . TSE. See Testicular self-examination Tuberous sclerosis . . . . . . . . . . . . Tubular carcinomas . . . . . . . . . . . . Tumor flare . . . . . . . . . . . . . . . . Tumor lysis syndrome . . . . . . . . . . Tumor markers . . . . . . . . . . . . . . Tumor necrosis factor (TNF) . . . . . . .
. . 1091 . . 1093 . . 1096
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1151 1152 1153 1154 1156 1157 1158 1158 1160 1161 1162 1164 1166 1167 1169 1172
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1174 1175 1177 1179 1180 1182 1183 1185 1186 1187
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1187 1188 1189 1189 1191 1193
Salem Health: Cancer Tumor-suppressor genes . . . . . . . . . . . . . . 1194 Turcot syndrome . . . . . . . . . . . . . . . . . . 1195 Tyrosine kinase inhibitors . . . . . . . . . . . . . 1196 Ultrasound, breast. See Breast ultrasound Ultrasound, endorectal. See Endorectal ultrasound Ultrasound, transrectal. See Transrectal ultrasound Ultrasound, transvaginal. See Transvaginal ultrasound Ultrasound tests . . . . . . . . . . . . . . . Ultraviolet radiation and related exposures Umbilical cord blood transplantation. . . . Upper gastrointestinal (GI) endoscopy . . . Upper gastrointestinal (GI) series . . . . . Urethral cancer . . . . . . . . . . . . . . . Urinalysis . . . . . . . . . . . . . . . . . . Urinary system cancers . . . . . . . . . . . Urography . . . . . . . . . . . . . . . . . Urologic oncology . . . . . . . . . . . . . Urostomy . . . . . . . . . . . . . . . . . . Uterine cancer . . . . . . . . . . . . . . . Vaccines, preventive . . . . . . . . . . . Vaccines, therapeutic . . . . . . . . . . . Vaginal cancer . . . . . . . . . . . . . . Vascular access tubes. . . . . . . . . . . Vasectomy and cancer . . . . . . . . . . Vegetables, cruciferous. See Cruciferous vegetables Veterinary oncology . . . . . . . . . . . VHL disease. See Von Hippel-Lindau disease Vinyl chloride . . . . . . . . . . . . . . Viral oncology . . . . . . . . . . . . . . Virus-related cancers . . . . . . . . . . .
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1199 1200 1201 1202 1203 1205 1207 1209 1213 1214 1216 1217
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1220 1221 1223 1225 1226
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Von Hippel-Lindau (VHL) disease. . . . . . . . . 1235 Vulvar cancer . . . . . . . . . . . . . . . . . . . . 1237 WAGR syndrome. See Wilms’ tumor aniridiagenitourinary anomalies-mental retardation syndrome and cancer Waldenström macroglobulinemia (WM) . . . . . . 1240 Watchful waiting . . . . . . . . . . . . . . . . . . 1242 Weight loss . . . . . . . . . . . . . . . . . . . . . 1243 Wilms’ tumor . . . . . . . . . . . . . . . . . . . . 1245 Wilms’ tumor aniridia-genitourinary anomaliesmental retardation (WAGR) syndrome and cancer . . . . . . . . . . . . . . . . . . . . . . 1248 Wine and cancer . . . . . . . . . . . . . . . . . . 1250 Wire localization . . . . . . . . . . . . . . . . . . 1250 WM. See Waldenström macroglobulinemia Wood dust . . . . . . . . . . . . . . . . . . . . . 1251 X-ray tests . . . . . . . . . . . . . . . . . . . . . 1252 Xeroderma pigmentosa . . . . . . . . . . . . . . . 1254 Yolk sac carcinomas . . . . . . . . . . . . . . . . 1256 Young adult cancers . . . . . . . . . . . . . . . . 1256 Zollinger-Ellison syndrome . . . . . . . . . . . . 1260 Drugs by Generic Name . . . Drugs by Trade Name . . . . Associations and Agencies . . Cancer Centers and Hospitals Cancer Support Groups . . . . Carcinogens. . . . . . . . . . Glossary . . . . . . . . . . . Bibliography . . . . . . . . .
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Category List . . . . . . . . . . . . . . . . . . . . 1409 Index . . . . . . . . . . . . . . . . . . . . . . . . 1419
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Complete List of Contents Volume 1 Alkylating agents in chemotherapy . . . . . . . ALL. See Acute lymphocytic leukemia Allicin, garlic and. See Garlic and allicin Alopecia . . . . . . . . . . . . . . . . . . . . . ALP. See Alkaline phosphatase test Alpha-fetoprotein (AFP) levels . . . . . . . . . Alternative therapies. See Complementary and alternative therapies Alveolar soft-part sarcomas . . . . . . . . . . . Amenorrhea . . . . . . . . . . . . . . . . . . . American Association for Cancer Research (AACR) . . . . . . . . . . . . . . . . . . . . American Cancer Society (ACS) . . . . . . . . American Institute for Cancer Research (AICR) 4-Aminobiphenyl . . . . . . . . . . . . . . . . AML. See Acute myelocytic leukemia Amputation . . . . . . . . . . . . . . . . . . . Amyloidosis . . . . . . . . . . . . . . . . . . . Anal cancer . . . . . . . . . . . . . . . . . . . Androgen drugs . . . . . . . . . . . . . . . . . Anemia . . . . . . . . . . . . . . . . . . . . . Anemia, aplastic. See Aplastic anemia Anemia, hemolytic. See Hemolytic anemia Angiogenesis . . . . . . . . . . . . . . . . . . Angiogenesis inhibitors . . . . . . . . . . . . . Angiography. . . . . . . . . . . . . . . . . . . Angiosarcomas . . . . . . . . . . . . . . . . . Anoscopy . . . . . . . . . . . . . . . . . . . . Anthraquinones . . . . . . . . . . . . . . . . . Anthrax . . . . . . . . . . . . . . . . . . . . . Antiandrogens . . . . . . . . . . . . . . . . . . Antidiarrheal agents . . . . . . . . . . . . . . . Antiestrogens . . . . . . . . . . . . . . . . . . Antifungal therapies . . . . . . . . . . . . . . . Antimetabolites in chemotherapy . . . . . . . . Antinausea medications . . . . . . . . . . . . . Antineoplastics in chemotherapy . . . . . . . . Antioxidants . . . . . . . . . . . . . . . . . . . Antiperspirants and breast cancer . . . . . . . . Antiviral therapies. . . . . . . . . . . . . . . . Anxiety . . . . . . . . . . . . . . . . . . . . . APBI. See Accelerated partial breast irradiation APC gene testing . . . . . . . . . . . . . . . . Aplastic anemia . . . . . . . . . . . . . . . . . Appendix cancer . . . . . . . . . . . . . . . . Appetite loss. . . . . . . . . . . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . . . v Publisher’s Note . . . . . . . . . . . . . . . . . . . . ix About the Editors . . . . . . . . . . . . . . . . . . . xi Contributors . . . . . . . . . . . . . . . . . . . . . xiii Complete List of Contents . . . . . . . . . . . . . . xv AACR. See American Association for Cancer Research ABCD. . . . . . . . . . . . . . . . . . . . . . . . . . 1 ACC. See Adenoid cystic carcinoma Abdominoperineal resection (APR) . . . . . . . . . . 1 Accelerated partial breast irradiation (APBI). . . . . . 3 Achlorhydria . . . . . . . . . . . . . . . . . . . . . . 4 Acoustic neuromas . . . . . . . . . . . . . . . . . . . 4 Acquired immunodeficiency disease-related cancers. See HIV/AIDS-related cancers Acrylamides . . . . . . . . . . . . . . . . . . . . . . 6 ACS. See American Cancer Society Acupuncture and acupressure for cancer patients . . . 8 Acute lymphocytic leukemia (ALL) . . . . . . . . . 11 Acute myelocytic leukemia (AML) . . . . . . . . . . 13 Adenocarcinomas . . . . . . . . . . . . . . . . . . . 16 Adenoid cystic carcinoma (ACC) . . . . . . . . . . . 17 Adenomatoid tumors . . . . . . . . . . . . . . . . . 18 Adenomatous polyps . . . . . . . . . . . . . . . . . 18 Adenoviruses . . . . . . . . . . . . . . . . . . . . . 19 Adjuvant therapy . . . . . . . . . . . . . . . . . . . 20 Adrenal gland cancers . . . . . . . . . . . . . . . . . 21 Adrenocortical cancer . . . . . . . . . . . . . . . . . 23 Advance directives . . . . . . . . . . . . . . . . . . 24 Aflatoxins . . . . . . . . . . . . . . . . . . . . . . . 26 AFP levels. See Alpha-fetoprotein levels African Americans and cancer . . . . . . . . . . . . 28 Africans and cancer . . . . . . . . . . . . . . . . . . 31 Afterloading radiation therapy . . . . . . . . . . . . 32 Agent Orange . . . . . . . . . . . . . . . . . . . . . 34 Aging and cancer . . . . . . . . . . . . . . . . . . . 34 AICR. See American Institute for Cancer Research Aids and devices for cancer patients . . . . . . . . . 38 AIDS-related cancers. See HIV/AIDS-related cancers Air pollution . . . . . . . . . . . . . . . . . . . . . . 39 Alcohol, alcoholism, and cancer . . . . . . . . . . . 42 Aleukemia . . . . . . . . . . . . . . . . . . . . . . . 43 Alkaline phosphatase test (ALP) . . . . . . . . . . . 44 lxxix
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64 66 68 69 70 71 71 72 73 75 76 78 81 83 86 88 90 93
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Salem Health: Cancer APR. See Abdominoperineal resection Arsenic compounds . . . . . . . . . . Arterial embolization . . . . . . . . . Artificial sweeteners . . . . . . . . . . Asbestos . . . . . . . . . . . . . . . . Ascites . . . . . . . . . . . . . . . . . Ashkenazi Jews and cancer . . . . . . Asian Americans and cancer. . . . . . Astrocytomas. . . . . . . . . . . . . . Ataxia telangiectasia (AT) . . . . . . . Autologous blood transfusion . . . . . Axillary dissection . . . . . . . . . . . Azathioprine . . . . . . . . . . . . . .
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Bacillus Calmette Guérin (BCG) . . . . . . . . Bacteria as causes of cancer . . . . . . . . . . . Barium enema . . . . . . . . . . . . . . . . . . Barium swallow . . . . . . . . . . . . . . . . . Barrett esophagus . . . . . . . . . . . . . . . . Basal cell carcinomas . . . . . . . . . . . . . . BCG. See Bacillus Calmette Guérin Beckwith-Wiedemann syndrome (BWS) . . . . Benign prostatic hyperplasia (BPH) . . . . . . . Benign tumors . . . . . . . . . . . . . . . . . . Benzene . . . . . . . . . . . . . . . . . . . . . Benzidine and dyes metabolized to benzidine . . Benzodiazepines . . . . . . . . . . . . . . . . . Bereavement, grief and. See Grief and bereavement Beryllium and beryllium compounds . . . . . . Beta-carotene . . . . . . . . . . . . . . . . . . Bethesda criteria . . . . . . . . . . . . . . . . . BHDS. See Birt-Hogg-Dubé syndrome Bile duct cancer . . . . . . . . . . . . . . . . . Bilobectomy . . . . . . . . . . . . . . . . . . . Bioflavonoids . . . . . . . . . . . . . . . . . . Biological therapy . . . . . . . . . . . . . . . . Biopsy. See also Computed tomography-guided biopsy; Core needle biopsy; Liver biopsy; Needle biopsies; Pleural biopsy; Stereotactic needle biopsy; Surgical biopsies . . . . . . . Birt-Hogg-Dubé syndrome (BHDS) . . . . . . . Birth control pills and cancer . . . . . . . . . . Bis(chloromethyl) ether and technical-grade chloromethyl methyl ether . . . . . . . . . . Bisphenol A (BPA) . . . . . . . . . . . . . . . Bisphosphonates . . . . . . . . . . . . . . . . . Bladder cancer . . . . . . . . . . . . . . . . . . Blood cancers . . . . . . . . . . . . . . . . . . BMT. See Bone marrow transplantation BNCT. See Boron neutron capture therapy
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Body image. See Self-image and body image Bone cancers . . . . . . . . . . . . . . . . . . . Bone marrow aspiration and biopsy . . . . . . . Bone marrow transplantation (BMT) . . . . . . Bone pain . . . . . . . . . . . . . . . . . . . . Bone scan . . . . . . . . . . . . . . . . . . . . Boron neutron capture therapy (BNCT) . . . . . Bowen disease . . . . . . . . . . . . . . . . . . BPA. See Bisphenol A BPH. See Benign prostatic hyperplasia BPI. See Brief Pain Inventory Brachytherapy . . . . . . . . . . . . . . . . . . BRAF gene . . . . . . . . . . . . . . . . . . . . Brain and central nervous system cancers . . . . Brain scan . . . . . . . . . . . . . . . . . . . . BRCA1 and BRCA2 genes . . . . . . . . . . . . Breakthrough pain . . . . . . . . . . . . . . . . Breast, calcifications of. See Calcifications of the breast Breast, medullary carcinoma of. See Medullary carcinoma of the breast Breast cancer, cutaneous. See Cutaneous breast cancer Breast cancer, estrogen-receptor-sensitive. See Estrogen-receptor-sensitive breast cancer Breast cancer in children and adolescents . . . . Breast cancer in men . . . . . . . . . . . . . . . Breast cancer in pregnant women . . . . . . . . Breast cancers . . . . . . . . . . . . . . . . . . Breast implants. . . . . . . . . . . . . . . . . . Breast reconstruction. . . . . . . . . . . . . . . Breast self-examination (BSE). . . . . . . . . . Breast ultrasound. . . . . . . . . . . . . . . . . Breslow’s staging . . . . . . . . . . . . . . . . Brief Pain Inventory (BPI) . . . . . . . . . . . . Brompton cocktail . . . . . . . . . . . . . . . . Bronchial adenomas . . . . . . . . . . . . . . . Bronchoalveolar lung cancer . . . . . . . . . . Bronchography. . . . . . . . . . . . . . . . . . Bronchoscopy . . . . . . . . . . . . . . . . . . BSE. See Breast self-examination Burkitt lymphoma . . . . . . . . . . . . . . . . 1,3-Butadiene . . . . . . . . . . . . . . . . . . 1,4-Butanediol dimethanesulfonate . . . . . . . BWS. See Beckwith-Wiedemann syndrome
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CA 15-3 test . CA 19-9 test . CA 27-29 test CA 125 test. . Cachexia . . . lxxx
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Complete List of Contents Cadmium and cadmium compounds. . . . . . . . Caffeine . . . . . . . . . . . . . . . . . . . . . . Calcifications of the breast. . . . . . . . . . . . . Calcium . . . . . . . . . . . . . . . . . . . . . . Cancell . . . . . . . . . . . . . . . . . . . . . . . Cancer biology . . . . . . . . . . . . . . . . . . . Cancer care team . . . . . . . . . . . . . . . . . . Cancer clusters . . . . . . . . . . . . . . . . . . . Cancer education. . . . . . . . . . . . . . . . . . Candidiasis . . . . . . . . . . . . . . . . . . . . . Carcinoembryonic antigen antibody (CEA) test . . . . . . . . . . . . . . . . . . . . . . . . Carcinogens, known . . . . . . . . . . . . . . . . Carcinogens, reasonably anticipated. . . . . . . . Carcinoid tumors and carcinoid syndrome . . . . Carcinoma of unknown primary origin (CUP) . . Carcinomas. . . . . . . . . . . . . . . . . . . . . Carcinomas, invasive ductal. See Invasive ductal carcinomas Carcinomas, invasive lobular. See Invasive lobular carcinomas Carcinomas, leptomeningeal. See Leptomeningeal carcinomas Carcinomatosis. . . . . . . . . . . . . . . . . . . Carcinomatous meningitis . . . . . . . . . . . . . Carcinosarcomas . . . . . . . . . . . . . . . . . . Cardiomyopathy in cancer patients . . . . . . . . Cardiopulmonary resuscitation (CPR) . . . . . . . Caregivers and caregiving . . . . . . . . . . . . . Caregiving, long-distance. See Long-distance caregiving Carney complex . . . . . . . . . . . . . . . . . . Carotenoids . . . . . . . . . . . . . . . . . . . . Cartilage supplements . . . . . . . . . . . . . . . Case management . . . . . . . . . . . . . . . . . Castleman disease . . . . . . . . . . . . . . . . . CBC. See Complete blood count CBE. See Clinical breast exam CDKN2A. See Cyclin-dependent kinase inhibitor-2A CEA test. See Carcinoembryonic antigen antibody test Cell phones. . . . . . . . . . . . . . . . . . . . . Cervical cancer. . . . . . . . . . . . . . . . . . . Chemoembolization . . . . . . . . . . . . . . . . Chemoprevention . . . . . . . . . . . . . . . . . Chemotherapy . . . . . . . . . . . . . . . . . . . Chemotherapy, cognitive effects of. See Cognitive effects of cancer and chemotherapy Chewing tobacco. . . . . . . . . . . . . . . . . . Childbirth and cancer . . . . . . . . . . . . . . .
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208 209 211 212 212 213 216 218 220 221
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Childhood cancers . . . . . . . . . . . . . . . . Chlorambucil. . . . . . . . . . . . . . . . . . . 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)1-nitrosourea (MeCCNU) . . . . . . . . . . . Cholecystectomy . . . . . . . . . . . . . . . . . Chordomas . . . . . . . . . . . . . . . . . . . . Choriocarcinomas . . . . . . . . . . . . . . . . CHPP. See Continuous hyperthermic peritoneal perfusion Chromium hexavalent compounds. . . . . . . . Chromosomes and cancer . . . . . . . . . . . . Chronic lymphocytic leukemia (CLL) . . . . . . Chronic myeloid leukemia (CML). . . . . . . . Cigarettes and cigars . . . . . . . . . . . . . . . Clinical breast exam (CBE) . . . . . . . . . . . Clinical trials . . . . . . . . . . . . . . . . . . . CLL. See Chronic lymphocytic leukemia CML. See Chronic myeloid leukemia Coal tars and coal tar pitches . . . . . . . . . . Cobalt 60 radiation. . . . . . . . . . . . . . . . Coenzyme Q10. . . . . . . . . . . . . . . . . . Cognitive effects of cancer and chemotherapy . Coke oven emissions. . . . . . . . . . . . . . . Cold nodule . . . . . . . . . . . . . . . . . . . Colectomy . . . . . . . . . . . . . . . . . . . . Coloanal anastomosis . . . . . . . . . . . . . . Colon polyps . . . . . . . . . . . . . . . . . . . Colonoscopy and virtual colonoscopy . . . . . . Colony-stimulating factors (CSFs) . . . . . . . Colorectal cancer. . . . . . . . . . . . . . . . . Colorectal cancer screening . . . . . . . . . . . Colostomy . . . . . . . . . . . . . . . . . . . . Colposcopy. . . . . . . . . . . . . . . . . . . . Comedo carcinomas . . . . . . . . . . . . . . . Complementary and alternative therapies . . . . Complete blood count (CBC) . . . . . . . . . . Computed tomography (CT)-guided biopsy . . . . . . . . . . . . . . . . . . . . . Computed tomography (CT) scan . . . . . . . . Conization . . . . . . . . . . . . . . . . . . . . Continuous hyperthermic peritoneal perfusion (CHPP) . . . . . . . . . . . . . . . . . . . . Cordectomy . . . . . . . . . . . . . . . . . . . Cordotomy . . . . . . . . . . . . . . . . . . . . Core needle biopsy. . . . . . . . . . . . . . . . Corticosteroids . . . . . . . . . . . . . . . . . . Coughing . . . . . . . . . . . . . . . . . . . . . Counseling for cancer patients and survivors . . Cowden syndrome . . . . . . . . . . . . . . . . COX-2 inhibitors. See Cyclooxygenase 2 inhibitors
249 251 253 254 257
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288 289 289 290 292 292 293 294 296 297 299 300 304 306 308 309 309 312
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318 318 319 321 321 322 324 326
Salem Health: Cancer CPR. See Cardiopulmonary resuscitation Craniopharyngiomas . . . . . . . . . . . . Craniosynostosis . . . . . . . . . . . . . . Craniotomy. . . . . . . . . . . . . . . . . Crohn disease . . . . . . . . . . . . . . . Cruciferous vegetables . . . . . . . . . . . Cryoablation . . . . . . . . . . . . . . . . Cryptorchidism. . . . . . . . . . . . . . . CSFs. See Colony-stimulating factors CT scan. See Computed tomography scan CTCL. See Cutaneous T-cell lymphoma Culdoscopy. . . . . . . . . . . . . . . . . CUP. See Carcinoma of unknown primary origin Curcumin. . . . . . . . . . . . . . . . . . Cushing syndrome and cancer . . . . . . . Cutaneous breast cancer . . . . . . . . . . Cutaneous T-cell lymphoma (CTCL) . . .
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Cyclin-dependent kinase inhibitor-2A (CDKN2A). . . . . . . . . . . . . . . Cyclooxygenase 2 (COX-2) inhibitors . Cyclophosphamide. . . . . . . . . . . . Cyclosporin A . . . . . . . . . . . . . . Cystography . . . . . . . . . . . . . . . Cystoscopy . . . . . . . . . . . . . . . . Cytogenetics . . . . . . . . . . . . . . . Cytokines . . . . . . . . . . . . . . . . Cytology . . . . . . . . . . . . . . . . . Cytology, sputum. See Sputum cytology
327 329 331 332 335 336 338
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344 344 345 346 347 347 348 350 350
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D&C. See Dilation and curettage Dana-Farber Cancer Institute . . . . . . . . . . . . 354 DCIS. See Ductal carcinoma in situ DEA. See Diethanolamine DEHP. See Di(2-ethylhexyl) phthalate Delta-9-tetrahydrocannabinol . . . . . . . . . . . . 355
339 340 341 342
Volume 2 Down syndrome and leukemia. . . . . . . . DPC4 gene testing . . . . . . . . . . . . . . DRE. See Digital rectal exam Drug resistance and multidrug resistance (MDR) . . . . . . . . . . . . . . . . . . . Dry mouth . . . . . . . . . . . . . . . . . . DSRCT. See Desmoplastic small round cell tumor Duct ectasia . . . . . . . . . . . . . . . . . Ductal carcinoma in situ (DCIS). . . . . . . Ductal lavage. . . . . . . . . . . . . . . . . Ductogram . . . . . . . . . . . . . . . . . . Duke Comprehensive Cancer Center . . . . Dukes’ classification . . . . . . . . . . . . . Duodenal carcinomas . . . . . . . . . . . . Dye, hair. See Hair dye Dysplastic nevus syndrome . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . xxxiii Complete List of Contents . . . . . . . . . . . . xxxvii Denys-Drash syndrome and cancer . . . . . . Depression . . . . . . . . . . . . . . . . . . . Dermatofibrosarcoma protuberans (DFSP) . . Dermatology oncology. . . . . . . . . . . . . DES. See Diethylstilbestrol Desmoid tumors . . . . . . . . . . . . . . . . Desmoplastic small round cell tumor (DSRCT) . . . . . . . . . . . . . . . . . . Developing nations and cancer . . . . . . . . DFSP. See Dermatofibrosarcoma protuberans Di(2-ethylhexyl) phthalate (DEHP) . . . . . . Diarrhea . . . . . . . . . . . . . . . . . . . . DIC. See Disseminated intravascular coagulation Dietary supplements . . . . . . . . . . . . . . Diethanolamine (DEA) . . . . . . . . . . . . Diethylstilbestrol (DES) . . . . . . . . . . . . Digital rectal exam (DRE) . . . . . . . . . . . Dilation and curettage (D&C) . . . . . . . . . Dioxins . . . . . . . . . . . . . . . . . . . . . Disseminated intravascular coagulation (DIC) . . . . . . . . . . . . . . . . . . . . Diverticulosis and diverticulitis . . . . . . . . DNR. See Do-not-resuscitate order Do-not-resuscitate (DNR) order . . . . . . . .
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386 387 389 389 390 392 393
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Eaton-Lambert syndrome. See Lambert-Eaton myasthenic syndrome EBRT. See External beam radiation therapy Edema . . . . . . . . . . . . . . . . . . . . . Education, cancer. See Cancer education Elderly and cancer . . . . . . . . . . . . . . . Electrolarynx . . . . . . . . . . . . . . . . . . Electromagnetic radiation . . . . . . . . . . . Electroporation therapy . . . . . . . . . . . . Electrosurgery . . . . . . . . . . . . . . . . .
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396 399 399 400 401
Complete List of Contents Embolization . . . . . . . . . . . . . . . . . . . . Embryonal cell cancer . . . . . . . . . . . . . . . End-of-life care . . . . . . . . . . . . . . . . . . Endocrine cancers . . . . . . . . . . . . . . . . . Endocrinology oncology . . . . . . . . . . . . . . Endometrial cancer . . . . . . . . . . . . . . . . Endometrial hyperplasia . . . . . . . . . . . . . . Endorectal ultrasound . . . . . . . . . . . . . . . Endoscopic retrograde cholangiopancreatography (ERCP) . . . . . . . . . . . . . . . . . . . . . Endoscopy . . . . . . . . . . . . . . . . . . . . . Endoscopy, upper gastrointestinal. See Upper gastrointestinal endoscopy Endotheliomas . . . . . . . . . . . . . . . . . . . Enteritis . . . . . . . . . . . . . . . . . . . . . . Enterostomal therapy . . . . . . . . . . . . . . . Eosinophilic leukemia . . . . . . . . . . . . . . . Ependymomas . . . . . . . . . . . . . . . . . . . Epidemiology of cancer . . . . . . . . . . . . . . Epidermoid cancers of mucous membranes . . . . Epstein-Barr virus . . . . . . . . . . . . . . . . . ERCP. See Endoscopic retrograde cholangiopancreatography ERD. See Estrogen receptor downregulator Erionite. . . . . . . . . . . . . . . . . . . . . . . Erythroplakia. . . . . . . . . . . . . . . . . . . . Esophageal cancer . . . . . . . . . . . . . . . . . Esophageal speech . . . . . . . . . . . . . . . . . Esophagectomy . . . . . . . . . . . . . . . . . . Esophagitis . . . . . . . . . . . . . . . . . . . . . Essiac . . . . . . . . . . . . . . . . . . . . . . . Estrogen receptor downregulator (ERD) . . . . . Estrogen-receptor-sensitive breast cancer . . . . . Ethnicity and cancer . . . . . . . . . . . . . . . . Ethylene oxide . . . . . . . . . . . . . . . . . . . Ewing sarcoma . . . . . . . . . . . . . . . . . . . Exenteration . . . . . . . . . . . . . . . . . . . . Exercise and cancer . . . . . . . . . . . . . . . . External beam radiation therapy (EBRT) . . . . . Eye cancers . . . . . . . . . . . . . . . . . . . . Eyelid cancer. . . . . . . . . . . . . . . . . . . .
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Fallopian tube cancer . . . . . . . Family history and risk assessment Fanconi anemia . . . . . . . . . . Fatigue . . . . . . . . . . . . . . . Fecal occult blood test (FOBT) . . Fertility drugs and cancer . . . . . Fertility issues . . . . . . . . . . . Fever . . . . . . . . . . . . . . . . Fiber . . . . . . . . . . . . . . . .
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402 403 404 406 409 412 414 416
. 417 . 417
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420 421 422 424 425 426 429 431
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433 433 434 436 438 439 441 441 442 444 447 447 450 451 454 455 458
. . . . . . . . .
460 461 464 466 467 469 471 472 474
Fibroadenomas . . . . . . . . . . . . . . . . Fibrocystic breast changes . . . . . . . . . . Fibrosarcomas, soft-tissue . . . . . . . . . . Financial issues . . . . . . . . . . . . . . . 5HIAA test. See 5-Hydroxyindoleacetic acid test 5Q minus syndrome . . . . . . . . . . . . . Flow cytometry . . . . . . . . . . . . . . . FOBT. See Fecal occult blood test Folic acid. . . . . . . . . . . . . . . . . . . Formaldehyde . . . . . . . . . . . . . . . . Fox Chase Cancer Center . . . . . . . . . . Fred Hutchinson Cancer Research Center . . Free radicals . . . . . . . . . . . . . . . . . Fruits . . . . . . . . . . . . . . . . . . . . .
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486 486 487 488 490 491
Gallbladder cancer . . . . . . . . . . . . . . Gallium scan . . . . . . . . . . . . . . . . . Gamma Knife . . . . . . . . . . . . . . . . Gardner syndrome . . . . . . . . . . . . . . Garlic and allicin . . . . . . . . . . . . . . . Gastric polyps . . . . . . . . . . . . . . . . Gastrinomas . . . . . . . . . . . . . . . . . Gastrointestinal cancers . . . . . . . . . . . Gastrointestinal complications of cancer treatment. . . . . . . . . . . . . . . . . . Gastrointestinal oncology . . . . . . . . . . Gastrointestinal stromal tumors (GISTs) . . GCTs. See Giant cell tumors Gene therapy . . . . . . . . . . . . . . . . . Genetic counseling . . . . . . . . . . . . . . Genetic testing . . . . . . . . . . . . . . . . Genetics of cancer . . . . . . . . . . . . . . Geography and cancer . . . . . . . . . . . . Germ-cell tumors . . . . . . . . . . . . . . Gerson therapy . . . . . . . . . . . . . . . . Gestational trophoblastic tumors (GTTs) . . Giant cell tumors (GCTs) . . . . . . . . . . Ginseng, panax. . . . . . . . . . . . . . . . GISTs. See Gastrointestinal stromal tumors Gleason grading system . . . . . . . . . . . Gliomas . . . . . . . . . . . . . . . . . . . Glomus tumors . . . . . . . . . . . . . . . . Glossectomy . . . . . . . . . . . . . . . . . Glutamine . . . . . . . . . . . . . . . . . . Gonioscopy . . . . . . . . . . . . . . . . . Grading of tumors . . . . . . . . . . . . . . Graft-versus-host disease (GVHD) . . . . . Granulosa cell tumors . . . . . . . . . . . . Green tea . . . . . . . . . . . . . . . . . . . Grief and bereavement . . . . . . . . . . . .
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493 495 497 498 499 500 501 502
lxxxiii
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475 476 478 481
. . . . 484 . . . . 484
. . . . 506 . . . . 508 . . . . 511 . . . . . . . . . .
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512 515 517 519 522 525 527 527 530 531
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532 533 534 535 536 536 537 538 540 540 541
Salem Health: Cancer GTTs. See Gestational trophoblastic tumors GVHD. See Graft-versus-host disease Gynecologic cancers . . . . . . . . . . . . . . . . . 543 Gynecologic oncology . . . . . . . . . . . . . . . . 547 H. pylori. See Helicobacter pylori HAI. See Hepatic arterial infusion Hair dye . . . . . . . . . . . . . . . . . . . . . . Hairy cell leukemia . . . . . . . . . . . . . . . . Hand-foot syndrome (HFS) . . . . . . . . . . . . HBV. See Hepatitis B virus HCG. See Human chorionic gonadotropin HCV. See Hepatitis C virus Head and neck cancers . . . . . . . . . . . . . . . Health maintenance organizations (HMOs) . . . . Helicobacter pylori. . . . . . . . . . . . . . . . . Hemangioblastomas . . . . . . . . . . . . . . . . Hemangiopericytomas . . . . . . . . . . . . . . . Hemangiosarcomas . . . . . . . . . . . . . . . . Hematemesis . . . . . . . . . . . . . . . . . . . . Hematologic oncology . . . . . . . . . . . . . . . Hematuria . . . . . . . . . . . . . . . . . . . . . Hemochromatosis . . . . . . . . . . . . . . . . . Hemolytic anemia . . . . . . . . . . . . . . . . . Hemoptysis. . . . . . . . . . . . . . . . . . . . . Hemorrhoids . . . . . . . . . . . . . . . . . . . . Hepatic arterial infusion (HAI) . . . . . . . . . . Hepatitis B virus (HBV) . . . . . . . . . . . . . . Hepatitis C virus (HCV) . . . . . . . . . . . . . . Hepatomegaly . . . . . . . . . . . . . . . . . . . HER2/neu protein . . . . . . . . . . . . . . . . . Herbs as antioxidants . . . . . . . . . . . . . . . Hereditary cancer syndromes . . . . . . . . . . . Hereditary diffuse gastric cancer . . . . . . . . . Hereditary leiomyomatosis and renal cell cancer (HLRCC) . . . . . . . . . . . . . . . . Hereditary mixed polyposis syndrome . . . . . . Hereditary non-VHL clear cell renal cell carcinomas . . . . . . . . . . . . . . . . . . . Hereditary pancreatitis . . . . . . . . . . . . . . . Hereditary papillary renal cell carcinomas . . . . Hereditary polyposis syndromes . . . . . . . . . . Herpes simplex virus. . . . . . . . . . . . . . . . Herpes zoster virus. . . . . . . . . . . . . . . . . HFS. See Hand-foot syndrome Hispanics and cancer. See Latinos/Hispanics and cancer Histamine 2 antagonists . . . . . . . . . . . . . . Histiocytosis X . . . . . . . . . . . . . . . . . . . HIV/AIDS-related cancers . . . . . . . . . . . . .
. 550 . 550 . 552
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554 557 558 559 559 560 561 562 564 565 566 566 567 568 569 570 571 573 573 574 576
. 577 . 579 . . . . . .
580 580 581 582 584 586
. 587 . 588 . 590
HLRCC. See Hereditary leiomyomatosis and renal cell cancer HMOs. See Health maintenance organizations Hodgkin disease . . . . . . . . . . . . . . . . . Home health services . . . . . . . . . . . . . . Hormonal therapies . . . . . . . . . . . . . . . Hormone receptor tests . . . . . . . . . . . . . Hormone replacement therapy (HRT) . . . . . . Horner syndrome. . . . . . . . . . . . . . . . . Hospice care . . . . . . . . . . . . . . . . . . . Hot flashes . . . . . . . . . . . . . . . . . . . . HPV. See Human papillomavirus HRAS gene testing . . . . . . . . . . . . . . . . HRT. See Hormone replacement therapy HTLV. See Human T-cell leukemia virus Human chorionic gonadotropin (HCG) . . . . . Human growth factors and tumor growth . . . . Human immunodeficiency virus-related cancers. See HIV/AIDS-related cancers Human papillomavirus (HPV) . . . . . . . . . . Human T-cell leukemia virus (HTLV) . . . . . Hydatidiform mole . . . . . . . . . . . . . . . . 5-Hydroxyindoleacetic acid (5HIAA) test . . . . Hypercalcemia . . . . . . . . . . . . . . . . . . Hypercoagulation disorders . . . . . . . . . . . Hyperthermia therapy . . . . . . . . . . . . . . Hyperthermic perfusion . . . . . . . . . . . . . Hypopharyngeal cancer . . . . . . . . . . . . . Hysterectomy . . . . . . . . . . . . . . . . . . Hysterography . . . . . . . . . . . . . . . . . . Hystero-oophorectomy. . . . . . . . . . . . . . Hysteroscopy. . . . . . . . . . . . . . . . . . . IEP. See Immunoelectrophoresis iFOBT. See Immunochemical fecal occult blood test Ileostomy. . . . . . . . . . . . . . . . . . . . . Imaging tests . . . . . . . . . . . . . . . . . . . Immune response to cancer . . . . . . . . . . . Immunochemical fecal occult blood test (iFOBT) . . . . . . . . . . . . . . . . . . . . Immunocytochemistry and immunohistochemistry . . . . . . . . . . . . Immunoelectrophoresis (IEP) . . . . . . . . . . Immunotherapy . . . . . . . . . . . . . . . . . IMRT. See Intensity-modulated radiation therapy Indoles . . . . . . . . . . . . . . . . . . . . . . Infection and sepsis . . . . . . . . . . . . . . . Infectious cancers . . . . . . . . . . . . . . . . Infertility and cancer . . . . . . . . . . . . . . .
lxxxiv
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593 597 599 601 603 605 606 608
. . 609
. . 609 . . 610
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611 612 612 613 614 615 617 618 619 620 621 622 623
. . 625 . . 626 . . 629 . . 632 . . 633 . . 634 . . 635
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638 638 641 643
Complete List of Contents Inflammatory bowel disease . . . . . . . . . . Informed consent. . . . . . . . . . . . . . . . Infusion therapies . . . . . . . . . . . . . . . Insurance . . . . . . . . . . . . . . . . . . . . Integrative oncology . . . . . . . . . . . . . . Intensity-modulated radiation therapy (IMRT) Interferon. . . . . . . . . . . . . . . . . . . . Interleukins. . . . . . . . . . . . . . . . . . . Invasive cancer. . . . . . . . . . . . . . . . . Invasive ductal carcinomas . . . . . . . . . . Invasive lobular carcinomas . . . . . . . . . . Ionizing radiation . . . . . . . . . . . . . . . Iridium seeds . . . . . . . . . . . . . . . . . . Islet cell tumors . . . . . . . . . . . . . . . . Isoflavones . . . . . . . . . . . . . . . . . . . Itching . . . . . . . . . . . . . . . . . . . . .
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645 646 647 648 651 652 653 654 655 656 657 657 658 659 661 661
Lambert-Eaton myasthenic syndrome (LEMS) Laparoscopy and laparoscopic surgery . . . . Laryngeal cancer . . . . . . . . . . . . . . . . Laryngeal nerve palsy . . . . . . . . . . . . . Laryngectomy . . . . . . . . . . . . . . . . . Laryngoscopy . . . . . . . . . . . . . . . . . Laser therapies . . . . . . . . . . . . . . . . . Latinos/Hispanics and cancer . . . . . . . . . Laxatives . . . . . . . . . . . . . . . . . . . . LCIS. See Lobular carcinoma in situ LDH test. See Lactate dehydrogenase test Leiomyomas . . . . . . . . . . . . . . . . . . Leiomyosarcomas . . . . . . . . . . . . . . . LEMS. See Lambert-Eaton myasthenic syndrome Leptomeningeal carcinomas . . . . . . . . . . Leukapharesis . . . . . . . . . . . . . . . . . Leukemia, Down syndrome and. See Down syndrome and leukemia Leukemia, eosinophilic. See Eosinophilic leukemia Leukemia, hairy cell. See Hairy cell leukemia Leukemias . . . . . . . . . . . . . . . . . . . Leukoencephalopathy . . . . . . . . . . . . . Leukopenia. . . . . . . . . . . . . . . . . . . Leukoplakia . . . . . . . . . . . . . . . . . . Leydig cell tumors . . . . . . . . . . . . . . . Li-Fraumeni syndrome (LFS) . . . . . . . . . Limb salvage . . . . . . . . . . . . . . . . . . Linear accelerator . . . . . . . . . . . . . . . Lip cancers . . . . . . . . . . . . . . . . . . . Liposarcomas . . . . . . . . . . . . . . . . . Liver biopsy . . . . . . . . . . . . . . . . . . Liver cancers . . . . . . . . . . . . . . . . . .
Jonsson Comprehensive Cancer Center (JCCC) . . . . . . . . . . . . . . . . . . . . . . 664 Journaling . . . . . . . . . . . . . . . . . . . . . . 665 Juvenile polyposis syndrome . . . . . . . . . . . . 665 Kaposi sarcoma . . . . . . . . . . . . . Karnofsky performance status (KPS) . . Keratosis . . . . . . . . . . . . . . . . . Ki67 test . . . . . . . . . . . . . . . . . Kidney cancer . . . . . . . . . . . . . . Klinefelter syndrome and cancer . . . . KPS. See Karnofsky performance status Krukenberg tumors . . . . . . . . . . .
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667 669 670 670 671 674
. . . . . . 675
Lacrimal gland tumors . . . . . . . . . . . . . . . . 677 Lactate dehydrogenase (LDH) test . . . . . . . . . 678 Laetrile . . . . . . . . . . . . . . . . . . . . . . . . 679
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679 681 682 685 686 687 688 690 692
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. . . 696 . . . 698
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698 702 704 704 706 706 708 709 710 712 714 715
Volume 3 Lumps . . . . . . . . . . . . . . Lung cancer, brochoalveolar. See Bronchoalveolar lung cancer Lung cancers . . . . . . . . . . . Lutein . . . . . . . . . . . . . . Lycopene . . . . . . . . . . . . . Lymphadenectomy. . . . . . . . Lymphangiography . . . . . . . Lymphangiosarcomas . . . . . . Lymphedema. . . . . . . . . . . Lymphocytosis . . . . . . . . . . Lymphomas . . . . . . . . . . .
Contents . . . . . . . . . . . . . . . . . . . . . . . . lv Complete List of Contents . . . . . . . . . . . . . . lix Living will . . . . . . . . . . . . . . . . . Living with cancer . . . . . . . . . . . . . Lobectomy . . . . . . . . . . . . . . . . . Lobular carcinoma in situ (LCIS) . . . . . Long-distance caregiving . . . . . . . . . Loop electrosurgical excisional procedure (LEEP) . . . . . . . . . . . . . . . . . Lumbar puncture . . . . . . . . . . . . . . Lumpectomy . . . . . . . . . . . . . . . .
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719 720 723 725 726
. . . . . 727 . . . . . 728 . . . . . 730 lxxxv
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733 737 737 738 740 741 742 743 744
Salem Health: Cancer M. D. Anderson Cancer Center . . . . . . . . . Macrobiotic diet . . . . . . . . . . . . . . . . . Magnetic resonance imaging (MRI) . . . . . . . Malignant fibrous histiocytoma (MFH) . . . . . Malignant rhabdoid tumor of the kidney . . . . Malignant tumors . . . . . . . . . . . . . . . . MALT lymphomas. See Mucosa-associated lymphoid tissue lymphomas Mammography . . . . . . . . . . . . . . . . . . Managed care . . . . . . . . . . . . . . . . . . Mantle cell lymphoma (MCL) . . . . . . . . . . Mastectomy . . . . . . . . . . . . . . . . . . . Mastocytomas . . . . . . . . . . . . . . . . . . Matrix metalloproteinase inhibitors . . . . . . . Mayo Clinic Cancer Center . . . . . . . . . . . MCC. See Merkel cell carcinomas MCL. See Mantle cell lymphoma MDR. See Drug resistance and multidrug resistance Mediastinal tumors. . . . . . . . . . . . . . . . Mediastinoscopy . . . . . . . . . . . . . . . . . Medical marijuana . . . . . . . . . . . . . . . . Medical oncology . . . . . . . . . . . . . . . . Medicare and cancer . . . . . . . . . . . . . . . Medullary carcinoma of the breast. . . . . . . . Medulloblastomas . . . . . . . . . . . . . . . . Melanomas . . . . . . . . . . . . . . . . . . . . Melphalan . . . . . . . . . . . . . . . . . . . . Memorial Sloan-Kettering Cancer Center . . . . MEN 1. See Multiple endocrine neoplasia type 1 MEN 2. See Multiple endocrine neoplasia type 2 Meningeal carcinomatosis . . . . . . . . . . . . Meningiomas. . . . . . . . . . . . . . . . . . . Merkel cell carcinomas (MCC) . . . . . . . . . Mesenchymomas, malignant. . . . . . . . . . . Mesothelioma . . . . . . . . . . . . . . . . . . Metastasis . . . . . . . . . . . . . . . . . . . . Metastatic squamous neck cancer with occult primary . . . . . . . . . . . . . . . . . . . . MFH. See Malignant fibrous histiocytoma Microcalcifications. . . . . . . . . . . . . . . . Microwave hyperthermia therapy . . . . . . . . Mineral oils . . . . . . . . . . . . . . . . . . . Mistletoe . . . . . . . . . . . . . . . . . . . . . Mitochondrial DNA mutations. . . . . . . . . . MLH1 gene. . . . . . . . . . . . . . . . . . . . Mohs surgery. . . . . . . . . . . . . . . . . . . Molecular oncology . . . . . . . . . . . . . . . Moles. . . . . . . . . . . . . . . . . . . . . . . Monoclonal antibodies . . . . . . . . . . . . . . Motion sickness devices . . . . . . . . . . . . .
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748 750 750 752 753 754
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754 757 759 761 763 764 765
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766 768 768 770 772 774 775 776 779 780
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781 782 783 785 786 788
. . 790 . . . . . . . . . . .
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790 791 792 793 794 795 796 796 798 800 802
MRI. See Magnetic resonance imaging MSH genes . . . . . . . . . . . . . . . . . . . . Mucinous carcinomas . . . . . . . . . . . . . . Mucosa-associated lymphoid tissue (MALT) lymphomas . . . . . . . . . . . . . . . . . . Mucositis . . . . . . . . . . . . . . . . . . . . . Mucous membranes, epidermoid cancers of. See Epidermoid cancers of mucous membranes Multiple endocrine neoplasia type 1 (MEN 1). . Multiple endocrine neoplasia type 2 (MEN 2). . Multiple myeloma . . . . . . . . . . . . . . . . Mustard gas . . . . . . . . . . . . . . . . . . . Mutagenesis and cancer . . . . . . . . . . . . . Myasthenia gravis . . . . . . . . . . . . . . . . MYC oncogene . . . . . . . . . . . . . . . . . . Mycosis fungoides . . . . . . . . . . . . . . . . Myelodysplastic syndromes . . . . . . . . . . . Myelofibrosis . . . . . . . . . . . . . . . . . . Myeloma . . . . . . . . . . . . . . . . . . . . . Myeloproliferative disorders. . . . . . . . . . . Myelosuppression . . . . . . . . . . . . . . . . 2-Naphthylamine. . . . . . . . . . . . . . . . Nasal cavity and paranasal sinus cancers . . . National Cancer Institute (NCI) . . . . . . . . National Science Foundation (NSF) . . . . . . Native North Americans and cancer . . . . . . Nausea and vomiting. . . . . . . . . . . . . . NCI. See National Cancer Institute Needle biopsies . . . . . . . . . . . . . . . . Needle localization. . . . . . . . . . . . . . . Nephroblastomas. . . . . . . . . . . . . . . . Nephrostomy . . . . . . . . . . . . . . . . . . Neuroblastomas . . . . . . . . . . . . . . . . Neuroectodermal tumors. . . . . . . . . . . . Neuroendocrine tumors . . . . . . . . . . . . Neurofibromatosis type 1 (NF1) . . . . . . . . Neurologic oncology. . . . . . . . . . . . . . Neutropenia . . . . . . . . . . . . . . . . . . NF1. See Neurofibromatosis type 1 Nickel compounds and metallic nickel . . . . Night sweats . . . . . . . . . . . . . . . . . . Nijmegen breakage syndrome . . . . . . . . . Nipple discharge . . . . . . . . . . . . . . . . Non-Hodgkin lymphoma . . . . . . . . . . . Nonsteroidal anti-inflammatory drugs (NSAIDs) . . . . . . . . . . . . . . . . . . NSAIDs. See Nonsteroidal anti-inflammatory drugs NSF. See National Science Foundation Nuclear medicine scan . . . . . . . . . . . . .
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. . 803 . . 803 . . 804 . . 806
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807 808 809 812 813 815 817 817 819 820 822 823 825
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826 826 829 830 832 834
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836 838 839 839 841 842 844 845 847 849
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851 852 853 854 855
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Complete List of Contents Nutrition and cancer prevention . . . . . . . . . . . 861 Nutrition and cancer treatment. . . . . . . . . . . . 864 Obesity-associated cancers . . . . . Occupational exposures and cancer . Occupational therapy . . . . . . . . OCs. See Organochlorines Oligodendrogliomas . . . . . . . . . Omega-3 fatty acids . . . . . . . . . Ommaya reservoir . . . . . . . . . . Oncogenes . . . . . . . . . . . . . . Oncogenic viruses . . . . . . . . . . Oncology . . . . . . . . . . . . . . . Oncology clinical nurse specialist . . Oncology social worker . . . . . . . Oophorectomy . . . . . . . . . . . . Ophthalmic oncology . . . . . . . . Opioids . . . . . . . . . . . . . . . . Oral and maxillofacial surgery. . . . Oral and oropharyngeal cancers . . . Orbit tumors . . . . . . . . . . . . . Orchiectomy . . . . . . . . . . . . . Organ transplantation and cancer . . Organochlorines (OCs) . . . . . . . Oropharyngeal cancers. See Oral and oropharyngeal cancers Orthopedic surgery. . . . . . . . . . Otolaryngology . . . . . . . . . . . Ovarian cancers . . . . . . . . . . . Ovarian cysts. . . . . . . . . . . . . Ovarian epithelial cancer . . . . . . Overtreatment . . . . . . . . . . . .
. . . . . . . . 868 . . . . . . . . 871 . . . . . . . . 873 . . . . . . . . . . . . . . . . .
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875 877 878 878 881 882 885 887 888 889 892 893 894 897 898 899 901
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902 903 905 908 909 911
Paget disease of bone . . . . . . . . . . . . . Pain management medications. . . . . . . . . Palliative treatment . . . . . . . . . . . . . . PALP. See Placental alkaline phosphatase Palpation . . . . . . . . . . . . . . . . . . . . Pancolitis . . . . . . . . . . . . . . . . . . . . Pancreatectomy . . . . . . . . . . . . . . . . Pancreatic cancers . . . . . . . . . . . . . . . Pancreatitis . . . . . . . . . . . . . . . . . . . Pap test . . . . . . . . . . . . . . . . . . . . . Paracentesis . . . . . . . . . . . . . . . . . . Paranasal sinus cancers. See Nasal cavity and paranasal sinus cancers Paraneoplastic syndromes . . . . . . . . . . . Parathyroid cancer . . . . . . . . . . . . . . . Pathology . . . . . . . . . . . . . . . . . . . PC-SPES . . . . . . . . . . . . . . . . . . . . PDT. See Photodynamic therapy
. . . 912 . . . 914 . . . 917 . . . . . . .
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920 920 921 923 927 928 929
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931 932 934 937
Pediatric oncology and hematology . . . . . . . . . 938 Pelvic examination . . . . . . . . . . . . . . . . . . 940 Penile cancer . . . . . . . . . . . . . . . . . . . . . 941 Percutaneous transhepatic cholangiography (PTHC) . . . . . . . . . . . . . . . . . . . . . . 943 Pericardial effusion . . . . . . . . . . . . . . . . . 944 Pericardiocentesis . . . . . . . . . . . . . . . . . . 946 Peritoneovenous shunts . . . . . . . . . . . . . . . 946 Personality and cancer . . . . . . . . . . . . . . . . 947 Pesticides and the food chain . . . . . . . . . . . . 948 PET. See Positron emission tomography Peutz-Jeghers syndrome (PJS) . . . . . . . . . . . . 951 Pharmacy oncology . . . . . . . . . . . . . . . . . 952 Phenacetin . . . . . . . . . . . . . . . . . . . . . . 955 Phenolics . . . . . . . . . . . . . . . . . . . . . . . 955 Pheochromocytomas . . . . . . . . . . . . . . . . . 956 Pheresis . . . . . . . . . . . . . . . . . . . . . . . 958 Photodynamic therapy (PDT) . . . . . . . . . . . . 959 Phyllodes tumors. . . . . . . . . . . . . . . . . . . 960 Phytoestrogens . . . . . . . . . . . . . . . . . . . . 962 Pineoblastomas. . . . . . . . . . . . . . . . . . . . 963 Pituitary tumors . . . . . . . . . . . . . . . . . . . 965 PJS. See Peutz-Jeghers syndrome Placental alkaline phosphatase (PALP) . . . . . . . 968 Plant alkaloids and terpenoids in chemotherapy . . . . . . . . . . . . . . . . . . . 968 Plasticizers . . . . . . . . . . . . . . . . . . . . . . 971 Pleural biopsy . . . . . . . . . . . . . . . . . . . . 972 Pleural effusion . . . . . . . . . . . . . . . . . . . 973 Pleurodesis . . . . . . . . . . . . . . . . . . . . . . 975 Pleuropulmonary blastomas . . . . . . . . . . . . . 975 PMS genes . . . . . . . . . . . . . . . . . . . . . . 976 Pneumonectomy . . . . . . . . . . . . . . . . . . . 977 Pneumonia . . . . . . . . . . . . . . . . . . . . . . 979 Polycyclic aromatic hydrocarbons . . . . . . . . . . 981 Polycythemia vera . . . . . . . . . . . . . . . . . . 981 Polypectomy . . . . . . . . . . . . . . . . . . . . . 982 Polyps . . . . . . . . . . . . . . . . . . . . . . . . 983 Polyps, colon. See Colon polyps Polyps, gastric. See Gastric polyps Positron emission tomography (PET) . . . . . . . . 984 Poverty and cancer . . . . . . . . . . . . . . . . . . 987 PPOs. See Preferred provider organizations Prayer and cancer support . . . . . . . . . . . . . . 989 Preferred provider organizations (PPOs) . . . . . . 990 Pregnancy and cancer . . . . . . . . . . . . . . . . 992 Premalignancies . . . . . . . . . . . . . . . . . . . 994 Prevent Cancer Foundation . . . . . . . . . . . . . 997 Prevention . . . . . . . . . . . . . . . . . . . . . . 999 Primary care physician . . . . . . . . . . . . . . . 1001
lxxxvii
Salem Health: Cancer Primary central nervous system lymphomas . . . . . . . . . . . . . . . . Progesterone receptor assay . . . . . . . . Prostate cancer . . . . . . . . . . . . . . . Prostate-specific antigen (PSA) test . . . . Prostatectomy. . . . . . . . . . . . . . . . Prostatitis . . . . . . . . . . . . . . . . . . Proteasome inhibitors. . . . . . . . . . . . Protein electrophoresis . . . . . . . . . . . Proteomics and cancer research . . . . . . Proton beam therapy . . . . . . . . . . . . Proto-oncogenes and carcinogenesis . . . . PSA test. See Prostate-specific antigen test Psycho-oncology . . . . . . . . . . . . . . Psychosocial aspects of cancer . . . . . . . PTHC. See Percutaneous transhepatic cholangiography Radiation, ionizing. See Ionizing radiation Radiation oncology . . . . . . . . . . . . . Radiation therapies . . . . . . . . . . . . . Radiation therapy, afterloading. See Afterloading radiation therapy Radical neck dissection . . . . . . . . . . . Radiofrequency ablation . . . . . . . . . . Radionuclide scan . . . . . . . . . . . . . Radiopharmaceuticals . . . . . . . . . . . Radon . . . . . . . . . . . . . . . . . . . . RB1 gene . . . . . . . . . . . . . . . . . . Receptor analysis . . . . . . . . . . . . . .
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1003 1003 1004 1006 1008 1009 1010 1010 1012 1014 1015
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1027 1027 1030 1030 1032 1032 1033
Reconstructive surgery . . . . . . . . . . . . . . Rectal cancer . . . . . . . . . . . . . . . . . . . Recurrence . . . . . . . . . . . . . . . . . . . . Rehabilitation . . . . . . . . . . . . . . . . . . . Relationships . . . . . . . . . . . . . . . . . . . Renal pelvis tumors. . . . . . . . . . . . . . . . Report on Carcinogens (RoC) . . . . . . . . . . Resveratrol . . . . . . . . . . . . . . . . . . . . Retinoblastomas . . . . . . . . . . . . . . . . . Rhabdomyosarcomas . . . . . . . . . . . . . . . RhoGD12 gene . . . . . . . . . . . . . . . . . . Richter syndrome . . . . . . . . . . . . . . . . . Risk assessment, family history and. See Family history and risk assessment Risks for cancer. . . . . . . . . . . . . . . . . . Robert H. Lurie Cancer Center . . . . . . . . . . RoC. See Report on Carcinogens Rothmund-Thomson syndrome . . . . . . . . . .
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Salivary gland cancer . . . . . . . . . . . . . Salpingectomy and salpingo-oophorectomy . Sarcomas, soft-tissue . . . . . . . . . . . . . Saw palmetto . . . . . . . . . . . . . . . . . Schwannoma tumors . . . . . . . . . . . . . SCLC1 gene. . . . . . . . . . . . . . . . . . Screening, colorectal cancer. See Colorectal cancer screening Screening for cancer . . . . . . . . . . . . . Second opinions . . . . . . . . . . . . . . . Self-image and body image. . . . . . . . . .
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1034 1036 1038 1038 1041 1043 1044 1045 1046 1048 1050 1050
. 1052 . 1054 . 1056 1058 1060 1062 1065 1066 1067
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Volume 4 Contents . . . . . . . . . . . . . . . . . . . . . . lxxvii Complete List of Contents . . . . . . . . . . . . . lxxix Sentinel lymph node (SLN) biopsy and mapping . . . . . . . . . . . . . . . Sepsis. See Infection and sepsis Sertoli cell tumors . . . . . . . . . . . Sexuality and cancer . . . . . . . . . . Sézary syndrome . . . . . . . . . . . . SIADH. See Syndrome of inappropriate antidiuretic hormone production Side effects . . . . . . . . . . . . . . . Sigmoidoscopy . . . . . . . . . . . . . Silica, crystalline . . . . . . . . . . . . Simian virus 40 . . . . . . . . . . . . . Singlehood and cancer . . . . . . . . .
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1078 1082 1083 1084 1084
Sjögren syndrome. . . . . . . . . . . . . . . . Skin cancers . . . . . . . . . . . . . . . . . . SLN biopsy and mapping. See Sentinel lymph node biopsy and mapping Small intestine cancer . . . . . . . . . . . . . Smoking cessation . . . . . . . . . . . . . . . Social Security Disability Insurance (SSDI) . . Soft-tissue fibrosarcomas. See Fibrosarcomas, soft-tissue Soots . . . . . . . . . . . . . . . . . . . . . . Soy foods . . . . . . . . . . . . . . . . . . . . Spermatocytomas . . . . . . . . . . . . . . . . Spinal axis tumors . . . . . . . . . . . . . . . Spinal cord compression . . . . . . . . . . . . Splenectomy . . . . . . . . . . . . . . . . . . Sputum cytology . . . . . . . . . . . . . . . .
lxxxviii
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1097 1098 1099 1100 1102 1103 1105
Complete List of Contents Squamous cell carcinomas . . . . . . . . . . . SRS. See Stereotactic radiosurgery SSDI. See Social Security Disability Insurance Staging of cancer . . . . . . . . . . . . . . . . Statistics of cancer . . . . . . . . . . . . . . . Stem cell transplantation . . . . . . . . . . . . Stent therapy . . . . . . . . . . . . . . . . . . Stereotactic needle biopsy . . . . . . . . . . . Stereotactic radiosurgery (SRS) . . . . . . . . Sterility . . . . . . . . . . . . . . . . . . . . . Stomach cancers . . . . . . . . . . . . . . . . Stomatitis . . . . . . . . . . . . . . . . . . . . Stress management . . . . . . . . . . . . . . . Sunlamps . . . . . . . . . . . . . . . . . . . . Sun’s soup . . . . . . . . . . . . . . . . . . . Sunscreens . . . . . . . . . . . . . . . . . . . Superior vena cava syndrome . . . . . . . . . Support groups . . . . . . . . . . . . . . . . . Surgical biopsies . . . . . . . . . . . . . . . . Surgical oncology. . . . . . . . . . . . . . . . Survival rates . . . . . . . . . . . . . . . . . . Survivorship issues . . . . . . . . . . . . . . . Symptoms and cancer. . . . . . . . . . . . . . Syndrome of inappropriate antidiuretic hormone production (SIADH) . . . . . . . . Synovial sarcomas . . . . . . . . . . . . . . . Taste alteration . . . . . . . . . . . . . . Teratocarcinomas . . . . . . . . . . . . . Teratomas . . . . . . . . . . . . . . . . . Testicular cancer . . . . . . . . . . . . . Testicular self-examination (TSE) . . . . Thermal imaging . . . . . . . . . . . . . Thiotepa. . . . . . . . . . . . . . . . . . Thoracentesis . . . . . . . . . . . . . . . Thoracoscopy . . . . . . . . . . . . . . . Thoracotomy . . . . . . . . . . . . . . . Throat cancer . . . . . . . . . . . . . . . Thrombocytopenia . . . . . . . . . . . . Thymomas . . . . . . . . . . . . . . . . Thymus cancer . . . . . . . . . . . . . . Thyroid cancer . . . . . . . . . . . . . . Thyroid nuclear medicine scan . . . . . . TNF. See Tumor necrosis factor TNM staging . . . . . . . . . . . . . . . Tobacco, chewing. See Chewing tobacco Tobacco-related cancers . . . . . . . . . Topoisomerase inhibitors . . . . . . . . . TP53 protein . . . . . . . . . . . . . . . Tracheostomy . . . . . . . . . . . . . . . Transfusion therapy. . . . . . . . . . . .
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1108 1111 1114 1116 1118 1119 1120 1121 1124 1125 1127 1128 1129 1130 1132 1135 1138 1140 1143 1144
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1151 1152 1153 1154 1156 1157 1158 1158 1160 1161 1162 1164 1166 1167 1169 1172
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1174 1175 1177 1179 1180
Transitional care . . . . . . . . . . . Transitional cell carcinomas . . . . . Transrectal ultrasound . . . . . . . . Transvaginal ultrasound . . . . . . . Trichilemmal carcinomas. . . . . . . TSE. See Testicular self-examination Tuberous sclerosis . . . . . . . . . . Tubular carcinomas . . . . . . . . . . Tumor flare . . . . . . . . . . . . . . Tumor lysis syndrome . . . . . . . . Tumor markers . . . . . . . . . . . . Tumor necrosis factor (TNF) . . . . . Tumor-suppressor genes . . . . . . . Turcot syndrome . . . . . . . . . . . Tyrosine kinase inhibitors . . . . . .
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1182 1183 1185 1186 1187
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1187 1188 1189 1189 1191 1193 1194 1195 1196
Ultrasound, breast. See Breast ultrasound Ultrasound, endorectal. See Endorectal ultrasound Ultrasound, transrectal. See Transrectal ultrasound Ultrasound, transvaginal. See Transvaginal ultrasound Ultrasound tests . . . . . . . . . . . . . . . Ultraviolet radiation and related exposures Umbilical cord blood transplantation. . . . Upper gastrointestinal (GI) endoscopy . . . Upper gastrointestinal (GI) series . . . . . Urethral cancer . . . . . . . . . . . . . . . Urinalysis . . . . . . . . . . . . . . . . . . Urinary system cancers . . . . . . . . . . . Urography . . . . . . . . . . . . . . . . . Urologic oncology . . . . . . . . . . . . . Urostomy . . . . . . . . . . . . . . . . . . Uterine cancer . . . . . . . . . . . . . . .
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1199 1200 1201 1202 1203 1205 1207 1209 1213 1214 1216 1217
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1220 1221 1223 1225 1226
Vaccines, preventive . . . . . . . . . . . Vaccines, therapeutic . . . . . . . . . . . Vaginal cancer . . . . . . . . . . . . . . Vascular access tubes. . . . . . . . . . . Vasectomy and cancer . . . . . . . . . . Vegetables, cruciferous. See Cruciferous vegetables Veterinary oncology . . . . . . . . . . . VHL disease. See Von Hippel-Lindau disease Vinyl chloride . . . . . . . . . . . . . . Viral oncology . . . . . . . . . . . . . . Virus-related cancers . . . . . . . . . . . Von Hippel-Lindau (VHL) disease. . . . Vulvar cancer . . . . . . . . . . . . . . .
lxxxix
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1230 1230 1232 1235 1237
Salem Health: Cancer WAGR syndrome. See Wilms’ tumor aniridiagenitourinary anomalies-mental retardation syndrome and cancer Waldenström macroglobulinemia (WM) . . . . . . 1240 Watchful waiting . . . . . . . . . . . . . . . . . . 1242 Weight loss . . . . . . . . . . . . . . . . . . . . . 1243 Wilms’ tumor . . . . . . . . . . . . . . . . . . . . 1245 Wilms’ tumor aniridia-genitourinary anomaliesmental retardation (WAGR) syndrome and cancer . . . . . . . . . . . . . . . . . . . . . . 1248 Wine and cancer . . . . . . . . . . . . . . . . . . 1250 Wire localization . . . . . . . . . . . . . . . . . . 1250 WM. See Waldenström macroglobulinemia Wood dust . . . . . . . . . . . . . . . . . . . . . 1251
Yolk sac carcinomas . . . . . . . . . . . . . . . . 1256 Young adult cancers . . . . . . . . . . . . . . . . 1256 Zollinger-Ellison syndrome . . . . . . . . . . . . 1260 Drugs by Generic Name . . . Drugs by Trade Name . . . . Associations and Agencies . . Cancer Centers and Hospitals Cancer Support Groups . . . . Carcinogens. . . . . . . . . . Glossary . . . . . . . . . . . Bibliography . . . . . . . . .
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1265 1309 1348 1352 1357 1362 1383 1400
Category List . . . . . . . . . . . . . . . . . . . . 1409 Index . . . . . . . . . . . . . . . . . . . . . . . . 1419
X-ray tests . . . . . . . . . . . . . . . . . . . . . 1252 Xeroderma pigmentosa . . . . . . . . . . . . . . . 1254
xc
Salem Health: Cancer
u ABCD Category: Procedures Also known as: Jewett staging system or the WhitmoreJewett staging system (for prostate cancer) Definition: There are two distinct ABCD rating systems for cancer. The first uses the symbols A, B, C, and D to define the stages of prostate cancer. The second uses these designations to describe the early warning signs of melanoma, the most serious type of skin cancer.
Abdominoperineal resection (APR)
•
A (asymmetry): The two halves of the skin lesion are dissimilar. • B (border irregularity): The lesion has ragged or poorly defined edges. • C (color): The color of the lesion is uneven with different shades of brown or black. • D (diameter): The lesion is usually greater than 6 millimeters or 0.25 inch. Anna Binda, Ph.D. See also Melanomas; Moles; Premalignancies; Prostate cancer.
Cancers monitored: Prostate cancer and melanoma (each with its own distinct ABCD rating) Why performed: After detecting prostate cancer, the physician will evaluate the stage of the tumor according to its size, its location, and the extent to which it may have spread to other parts of the body. This information is important for choosing the best treatment plan. Staging of prostate cancer is based on the findings of clinical tests, mainly a digital rectal examination, a test to measure the level of prostate-specific antigen (PSA) in the blood, and transrectal ultrasonography. For melanoma prevention, the American Cancer Society recommends monthly skin self-examinations. The ABCD guideline serves as a reference when looking for any suspicious changes in the appearance of spots or sores that do not heal. Usually, this means monitoring any variation in the size, shape, or color of a mole. Any suspicious mole should be checked by a physician, who may decide to resect an abnormal-looking lesion and send the tissue for pathological review. Results: The ABCD rating for prostate cancer is used to classify the disease into four basic stages. • Stage A: Localized disease in which the cancer is very small, confined to the prostate gland, not palpable during a rectal examination, and identified by high PSA levels and biopsy. • Stage B: Localized disease in which the cancer is larger and confined to the prostate gland, but a lump is palpable during a rectal examination. • Stage C: Regional disease in which the cancer has grown through the prostate capsule and into surrounding tissues, perhaps into the seminal vesicles. • Stage D: Metastatic disease in which the cancer has grown into the pelvic area or has spread to the lymph nodes, bones, or other parts of the body. The ABCD rule for melanoma detection lists the four usual warning signs of the disease for most types of melanoma.
u Abdominoperineal resection
(APR) Category: Procedures Also known as: Abdominoperineal excision, anorectal excision, anoproctectomy Definition: Abdominoperineal resection (APR) is the surgical removal of the anus, rectum, and surrounding membrane called the mesentery, as well as the lower part of the colon supported by that mesentery. The upper part of the colon is rerouted through a new opening (ostomy) in the lower abdomen, forming an opening called a stoma. Cancers treated: Low rectal cancer, advanced anal cancer, metastatic pelvic disease Why performed: APR is performed to remove cancerous tissue, thereby curing or controlling the cancer or relieving symptoms of advanced disease. APR is the preferred procedure for large rectal tumors and tumors near the anal sphincter, but other tumor characteristics and patientspecific factors are also considered. Patient preparation: A series of medical tests are completed to plan effective treatment and to evaluate the patient’s fitness for major surgery. A specialist counsels the patient and helps choose the location for the stoma required by an APR. Radiation therapy, chemotherapy, or both may be recommended before the procedure. Certain patient medications may need to be stopped, the patient’s bowel must be cleaned, and the patient’s stomach must be empty. Steps of the procedure: APR is scheduled in a hospital. Sensors are placed to monitor the patient’s condition. An intravenous line is started, and an antibiotic is infused. General anesthetic is administered, and a breathing tube is 1
Abdominoperineal resection (APR) placed. The patient is positioned, a urinary catheter is inserted, and the incision sites are prepared. APR is a complex operation requiring incisions first on the abdomen (abdominal resection) and then on the perineum (perineal resection), which may be performed by one or two surgeons. Abdominal resection prepares the lower colon and rectum for removal during the perineal resection and forms the stoma. Perineal resection frees the anus and removes all the diseased tissue. In some instances, the abdominal resection may be performed laparoscopically; however, this approach will remain controversial until long-term studies prove its safety and efficacy for APR. To begin, the surgeon makes an midline incision in the abdomen large enough to see the tumor and to examine lymph nodes and other organs for metastases. If the tumor is removable, then the procedure continues. Within the abdomen, rectal blood vessels are tied, and the mesentery is clamped. The lower colon is freed from attachments. The peritoneum is divided, enabling the surgeon to free the rectum. The tied blood vessels and clamped mesentery are divided and sealed. Then, the ostomy opening is made in the abdomen. The colon is divided. The lower end of the colon is covered and tucked below the peritoneum for removal during the perineal resection, and the peritoneum is closed. The upper end of the colon is passed through the ostomy opening, the colon segment is sized to an appropriate length, and the edge of the cut end is folded back and stitched to the abdomen, forming a stoma. Next, other organs are examined for cancer; if other lesions or metastases are found, then they may also be removed. Finally, the abdominal cavity is inspected and cleaned, and the abdominal incision is closed. On the perineum, the surgeon makes an elliptical incision around the anus. Blood vessels are clamped, then tied as needed. The anus is freed from attachments, including as much surrounding tissue as possible without disturbing major blood vessels, nerves, and healthy organs; however, if the cancer has spread into these structures, then part or all of these structures may be included. The anus is pulled out, as well as the rectum and lower colon freed during the abdominal resection. All tissues are taken to the laboratory for histopathologic evaluation. Finally, the pelvic cavity is inspected and cleaned, and the perineal incision is closed, with a small tube inserted to drain excess fluid. After the procedure: Anesthetic is stopped, and the breathing tube is removed. The urinary catheter and the intravenous line are kept. A clear collection pouch (ostomy appliance) is fitted over the stoma. The patient is trans2
Salem Health: Cancer ferred to the recovery room, then to a hospital room. Medications are given to control pain and infection. The patient slowly progresses to a normal diet. The ostomy is monitored; once it starts functioning, the patient learns how to care for the stoma, empty and change pouches, and manage bowel function. At home, the patient follows the physician’s instructions about medications, activities, and diet. Further treatment with radiation therapy, chemotherapy, or both may be recommended. Risks: APR is moderately safe, with low mortality. Risks relate to anesthesia, infection, and inadvertent damage to other structures. Side effects are common because of the complex anatomy and the difficulty of operating within the bony pelvis. The most frequent side effects are urinary dysfunction and infection, perineal infections or bleeding, and ostomy-related problems. Less frequent side effects are male impotence and infertility, abdominal wound infection, and intestinal obstruction. Results: The long-term outcome varies considerably with patient-specific factors (such as disease stage, overall health, and body characteristics), among medical institutions (as a result of surgical protocol and specialized experience), and with therapeutic combinations. The five-year survival rate has increased as the recurrence rate has decreased because of more complete removal of diseased tissue and more effective therapeutic combinations. Survival is improved significantly by the removal of metastases. Patricia Boone, Ph.D. u
For Further Information American Cancer Society. Detailed Guide: Colon and Rectum Cancer Surgery. Available online at http:// www.cancer.org. American Cancer Society and National Comprehensive Cancer Network. Colon and Rectal Cancer: Treatment Guidelines for Patients. Version IV. Atlanta: American Cancer Society, 2005. Available online at http://www .nccn.org. Levin, Bernard, et al., eds. American Cancer Society’s Complete Guide to Colorectal Cancer. Atlanta: American Cancer Society, 2006. See also Anal cancer; Anoscopy; Appendix cancer; Colectomy; Coloanal anastomosis; Colorectal cancer; Colostomy; Crohn disease; Enterostomal therapy; Ileostomy; Laparoscopy and laparoscopic surgery; Rectal cancer; Sexuality and cancer.
Salem Health: Cancer
u Accelerated partial breast
irradiation (APBI) Category: Procedures Definition: Accelerated partial breast irradiation (APBI) is an alternative to traditional radiation therapy after lumpectomy that can reduce the time of treatment from weeks to days. It is considered an experimental procedure by many doctors. Cancers treated: Breast cancer Why performed: Radiation therapy is given after a lumpectomy to kill any cancer cells that remain in the breast. Accelerated partial breast irradiation is an alternative therapy that delivers radiation in a way that reduces the time and number of treatments required. Radiation therapy usually requires visits to the outpatient center or clinic five days a week for six or seven weeks. APBI reduces the amount of time required for treatment to about five days in total. Patient preparation: Patients who are undergoing accelerated partial breast irradiation treatment are generally enrolled in a clinical trial, because the procedure is still considered experimental. A clinical trial is a carefully controlled study, supervised by doctors who are also researchers, that is designed to investigate the risks or benefits of a new or experimental procedure. Different types of APBIs are being investigated in clinical trials, using different methods and techniques. As a result, the patient preparation for APBI will differ depending on the specifics of the therapy. In general, the preparation for APBI is the same as for any other radiation therapy treatment. Steps of the procedure: Just as with traditional radiation therapy, the actual time elapsed during a treatment of accelerated partial breast irradiation is usually very short. The time that it takes to get the equipment and patient set up, however, may be significant. First, the patient and the patient’s breast are positioned appropriately for the machine. During traditional radiation therapy, the entire breast receives radiation. During APBI, however, the only part of the breast that receives radiation is the area around the lumpectomy site. Therefore, the breast must be positioned very exactly so that the right area receives the radiation. To place the breast in the correct position, the cancer care team may label the breast with marker or tattooing. The patient should check with her cancer care team to see if these marks are temporary. Once the breast and equipment are correctly positioned, a dose of radiation is given to the breast. Radiation machines deliver beams of high-energy particles to the tis-
Accelerated partial breast irradiation (APBI) sue that destroy cancer cells. Accelerated partial breast irradiation uses amounts of radiation during treatment that are higher than those used by traditional radiation therapy. This is part of the reason that the treatment time of APBI is so short. After the procedure: After the procedure, the patient may experience fatigue, as well as pain or swelling in the breast. Aftercare depends on the procedure that is used. Patients should discuss aftercare with their cancer care team before the day of the first procedure so that anything needed, such as transportation home after the procedure, can be arranged in advance. Risks: Some risks are associated with any procedure involving radiation. With an experimental therapy such as APBI, ongoing clinical trials are trying to determine any long-term side effects that may result from the procedure. Most studies, however, have found the risks associated with APBI to be relatively mild, not greater than risks associated with traditional radiation therapy, and decreasing over time. The most common side effects of APBI are believed to be fatigue, skin changes similar to sunburn in the treated area, swelling in the breast, breast heaviness, and breast discoloration. The creation of small, hard nodes in the breast is also possible. These nodes are not dangerous, but they can occasionally be mistaken for a return of the breast cancer when felt or seen on a mammogram. A very rare but extremely serious possible complication of any radiation to the breast is the development of angiosarcoma, an aggressive form of cancer. Results: Studies done comparing women who received APBI and those who received traditional radiation therapy after lumpectomy have generally found comparable rates of recurrence, even after many years. Researchers, however, are still conducting more studies and clinical trials. Most studies have been conducted only on very specific groups of women, and more research is being done to study the larger population of women with breast cancer to help determine whether APBI is a technique that could be beneficial to all women, and should be integrated into standard breast cancer treatment practices. The results that any individual woman experiences after APBI will depend on many different factors, including genetics, the type of original cancer, and the size of the original cancer. Helen Davidson, B.A. u
For Further Information Pasqualini, Jorge R., ed. Breast Cancer: Prognosis, Treatment, and Prevention. 2d ed. New York: Informa Healthcare, 2008. 3
Achlorhydria Smith, Terry L. Breast Cancer: Current and Emerging Trends in Detection and Treatment. New York: Rosen, 2006. Torosian, Michael H., ed. Breast Cancer: A Guide to Detection and Multidisciplinary Therapy. Totowa, N.J.: Humana Press, 2002. Winchester, David J., et al. Breast Cancer. 2d ed. Hamilton, Ont.: BC Decker, 2006. See also Afterloading radiation therapy; Breast cancer in children and adolescents; Breast cancer in men; Breast cancer in pregnant women; Breast cancers; Cutaneous breast cancer; Ductal carcinoma in situ (DCIS); Invasive ductal carcinomas; Invasive lobular carcinomas; Lobular carcinoma in situ (LCIS); Lumpectomy; Lumps; Mastectomy; Medullary carcinoma of the breast; Radiation therapies; Radiofrequency ablation.
u Achlorhydria Category: Diseases, symptoms, and conditions Also known as: Profound hypochlorhydria Related conditions: Helicobacter pylori infection, chronic atrophic gastritis, gastric adenocarcinoma, gastric carcinoid Definition: Achlorhydria is the absence of acid secretion by the stomach caused by either atrophy of the acid-producing parietal cells or direct inactivation of the protonpumping enzyme in parietal cells responsible for acid secretion. Risk factors: The risk of achlorhydria increases with age and with long-term, untreated infection with the bacteria Helicobacter pylori. Patients with autoimmune conditions are also at increased risk. The condition has no predilection for sex or race. Etiology and the disease process: Chronic inflammation of the stomach in response to untreated H. pylori infection lasting many years leads to the atrophy of stomach cells and a corresponding loss of acid-secreting capacity. Some patients may be more predisposed to achlorhydria in the presence of H. pylori because they respond to the infection by producing a specific inflammatory agent that is also a potent proton pump inhibitor. Autoimmune disease can also produce achlorhydria if the body makes antibodies that inactivate parietal cell proteins. Achlorhydria is associated with the development of malignant cancer of the stomach. Over 60 percent of patients with gastric cancer have achlorhydria compared with 20 percent of healthy individuals. Acid normally acts 4
Salem Health: Cancer as a disinfectant to prevent overgrowth of harmful bacteria; achlorhydria contributes to cancer development because the bacteria synthesize carcinogenic chemicals from nitrates present in food. Achlorhydria is also associated with the formation of gastric carcinoid tumors. If acid output by the stomach is disrupted, the body overproduces the hormone gastrin, which stimulates overgrowth of enterochromaffinlike (ECL) cells in the stomach. This overgrowth may progress to carcinoid formation. Incidence: Gastric carcinoids constitute 0.5 percent of gastric cancers. They are typically associated with autoimmune conditions and have a low risk of malignancy. Symptoms: Achlorhydria itself causes no symptoms; rather, symptoms are secondary to the absence of acid. Lack of acid can cause vitamin B12 or calcium deficiency. Diarrhea may occur because of the overgrowth of bacteria. Screening and diagnosis: Diagnosis is made by measuring the acidity of a stomach fluid sample after an intravenous injection of pentagastrin, which stimulates acid secretion in normal patients. Acidity will not increase in the stomach fluid of achlorhydric patients. Treatment and therapy: Treatment focuses on addressing the underlying condition causing achlorhydria. Because vitamin B12 and calcium absorption are decreased, supplementation or injections of B12 may be necessary. Prognosis, prevention, and outcomes: Restoration of normal acid production depends on prognosis and treatment for the underlying condition responsible for achlorhydria. Pamela S. Cooper, Ph.D. See also Adenocarcinomas; Bacteria as causes of cancer; Gastric polyps; Gastrointestinal cancers; Helicobacter pylori; Hereditary diffuse gastric cancer; Premalignancies; Stomach cancers.
u Acoustic neuromas Category: Diseases, symptoms, and conditions Also known as: Vestibular schwannomas Related conditions: Neurofibromatosis type 2 Definition: Acoustic neuromas are benign (or nonmalignant) tumors that originate from Schwann cells surrounding the vestibular nerve (eighth cranial nerve) in the internal auditory canal. The term “neuroma” is somewhat misleading, as the tumors are not neuromas, nor do they
Salem Health: Cancer arise from the acoustic or cochlear nerve. Acoustic neuroma typically occurs as unilateral (one-sided) sporadic tumors in 95 percent of all cases, but in rare cases tumors can be bilateral (two-sided) and are associated with an inherited syndrome called neurofibromatosis type 2 (NF2). Approximately 2 to 4 percent of patients diagnosed with acoustic neuromas have NF2 type, a prevalence of 1 in 50,000 in the general population. Risk factors: Although high-dose ionizing radiation is a known risk factor of acoustic neuroma, environmental factors including noise exposure, radio frequency electromagnetic fields, and allergens have been reported as potential sources that may contribute to the formation of acoustic neuroma. One publication has reported the findings from an international multicenter case-control study that investigated the effects of these environmental factors in ninety-seven patients with acoustic neuroma and in agematched control subjects. The study reported that increased risks were found for exposure to persistent noise and hay fever, but not for ionizing radiation or for regular mobile phone use. Etiology and the disease process: Currently, the etiology of acoustic neuroma is not known. However, as an anomaly, it is rarely inherited. Nonetheless, neurofibromatosis type 2 should be suspected in young patients and those with family history. Neurofibromatosis is an autosomal dominant disease; thus patients who inherit a defective copy of the NF2 tumor-suppressor gene have a 95 percent chance of developing bilateral tumors; however, half of the cases have no family history of NF2, which could indicate mutations in the germline that were not inherited. Incidence: Sporadic acoustic tumors, the most common form of manifestation, occur in approximately 10 per 1 million persons per year—in other words the chance of an average person developing an acoustic neuroma in his or her lifetime is about 1 in 100,000. Neurofibromatosis is rarer, with only several thousand affected persons in the entire United States, corresponding to 1 in 40,000 individuals. However, a study has highlighted that the true incidence of acoustic neuroma may be higher than what has been envisaged, as 7 unsuspected schwannomas per 10,000 brain magnetic resonance imaging studies were identified, an equivalent of 0.07 percent. Acoustic neuromas, or schwannomas, occur largely in adults, typically in the fourth and fifth decades, with a mean presentation age of fifty years. They are uncommon in children; only thirty-nine cases had been reported as of 2007. Symptoms: Acoustic neuromas are histologically benign; however, if large, they can cause hydrocephalus, brain-
Acoustic neuromas stem compression, herniation, and eventually death. Hearing loss is the most prevalent symptom, occurring in more than 95 percent of patients, and the duration of hearing loss may extend to three or four years before clinical diagnosis is made—a majority of the patients experience one-sided, slowly progressing hearing impairment associated with high-frequency sounds. Alternative complaints or accompanying symptoms include tinnitus, dizziness, vertigo, and a sensation of fullness in the ear. With the progression of the tumor, patients may experience facial numbness, headaches, loss of coordination, and difficulty in swallowing. Vertigo is prevalent with smaller tumors, while unsteadiness, headache, and facial sensory disturbance are associated with large tumors. Screening and diagnosis: Acoustic neuroma can be diagnosed by a number of screening methods. These include conventional audiometry, auditory brainstem response (ABR), and gadolinium-enhanced magnetic resonance imaging (MRI). Among these, gadolinium-enhanced MRI is the optimal diagnostic test. Typically, on MRI scans acoustic neuromas appear as dense and uniformly enhanced. Acoustic neuromas are staged according to their location and size. Small tumors are less than 1.5 centimeters (cm), moderate tumors between 1.5 and 3 cm, and large tumors greater than 3 cm in size. Based on the location, they are staged as intracanalicular (located in the internal auditory canal), cisternal (extending outside the internal auditory canal), compressive (having progressed to touch the cerebellum or brainstem), and hydrocephalus (having progressed to obstruct the drainage of cerebrospinal fluid in the fourth ventricle). Treatment and therapy: The treatment options for acoustic neuroma include observation, microsurgery, stereotactic radiosurgery, and radiotherapy. Patients with advanced age or those deemed unfit for surgical intervention with small tumors at diagnosis are observed; treatment is withheld while tumor progression is monitored in serial imaging studies. However, treatment by observation has its own risks, as there is a greater risk of losing useful hearing. If microsurgery is the choice for treatment, many factors need to be assessed when evaluating its primary and secondary outcomes. First, there are three standard surgical approaches, each with its own advantages and disadvantages: suboccipital, middle fossa, and translabyrinthine. In the suboccipital approach, the tumor is reached through the skull behind the ear. As the procedure involves the retraction of the cerebellum, the approach is intrinsically dangerous and prone to complications. Although the middle fossa method can preserve hearing in theory, this 5
Acrylamides approach is also dangerous as it too requires the retraction of part of the brain. In the translabyrinthine approach, the tumor is accessed through the inner ear, and thus hearing loss is expected and inevitable. However, this method is unsuitable for large tumors. Second, microsurgery is technically challenging; therefore the rate of success is lower with a less experienced surgeon. Third, large tumors (greater than 3 cm) are difficult to resect without concomitant morbidity, such as facial palsy. Some of the complications that may arise from microsurgery are cerebrospinal fluid leak (12 percent of all cases), meningitis (5 percent), intracranial hemorrhage (2 percent), facial weakness with complete paralysis (31 percent), and delayed or partial paresis (50 percent). Radiosurgery refers to the administration of a single fraction of radiotherapy using stereotactic techniques to localize the tumor and align the fields. Radiosurgery may be performed either with a Gamma Knife or a linear accelerator (linac) based system. Gamma Knife is an emerging treatment option for those who are at high risk during microsurgery. High-dose Gamma Knife procedures are less favored due to the possibility of radiation complications; thus low-dose radiation (for example, 13 gray, or Gy) therapies are advised because of safety and lower risk of facial weakness. Radiotherapy refers to the administration of fractionated radiotherapy and includes stereotactic radiotherapy (radiation with other than gamma rays) and conventional radiotherapy techniques. Complications of Gamma Knife radiosurgery include injury to facial and trigeminal nerves. However, with the current dosing regimen of 12.5 Gy, the risk of trigeminal or facial nerve injury has decreased significantly. Although the potential for complications is higher with microsurgical procedures than with radiotherapy or radiosurgery, an important issue that should be considered with irradiation therapies is the low risk of inducing malignancies within the radiation area. Current recommendations are to offer microsurgery and radiosurgery options for patients with definite treatment indications. While microsurgery is the treatment of choice for large tumors because of the low risk of radiation-induced malignancies, microsurgery is also considered for younger patients. Prognosis, prevention, and outcomes: The microsurgical techniques for acoustic neuroma have improved the anatomical and functional preservation of the facial and cochlear nerves. These techniques, accompanied by continuous electrophysiological monitoring, have resulted in marked changes in the primary goals of management. In the past, the primary goal of acoustic neuroma manage6
Salem Health: Cancer ment was to preserve the patient’s life, whereas the objective today is to preserve the neurological function. Long-term follow-ups show negligible recurrence rates, suggesting that the preservation of neurological function does not restrict the tumor removal. Despite these advances, loss of nerve function and even deafness may occur postoperatively in some cases. Bagirathy Ravishankar, Ph.D. u
For Further Information Battaglia, A., et al. “Comparisons of Growth Patterns of Acoustic Neuromas with and Without Radiosurgery.” Otology and Neurotology 27 (2006): 705-712. Mendenhall, W., et al. “Management of Acoustic Schwannoma.” American Journal of Otolaryngology 25 (2004): 38-47. Neff, B., et al. “The Molecular Biology of Vestibular Schwannomas: Dissecting the Pathogenic Process at the Molecular Level.” Otology and Neurotology 27 (2006): 197-208. Schlehofer, B., et al. “Environmental Risk Factors for Sporadic Acoustic Neuroma.” European Journal of Cancer 43 (2007): 1741-1747. Yohay, K. “Neurofibromatosis Types 1 and 2.” The Neurologist 12 (2006): 86-93.
u
Other Resources
Acoustic Neuroma Association http://anausa.org American Cancer Society http://www.cancer.org See also Ependymomas; Neurofibromatosis type 1 (NF1); Schwannoma tumors; Stereotactic radiosurgery (SRS).
u Acrylamides Category: Carcinogens and suspected carcinogens RoC status: Reasonably anticipated human carcinogen since 1991 Also known as: 2-propenamide, propenamide, acrylic amide, vinyl amide, ethylene carboxamide Related cancers: Although an acrylamide-cancer connection in humans has not been established with certainty, the level of suspicion is high because under laboratory conditions in rats and mice, the following cancers have been associated with acrylamide: adrenal pheochromocytomas and mesotheliomas in the testes; adenomas in the
Salem Health: Cancer
Acrylamides
pituitary and mammary glands; adenocarcinomas of the clitoris, uterus, and thyroid gland; squamous cell carcinoma of the skin; and adenomas of the lung. Definition: Acrylamide is a compound of carbon, hydrogen, nitrogen, and oxygen resulting in the chemical formula, C3H5NO. This white, odorless, and crystalline compound is soluble in water, ethanol, ether, and chloroform, accounting for not only its many industrial uses but also its potential for uncomplicated entry into the human body. Many of its industrial and agricultural uses require the conversion of acrylamide to the polymer polyacrylamide. Exposure routes: Experimentally in rats and mice, cancer-inducing exposure routes include administration in the drinking water, intraFrench fries contain high levels of acrylamide. (©Birgit Reitz-hofmann/ Dreamstime.com) peritoneal injection, and topical application. In humans, during everyday activity and work, acrylamide gains entrance through unbroken At risk: Because of its almost ubiquitous presence at skin, mucous membranes, lungs, and the gastrointestinal the dinner table and its known neurotoxic and carcinotract. The primary occupational exposure routes are skin genic potential, acrylamide poses a health risk to humans. contact and through the inhalation of dust and vapor. Microwaving, baking, and frying will produce acrylamide, and as the food continues to cook, ever larger amounts Where found: Acrylamides are used in the treatment of of acrylamide are produced. As the risk potential for wastewater, drinking water, and sewage; in the production acrylamides in foods becomes more publicized, some of paper, plastics, and dyes; and in the manufacture of persteps are under way to modify food production methods, manent press fabrics, adhesives, and food packaging. It is such as using vacuum frying at lower temperatures. Raw also fundamental to ore processing. Acrylamide finds its or boiled foods pose little risk for acrylamides. way into a number of everyday products such as building Workers engaged in oil drilling, paper and pulp manumaterials, contact lenses, textiles, soap, food, and gelatin facture, general construction, plastics manufacture, mincapsules. Acrylamides have also established a place on ing, food processing, textile and cosmetics processing, and people’s dining tables: It is found in fried and baked agricultural industries are at increased risk of acrylamide goods, coffee, olives, and prune juice. Smoking is also a exposure. major acrylamide producer. Some acrylamide contaminates drinking water because Etiology and symptoms of associated cancers: Although of its use in water treatment facilities, but curiously, the research has not firmly established the acrylamide-cancer amount of acrylamide in a large order of fast-food french connection in humans, there is no question that acrylamide fries is more than three hundred times what the U.S. Enviis a serious neurotoxin. Depending on dosage levels, exporonmental Protection Agency allows in a single glass of sure can cause damage to the male reproductive glands, water. This pervasiveness of acrylamide prompted Dale skin, and eyes. Additionally, it may result in urinary inconHattis, a risk analysis expert at Clark University, to specutinence, numbness, weakening in the legs and hands, and late that “acrylamide causes several thousand cancers per irritation of the mucous membranes. year in Americans.” The National Institute for Occupational Health and Additionally, polyacrylamide, the polymer of acrylamSafety (NIOSH) lists the common acrylamide exposure ide, finds widespread global use in pesticides and in soil symptoms in an industrial setting: irritation of the eyes and treatment formulations. This has resulted in notable resiskin, ataxia, numbness of the limbs, paresthesia, muscle dues of polyacrylamide in the most widely consumed vegeweakness, absent deep tendon reflex, hand sweating, lassitables such as potatoes and grains. There is little governtude (weakness, exhaustion), drowsiness, and reproducment oversight or measurement of polyacrylamide in foods. 7
Acupuncture and acupressure for cancer patients tive effects. The institute further cautions that acrylamide is a potential occupational carcinogen. History: Production of acrylamide in the United States exceeds one million pounds per year. It was not until 2002 that Swedish scientists found high levels of acrylamide in certain fried and baked starchy foods. In the same year, the Center for Science in the Public Interest in the United States reported finding high levels of acrylamide in popular brands of snack chips, french fries, taco shells, and breakfast cereals. Government action concerning these findings has been very slow, but in 2005 the California attorney general filed a lawsuit requiring a warning label for french fries and potato chips. Although NIOSH considers the compound dangerous to life and health, the Food and Drug Administration allows acrylamide to be used for packaging, in plastics that are in contact with food, and in treating food to maximum levels ranging up to 0.20 percent. Although research has firmly established the canceracrylamide connection in rats and mice, the findings are still mixed in human studies. Some experts claim the very pervasiveness of acrylamide in the Western diet confuses the results. Richard S. Spira, D.V.M. u For Further Information Brown, L., M. M. Rhead, K. C. C. Bancroft, and N. Allen. “Model Studies of the Degradation of Acrylamide Monomer.” Water Research 14, no. 7 (1980): 775-778. Rice, Jerry M. “The Carcinogenicity of Acrylamide.” Mutation Research/Genetic Toxicology and Environmental Mutagenesis 580, nos. 1/2 (2005): 3-20. Smith, E., S. Prues, and F. Ochme. “Environmental Degradation of Polyacrylamides: Effect of Artificial Environmental Conditions.” Ecotoxicology and Environmental Safety 35 (1996): 121-135. Tareke, E., et al. “Analysis of Acrylamide, a Carcinogen Formed in Heated Foodstuffs.” Journal of Agriculture and Food Chemistry 50, no. 17 (2002): 4998-5006. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Eleventh Report on Carcinogens. Research Triangle Park, N.C.: Author, 2005. Weiss, G. “Acrylamide in Food: Uncharted Territory.” Science 27 (2002): 297. u
Other Resources
National Institute for Occupational Safety and Health http://www.cdc.gov/niosh 8
Salem Health: Cancer National Library of Medicine Toxicology Data Network http://toxnet.nlm.nih.gov U.S. Food and Drug Administration Draft Action Plan for Acrylamide in Food http://www.cfsan.fda.gov/~dms/acrypla3.html See also Adenocarcinomas; Endocrine cancers; Testicular cancer; Vulvar cancer.
u Acupuncture and acupressure
for cancer patients Category: Procedures Also known as: Traditional Chinese medicine (TCM), complementary and alternative medicine (CAM), Oriental medicine (OM) Definition: Acupuncture is a technique in which hair-thin, sterile, disposable needles of varying lengths are inserted into the skin and muscles at specific anatomical points (called acupoints) in order to treat ailments, including pain and certain diseases. It is one branch of traditional Chinese medicine (TCM) that originated in China around four thousand years ago to prevent, diagnose, and treat diseases in both humans and animals. Acupressure is a variation of acupuncture, in which therapists or patients press on acupoints with their fingers instead of inserting needles. Only specifically trained, licensed professionals can treat patients using acupuncture needles, but patients can be taught (preferably by a licensed professional) to perform acupressure on themselves. In 1996, the Food and Drug Administration (FDA) approved the acupuncture needle as a medical device. In 1997, the National Institutes of Health (NIH) began evaluating the safety and effectiveness of acupuncture as a complementary and alternative treatment. According to TCM principles, fourteen meridians are theorized to course invisibly along the body surface, including six paired and two unpaired channels. These meridians correspond to and connect with certain internal organs and physiological systems as understood in both traditional Chinese and Western medicine. Every acupoint is named and numbered according to its location on a specific meridian (for example, P6, or pericardium 6). Upon needling, the acupuncturist attempts to unblock, move, or alter what TCM refers to as the qi or chi (pronounced “chee”) of the body. This qi is a vital force that is thought to flow along the meridians and throughout the
Salem Health: Cancer body and organ systems. TCM posits that qi is formed from a merging of yin and yang, which are opposite energy states that permeate the universe. An imbalance of yin and yang in the body is thought to lead to a disruption of qi, leading to disharmony in physical and psychic well-being and thus to certain ailments or diseases. The acupuncturist (or acupressure practitioner) tries to restore a healthier balance of yin and yang in the patient. Many Western and Eastern acupuncturists currently blend TCM theory with modern understanding of neuroanatomy and the immune and other physiological systems. Cancers diagnosed or treated: In Western cancer management, acupuncture and acupressure are primarily used to mitigate the side effects related to conventional cancer treatments such as chemotherapy, radiation treatment, and surgery, or side effects of the disease itself. These side effects include chemotherapy-related nausea and vomiting, dyspnea (shortness of breath in advanced cancer cases), pain (either from a conventional treatment or the cancer itself), fatigue, depression, vasomotor symptoms (hot flashes), and treatment- or cancerrelated immunosuppression. In most instances, the acupuncture or acupressure interventions are used in addition to state-of-the-art pharmaceutical treatments, such as antiemetic therapy (such as Odansetron) for nausea and vomiting. Why performed: Cancer patients and their clinicians often resort to acupuncture and acupressure (and other alternative medical treatment modalities) for symptoms that are not amenable or are unresponsive to traditional therapies. Sometimes they are used to augment the effectiveness of conventional medicines, as in the case of antiemetic therapies for nausea and vomiting, which can lead to weight loss and depression. Some patients (and their clinicians) are seeking a more holistic approach to healing, viewing acupuncture and acupressure as methods that restore harmony to the body, treating the whole person instead of just the disease. Often patients take solace in the “mysterious” mechanisms underlying alternative treatments. Many acupuncturists are intrigued by the TCM philosophies and theories, at the same time applying current Western knowledge of anatomy and neurophysiology to their techniques. Most acupoints correspond to specific nerve pathways or receptors and/or highly vascular areas. There is strong evidence that acupuncture modulates neurotransmitters, leading to the release of endogenous opioids (endorphins and
Acupuncture and acupressure for cancer patients enkephalins) for analgesia (pain relief). Manipulation of certain acupoints stimulates the autonomic nervous system, leading to changes in blood circulation and engaging components of the immune and endocrine systems (proteins called cytokines or the release of endogenous corticosteroids and other hormones). These procedures can also alter blood pressure, heart rhythms, and body temperature. Not all the mechanisms involved in successful acupuncture and acupressure treatment are understood, and they remain a subject of scientific investigation. Some skeptics still believe that they work primarily via the placebo effect. Patient preparation: Very little patient preparation is required for these procedures. The patient disrobes to the extent required for examination and the placement of acupuncture needles or accessibility to acupressure points. Some acupuncturists will take a patient’s medical history
A patient receives an acupuncture treatment. (PhotoDisc)
9
Acupuncture and acupressure for cancer patients and ask questions about diet and exercise. Some will also look at the patient’s tongue and feel his or her pulse in order to make a TCM diagnosis and appropriate acupoint prescription tailored to the patient’s needs. A more Westernized approach would be to apply a standard point prescription for a particular malady, omitting such TCM elements as tongue and pulse exams. Steps of the procedure: The acupuncturist will feel for the appropriate acupoints, often massaging the area prior to needle insertion. The skin is then cleaned with an alcohol wipe and the needle is inserted until the practitioner feels some resistance and/or the patient feels a tingling or cramping sensation. This is referred to as “obtaining the qi,” or De Qi. Many practitioners then manipulate the needle, using hand technique (shou fa) to move, supplement or drain the qi and/or yin and yang. The needles are then usually left in place for ten to twenty minutes. In acupressure, the patient or practitioner applies pressure to the acupoints for a few minutes, repeating this action at intermittent intervals over a specified period of time. Sometimes a band with an attached stud is applied over an acupoint and the patient is instructed to press the stud into the point at prescribed intervals in an effort to obtain a De Qi response during point stimulation. Sometimes an acupuncturist will apply a small electric current to the needles in a technique called electroacupuncture. This is another method of stimulating the acupoints. Various other methods of stimulation are employed as well. Moxibustion applies heat to the acupoints using burning mugwort herb (Artemisia vulgaris). Aquapuncture is a technique in which acupoints are injected with drugs, vitamins, flower essences, herbal extracts, or other fluids for longer-term stimulation of acupoints. After the procedure: A properly treated patient should experience relaxation, deeper respiration, and increased vitality following acupuncture, since energetic balance has supposedly been restored. For treatment of specific cancer-related symptoms, some immediate relief is expected, followed by delayed improvement, especially after multiple acupuncture or acupressure sessions. Risks: Acupuncture should be avoided in patients with thromobocytopenia or aplasia or in those treated with anticoagulants. Some common side effects are bruising, local bleeding, and mild pain in the treated areas. The risk of infection is small if sterile, disposable needles are used. There is a very small risk that the lungs or other internal organs can be punctured if a needle is placed too deep. 10
Salem Health: Cancer Results: The results of many random, controlled clinical trials have demonstrated that acupuncture is effective for reducing episodes of acute vomiting following chemotherapy for breast and other cancers. The same and other studies have shown that acupressure at certain acupoints is effective for reducing episodes of acute nausea following chemotherapy. Both acupuncture and acupressure have been more effective for prophylactic treatment of vomiting and nausea following conventional cancer treatment rather than stopping these symptoms once they have started. One study indicated that the effectiveness of acupuncture for reducing vomiting episodes following chemotherapy was increased for up to twenty-four hours when acupressure followed needling therapy. One review of acupuncture for the relief of cancerrelated pain found that ear acupuncture (stimulation of acupoints corresponding to different body areas on the ear) was effective for reducing cancer-related pain. Other clinical trials have shown that acupuncture helps reduce the number of hot flashes in men being treated with hormones or surgery for prostate cancer and women being treated with tamoxifen or related hormone therapies for breast cancer. Investigators, however, have noted a dearth of random, double-blind, controlled clinical trials for proving the effectiveness of these alternative therapies. The development of a sham acupuncture needle (the needle withdraws into the shaft upon “insertion” at true acupoints) is expected to improve the rigorousness of these trials and to provide substantive evidence for or against acupuncturerelated therapies. Lisa J. Shientag, V.M.D. u
For Further Information Ezzo, J. M., M. A. Richardson, and A. Vickers. “Acupuncture Point Stimulation for Chemotherapy-Induced Nausea or Vomiting.” The Cochrane Database of Systematic Reviews 2 (2007). Hyangsook, L., K. Schmidt, and E. Ernst. “Acupuncture for the Relief of Cancer-Related Pain: A Systematic Review.” European Journal of Pain 9, no. 4 (August, 2005): 437-444. Sagar, Stephen M. Restored Harmony: An Evidence Based Approach for Integrating Traditional Chinese Medicine into Complementary Cancer Care. Hamilton, Ont.: Dreaming DragonFly Communications, 2001. See also Bone cancers; Bone pain; Complementary and alternative therapies; Home health services; Integrative oncology; Living with cancer; Pneumonia; Side effects; Smoking cessation.
Salem Health: Cancer
Acute lymphocytic leukemia (ALL)
u Acute lymphocytic leukemia
(ALL) Category: Diseases, symptoms, and conditions Also known as: Acute childhood leukemia, acute lymphoblastic leukemia, acute lymphoid leukemia Related conditions: Acute myeloid leukemia, chronic lymphocytic leukemia, chronic myeloid leukemia Definition: Acute lymphocytic leukemia (ALL) is a cancer of the white blood cells. A lymphocyte is a type of white blood cell made in the bone marrow that helps fight infection. In this fast-growing type of cancer, for unknown reasons, the bone marrow begins to make lymphocytes that develop abnormally. “Acute” means that the disease affects lymphocytes before they are fully formed and that it progresses rapidly if not treated. Risk factors: Few risk factors exist for ALL. Receiving high doses of radiation, usually as treatment for another type of cancer, is one risk factor. Exposure to benzene may also be a factor. Risk increases in people with certain other diseases, such as Down syndrome, Fanconi anemia, Bloom syndrome, and some other genetic diseases. In about 25 percent of ALL cases, the patient has a chromosome mutation in which parts of chromosome 9 and chromosome 22 have changed places. Having a sibling, especially a twin, with ALL also increases the risk for this disease. Researchers are exploring lifestyle or environmental relationships, but it appears that many factors, including a combination of genetic and environmental factors, may be involved in developing ALL.
and slightly more common in white children than in children of other races. ALL occurs in people of all ages but has a peak incidence in children between the ages of two and five. After age five, risk decreases, then increases again in people over age fifty. It is the most common type of leukemia in children under the age of fifteen, accounting for about 80 percent of childhood leukemias. It occurs more often in developed countries and in people with higher socioeconomic status. Symptoms: Symptoms of ALL include anemia, body aches, bone pain, bruises without any injury, enlarged lymph nodes, an enlarged spleen, excessive bleeding from minor injuries, fever with no illness or lasting low-grade fever, frequent infections, headaches, joint pain, nosebleeds, paleness, shortness of breath during activity, tiredness, vomiting, and unexplained weight loss. Screening and diagnosis: There is no screening test for ALL. Blood and bone marrow tests are necessary to diagnose ALL. These tests look for abnormal lymphocyte cells. A bone marrow aspirate test (using a long needle to take marrow out of the bone) and a bone marrow biopsy (surgical removal of some bone marrow) are two possible tests. The bone marrow aspirate test looks for abnormal
Etiology and the disease process: Through a genetic process that is not completely understood, cells in bone marrow begin to form abnormally. ALL can begin in two different types of lymphocytes, either B cells or T cells. As the abnormal lymphocytes quickly grow, they crowd out the red and white blood cells and platelets that the body needs and that are also created in the bone marrow. The symptoms of ALL come from the crowding out of these normal, healthy cells. These cells may then spread into the lining of the spine and brain. Incidence: About 5,200 people in the United States were diagnosed with ALL in 2007. It is slightly more common in men than in women
A nine-year-old girl with acute lymphocytic leukemia describes her condition to a health care worker. (Simon Fraser/Photo Researchers, Inc.)
11
Acute lymphocytic leukemia (ALL)
Age at Death for Acute Lymphocytic Leukemia, 2001-2005 Age Group
Deaths (%)
Under 20 20-34 35-44 45-54 55-64 65-74 75-84 85 and older
21.4 15.9 9.7 11.2 11.7 12.7 11.5 5.8
Source: Data from National Cancer Institute, Surveillance Epidemiology and End Results, Cancer Stat Fact Sheets, 2008 Note: The median age of death from 2001 to 2005 was fortyseven, with an age-adjusted death rate of 0.5 per 100,000 men and women.
cells in the bone marrow and can also be used for other types of analysis. A bone marrow biopsy can show how much disease is already in the bone marrow. The results of these tests help determine which type of drug therapy to use and how long treatment should last. If a patient has been diagnosed with ALL, a lumbar puncture may be performed to see if the abnormal cells have moved into the fluid surrounding the spine and brain. Chest X rays, ultrasounds, or additional blood tests may also be used to determine the spread of the disease. Depending on where the cancer started and the results of testing, ALL may be categorized into early pre-B-cell ALL, common ALL, pre-B-cell ALL, mature B-cell ALL, pre-T-cell ALL, or mature T-cell ALL. The type of ALL helps determine which therapy to use and how long treatment should last. About 85 percent of ALL cases begin in B cells, and these cases are generally classified as lower risk. ALL may also be classified or staged using the FrenchAmerican-British (FAB) classification system. In this older system, ALL is classified according to the type of abnormal cells as follows: • ALL-11: small, uniform abnormal cells • ALL-12: large, varied abnormal cells • ALL-13: large, varied, bubble-like cells Treatment and therapy: Patients diagnosed with ALL should start treatment immediately. The course and length of treatment chosen depend on the results of the patient’s bone marrow tests, the patient’s age, the number of ALL cells in the blood, whether certain chromosomal changes 12
Salem Health: Cancer have already happened, whether ALL cells began in the B cells or the T cells, and whether ALL has spread to the brain covering or spinal cord. During therapy, bone marrow tests may be done again to make sure the treatment is destroying the cancer cells. The first part of treatment for ALL is called induction therapy. This therapy helps kill ALL cells and get a patient’s blood counts back to normal (remission). Some of the drugs used in induction therapy are given by mouth. Others are given in a vein, usually through the patient’s chest. Most often, this chemotherapy for ALL involves combining drugs to improve the effects of the drugs. Often, ALL spreads into the lining of the spinal cord and the brain. To kill these ALL cells, drugs are injected directly into the spinal fluid. Radiation therapy may be used on the spine and brain either with or without the injected drugs. Post-induction therapy, the second part of treatment for ALL, begins when a patient has reached remission. This type of therapy is needed because usually some ALL cells that cannot be detected by tests remain in the body. Postinduction therapy usually happens in two- or three-year cycles. The drugs used in post-induction therapy are usually different from those used in induction therapy, and the type of drugs used depends on how the patient responded to induction therapy and whether the patient has certain chromosome abnormalities. A patient may also need maintenance therapy after post-induction therapy to prevent the cells from regrowing. T-cell ALL, infant ALL, and adult ALL are all forms of high-risk ALL. These types of ALL are usually treated with higher doses of drugs during both induction and postinduction therapy. Some patients with high-risk types of ALL may respond well to bone marrow or cord blood transplant therapy. A bone marrow or cord blood transplant may be used when high doses of drugs are given to kill the ALL cells. These high doses of drugs may also kill healthy cells in the bone marrow. This transplant gives a patient healthy cells to replace the killed bone marrow cells. A transplant is a high-risk procedure and will probably not be used unless a patient does not have a good possibility of long-term remission with chemotherapy. High-risk ALL patients are more likely to have a transplant. The timing of a transplant is important; a patient has a better chance of a successful transplant when he or she is in remission at the time of transplant. Prognosis, prevention, and outcomes: There is no known way to prevent ALL. Most children with ALL can be cured of this disease with proper treatment. The overall survival rate for children after chemotherapy is nearly 80 percent.
Salem Health: Cancer Children with low-risk ALL have even higher survival rates. Most adults also improve with treatment; the number of adults who have remissions has increased, and the length of adult remissions has improved. The overall survival rate for adults after chemotherapy is about 40 percent, and adults with low-risk ALL have even higher survival rates. Marianne M. Madsen, M.S. u For Further Information Abeloff, M. D., et al. Clinical Oncology. 3d ed. Orlando, Fla.: Churchill Livingstone, 2004. Hoffman, R., et al. Hematology: Basic Principles and Practice. 4th ed. Orlando, Fla.: Churchill Livingstone, 2005. Lichtman, M. A., et al., eds. William’s Hematology. 7th ed. New York: McGraw-Hill, 2006. Pui, C-H, ed. Childhood Leukemias. 2d ed. New York: Cambridge University Press, 2006. u
Other Resources
Association of Cancer Online Resources http://www.acor.org CureSearch: National Childhood Cancer Foundation, Children’s Oncology Group http://www.curesearch.org Leukemia and Lymphoma Society http://www.leukemia-lymphoma.org National Cancer Institute http://www.cancer.gov/cancertopics/treatment/ See also Acute myelocytic leukemia (AML); Aleukemia; Blood cancers; Childhood cancers; Chronic lymphocytic leukemia (CLL); Chronic myeloid leukemia (CML); Hemolytic anemia; Leukemias; Myelodysplastic syndromes; Myelofibrosis; Myeloproliferative disorders; Topoisomerase inhibitors.
u Acute myelocytic leukemia
(AML) Category: Diseases, symptoms, and conditions Also known as: Acute myeloid leukemia, acute myelogenous leukemia, acute myeloblastic leukemia, acute myelomonocytic leukemia, granulocytic leukemia, acute nonlymphocytic leukemia, acute promyelocytic leukemia
Acute myelocytic leukemia (AML) Related conditions: Acute lymphoblastic leukemia, myelodysplastic syndrome Definition: Acute myelocytic leukemia (AML) describes a malignant proliferation in the bone marrow of an undifferentiated blood-forming cell of the myeloid line. AML begins with the genetic alteration of a single cell. That cell, called a blast cell, is the foundation from which the leukemia follows. The process of normal blood cell formation, or hematopoiesis, begins with undifferentiated cells, known as stem cells, inside the bone marrow. Stem cells differentiate into blasts, and these primitive blast cells give rise to red blood cells, platelets, and white blood cells. It is the accumulation of blast cells in the bone marrow and their failure to differentiate that has lethal consequences within just a few weeks or months if unchecked. Although the rate of cure has improved, treatment is still associated with high morbidity and mortality. Risk factors: Certain genetic disorders have an associated AML risk, including Down syndrome, Fanconi anemia, and Shwachman-Diamond syndrome. Other risk factors include some forms of chemotherapy, radiation therapy, and exposure to tobacco smoke and benzene. Etiology and the disease process: The process leading to acute myelocytic leukemia involves the interruption in the progression of an undifferentiated progenitor cell in the bone marrow that normally matures into red blood cells, white blood cells (neutrophils, eosinophils, basophils, and monocytes), and megakaryocytes. Megakaryocytes are bone marrow cells responsible for the production of the blood platelets necessary for blood clotting. Bone marrow is the soft interior of some bones, such as the skull, shoulder blades, ribs, pelvis, and backbones. It comes in two varieties: red marrow and yellow marrow. The red marrow, also called myeloid tissue, is the source of AML activity. Red blood cells, platelets, and most white blood cells arise from a parent cell in the red marrow. Many references limit discussion of AML to only the direct descendants of the myeloid line; these are the neutrophils, eosinophils, and basophils. When blast cells do not mature properly, they accumulate in the bone marrow. It is the proliferation and the accumulation of this hemopoietic cell in the bone marrow that defines AML. Although research has not completely unraveled the process of this leukemic transformation, there is strong evidence of underlying chromosomal damage. For example, a variety of mutations are associated with AML, with damage to the gene for FMS-related tyrosine kinase (FLT3) being the most prominent. Normally, the receptor encoded by FLT3 signals undifferentiated blast 13
Acute myelocytic leukemia (AML) cells in the bone marrow to proliferate when there is a need for additional circulating blood cells. The signal stops when the supply is sufficient, but in AML, the switch stays on, and unconstrained blast cell proliferation follows. Although AML begins with defective bone marrow cells, it generally moves quickly into the peripheral blood and may spread to other parts of the body, such as the liver, spleen, testes, brain, spinal cord, and lymph nodes. Incidence: Because AML is associated with accumulating genetic defects, the incidence increases with age. AML ranges from 0.7 to 3.9 cases per 100,000 in people up through the age of sixty and increases to 6.7 to 19.2 cases per 100,000 in people who are over sixty. The median age of onset is more than sixty-seven years. Each year AML will strike about 13,400 adults and 650 children in the United States. Symptoms: Clinical findings reflect the replacement of normal bone marrow elements with malignant blast cells. Probably the most consistent early complaints in AML are a history of increasing lethargy later followed by skin, soft-tissue, or respiratory infection. Some patients will have small red or purple spots on the body, called petichia, resulting from broken blood vessels. Liver, spleen, and lymph node enlargement is common, as is weight loss. Some symptoms are nonspecific but quite common in AML patients. These include swollen gums; pale skin; black-and-blue marks; achiness in the knees, hips, or shoulder; mild fever; shortness of breath during even light exertion; and the slow healing of cuts. Screening and diagnosis: The diagnostician must distinguish AML from other myeloproliferative disorders,
Age at Diagnosis for Acute Myelocytic Leukemia, 2001-2005 Age Group
Diagnosed (%)
Under 20 20-34 35-44 45-54 55-64 65-74 75-84 85 and older
6.3 6.3 6.8 10.9 14.8 21.1 24.6 9.2
Source: Data from National Cancer Institute, Surveillance Epidemiology and End Results, Cancer Stat Fact Sheets, 2008
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Salem Health: Cancer chronic myelogenous leukemia, and myelodysplastic syndrome. Although many supporting tests and symptoms point toward a diagnosis, the definitive finding of AML will require bone marrow aspirate and biopsy. Short of biopsy examination, other indicators will raise suspicion. About one-third of AML patients will have an enlarged spleen and high levels of uric acid in the blood. The peripheral white blood cell count is not a good indicator, as it may be increased, decreased, or normal. However, there usually will be reduced numbers of granulocytes (neutrophils, basophils, and eosinophils) and platelets in the blood. Blast cells in the peripheral blood appear in only 15 percent of AML patients initially, but this number rises to half of those patients with decreased number of circulating white blood cells (leukopenia). There is no standard staging system for AML. Generally, doctors describe the status of the condition as untreated, in remission, or recurrent. However, bone marrow examination more closely defines AML as belonging to one of eight cell subtypes. Doctors tailor the treatment to the subtype. The subtypes are as follows:
• • • • • • • •
M0: Myeloblastic, on special analysis M1: Myeloblastic, without maturation M2: Myeloblastic, with maturation M3: Promyeloctic M4: Myelomonocytic M5: Monocytic M6: Erythroleukemic M7: Megakaryocytic
Treatment and therapy: The goal of AML treatment is the destruction of the leukemic cells. However, this requires the suppression of bone marrow activity, which brings unfortunate side effects. With the bone marrow suppressed, fewer white cell are available to fight infection and fewer red cells and platelets are present to maintain a healthy oxygen exchange and clot formation. This almost always requires treatment with antibiotics and blood transfusions. Initial treatment or induction therapy begins with a hospital stay of about a week using chemotherapy in a combination of drug types. Generally induction therapy requires more than one round of treatment, as it is likely that some AML cells will survive. Even if the induction therapy seems successful, the doctors assume that leukemic cells still exist though unrevealed on biopsy examination. In the unusual event that leukemia has spread to the brain or spinal cord, chemotherapy is also introduced into the cerebrospinal fluid. At a later date, a follow-up round of less intensive treat-
Salem Health: Cancer
Acute myelocytic leukemia (AML)
ments called consolidation therapy brings the patient back to the hospital to maintain remission status. Remission describes a normal peripheral blood profile, a normal bone marrow free of excess blasts, and a normal clinical status. Doctors generally reserve stem cell transplantation with more vigorous chemotherapy for those patients susceptible to relapse, although it is sometimes part of the consolidation regimen. However, there is some debate among doctors as to the risks and benefits of this treatment. For relapsed patients who are unable to undergo the rigors of stem cell transplantation, additional chemotherapy is generally not well tolerated or effective. Doctors adapt specific chemotherapies Human cells with acute myelocytic leukemia in the pericardial fluid. (National Cancer Institute) to the subtype of the leukemia. Usually this will be some combination of an anthracycline class agent with cytabrine. In u For Further Information some cases a third drug, 6-thioguanine, is added. Also facEzzone, Susan, and Kim Schmit-Pokorny, eds. Blood and tored into the treatment strategy are the patient’s age, cliniMarrow Stem Cell Transplantation: Principles, Praccal status, and leukemia profile. Although quite variable, tices, and Nursing Insights. Sudbury, Mass.: Jones and hospital stays for induction and consolidation therapies Bartlett, 2007. may require weeks or even months. Typically, chemotherHoffman, Ronald, et al. Hematology: Basic Principles and apy will drive the patient’s blood cell counts down to danPractice. 4th ed. St. Louis: Elsevier Churchill Livinggerously low levels. This will require drugs to elevate stone, 2005. white blood cell counts as well as antibiotics and blood Hutton, John J. “The Leukemias and Polcythemia Vera.” transfusions to protect against complications. In Internal Medicine, edited by Jay H. Stein. 5th ed. St. Louis: Mosby, 1998. Prognosis, prevention, and outcomes: The prognosis of Lichtman, Marshall A., and Jane A. Liesvelt. “Acute patients with AML largely depends on the patient’s age. In Myelogenous Leukemia.” In Williams Hematology, part this is due to chemoresistance or the biological reedited by Marshall A. Lichtman, et al. 7th ed. New sponse of cells to survive the toxic stress of chemotherapy. York: McGraw-Hill, 2006. Because chemoresistance tends to increase with age, important therapies are less effective in older patients. Also, the difference in the mechanisms of chromosome translou Other Resources cations in the young and older patients allows for a more The Leukemia and Lymphoma Society favorable outcome in the younger patient. Acute Lyelogenous Leukemia In the absence of treatment, most people stricken with http://www.leukemia-lymphoma.org/all_mat_toc AML will die less than two months after the diagnosis. .adp?item_id=3113 With therapy, between 20 and 40 percent of people survive for at least five years. The poorest prognoses are reserved National Marrow Donor Program for those patients older than sixty and for those developing Acute Myelogenous Leukemia AML following chemotherapy and radiation therapy for http://www.marrow.org/PATIENT/Undrstnd_ other cancers. In general, four years following consolidaDisease_Treat/Lrn_about_Disease/AML/index.html tion therapy, approximately 40 percent of patients under sixty years of age will be free of any signs of leukemia, See also Acute lymphocytic leukemia (ALL); Blood cancers; Childhood cancers; Chronic lymphocytic leukemia with that number dropping to 15 percent in older patients. (CLL); Chronic myeloid leukemia (CML); Fanconi aneRichard S. Spira, D.V.M. 15
Adenocarcinomas mia; Genetics of cancer; Leukemias; Leukopenia; Myelodysplastic syndromes; Myeloproliferative disorders; Myelosuppression.
u Adenocarcinomas Category: Diseases, symptoms, and conditions Also known as: Malignant adenomas, other names vary by type Related conditions: Lung cancer, breast cancer, colon cancer, renal cell carcinomas Definition: Adenocarcinoma is a type of cancer that develops in the epithelial tissue of glandular (secretory) organs. Although it is commonly associated with lung cancer (and is the most common form of lung cancer), adenocarcinoma can also develop in such organs as the breast, colon, kidney, liver, pancreas, prostate, and stomach. It is classified according to the kind of tissue from which it
Salem Health: Cancer arose (such as lung or breast) or according to a particular product of the cells (such as mucinous adenocarcinoma). Adenocarcinoma can spread (metastasize) to other parts of the body and also destroy surrounding tissues. Risk factors: Smoking increases the risk of almost every type of cancer. Other risk factors for adenocarcinoma vary by organ site. Age, race, family history, medication use, and lifestyle factors such as diet have been implicated in certain forms of adenocarcinoma. Etiology and the disease process: Etiology of and the disease process for adenocarcinoma vary with the involved organ. Incidence: Incidence of adenocarcinoma varies by type. Adenocarcinoma is the most common form of lung, pancreatic, prostate, and stomach cancer. Symptoms: Symptoms of adenocarcinoma vary by type. Small adenocarcinomas may produce only mild symptoms that go undetected. Large adenocarcinomas produce more noticeable symptoms that vary with the site of in-
A surgical specimen showing colonic adenocarcinoma. (Centers for Disease Control and Prevention)
16
Salem Health: Cancer volvement. The first signs of adenocarcinoma may be a noticeable lump and pain or discomfort. Screening and diagnosis: Diagnosis of adenocarcinoma begins with a medical history and physical examination. Lumps are commonly biopsied, and specialized imaging techniques, such as X rays and computed tomography (CT) scans, are used to determine the extent of the disease (staging). Staging of adenocarcinoma varies by type. Treatment and therapy: Specific treatment protocols vary by adenocarcinoma type and other factors, such as overall patient health and extent of the disease. Conventional treatment options include surgery, chemotherapy, and radiation therapy. Early-stage, localized disease may be treated by surgery alone (surgical removal of the tumor and surrounding tissue) or surgery with adjuvant chemotherapy or radiation therapy. Advanced adenocarcinoma has no cure. Newly emerging treatments for adenocarcinoma include hormone therapy and stem cell transplantation. Prognosis, prevention, and outcomes: Without treatment, adenocarcinoma is fatal. Routine physical examinations and avoidance of risk factors, such as smoking, are keys to early detection and prevention. Jaime Stockslager Buss, M.S.P.H., ELS See also Adenoid cystic carcinoma (ACC); Appendix cancer; Bile duct cancer; Breast cancer in children and adolescents; Bronchoalveolar lung cancer; Carcinomas; Duodenal carcinomas; Esophageal cancer; Fallopian tube cancer; Gallbladder cancer; Gastrointestinal cancers; Granulosa cell tumors; Head and neck cancers; Helicobacter pylori; Lung cancers; Mesothelioma; Mucinous carcinomas; Nasal cavity and paranasal sinus cancers; Oncogenic viruses; Pancreatic cancers; Prostate cancer; Rectal cancer; Salivary gland cancer; Small intestine cancer; Stomach cancers; Throat cancer; Urethral cancer; Urinary system cancers; Uterine cancer; Vaginal cancer; Vulvar cancer.
u Adenoid cystic carcinoma
(ACC) Category: Diseases, symptoms, and conditions Also known as: Adenocystic carcinoma, cribriform carcinoma, cylindroma, malignant cylindroma, AdCC Related conditions: Adenoma, adenocarcinoma Definition: Adenoid cystic carcinoma (ACC) is a rare malignant cancer of the secretory glands. Neoplasms usually
Adenoid cystic carcinoma (ACC) originate in the major and minor salivary glands of the head and neck region but can also occur in places such as in the trachea, lacrimal glands, breast, skin, and vulva. Risk factors: Environmental and genetic risk factors have not been identified. Etiology and the disease process: There is little information available regarding pathogenesis except for some evidence suggesting that the TP53 tumor-suppressor gene is inactivated in the most aggressive forms or stages of ACC. Incidence: Both children and adults may develop ACC; however, most patients are diagnosed between the fourth and sixth decades of life. ACC affects more women than men at a ratio of approximately 3:2. Symptoms: Signs and symptoms depend on the origin of the neoplasm. Screening and diagnosis: Unfortunately, no screening tests exist because of a lack of serum markers. Diagnosis is made after histologic analysis obtained through biopsy or resection of a tumor. ACC is classified into three major groups according to distinctive histologic growth pattern: cribriform, tubular, and solid. Treatment and therapy: The primary treatment option for adenoid cystic carcinoma is surgery. Postoperative radiotherapy or neutron beam therapy is sometimes recommended to help limit local failure. There is no effective chemotherapy for metastatic or unresectable ACC; however, several clinical trials are testing the effectiveness of new chemotherapeutic drugs (for example, paclitaxel and gemcitabine) when used alone or in combination with other drugs. Radiofrequency ablation and cryoablation are also being explored as treatment options. Prognosis, prevention, and outcomes: ACC growth and disease progression tend to be slow but relentless. ACC is atypical of carcinomas and seldom metastasizes to regional lymph nodes. Distant metastasis is the predominant reason for treatment failure and occurs most frequently in the lung, followed by the liver. Tumors with solid growth patterns and perineural invasion of major nerves or positive margins tend to have poor prognosis. In one study that followed 160 ACC patients, disease-specific survival was 89 percent at five years and 40 percent at fifteen years. Rena C. Tabata, M.Sc. See also Bronchial adenomas; Lacrimal gland tumors; Lung cancers; Nasal cavity and paranasal sinus cancers; Salivary gland cancer; Throat cancer. 17
Adenomatoid tumors
u Adenomatoid tumors Category: Diseases, symptoms, and conditions Also known as: Adenofibromyomas, Recklinghausen’s tumors Related conditions: None Definition: An adenomatoid tumor is a small benign tumor of mesothelial origin usually occurring in the male epididymis or female Fallopian tube, ovary, or uterus. Rarely, these tumors can be seen within the testes and prostate. Extragenital adenomatoid tumors have also been identified in the heart, mesentery, pleura, lymph nodes, omentum, and adrenal glands. Because of its glandular appearance, it may be confused with an adenocarcinoma or metastatic carcinoma, especially signet ring cell carcinoma. Risk factors: There are no known risk factors for adenomatoid tumors. Etiology and the disease process: An adenomatoid tumor is a benign hamartoma that is a malformation resulting from faulty development in an organ and is made up of an abnormal mixture of tissue elements normally present at that site. Most adenomatoid tumors are composed of fibrous tissue separated by numerous slitlike pseudotubular spaces crossed by peculiar threadlike bridging strands, which are their typical morphologic feature. The most common benign tumor of the epididymis, adenomatoid tumors usually arise in the tail of the epididymis and may rarely invade adjacent testicular parenchyma. Although they may occur at any age, they are most commonly seen in patients between twenty and fifty years of age and are usually asymptomatic. Although usually under 5 centimeters (cm) in size, they can grow quite large under hormonal influence. Incidence: In one study, the reported incidence of adenomatoid tumors is 1.2 percent, although the true incidence is probably greater, as most tumors are never biopsied because of their small size and similarity to leiomyomas of the uterus. When found in the male genital tract, these tumors are usually seen in an extratesticular location, usually involving the epididymis, representing approximately 30 percent of tumors arising in the paratesticular area. Symptoms: Adenomatoid tumors usually are asymptomatic. However, when adenomatoid tumors occur in the genital tract, they can grow quite large and can be painful. Screening and diagnosis: Often mistaken for uterine fibroids on magnetic resonance imaging, the radiologic appearance can vary from solid to cystic depending on the 18
Salem Health: Cancer relative amounts of cystic spaces, smooth muscle, and fibrous tissue contained within the tumor. Ultrasound is useful in diagnosing adenomatoid tumors of epididymal origin. They usually appear as a round or oval, solitary, solid, well-circumscribed mass of variable echogenicity measuring between 5 millimeters (mm) and 5 cm. Occasionally they may appear cystic sonographically and rarely appear plaquelike and ill-defined. Treatment and therapy: Surgical removal. Prognosis, prevention, and outcomes: Excellent. Debra B. Kessler, M.D., Ph.D. See also Endometrial cancer; Fallopian tube cancer; Fibrosarcomas, soft-tissue; Gynecologic cancers; Oophorectomy; Ovarian cancers; Ovarian cysts; Testicular cancer.
u Adenomatous polyps Category: Diseases, symptoms, and conditions Also known as: Colorectal adenomas Related conditions: Colon cancer, benign polyps, familial adenomatous polyposis (FAP) Definition: Polyps are abnormal tissue growths stemming from the lining of mucous membranes. Colorectal adenomatous polyps are benign (noncancerous) polyps that project from the inner lining of the colon or rectum and protrude into the lumen of the intestines. Despite their benign characteristics, adenomatous polyps can become cancerous if not removed. Risk factors: Adenomatous polyps are one of the most common types of colon polyp. Individuals over the age of fifty years are much more likely to develop these growths, as are those people with a family history of colon polyps. Additionally, having a mutation in the APC gene can cause a condition named familial adenomatous polyposis (FAP), a disorder that causes numerous polyps to grow in the intestines and almost always develop into tumors. Etiology and the disease process: Adenomatous polyps are a collection of cells that display uncontrolled proliferation, forming a growth that stems from the inner lining of the colon. Incidence: The prevalence of adenomatous polyps ranges from 10 to 25 percent of the population, depending on the type of screening procedure used. Symptoms: Most adenomatous polyps are asymptomatic, and patients are unaware of their presence until they are
Salem Health: Cancer identified through screening. When adenomatous polyps are not removed and continue to grow larger, they can eventually induce rectal bleeding, diarrhea, or constipation. Screening and diagnosis: The most common screening method to detect adenomatous polyps is colonoscopy, a procedure by which a doctor inserts a viewing tube into the colon and removes any visually identified polyps. Other screening methods that may be used are flexible sigmoidoscopy and barium enema. Removed polyps are then biopsied to determine if they are benign or have developed into precancerous or cancerous lesions. Treatment and therapy: When identified through screening, the general treatment is immediate removal of adenomatous polyps to prevent their possible development into cancer. Most doctors recommend that patients undergo subsequent colorectal screening on a regular basis for several years following the removal of adenomatous polyps. Prognosis, prevention, and outcomes: When discovered and removed, adenomatous polyps do not significantly change a patient’s quality of life. However, if left undetected, some of these polyps can develop into colon cancer, which has a higher mortality rate than any other cancer type in the United States. Some possible ways to prevent the development of adenomatous polyps is to maintain a diet that is high in fiber and low in fat, as well as refraining from smoking and excessive drinking. Lisa M. Cockrell, B.S.
Adenoviruses human viruses in the family Adenoviridae. Adenoviruses can be genetically engineered to serve as vectors that deliver targeted gene therapy to human cells. Cancers treated: Breast, colorectal, head and neck, liver, and prostate cancers Delivery routes: Injection How these agents work: Adenoviruses are nonenveloped, or naked, viruses, meaning that they lack a lipid and protein outer covering. Counterintuitively, viruses without this outer covering are better able to withstand environmental stressors such as an acidic environment, drying, and heat—and therefore may live longer outside a host cell. Most adenoviruses cause respiratory illnesses, conjunctivitis (pinkeye), or gastroenteritis and are transmitted via respiratory droplets or through fecal-oral transmission. Adenoviruses are well suited to gene therapy because of their environmental robustness, the ease of manipulating the adenovirus genome, and their ability to infect a number of different kinds of tissue. The DNA inside the adenovirus may one day be altered to encode up to forty genes.
See also Colon polyps; Colorectal cancer; Desmoid tumors; Duodenal carcinomas; Enterostomal therapy; Gardner syndrome; Gastric polyps; Genetics of cancer; Hereditary cancer syndromes; Hereditary polyposis syndromes; Polyps; Small intestine cancer; Stomach cancers; Turcot syndrome.
u Adenoviruses Category: Chemotherapy and other drugs Also known as: Adenoviridae viruses Definition: An adenovirus is a twenty-sided symmetrical icosahedron measuring between 80 and 100 nanometers in diameter with 252 capsomers forming its outside “capsid,” or protein shell. Adenoviruses contain double-stranded, linear deoxyribonucleic acid (DNA), sometimes referred to as dsDNA. These viruses are named for the the adenoids, as they were first isolated from human tonsils in the 1950’s. There are now more than forty identified types of
An electron micrograph of an adenovirus. (Centers for Disease Control and Prevention)
19
Adjuvant therapy In cancer therapy, adenoviruses are first inactivated to make them incapable of causing infection once inside the body. When injected into cancer cells, the virus can cause cell death or tumor suppression by producing toxic proteins, flagging cells for destruction by the immune system, breaking the cell apart (cell lysis), or activating genes that will cause the cell to die (apoptosis) or stop replicating. To gain access to host cells, adenoviruses attach to a receptor on the host cell, which triggers the host cell to surround, engulf, and coat the virus with chemicals. Once the virus is inside the host, the coating dissolves and the virus releases into the host cell cytoplasm. The virus makes its way to the host cell nucleus, where it disassembles itself and releases viral DNA into the host’s nuclear pores. Soon the host cell nucleus stops replicating its DNA and instead begins replicating the DNA of the adenovirus. Eventually the host cell breaks apart (lyses) and releases the newly created adenoviruses. Since most people have been exposed to adenoviruses, the immune system can mount an immune response to the adenoviruses before they have a chance to target the cancer cells. With more research into the specific targeting of cancer cells, however, a vigorous immune response may serve as a beneficial side effect of treatment. Side effects: The side effects of adenovirus use in cancer therapy include inflammation at site of injection, inappropriate immune response, fever, and coldlike symptoms. Pamela Richardson, M.S. See also Gene therapy; Oncogenes; Oncogenic viruses; Simian virus 40.
u Adjuvant therapy Category: Procedures Definition: An adjuvant therapy is any treatment given after the primary treatment to increase the likelihood of killing all cancer cells. Cancers treated: Many types, including cancers of the breast, colon, kidney, ovary, and testicle Why performed: After the primary treatment removes or kills a detected primary tumor, additional cancerous cells or microtumors may still be present in the body. Adjuvant therapy may be administered to help prevent the recurrence of cancer after the primary tumor is removed. Generally, the larger the primary tumor size at detection, the larger is the probability that residual cancer cells may be left behind following surgery. Cancer cells can break away 20
Salem Health: Cancer from the primary tumor and metastasize even when the disease is in an early stage, and they exist in a form too small to detect by radiological or laboratory testing. Patient preparation: In the decision regarding whether to undergo adjuvant therapy, a number of prognostic factors enter into the determination, such as patient age, size of primary tumor, spread to lymph nodes, and microscopic appearance of the cancer cells. Doctors consider these factors and others in order to estimate the likelihood of recurrence. The higher the risk for recurrence, the greater is the motivation to pursue adjuvant therapy options. Local adjuvant radiation treatment typically commences about three to six weeks following the primary treatment. If a combination of chemotherapy and radiotherapy as adjuvant therapy is chosen, then usually chemotherapy is received first followed by radiation, although they may be administered simultaneously in some cases. It is not known how effective adjuvant therapy may be if started later than six weeks following primary therapy. Steps of the procedure: The term “adjuvant therapy” actually encompasses many different treatment forms, including chemotherapy, radiation, hormonal therapy, targeted therapy, or some combination thereof. Adjuvant therapy can be either systemic or local. Chemotherapy, for instance, is given by mouth or injected into the bloodstream. Adjuvant chemotherapy is administered in cycles of treatment followed by recovery and typically lasts for three to six months. Side effects from adjuvant therapy such as chemotherapy or radiation may be experienced. For example, the effects of adjuvant chemotherapy may include loss of hair, loss of appetite, vomiting, diarrhea, mouth sores, psychological distress, and some loss of cognitive brain function. Medications are available to help control vomiting and nausea induced by chemotherapy. Researchers at the University of Rochester have reported that treatment with modafinil (Provigil) can alleviate the cognitive symptoms of so-called chemo brain experienced in certain cancer treatment regimens. Longer-term side effects may include infertility. Another example of adjuvant therapy is hormone adjuvant therapy to treat breast cancer. Hormone adjuvant therapy is used on breast cancer cells that have been found to be estrogen or progesterone receptor positive. Some standard hormone therapies include the synthetic hormone tamoxifen and aromatase inhibitors. Tamoxifen as an adjuvant therapy has been found to decrease the chance of recurrence in women with early-stage hormone receptor positive breast cancer. It is also used to treat women who are at risk of one day developing breast cancer. Aromatase inhibitors are used as adjuvants to reduce the levels of es-
Salem Health: Cancer trogen in postmenopausal women; they include anastrozole (Arimidex), exemestane (Aromasin), and letrozole (Femara). These drugs are not to be used by premenopausal women. Combination adjuvant therapies comprising hormone treatment together with chemotherapy are also available for some patients. After the procedure: It is advised that patients undergo regular checkups following adjuvant therapy in order to monitor any cancer recurrence. Hormone adjuvant therapy, such as used to treat some forms of breast cancer, involves longer-term procedures, with five-year regimens recommended. Risks: The risks associated with different forms of adjuvant therapy are similar to the risks of corresponding primary treatments with chemotherapy, radiotherapy, or hormone therapy. The main risk of declining to participate in adjuvant therapy is the possibility of cancer cells spreading undetected to other parts of the body. While patients with invasive cancers are often urged to consider undergoing adjuvant therapy, other options are available. Patients who turn down the option of adjuvant therapy are advised to participate in regular follow-up clinical examinations to facilitate the detection of new tumors. This alternative is often referred to as “watchful waiting.” Some of the side effects of hormone adjuvant therapy mimick the symptoms of menopause, such as hot flashes and an increased risk for the development of osteoporosis. Results: The goal of adjuvant therapy is to make primary treatment more effective and result in years of disease-free survival. Successful adjuvant therapy is marked by a lack of detectable tumor recurrence or metastasis formation in the months and years following primary therapy. Michael R. King, Ph.D. u For Further Information Henderson, I. Craig, ed. Adjuvant Therapy of Breast Cancer. Boston: Kluwer Academic, 1992. Kirkwood, John M., ed. Strategies in Adjuvant Therapy. Malden, Mass.: Blackwell, 2000. Murphy, Kevin. Adjuvant Chemotherapy Guide. Available online at http://www.cancerguide.org. Salmon, Charles G. Adjuvant Therapy of Cancer. Philadelphia: Lippincott Williams & Wilkins, 1993. u
Other Resources
Mayo Clinic Adjuvant Therapy for Breast Cancer Guide http://www.MayoClinic.com
Adrenal gland cancers National Cancer Institute http://www.cancer.gov See also Biological therapy; Chemotherapy; Hormonal therapies; Pain management medications; Radiation therapies; Watchful waiting.
u Adrenal gland cancers Category: Diseases, symptoms, and conditions Also known as: Pheochromocytoma, adrenal cortical cancer, adrenocortical cancer, neuroblastoma Related conditions: Cushing syndrome, Conn syndrome, adrenogenital syndrome Definition: The adrenal glands are hormone-producing endocrine glands located directly above the kidneys. The outer layer of each gland is called the adrenal cortex. Hormones produced in the adrenal cortex include cortisol (aids in regulating blood sugar level), aldosterone (aids in regulating fluid and electrolyte balance and blood pressure), and testosterone and estrogen (male and female sex hormones). A primary malignant tumor in the adrenal cortex—one that originates in that location—is called adrenocortical cancer. The inner area of each gland is called the adrenal medulla. Hormones produced in the medulla include epinephrine and norepinephrine, which help regulate the body’s response to physical and emotional stress. A primary malignant tumor that originates in the medulla is called a pheochromocytoma. Another form of cancer that originates in the medulla is neuroblastoma, typically found in infants and children younger than age ten. Adrenal tumors are commonly classified by their effect on hormone production in the affected area. Adrenal tumors that increase hormone production are called functioning tumors; those that do not produce hormones are called nonfunctioning tumors. Risk factors: Although specific risk factors for adrenal cancers have not been identified, they have been associated with genetically linked familial syndromes, such as Li-Fraumeni syndrome, Beckwith-Wiedemann syndrome, and Carney complex. Etiology and the disease process: The cause of adrenal cancer is unknown. Functioning tumors that secrete hormones produce changes in the body systems affected by those hormones. Nonfunctioning tumors typically grow large enough to produce pressure on other organs, causing discomfort or pain in the abdomen or flank. 21
Adrenal gland cancers
Salem Health: Cancer
Incidence: Primary adrenal gland cancers are rare, affecting only 1 or 2 persons per 1 million people. Approximately 60 to 80 percent of adrenal cancers are functional, secreting large amounts of adrenal hormones. Adrenocortical cancer is most common in men between the ages of forty and fifty; neuroblastoma most commonly affects children younger than age five; and pheochromocytoma is most common between ages thirty and forty. Symptoms: A functioning adrenocortical cancer tumor typically produces excess amounts of cortisol and aldosterone, which can cause elevated blood pressure, weight gain, thirst, urinary frequency, facial swelling (moon face), cramping of the muscles in the arms and legs, and increased hair growth on the face, arms, and back. If the tu-
mor produces sex hormones, men may develop a loss of sex drive, impotence, and enlarged breasts; women may develop a deeper voice, menstrual irregularities, and increased facial hair; and children may experience early puberty. A neuroblastoma can cause an unusual abdominal lump or fullness, weight loss, extreme tiredness, persistent diarrhea, flushing, sweating, elevated blood pressure, and behavior indicating the presence of abdominal pain. A pheochromocytoma can cause elevated blood pressure that is resistant to treatment, excessive sweating, severe headaches, tremors, rapid pulse, palpitations, and extreme anxiety. A nonfunctioning adrenal cancer may not produce symptoms until the cancer is advanced or has metastasized. Typical symptoms are caused by the tumor pressing on
Adrenal Glands
Kidney
Kidney
The adrenal glands are located on top of the kidneys. (LifeART© 2008 Wolters Kluwer Health, Inc.-Lippincott Williams &Wilkins. All rights reserved.)
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Salem Health: Cancer
Adrenocortical cancer therapy may be used after surgery or to treat metastatic pheochromocytoma.
Relative Survival Rates for Adrenal Gland Cancers, 1988-2001
Prognosis, prevention, and outcomes: There is no known prevention for adrenal cancer. The prognosis for adrenal cancer depends on the type of tumor and the stage of the disease. The five-year survival rate after surgery for adrenocortical cancer is approximately 10 to 35 percent; for localized pheochromocytomas it is about 95 percent. The prognosis for neuroblastoma varies widely depending on the child’s risk grouping. The five-year survival rate ranges from about 95 percent for a low-risk child to about 30 percent for a high-risk child. Metastatic tumors of all types have a poor prognosis. Dorothy P. Terry, R.N.
Survival Rates (%) Cancer Type Adrenal gland (all) Adrenocorticol Pheochromocytoma
1-Year
3-Year
5-Year
10-Year
59.4 66.0 84.5
45.5 48.5 73.0
38.7 41.2 64.8
29.6 31.3 44.0
Source: Data from L. A. G. Ries et al., eds., Cancer Survival Among Adults: U.S. SEER Program, 1988-2001—Patient and Tumor Characteristics, NIH Pub. No. 07-6215 (Bethesda, Md.: National Cancer Institute, 2007)
other abdominal organs, causing pain or an abnormal feeling of fullness. Tiredness, fever, and weight loss may also be present. Screening and diagnosis: There are no screening tests for adrenal cancer. Diagnosis begins with a thorough patient and family medical history and physical examination. If adrenal cancer is suspected, the patient’s blood and urine are tested for elevated levels of adrenal hormones, and computed tomography scanning and magnetic resonance imaging are performed to identify tumors. The metaiodobenzylguanidine (MIBG) scan, during which images are taken after the injection of small amounts of radioactive materials, is used to detect the presence and location of a pheochromocytoma. Staging of adrenal cancer depends on the specific type of tumor. Treatment and therapy: Treatment for adrenal cancer usually includes surgery to remove the affected gland, followed by chemotherapy to destroy any remaining cancer cells. The type and combination of chemotherapeutic drugs used varies with the type of tumor. Mitotane, most commonly used after surgery for adrenocortical cancer, blocks hormone production and destroys adrenal cancer cells. It is also used to treat inoperable, recurrent, and metastatic adrenocortical cancer. If the patient cannot tolerate mitotane therapy or it is ineffective, cisplatin is typically used, either alone or combined with cyclophosphamide and doxorubicin, fluorouracil and doxorubicin, or VP-16. Following surgery, neuroblastoma may be treated with chemotherapy using carboplatin, doxorubicin, cyclophosphamide, and etoposide. Surgery to remove a pheochromocytoma is typically preceded by the administration of medication to block the secretion of adrenalin, which can cause very high blood pressure and serious surgical complications. MIBG radio-
u
For Further Information Bertagna, Xavier, ed. Adrenal Cancer. Montrouge, France: John Libbey Eurotext, 2006. Souhami, Robert, and Jeffrey Tobias. Cancer and Its Management. Malden, Mass.: Blackwell, 2005. Stern, Theodore A., and Mikkael A. Sekeres. Facing Cancer: A Complete Guide for People with Cancer, Their Families, and Caregivers. New York: McGraw-Hill, 2004.
u
Other Resources
American Cancer Society http://www.cancer.org Endocrine Web http://www.endocrineweb.com National Cancer Institute http://www.nci.nih.gov/cancertopics See also Adrenocortical cancer; Computed tomography (CT) scan; Cushing syndrome and cancer; Endocrine cancers; Endocrinology oncology; Hepatomegaly; Radiofrequency ablation.
u Adrenocortical cancer Category: Diseases, symptoms, and conditions Also known as: Adrenal cortex carcinoma Related conditions: Cushing syndrome, Conn syndrome, virilization Definition: Adrenocortical cancer is an aggressive malignancy that occurs when a tumor develops in the tissue of 23
Advance directives the adrenal cortex, the outer layer of tissues that surround the adrenal gland and produce steroid hormones. Risk factors: Certain hereditary diseases, including LiFraumeni syndrome, Beckwith-Wiedemann syndrome, and Carney complex, are the main known risk factors. Etiology and the disease process: The cause of these tumors is unknown. An adrenocortical cancer tumor is either nonfunctioning or functioning, meaning that it overproduces certain hormones that the adrenal cortex normally produces. These hormones include cortisol, aldosterone, testosterone, and estrogen. Adrenocortical cancer commonly becomes malignant, spreading to the lung, liver, bone, and peritoneum (lining of the abdominal cavity). Incidence: Adrenocortical cancer is relatively rare, affecting only 1 to 2 people out of 1 million every year. Although it generally occurs in adults between the ages of thirty and forty years, children can develop this cancer, usually under the age of six.
Salem Health: Cancer of the cancer at diagnosis, the general health of the patient, and whether the tumor is recurrent. Lisa M. Cockrell, B.S. See also Adrenal gland cancers.
u Advance directives Category: Social and personal issues Also known as: Living wills, durable powers of attorney for health care (DPOA), do-not-resuscitate (DNR) orders Definition: Advance directives are written instructions in the form of legal documents that allow people to communicate their desires about medical care and treatment if they cannot speak for themselves due to a terminal condition. Patients with advanced cancer may use them to allow their wishes to be known and followed.
Treatment and therapy: When discovered early, adrenocortical cancer can be cured through surgical removal of the tumor. However, because most tumors are not diagnosed until they are advanced, other treatment strategies such as radiation therapy and chemotherapy must be used. Most chemotherapy regimens to treat adrenocortical cancer include the drug mitotane, which is toxic to adrenal cortex cells, in addition to other chemotherapeutic agents such as cisplatin, doxorubicin, and etoposide.
Purposes: Advance directives are designed to allow competent patients an opportunity to express their wishes for future health decisions in the event that they are unable to participate in medical decision making because of their poor state of health. Advance directives take the pressure off family and friends by letting them know what care and services the cancer patient prefers and what treatment the patient would refuse in the event that communication is not possible. The patient can also designate a person or persons to make decisions. In families in which there is disagreement about what an ill relative would prefer, the advance directive provides clarification. If there is no advance directive and the patient becomes incapacitated with no surrogate designated, state law will dictate the order of surrogate decision makers, usually other family members. By designating a surrogate decision maker, the patient’s choice supersedes that of the state. This is particularly valuable for people without close family or in nontraditional relationships. Advance directives are important because complex choices about end-of-life care are difficult and can seem overwhelming if a someone close to the decision maker is involved. Avoiding these decisions during healthy times will place a heavy burden on family and friends later. Communicating wishes about end-of-life care will ensure that the cancer patient’s wishes are respected.
Prognosis, prevention, and outcomes: The prognosis for patients diagnosed with adrenocortical cancer is generally very poor, and dependent on several factors. These include the ability of the tumor to be surgically removed, the stage
Types: Advance directives emerged in the late 1960’s and early 1970’s as a major social and medical phenomenon resulting from the conflict between professional ethics based on the Hippocratic oath and the physician’s duty to
Symptoms: Nonfunctioning adrenocortical cancer tumors usually do not have symptoms. Functioning adrenocortical cancer tumors can generate many symptoms, owing to their overproduction of steroid hormones. Depending on the hormone, symptoms can include weight gain, high blood pressure, muscle weakness, acne, and changes in menstrual cycles. Screening and diagnosis: Laboratory testing can be used to confirm changes in steroid hormone production. Abdominal radiological examination, such as computed tomography scanning and magnetic resonance imaging, can be used to determine the exact location and extent of the tumor. Adrenocortical cancer tumors are staged on a scale of I to IV, according to the size of the tumor and the degree of invasion, both locally and to distant sites.
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Advance directives
dated, witnessed, notarized, copied, and incorporated into benefit the patient according to the physician’s own ability the patient’s medical record. A copy should be placed in and judgment and the patient’s autonomy. In Schloendorff the chart and given to the patient’s physician and attorney. v. Society of New York Hospital (1914), the Supreme Court Advance directives should be reviewed periodically and ruled that patients were entitled to complete information kept current. Some people even take their directives with about their illness and shared decision making. The Patient them when they travel. Advance directives remain in efSelf-Determination Act of 1991 mandated that all patients fect until they are revoked. admitted to acute care hospitals, long-term care facilities, health maintenance organizations, and home care proConditions: Advance directives are recognized in all fifty grams are to be informed about their rights under state law states and can be considered legally binding, provided to participate in health care decision making, including they are executed in accordance with state guidelines. their right to have written directives. Some directives are written only to apply in particular clinDespite widespread media attention, the majority of seical situations, such as when the patient has a terminal type riously ill patients do not have a written advance directive. of cancer or an incurable illness (advanced or aggressive For those without directives, family members collaborate cancers would fit these categories). Ambiguous terms with a health care provider to make decisions generally resuch as “extraordinary means” and “unnaturally prolongflective of substituted judgment or best-interest principles ing my life,” should be placed within the context of the pa(that is, what the patient would have wanted based on pretient’s values to be understood. Because these ambiguous vious statements and values). This approach, of course, is terms necessitate interpretation by caregivers, revised state problematic because often there is little evidence about the forms have attempted to overcome this problem by adpreferences of any particular patient. dressing specific interventions that are to be withheld in all Advance directives include living wills, durable powers circumstances (for example, blood transfusions, dialysis, of attorney for health care (DPOA), and do-not-resuscitate ventilators and respirators, CPR, artificial nutrition and (DNR) orders. There are two broad categories of advance hydration, withholding of food and fluids, and organ and directives: instructive and proxy. Instructive directives altissue donation). low an opportunity to express preferences regarding the It is important to understand that a decision not to reprovision of particular treatment options. Living wills ceive “aggressive medical care” is not the same as withare the most common examples of instructional directives holding all medical care. A cancer patient can still receive in which the patient’s preferences are specified, but there antibiotics, nutrition and hydration, medication, radiation are also other types such as no transfusion or no cardiopultherapy, and pain management (palliative or comfort care). monary resuscitation (CPR) directives. The proxy direcAnother approach can provide instructions in the event of tive, generally a durable power of attorney for health a specific circumstance or diagnosis (such as a prolonged care, allows the patient to designate a surrogate decision maker of the patient’s choosing. This surrogate makes health care decisions for the patient in the case of incapacity. Choosing a Surrogate Decision Maker It should be noted that advance directives Picking a proxy decision maker can be a difficult task. Generally, experts are applicable only in situations in which parecommend that the proxy has the following qualities: tients are unable to participate in their health care decision making. The assessment of ca• shares the patient’s values and beliefs about end-of-life care and death pacity for decision making is sometimes dif• is a person with whom the patient can comfortably talk about difficult ficult and may involve a psychiatric evaluaissues tion and even a legal determination. If a • is a responsible, calm, mature person patient is competent and communicative, • is willing to assume this responsibility however, the advance directive will not • ideally is a person who lives close or is able to travel to the patient’s apply. location A health care proxy or surrogate is a per• is not the patient’s health care provider (for legal reasons) son appointed to make a patient’s medical • is chosen separate from considerations of who will handle the patient’s financial issues decisions if and when the patient is unable to do so. The durable power of attorney for • is the person, whether relative or friend, that the patient trusts the most to make medical decisions health care is the legal document that names the health care proxy. It should be signed, 25
Aflatoxins state of unconsciousness, trauma, or a diagnosis of dementia). Some living wills state that patients do not want lifeprolonging treatments if their condition necessitates constant care and supervision. Alternatively, others can state that patients wish their lives to be prolonged as long as possible. Advance directives can be revised or revoked as long as the patient remains competent to participate in medical decisions. Decisions by competent patients always supersede written directives. If there is disagreement among family members about the interpretation or authority of a patient’s advance directive, the medical team or a medical ethicist should meet with the family, clarify, and attempt to resolve the issue. Limitations: Living wills cannot possibly be made allencompassing because of the great variability in end-oflife care. Pain alleviation or management is among the most controversial end-of-life issues. Laws regulating drug addiction are inconsistent among the states, and the role of lethal drugs in the management of end-of-life pain and discomfort is being debated in Congress. Cancer patients making or considering writing advance directives are encouraged to communicate their preferences with their medical providers and surrogate decision makers. Most states ensure that patients remain in charge of their medical care until at least two physicians declare them to be incapacitated. Health care providers may refuse to honor the patient’s stated wishes or decisions because of personal standards or institutional policies. If either is the case, it is up to the individual health care provider to inform the surrogate immediately and transfer the patient to another provider. Marcia J. Weiss, J.D. u
For Further Information King, Nancy. Making Sense of Advance Directives. Dordrecht, Netherlands: Kluwer, 1991. Mappes, Thomas A., and David De Grazia. Biomedical Ethics. 6th ed. New York: McGraw-Hill, 2006. Sass, Hans-Martin, Robert M. Veatch, and Ribito Kimura, eds. Advance Directives and Surrogate Decision Making in Health Care: United States, Germany, and Japan. Baltimore: Johns Hopkins University Press, 1998. Ulrich, Lawrence P. The Patient Self-Determination Act: Meeting the Challenges in Patient Care. Washington, D.C.: Georgetown University Press, 1999. Weir, Robert F. Abating Treatment with Critically Ill Patients: Ethical and Legal Limits to the Medical Prolongation of Life. New York: Oxford University Press, 1989. 26
Salem Health: Cancer u
Other Resources
American Cancer Society Advance Directives http://www.cancer.org/docroot/MIT/mit_3_1_1.asp National Cancer Institute End-of-Life Decisions http://www.cancer.gov/cancertopics/pdq/ supportivecare/transitionalcare/HealthProfessional/ page9 See also Cardiopulmonary resuscitation (CPR); Do-notresuscitate (DNR) order; End-of-life care; Living will; Long-distance caregiving; Transitional care.
u Aflatoxins Category: Carcinogens and suspected carcinogens RoC status: Known human carcinogen since 1980 Also known as: Aflatoxin B1, aflatoxin B2, aflatoxin G1, aflatoxin G2, aflatoxin M1 Related cancers: Liver cancer, primary liver cell cancer, hepatocellular carcinoma, lung cancer Definition: Aflatoxins are naturally occurring toxic metabolites produced by certain fungi that grow on some agricultural products. At least thirteen different aflatoxins are produced in nature, with the four major aflatoxins called aflatoxin B1, B2, G1, and G2. Aflatoxin B1 is typically the most predominant as well as the most toxic. Aflatoxin M1 is found primarily in milk. Exposure routes: Ingestion and inhalation Where found: Numerous agricultural commodities, including corn and other grains, peanuts, tree nuts, and cottonseed meal. Milk, eggs, and meat products can be contaminated if animals consume aflatoxin-contaminated feed. At risk: Those living in countries where agricultural products that readily support the growth of aflatoxin-producing fungi are a dietary staple. Farmers and other agricultural workers are at risk for occupational exposure through inhalation of dust generated during handling of contaminated crops and feeds. Etiology and symptoms of associated cancers: Aflatoxin-producing fungi can grow on a wide range of agricultural products. Corn and groundnuts are major sources of human exposure because of greater susceptibility to contamination and widespread consumption. Worldwide,
Salem Health: Cancer
Aflatoxins
These peanuts are contaminated with aflatoxins. (AP/Wide World Photos)
corn is probably of greatest concern because it is grown in climates that readily support the growth of fungi and is a dietary staple in many countries. Aflatoxin-producing fungi often grow on crops in the field before harvest, particularly if the crops have experienced drought stress. After harvest, contamination can occur during storage. The growth of aflatoxin-producing fungi and subsequent production of aflatoxins are influenced by weather conditions such as temperature and humidity. As a result, aflatoxin contamination varies with geographic location, agricultural and agronomic practices, and the susceptibility of crops to fungal growth. Exposure to aflatoxins occurs primarily by consuming contaminated food. Aflatoxin consumption is commonplace in developing countries where food supplies are limited and regulations of aflatoxin levels are not enforced or nonexistent. In developed countries, food supplies are generally more abundant and diverse, and aflatoxin levels are monitored to limit toxin ingestion. Although the sale of heavily contaminated food supplies is not permitted in
developed countries, chronic exposure to low levels of aflatoxins may still be a concern. The most common aflatoxin-producing fungi are Aspergillus flavus and Aspergillus parasiticus. Although many aflatoxins are produced by these fungi, aflatoxin B1 is the most prevalent and the most toxic. Aflatoxin B1 is also the most potent naturally occurring carcinogen. Aflatoxins are both toxic and carcinogenic, with exposure to high levels resulting in toxic effects referred to as aflatoxicosis and chronic exposure to low levels potentially resulting in cancer. Susceptibility to aflatoxin-related diseases is influenced by many factors, including age, exposure level, duration of exposure, health, nutritional status, and exposure to other agents, such as the hepatitis B virus (HBV). The liver is the primary target organ of aflatoxin exposure, although other organs can also be affected. Metabolic activation by liver enzymes is required for the carcinogenic effects of aflatoxin B1. In the liver, aflatoxin B1 is metabolized to a highly reactive form that readily binds deoxyribonucleic acid (DNA) and proteins and can lead to 27
African Americans and cancer liver damage and subsequent formation of tumors in the liver. Exposure to aflatoxins in the diet has been shown to be one of the major etiological factors in the development of primary hepatocellular carcinoma in some countries, such as China and many African countries. Concurrent infection with HBV and exposure to aflatoxins results in significantly greater liver damage than either infection or exposure alone, a synergy that is likely produced because HBV interferes with the liver’s ability to detoxify aflatoxins. Although aflatoxin is most well known as an agent that promotes liver cancer, inhalation of contaminated grain dust has been associated with an increased incidence of lung cancer. Liver cancer is not associated with any symptoms in the early stages. As the cancer progresses, symptoms may include pain in the upper abdomen on the right side, which may also extend to the back and shoulder. Other symptoms include a swollen or bloated abdomen, weight loss, loss of appetite, feeling of fullness, weakness, fatigue, nausea and vomiting, yellowish skin and eyes, dark urine, and fever. History: Aflatoxins have been recognized as a significant contaminant since the 1960’s, when more than 100,000 young turkeys on poultry farms in England died from what was termed turkey X disease. The mortalities were traced to consumption of mold-contaminated peanut meal. In 1961 the toxin-producing fungus, A. flavus, was identified and the toxin given the name aflatoxin. The International Agency for Research on Cancer (IARC) first recognized aflatoxins as carcinogenic in 1976. In 1987 naturally occurring mixtures of aflatoxins and AFB1 were classified as Group I carcinogens. Aflatoxins are considered unavoidable contaminants of food and feed, even when good manufacturing practices have been followed. Although absolute safety can never be achieved, many countries have attempted to limit exposure to aflatoxins by imposing regulatory limits on commodities intended for consumption. The Food and Drug Administration has established specific guidelines that regulate this toxin to very low concentrations in human food and animal feed. Catherine J. Walsh, Ph.D. u
For Further Information Bennet, J. W., and M. Klich. “Mycotoxins.” Clinical Microbiology Reviews 16, no. 3 (2003): 497-516. Eaton, D. L., and J. D. Groopman. The Toxicology of Aflatoxins. New York: Academic Press, 1994. Goldblatt, L., ed. Aflatoxin: Scientific Background, Control, and Implications. New York: Academic Press, 1969. 28
Salem Health: Cancer U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Eleventh Report on Carcinogens. Research Triangle Park, N.C.: Author, 2005. u
Other Resources
Centers for Disease Control and Prevention http://www.cdc.gov National Cancer Institute http://www.cancer.gov National Toxicology Program http://ntp.niehs.nih.gov U.S. Food and Drug Administration Center for Food Safety and Nutrition http://www.cfsan.fda.gov See also Free radicals; Hepatomegaly; Infectious cancers; Liver cancers; Risks for cancer.
u African Americans and cancer Category: Social and personal issues Definition: Cancer is the second leading cause of death among African Americans. African Americans experience higher cancer rates than any other racial or ethnic group in the United States, as well as higher mortality rates from those cancers. Description of the population: The U.S. government identifies as African Americans “individuals whose origins are from any of the black racial groups of Africa,” including people who self-report their ethnicity as “Black, African American, or Negro” or who describe themselves as African American, Afro-American, Angolan, Negro, West Indian, Afro-Caribbean, Nigerian, Haitian, Gullah, Creole, West African, Afro-Latin, Afro-Brazilian, Congolese, Americo-Liberian, Bantu, Guinean, Moor, Pygmy, or Liberian. According to the Census Bureau, African Americans represented more than 13 percent of the U.S. population as of 2006. Incidence, death, and survival statistics: The average U.S. life expectancy was 49.2 years in the nineteenth century. The National Vital Statistics Reports (vol. 47, no. 28) note that African American life expectancy is 70.2 years, as opposed to 76.5 years for the U.S. population overall. African American men have a life expectancy of only 66.1 years; for all U.S. men it is 73.6 years. These statistics are
Salem Health: Cancer reflected in the cancer morbidity rates for African Americans: In 2003, for example, cancer was the second leading cause of death of African Americans (topped only by heart disease). The death rate outstripped that of whites, with 234.5 African Americans (versus 188.3 whites) dying of cancer per every 100,000 in the U.S. population. Overall, African Americans have higher cancer rates than any other racial or ethnic group in the United States, and their death rates from those cancers are also higher. The five-year survival rate among African Americans for all cancers improved from 27 percent in 1960-1963 to 57 percent in 1996-2002. Nevertheless, at more than 63 percent, whites were still more likely to survive five years after diagnosis. African American men are more likely to succumb to cancer than are white men, although this disparity, after peaking in the early 1990’s, has begun to decline. Death rates for African American women are closer to those for white women—although still higher. The fact that African Americans are more likely to be diagnosed with cancer later in the disease process and have less access to high-quality care in part explains their increased likelihood of death. The American Cancer Society reported that between 2000 and 2003, the cancers afflicting African American men most often were, from highest to lowest incidence, prostate cancer, lung and bronchial cancers, colorectal cancer, kidney and renal pelvic cancers, urinary bladder cancer, oral cavity and pharyngeal cancers, stomach cancer, non-Hodgkin lymphoma, pancreatic cancer, myeloma, leukemia, liver and intrahepatic bile duct cancers, laryngeal cancer, esophageal cancer, brain and other nervous system cancers, small intestinal cancer, soft-tissue (including heart) cancers, Hodgkin disease, Kaposi sarcoma, thyroid cancer, testicular cancer, melanoma of the skin, and mesothelioma. For all these cancers combined, African American men were afflicted, on average, 1.2 times more often than white men, with particularly noticeable disparities in Kaposi sarcoma, myeloma, and small intestinal cancers. For the same period, cancers afflicting African American women were, from highest to lowest incidence, breast cancer, colorectal cancer, lung and bronchial cancers, uterine corpus cancer, pancreatic cancer, non-Hodgkin lymphoma, uterine-cervical cancer, ovary, kidney and renal pelvic cancers, stomach cancer, myeloma, leukemia, urinary bladder cancer, thyroid cancer, oral cavity and pharyngeal cancers, brain and other nervous system cancers, liver and intrahepatic bile duct cancers, esophageal cancer, soft-tissue (including heart) cancers, small intestinal cancer, Hodgkin disease, laryngeal cancer, and melanoma of the skin. The overall incidence for African Amer-
African Americans and cancer
Five-Year Relative Survival Rates for Selected Cancers for African Americans and Whites in the United States, 1996-2002 Survival Rates (%) Cancer Type Prostate Female breast Bladder Uterus Cervix Colon and rectum Non-Hodgkin lymphoma Leukemia Mouth Lungs and bronchi Esophagus
African American
White
98 77 64 60 63 55 54 40 40 12 11
100 90 82 85 73 65 64 49 61 15 16
Source: Data from National Cancer Institute, Surveillance Epidemiology and End Results, Cancer Stat Fact Sheets, 2008 Note: Based on cancer patients diagnosed between 1996 and 2002 and followed through 2003
ican women was, on average, slightly less than for white women, although the incidence of myeloma, stomach cancer, and small intestinal cancer among African American women was more than twice that among white women— balanced by lower incidence rates for other cancers, including breast and uterine corpus. For 1996-2002 (in descending order), survival rates among African Americans as a whole were best for prostate, female breast, urinary bladder, uterine corpus, uterine cervical, colorectal, non-Hodgkin lymphoma, leukemia, oral cavity, lung and bronchial, and esophageal cancers. For these same cancers combined, white survival rates exceeded those of African Americans by an average of 11.45 percent (ranging from 2 to 25 percent). The greatest disparities in survival rates could be seen in uterine corpus and oral cavity cancers: Whites outlived blacks by 25 percent and 21 percent, respectively. For 2007, the cancers projected to be diagnosed most often in African American men were prostate (37 percent), lung (15 percent), and colorectal (12 percent) cancers. African American women were expected to be diagnosed most often with breast (27 percent), lung (13 percent), and colorectal (12 percent) cancers. Risk statistics: The major risk factors for cancer in all populations are socioeconomic status, tobacco use, and 29
African Americans and cancer being overweight or obese. African Americans are disproportionately poor: In 2004, more than 29 percent of African Americans fell below the poverty line, as opposed to 13 percent of whites. Because one-fifth of African Americans are uninsured, access to care, particularly preventive and screening care, is limited relative to the rest of the population. Limited detection, in turn, leads to later diagnoses and thus cancers that are more difficult to treat and to survive. Tobacco use—the biggest risk factor for the deadliest cancer, lung cancer—accounts for about 30 percent of cancer deaths overall. Among African Americans, lung cancer death rates are higher than those of whites, even though most African Americans begin smoking at a later age and smoke fewer cigarettes per day. The amount of each cigarette smoked, the type of cigarettes commonly smoked (mentholated, with higher concentrations of carbon monoxide), and the condition of the individuals who smoke (nutritional status and genetic differences) are predicted to account for the higher death rates. Overweight and obesity, which constitute a growing pandemic in American society generally, are defined as a body mass index (BMI) greater than 25 (overweight) or greater than 30 (obese). After tobacco use, obesity is the second leading cause of preventable deaths in the United States. According to the 2003 National Health and Nutrition Examination Survey, nearly 33 percent of U.S. adults were obese, and as early as 2002, overweight individuals formed 65 percent of the U.S. population. Among African Americans, 76 percent were either overweight or obese as of the year 2004. Obesity is positively correlated with certain cancers, particularly breast, endometrial, and colon cancers. Perspective and prospects: From the early 1970’s to 1992, rates of both incidence of and deaths from cancer increased among African Americans. After 1992, both death and incidence rates for all cancers among both sexes of African Americans, fortunately, declined. Five-year survival rates also improved, from only 27 percent in the early 1960’s to 57 percent by 2002. Nevertheless, to bring about parity with the rest of the population, some key factors must be addressed: The current health care system must educate, train, and prepare a health care workforce that is intimately aware of African American health issues and must be sensitive to perceptions, concerns, and fears that may exist in the African American population. A concerted effort must also be made to educate African Americans regarding the role they play in improving their own health. They must understand the importance of health care screenings, weight re30
Salem Health: Cancer duction and management, exercise, and regular physical examinations. Beyond prevention, however, African Americans continue to need better access to the health care system, improved medical insurance, more routine screenings, earlier detection, and better treatments upon diagnosis. With better access, informed African Americans can become empowered to take control of their health by seizing every opportunity to improve it. Christina J. Moose, M.A. u
For Further Information American Cancer Society. Cancer Facts and Figures for African Americans. Atlanta: Author, 2007. Bailey, Eric J. Medical Anthropology and African American Health. Westport, Conn.: Bergin & Garvey, 2000. Byrd, W. Michael, and Linda A. Clayton. A Medical History of African Americans and the Problem of Race, Beginnings to 1900. Foreword by Robert J. Blendon. New York: Routledge, 2000-2002. Collins, Catherine Fisher. African American Women’s Health and Social Issues. Foreword by Vivian W. Pinn. Westport, Conn.: Praeger, 2006. Rawls, George, Frank P. Lloyd, Jr., and Herbert Stern. Managing Cancer: The African American’s Guide to Prevention, Diagnosis, and Treatment. Roscoe, Ill.: Hilton, 2001. Reed, James, Neil Shulman, and Charlene Shucker. The Black Man’s Guide to Good Health: Essential Advice for the Special Concerns of African-American Men. New York: Berkley, 1994. Williams, Christopher Kwesi O., Olufunmilayo I. Olopade, and Carla I. Falkson, eds. Breast Cancer in Women of African Descent. London: Springer, 2006. u
Other Resources
African American Health Network http://www.aahn.com MedlinePlus African-American Health http://www.nlm.nih.gov/medlineplus/ africanamericanhealth.html National Cancer Institute Center to Reduce Cancer Health Disparities http://crchd.cancer.gov/index.html NetWellness African American Health Center http://www.netwellness.org/healthtopics/aahealth
Salem Health: Cancer
Africans and cancer
See also Africans and cancer; Asian Americans and cancer; Epidemiology of cancer; Ethnicity and cancer; Geography and cancer; Latinos/Hispanics and cancer; Polyps; Sézary syndrome; Smoking cessation; Statistics of cancer; Stomach cancers; Survival rates; Testicular cancer.
million people. In contrast, the average radiation machine in Europe serves a population of only about 250,000 people. Additionally, only fifteen countries in Africa have any radiation machines at all. The United Nations estimates that only about 20 percent of Africa’s population has any kind of radiation therapy available to them, and in many cases, available can mean hundreds of miles away.
u Africans and cancer
Problems of prevention and treatment: Africa faces many significant challenges to the successful prevention, early diagnosis, and treatment of cancer. Prevention of cancer requires education of the population about what types of things may increase the risks of developing cancer, and what things and lifestyle choices are believed to reduce the risk of cancer. Smoking and use of tobacco products in any form have been linked to cancer for many years. However, public education about the perils of smoking can be difficult, time-consuming, and expensive. Most African governments are already highly burdened, and there are rarely any budget dollars left to go to public education about something as intangible as smoking or tobacco use and its correlation with an increased risk for cancer. Another barrier to prevention in Africa is that what is considered a healthy lifestyle for cancer prevention is not accessible to many Africans. Most African countries have a per capita national income that labels them as low- or very low-income countries. Fresh, clean water and many different fruits, vegetables, whole grains, and lean proteins, all considered part of a healthy lifestyle in the United States and other developed countries, are not reasonably accessible to many people living in Africa. The opportunity for early diagnosis is severely lacking in most areas of Africa. Diagnosing cancer when it is in its earliest stages leads to the most positive prognosis. Many cancers that are treatable if found early are almost never treatable when diagnosed in a very late stage. Preventive health care is not readily accessible in most parts of Africa, and many people seek medical attention only when there is an obvious problem. Unfortunately, because many cancers produce severe symptoms only when in the later stages, this means that most cancers diagnosed in Africa are diagnosed at a stage too late to be treated successfully. This problem is caused by many interacting factors, including many people living too far from health care to reasonably get preventive screenings, lack of education about the benefits of early detection, and lack of medical professionals and facilities to do the screenings. The cost of preventive medicine and screenings is also often a barrier to early diagnosis. Even when an early diagnosis is made, there are many
Category: Social and personal issues Definition: According to the World Health Organization, cancer is the leading cause of death worldwide, and more than 70 percent of those deaths occur in countries that are considered low or middle income. Cancer is one of the top health problems in Africa, where access to quality health care is often barred by distance, availability, and income. Statistics: There are many barriers to good statistical analysis of cancer trends in Africa. There are no governmental agencies charged with the collection and monitoring of cancer statistics and trends as there are in the United States. In addition, many Africans live in remote areas and do not necessarily seek treatment in hospitals or clinics, so data about cancer incidence and mortality are difficult to collect and assess accurately. However, the World Health Organization (WHO) did compile statistics about cancer incidence and mortality in Africa as a whole in 2002. In that year, about 582,000 people (283,000 men and 299,000 women) living in sub-Saharan Africa developed cancer. Also in 2002, 412,100 in the same area died due to cancer. The most common forms of cancer in Africa among women were breast cancer, cervical cancer, and Kaposi sarcoma (a form of cancer common in individuals with acquired immunodeficiency syndrome, or AIDS). In men the most common cancers were Kaposi sarcoma, prostate cancer, and liver cancer. Lung cancer and stomach cancer were also very common and were especially likely to result in death. It is estimated that in 2020 804,000 people living in sub-Saharan Africa will develop cancer, and that 624,000 will die of it that year. There are many barriers to the successful treatment of cancer in Africa. In August, 2007, the World Health Organization estimated that 80 to 90 percent of the cancer cases that are encountered by doctors and hospital personnel in Africa are diagnosed when the cancer has developed and spread too far to be successfully treated. Additional difficulties occur because of significant lack of resources. According to the United Nations, Ethiopia did not receive a radiation therapy machine until 1997, and many years later it still had only one machine to serve a population of 65
31
Afterloading radiation therapy barriers to effective cancer care in Africa. There is a significant lack of the resources and equipment necessary for the treatment of cancer. Treating cancer is a process that requires many experts and technologically advanced equipment and drugs. Unfortunately, much of the necessary equipment is prohibitively expensive for most hospitals and clinics in Africa. Additionally, there is a lack of training programs and trained health professionals to run the equipment, administer medication, and oversee treatment. The dispersed nature of the population over most of Africa is also a barrier to effective care. Even if a country does have a few hospitals or centers with the staff and equipment necessary for cancer treatment, many millions of individuals may live too far from the center to be able to make effective use of what it offers. Another problem facing the African health care community in its attempts to successfully treat cancer is the AIDS epidemic. Millions of Africans are infected with the human immunodeficiency virus (HIV) or have AIDS, and it contributes to problems for cancer treatment in a number of ways. The AIDS epidemic is stretching the resources of the health care systems in most African countries very thin. Because AIDS impairs the immune system’s ability to function properly and ward off disease, individuals with AIDS need significant medical treatment for the many complications that occur. Individuals with AIDS are also more likely to develop cancer, especially Kaposi sarcoma, one of the most common cancers in Africa. This stretches the cancer resources that do exist even more thinly.
Salem Health: Cancer too bright, even small improvements in resources and education can make a huge difference in the number of Africans affected by cancer. Cancers that are usually detected early and cured in the United States and Europe could also be cured in Africa if they were detected early enough and the right treatment options were available. Progress made in improving the AIDS epidemic may also have beneficial effects on the rates of cancer incidence and mortality in Africa. As Kaposi sarcoma, a cancer common among those with AIDS, is one of the leading cancers in Africa, reducing the number of individuals infected with HIV should cause a reduction in the number of individuals with AIDS-related cancers. Helen Davidson, B.A. u
For Further Information O’Keefe, Stephen J. D., et al. “Why Do African Americans Get More Colon Cancer than Native Africans?” Journal of Nutrition 137, no. 1 (January, 2003): 175183. Sloan, Frank A., and Hellen Gelband, eds. Cancer Control Opportunities in Low- and Middle-Income Countries. Washington, D.C.: National Academies Press, 2007. U.S. Department of Health and Human Services, National Institutes of Health, and the National Cancer Institute. NCI International Portfolio: Addressing the Global Challenge of Cancer. Bethesda, Md.: National Cancer Institute, 2006.
u
Outlook for the future: The outlook for the future of cancer in Africa is not excellent, but it is improving. Although estimates suggest that there will be increasing numbers of cancer cases in Africa over the next decades, some organizations and groups are making strong efforts to stop the problem. Many of these efforts focus on increased access to prevention, early diagnosis, and access to treatment. In May, 2005, the World Health Organization adopted a resolution on cancer prevention and control. The resolution called on member states of the organization to take steps to reduce cancer incidence and mortality by creating and putting into action programs of cancer control. The WHO breaks down the areas of concern for countries that are working to stop cancer into four broad categories: prevention, early detection, diagnosis and treatment, and palliative care. Some private and corporate organizations are also working to help prevent and treat cancer in Africa. Various programs work to raise awareness of the problem of cancer in Africa and to raise money for desperately needed equipment, training, and education. Although the outlook is not 32
Other Resources
Cancer-Africa http://www.ialphan.com/cancerafrica/ World Health Organization http://www.who.int See also African Americans and cancer; HIV/AIDS-related cancers; Kaposi sarcoma; Rectal cancer.
u Afterloading radiation
therapy Category: Procedures Also known as: High dose rate remote afterloading (HDR) Definition: Afterloading radiation therapy is a form of high dose rate brachytherapy that uses a computer-controlled machine called an afterloader to deliver radiation from iridium 192 directly to a tumor. Iridium 192 is a radioac-
Salem Health: Cancer tive source that emits high-energy gamma rays, a type of radiation that is used to kill cancer cells. The radioactive source is contained in the lead-shielded machine and welded to a stainless steel cable that is inserted into the tumor through catheters, needles, or balloons placed in the tumor or tumor bed. Afterloading radiation therapy is considered a temporary implant because the radioactive source does not remain in the patient, and the patient is not radioactive. Cancers treated: Lung cancer, breast cancer, prostate cancer, head and neck cancers, uterine cancer, cervical cancer, esophageal and bile duct cancers, soft-tissue sarcoma, rectal cancer, others under study Why performed: The use of a high-dose remote afterloader provides more targeted therapy to the tumor, or to the tumor bed after the bulk of the tumor is removed in surgery. The afterloader provides more accurate dose delivery to the target site while better protecting normal tissue. Its use also provides a shorter course of therapy of approximately one week, as compared to external beam radiation therapy, which takes place over four to six weeks. The dose distribution is more even, and there are fewer hot (overdose) spots or cold (underdose) spots. Side effects occur less often with HDR therapy. Patient preparation: Planning for the use of afterloading radiation therapy often begins before an initial surgery, depending on the type of cancer and its site. The surgeon and the radiation oncologist will confer, as the catheters used in administering the radiation may be placed at the time of the initial surgery for the cancer. Catheters or needles may also be placed in an outpatient setting under local anesthesia or other sedation. Imaging or radiology studies may be used to assist in treatment planning for the optimal radiation dose delivery to the tumor site and to verify the location of the catheters, especially if it has been a few weeks since their placement. A simulation is done to visualize the tumor or tumor site in comparison to adjacent organs and tissues using a computed tomography (CT) scan or X ray. This procedure assists the radiation oncologist in planning the amount of dose that the afterloader will deliver. The simulation data are then loaded into a treatment-planning computer, which calculates the dose needed. Steps of the procedure: The patient arrives in the radiation oncology center and may change into a gown prior to receiving treatment. For some prostate treatments, needles may be placed prior to the treatment under local anesthesia. Upon entering the treatment room, the patient is assisted to a comfortable position that also allows access to
Afterloading radiation therapy the ends of the catheters or needles. The treatment catheters or needles from the patient are attached to the transfer tubes from the afterloader. The treatment personnel leave the room but can observe the patient using closed-circuit television and an intercom for communication. The treatment data loaded into the HDR unit control the movement of the source into the patient and the time that the source remains at various stops along the catheters or needles in order to achieve the distribution of dose planned. The source is placed in the patient for approximately ten to fifteen minutes, but a single treatment may take up to one hour or more. The complexity of the treatment, the site being treated, and the strength of the radioactive source will dictate the time involved. The radiation oncologist will discuss the number of treatments needed based on the disease, but treatment times vary from a few days to slightly more than a week. After the procedure: Depending on the site being treated, the patient may need to stay in the hospital or may be allowed to go home between treatments. A bandage may be placed over the catheters. After all treatments are complete, the catheters are removed by clipping the sutures holding the catheters, and they are withdrawn. A small amount of bleeding may occur, but it is quickly controlled with direct pressure, and a bandage is applied over the site. Risks: Risks are related to catheter movement out of the site being treated. It is important for patients to tell the radiation staff if a catheter seems to have moved, or if it gets snagged on clothing or the bandage at any time. A misplaced catheter or needle may deliver radiation to normal tissues or organs, causing radiation burns. There is a risk that cancer cells may be missed by the radiation. Results: Outcomes vary by the disease being treated, but success rates for HDR treatments are comparable to other forms of treatment in most instances. Patricia Stanfill Edens, R.N., Ph.D., FACHE u
For Further Information Hoskin, P. J., and P. Bownes. “Innovative Technologies in Radiation Therapy: Brachytherapy.” Seminars in Radiation Oncology 16, no. 4 (October, 2006): 209-217. Hoskin, P. J., K. Motohashi, P. Bownes, L. Bryant, and P. Ostler. “High Dose Rate Brachytherapy in Combination with External Beam Radiotherapy in the Radical Treatment of Prostate Cancer: Initial Results of a Randomized Phase Three Trial.” Radiotherapy & Oncology 84, no. 2 (August, 2007): 114-120. 33
Agent Orange National Cancer Institute. Radiotherapy and You: Support for People with Cancer. Available online at http://www .cancer.gov/cancertopics/radiation-therapy-and-you. u
Other Resources
American Cancer Society http://www.cancer.org American Society for Therapeutic Radiology and Oncology Patient Web Site http://www.rtanswers.org See also Brachytherapy; Cobalt 60 radiation; External beam radiation therapy (EBRT); Intensity-modulated radiation therapy (IMRT); Iridium seeds; Proton beam therapy; Radiation therapies; Radiofrequency ablation; Stereotactic radiosurgery (SRS).
u Agent Orange Category: Carcinogens and suspected carcinogens Also known as: Super Orange Related cancers: Soft-tissue sarcoma, non-Hodgkin lymphoma, Hodgkin disease, chronic lymphocytic leukemia (CLL), acute myelogenous leukemia (AML) Definition: Agent Orange was a chemical mixture used in the United States to control weeds and in Vietnam during the Vietnam War to remove forest cover. So named because of the orange stripes painted on its storage drums, Agent Orange is a blend of two herbicides: 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T). Although 2,4,5-T is not highly poisonous, the manufacturing process generates a toxic by-product called TCDD, or 2,3,7,8-tetrachlorodibenzop-dioxin. This dioxin, classified as a human carcinogen, tainted Agent Orange formulations. Exposure routes: Inhalation, ingestion, skin contact, ocular absorption Where found: Herbicide mixtures formerly used for agricultural, forestry, and military purposes At risk: Combatants and civilians exposed to Agent Orange during the Vietnam War and their children, workers occupationally exposed to the chemical, and populations exposed through domestic herbicide spraying Etiology and symptoms of associated cancers: Because epidemiologic data on Vietnam veterans is limited, the 34
Salem Health: Cancer health effects of Agent Orange have been studied indirectly in certain populations highly exposed to dioxin or dioxin-tainted herbicides. These studies provide sufficient evidence linking Agent Orange to chloracne, an acnelike skin disorder, and to certain cancers, induced when TCDD activates a protein receptor in target cells. The soft-tissue sarcomas develop from fat, muscle, or deep body tissues and usually appear as a lump. Hodgkin disease (highly curable) and non-Hodgkin lymphoma originate in lymphatic tissue and result in painless swelling of lymph nodes under the skin. Chronic lymphocytic leukemia, which develops from white blood cells, is often asymptomatic, but later is marked by enlarged lymph nodes. Paternal exposure to Agent Orange has been associated with acute myelogenous leukemia in children. This fastgrowing cancer of the bone marrow produces abnormal white blood cells and results in fatigue, shortness of breath, and increased susceptibility to infection. Only limited evidence links Agent Orange to respiratory cancer, prostate cancer, and multiple myeloma. History: Phenoxy herbicides, including the 2,4,5-T component of Agent Orange, were developed in the 1940’s and widely used in agriculture and forestry. Starting in 1960 during the Vietnam War, the United States military sprayed Agent Orange onto lands in Vietnam and Laos. It suspended this activity in 1970, after a study in laboratory animals linked 2,4,5-T to birth defects. Since the 1980’s, various groups of Vietnam veterans have filed lawsuits against the makers of Agent Orange. The United States has permanently banned all uses of 2,4,5-T and, consequently, Agent Orange. Anna Binda, Ph.D. See also Dioxins; Multiple myeloma; Mycosis fungoides; Organochlorines (OCs); Pesticides and the food chain.
u Aging and cancer Category: Social and personal issues Definition: The most significant risk factor associated with developing cancer is age, with 60 percent of all cancers occurring in people who are sixty-five and over. Mortality rates are also highest in this age group; older individuals typically have additional chronic medical conditions that enhance the risk for simultaneously occurring psychiatric morbidity. These complex and potentiating trends are creating new clinical challenges that threaten to overwhelm the current health care system. Based on projections that 1 in 5 Americans will be over the age of
Salem Health: Cancer
Aging and cancer
Cancer is more common and deadlier in the elderly. (Digital Stock)
sixty-five by 2030, there is an immediate need to better understand the influence of age on cancer detection, diagnosis, and treatment, with the goal of modifying infrastructure, practices, and the educational preparation of future health care providers. Biology of aging and cancer: Based on the population trends, research aimed at illuminating the biology of aging and mechanisms that enhance cancer susceptibility are increasing. A clearer understanding of the well-documented age-related increase in cancer incidence is needed to develop well-conceived primary cancer prevention strategies. This line of research has been designated as a priority by the National Cancer Institute. At present, there are three major hypotheses that explain the association between cancer and age: Hypothesis 1 holds that the link between aging and cancer is simply related to duration of carcinogenesis. In other words, the high prevalence of cancer in older individuals simply reflects more prolonged exposure to carcinogens. Hypothesis 2 proposes that age-related, progressive changes within the human organism may provide an in-
creasingly favorable environment for the induction of new cancers and the growth of preexisting but latent malignant cells. These mechanisms may be related to proliferative senescence, whereby aging cells lose their ability to undergo apoptosis (a form of cell death that leads to the sequential elimination of cells without releasing harmful substances into the body). When apoptosis does not work right, cells that should be eliminated become immortal, stimulating cancer-related mutations at the cellular level. Hypothesis 3 combines aspects of the first two hypotheses and proposes that the aging, cancer-prone human phenotype is characterized by an accumulation of dysfunctional senescent cells. These cells proliferate via synergistic, simultaneous physiologic processes that foster progressive accumulation of cancer-prone mutations; silencing of genes that previously functioned to prevent cancerpredisposing mutations from developing in response to carcinogens (failure of epigenetic gene silencing); and telomere dysfunction (telomeres are specialized structures at chromosome ends that regulate their replication and stability). These changes are particularly relevant to the production of malignancies because they occur within the 35
Aging and cancer context of an aging microenvironment of surrounding tissues. Cancer, aging, and psychiatric comorbidity: As increased longevity contributes to rising cancer incidence, those diagnosed often have one or more additional chronic medical conditions. Paradoxically, new treatment discoveries have extended survival for multiple medical illnesses but often within the context of troubling side effects and consequences that in turn have led to documented increases in the incidence of psychiatric morbidity. The incidence of psychiatric morbidity is further enhanced as the burden of cancer care progressively shifts from the health care system to family caregivers. Family caregivers are usually aging spouses with medical problems of their own or adult children, with their own families, jobs, responsibilities, and problems. When the role of providing complex cancer care for a loved one is added to their already stressful lives, risk for psychiatric morbidity is significantly enhanced. Although the preceding issues have been largely ignored, they continue to strain the U.S. health care system to its limit. The preceding trends are occurring within a system in which mental health services are a low priority. Stigma, limited knowledge regarding the nature and intensity of psychiatric symptoms associated with clinical need, and inconsistent, generally inadequate reimbursement mechanisms are a sampling of the multiple issues contributing to
Problems to Consider in Treating Pain in Older Cancer Patients Other chronic illnesses: Patients taking multiple medications may be at risk for drug interactions. Impairments in hearing, vision, and mental function: Patients may need to be monitored more frequently and tests may need to be simplified. Patient-controlled analgesia: Patients are more sensitive to the side effects of these drugs, which remain in their bodies longer. Opioids: Patients may be more sensitive to the effects of these drugs and experience longer periods of pain relief. Side effects from nonsteroidal anti-inflammatory drugs (NSAIDs): Stomach and kidney toxicity, constipation, headaches, and difficulties with the ability to think may arise. Administration of medicine: Some older patients may not be able to administer some drugs as directed (for example, inserting a drug into the rectum). Source: National Cancer Institute
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Salem Health: Cancer our dismal state of mental health services. Research, professional education, and clinical services are most deficient with regard to the psychiatric morbidity that occurs within the context of a chronic medical illness. Psychiatric symptoms are typically treated only when they emerge as disease states within an expensive, fragmented, specialtyoriented system. Reimbursement for psychiatric treatment is difficult to obtain, yet paying out of pocket is prohibitive and biases care toward the affluent. Limited solutions to these consequential problems potentiate untold human suffering, negative clinical outcomes, and high resource utilization that could be avoided if problems were dealt with before they got out of hand. Cancer screening in the elderly: Considerable uncertainty regarding the use of cancer screening procedures in the elderly is illustrated by the range of age cutoffs recommended by various guideline panels. To address inconsistencies, it has been suggested that a comprehensive framework rather than specific age parameters should inform individual screening decisions in older cancer patients. Screening decisions should encompass estimates of life expectancy, risk of cancer death, documented screening outcomes, and a risk-benefit screening ratio. For example, harm may result from screening practices that detect and treat cancers that never would have become clinically significant. Because many cancer screening decisions in older adults cannot be answered solely by quantitative estimates of benefits and harms, consideration of predicted outcomes within the context of an individual’s values and preferences is an important aspect of informed screening decisions. Statistics reveal considerable underutilization of cancer screening practices in the United States. Having health insurance, a regular doctor, and a point of usual care all are associated with higher cancer screening rates and better preventive health care overall. When these supports are absent, cancer screening rates drop considerably. The lack of preventive services reimbursed by Medicare, the limited number of elders with comprehensive, employerprovided health coverage, and growing numbers of elders who are homebound or lack a regular physician and point of care make elderly Americans especially prone to lacking supports that facilitate cancer screening practices. Age-related differences in cancer treatment: Cancer treatments may produce different therapeutic and adverse responses based on patient age. For example, chemotherapy resistance and toxicity have been shown to vary by age, being more common and severe in the elderly. Treatment toxicities may develop in old versus young recipients because of increased vulnerability of target organs and de-
Salem Health: Cancer layed renal excretion of treatment agents and metabolites. These problems should be managed with treatment modifications determined by kidney function and other relevant parameters of individual health status and treatment response. Aging cancer patients often do not receive adequate information to assist with or inform a definitive treatment plan. Understanding why these deficiencies exist is vital to reducing disparities in cancer mortality between young and old. Studies suggest that treatment uncertainty could be better addressed if elderly cancer patients were offered a choice from a group of definitive therapies. Treatment discussions should also address common concerns related to the costs and functional consequences of each treatment in relation to expected benefits. Current understanding of age-related differences in pharmacokinetics, drug interactions, adverse events, and treatment adherence is extremely limited. Palliative cancer care of the elderly: Despite ambitious research, treatment, and educational initiatives, the quality of palliative care provided to the elderly has historically been and remains poor. Research consistently demonstrates unnecessary suffering among elderly patients with advanced cancer. Their suffering is related to myriad issues, including uncontrolled physical symptoms, depression, and unaddressed existential concerns. Wide gaps in palliative care services targeted to elderly patients with cancer occur across a range of settings, including hospice, where the approach to palliative care has been largely insufficient. Some studies report lower levels of psychological distress in elderly versus young cancer patients, which has been erroneously interpreted to mean that elders are better equipped to manage existential concerns because they are at a stage in life when death is expected. However, data may more accurately reflect age-related differences in exposure to prevention, screening, and treatment practices; the resultant cancer course; and symptom profiles. Results therefore indicate the need for ongoing research and education targeted to unraveling complex relationships between aging and cancer. Knowledge development and dissemination must be met aggressively with clinical initiatives throughout the twenty-first century and beyond as population, demographic, and clinical trends continue to outpace the availability of resources for elderly individuals with cancer. Jeannie V. Pasacreta, Ph.D., A.P.R.N. u For Further Information Hassett, M. J., et al. “Frequency and Cost of Chemotherapy-Related Serious Adverse Effects in a Population
Aging and cancer Sample of Women with Breast Cancer.” Journal of the National Cancer Institute 98, no. 16 (2006): 11081117. Kumar, H., P. Soares, L. Balducci, and B. Djulbegovic. “Treatment Tolerance and Efficacy in Geriatric Oncology: A Systematic Review of Phase III Randomized Trials Conducted by Five National Cancer InstituteSponsored Cooperative Groups.” Journal of Clinical Oncology 25, no. 10 (2007): 1272-1276. Lichtman, S. M., et al. “International Society of Geriatric Oncology Chemotherapy Taskforce: Evaluation of Chemotherapy in Older Patients—An Analysis of the Medical Literature.” Journal of Clinical Oncology 25, no. 14 (2007): 1832-1843. Muss, H. B. “Older Age: Not a Barrier to Cancer Treatment.” New England Journal of Medicine 345 (2001): 28-29. Talarico, Lilia, Gang Chen, and Richard Pazdur. “Enrollment of Elderly Patients in Clinical Trials for Cancer Drug Registration: A Seven-Year Experience by the U.S. Food and Drug Administration.” Journal of Clinical Oncology 22, no. 22 (2004): 4626-4631. Trimble, E. L., and M. C. Christian. “Cancer Treatment and the Older Patient.” Clinical Cancer Research 12, no. 7 (2006): 1956-1957. Yancik, R., et al. “Perspectives on Comorbidity and Cancer in Older Patients: Approaches to Expand the Knowledge Base.” Journal of Clinical Oncology 19 (2006): 1147-1151. u
Other Resources
AARP Foundation http://www.aarp.org/foundation American Cancer Society http://www.cancer.org American Geriatrics Society/Foundation http://www.americangeriatrics.org Family Caregiver Alliance http://www.caregiver.org Geriatric Mental Health Foundation http://www.gmhfonline.org/gmhf Medicare.gov http://www.medicare.gov National Institute on Aging http://www.nih.gov/nia See also Advance directives; Aids and devices for cancer patients; Caregivers and caregiving; Childbirth and can37
Aids and devices for cancer patients cer; Counseling for cancer patients and survivors; Do-notresuscitate (DNR) order; Elderly and cancer; End-of-life care; Living will; Medicare and cancer; Nutrition and cancer prevention; Occupational therapy; Overtreatment; Palliative treatment; Self-image and body image; Singlehood and cancer; Support groups; Survivorship issues; Young adult cancers.
u Aids and devices for cancer
patients Category: Social and personal issues Also known as: Prostheses, breast forms, positioning aids, nutritional aids, braces, canes, walkers, wheelchairs, aromatherapy products, music therapy products Definition: Aids and devices for cancer patients are designed to help a person live a more comfortable and enjoyable life in spite of the side effects of cancer treatment. Some aids and devices help temporarily hide the effects of a cancer treatment while others can improve mobility or provide comfort permanently.
Salem Health: Cancer Another side effect of cancer treatment can be difficulty swallowing and keeping food down. To help people facing this situation get proper nutrition, there are thickening products available to add substance to liquefied foods. These products include gelatin, tapioca flour, cornstarch, commercial thickeners, pureed vegetables, instant potatoes, and baby cereal. There are also a number of liquid nutritional supplement drinks, many available at local grocery stores, that can provide needed nutrition when other types of food cannot be eaten. Some cancer patients experience sun sensitivity. Sunscreen or protective clothing can help protect sensitive skin from the sun. Sunscreens can be found at drug and grocery stores, and a number of companies create clothing—pants, shirts, hats, and gloves—that has built-in sun protection. For both men and women, making an extra effort to maintain personal grooming routines can be a way to maintain a positive attitude. Organizations such as the American Cancer Society provide classes that address special concerns cancer patients may have about their grooming and beauty routines (for example, how to deal with thinning hair). Music can be a wonderful aid in lowering stress levels and helping cancer patients sleep better. It is also shown to reduce pain by increasing endorphins and boosting immunity. It is recommended that the music be sixty beats or less per minute to provide relaxation. Much classical music falls into this category. Many hospitals offer group music therapy sessions.
Comfort aids and devices: A number of products can help cancer patients with some of the physical and emotional discomfort they may experience because of their cancer treatment. Specialty positioning pillows and foam wedges can help patients on bed rest prevent bedsores. In addition, special seat cushions for wheelchair users can help distribute their weight evenly over a large area, preventing sores and easing discomfort. These cushions tend to be filled with either water or gel. Water-filled products help decrease body temperature and gel-filled help maintain body temperature. A simple straw can make drinking beverages easier for cancer patients with sores in the mouth. If dry mouth is a problem after the salivary glands have been removed or damaged by radiation, saliva substitute products can add moisture to a cancer patient’s mouth. A cool-mist humidifier can also help prevent dry mouth by moistening the air within a room. Note that it is important to keep the humidifier clean so that germs are not spread. A wheelchair can provide mobility for a cancer patient. (PhotoDisc) 38
Salem Health: Cancer Aromatherapy may also help ease discomfort. Scents are available to help with all kinds of ailments, from pain and discomfort to lethargy. For example, lavender is a calming scent and can help ease anxiety or sleeplessness. Aromatherapy products and books explaining how to use scents can be found at many health food stores and online. Patients should check for any side effects or interactions with medical conditions before using a particular scent. An inexpensive way that many cancer patients deal with their emotions is to keep a journal. Writing down their thoughts about their situation can be very therapeutic and make it easier to keep a positive outlook. Prosthetic devices: A second category of aids and devices includes prosthetic body parts. Prostheses are available for a large number of body parts, and cancer patients should discuss with their doctors the options available to them for replacing amputated extremities. These products can help individuals regain mobility or provide cosmetic benefits. Braces, canes, walkers, and wheelchairs can improve mobility, whether used on their own or in combination with prosthetic limbs. For breast cancer patients who have undergone mastectomies, prostheses provide more than cosmetic benefits. They can provide protection and pain relief during healing, help maintain proper posture, and help prevent back and shoulder pain. Breast forms made of silicone or fiber can be inserted into a specially made mastectomy bra or worn next to the skin with a special adhesive. Cooling pads can also be inserted into bras to help relieve pain while the area heals. Specialty vests with flat panels can provide post-radiation treatment comfort. In addition, special arm sleeves can be worn to help reduce swelling by providing graduated compression. Cancer patients experiencing hair loss may want to try using a satin pillowcase to help minimize loss and to provide comfort to their sensitive scalps. Head scarves and wigs can be worn to hide hair loss. Sleep and swim caps are also available to protect remaining hair and minimize additional hair loss. Cost and insurance coverage: Some comfort and prosthetic devices are covered by public and private insurance providers. Patients should contact the insurance company before purchasing an item to find out whether the device in question is covered and if any paperwork or special authorization is needed. Some companies may require a prescription from a physician and preauthorization before they will pay for a device. Other insurance companies ask patients to pay up front for an item and then be reimbursed. If an insurance company will not cover a product and the patient cannot afford it, sometimes local cancer sup-
Air pollution port agencies such as the American Cancer Society or CancerCare can help obtain the needed item or suggest other ways to get the necessary money to pay for the item. Jennifer M. Hickin, B.S. u
For Further Information Garrison, Kevin S. It’s Just a Matter of Balance. Baltimore: Gateway Press, 2005. Gaynor, Mitchell L. The Healing Power of Sound: Recovery from Illness by Using Sound, Voice, and Music. Boulder, Colo.: Shambhala, 2002. Kelly, Mary Olson. Number One Best Tools and Tips from the Trenches of Breast Cancer. Austin, Tex.: Books Beyond Borders, 2006. Klein, Karen. Mama Said There’d Be Days like This: A Twelve-Step Guide to Surviving a Mastectomy. Farmington, Conn.: Variegate Press, 2001. Oritz, Lori M. Facing the Mirror with Cancer: A Guide to Using Makeup to Make a Difference. Chicago: Belle Press, 2004. Shurr, Donald G., and John W. Michael. Prosthetics and Orthotics. Upper Saddle River, N.J.: Prentice Hall, 2001. Wilson, A. Bennett, Jr. A Primer on Limb Prosthetics. Springfield, Ill.: Charles C Thomas, 1998. u
Other Resources
American Cancer Society http://www.cancer.org CancerCare http://cancercare.org TLC http://www.tlcdirect.org See also Breast implants; Breast reconstruction; Caregivers and caregiving; Electrolarynx; Esophageal speech; Home health services; Hospice care; Integrative oncology; Living with cancer; Reconstructive surgery; Self-image and body image; Side effects.
u Air pollution Category: Carcinogens and suspected carcinogens RoC status: Asbestos, known human carcinogen since 1980; diesel exhaust particulate, reasonably anticipated human carcinogen since 2000. Other air pollutants that are known human carcinogens include benzene, 1,3-butadiene, radon, and tobacco smoke; 39
Air pollution
Salem Health: Cancer
those that are reasonably anticipated human carcinogens include formaldehyde and polycyclic aromatic hydrocarbons. Air pollutants such as ozone, oxides of nitrogen, and sulfur oxides are not listed in the Report on Carcinogens (RoC); however, epidemiologic studies (studies on populations) provide some evidence of their association with lung cancer. Of the many components of particulate matter (PM), only diesel exhaust particulate has been the subject of studies that led to its current classification. Also known as: Criteria air pollutants, toxic air pollutants Related cancers: Lung cancer, pleural and peritoneal mesotheliomas, gastrointestinal cancers, laryngeal cancer, cancers of the lymphatic and blood-forming systems (1,3butadiene) Definition: Air pollution is the presence of contaminants, many of which are carcinogens, in the air. Outdoors, pollution is largely a consequence of the combustion of fossil fuels for transport, power generation, and other human activities. Indoors, pollution is generated by burning solid
fuels, and the air may also contain asbestos, radon gas, environmental tobacco smoke, formaldehyde, and volatile organic compounds. Exposure routes: Inhalation Where found: Indoor and outdoor air. Outdoor pollutants can be carried far from their original source by air currents. At risk: Populations exposed to smog and particulate matter in air pollution, including inner-city residents; people living near electric-power-generating plants, factories, and refining plants; occupationally exposed railroad workers and synthetic rubber industry workers; people cooking indoors with solid fuels Etiology and symptoms of associated cancers: According to the World Health Organization, the air contains a complex mixture of pollutants, including primary emissions such as diesel soot particles and oxides of nitrogen produced during combustion processes, the products of atmospheric transformation such as ozone, and the sulfate particles formed by burning sulfur-containing fuels. Although air pollution is a minor contributor to lung
Exhaust from cars on congested freeways contains carcinogens. (©iStockphoto.com/Dan Eckert)
40
Salem Health: Cancer cancer compared with tobacco smoke, it can affect entire populations, and components of the pollutant mix might interact with other carcinogens, possibly increasing their effects. In 1995 researchers Aaron Cohen and C. Arden Pope III analyzed epidemiological studies and found that they consistently suggested that ambient air pollution, chiefly as a result of the incomplete combustion of fossil fuels, is responsible for increased rates of lung cancer. A study published in 1998 of nonsmoking adults over a fifteen-year period by David Abbey and his coworkers showed a strong association between ozone levels and lung cancer. The ozone at ground level (which people inhale) is not emitted directly into the air. It is created by chemical reactions between oxides of nitrogen, emitted in motor vehicle exhaust and by industrial facilities, and volatile organic compounds from many sources, including gasoline vapors and chemical solvents. The relation between ozone levels and lung cancer has been reported in many additional scientific studies. The major outdoor air pollutants linked to lung cancer are particulate matter, sulfur oxides, ozone, oxides of nitrogen, and volatile organic compounds. Particulate matter is the term for a mixture of solid particles and liquid droplets found in the air that come from soot, smoke, and diesel exhaust. The particles of most concern are those smaller than 10 micrometers in diameter. Once inhaled, the smaller particles can travel to the deepest regions of the lungs, where chemicals (such as those adsorbed to diesel exhaust particulate) can be released. Some of these chemicals cause deoxyribonucleic acid (DNA) mutations, which can lead to cancer. Many studies have demonstrated that exposure to indoor air pollutants has adverse effects on health. More than three billion people worldwide depend on solid fuels, including biomass fuels and coal, for their cooking and energy needs. Combustion of these materials indoors produces high levels of smoke that contains many pollutants, and there is consistent evidence of lung cancer in adults exposed to coal-generated pollutants, according to the World Health Organization. Inhaling asbestos fibers released from damaged or crumbled insulating materials or other products containing this material can lead to mesothelioma and several other cancers. Other common indoor air pollutants include formaldehyde, environmental tobacco smoke, radon gas, and polycyclic aromatic hydrocarbons (a class of volatile organic compounds). History: Many of the components of air pollution are recognized as known or reasonably anticipated carginogens, such as asbestos, benzene, 1,3-butadiene, radon, tobacco
Air pollution smoke, diesel exhaust particulate, formaldehyde, and polycyclic aromatic hydrocarbons. Other components have scientific research supporting their link to human cancer. The Clean Air Act as amended in 1990 requires the U.S. Environmental Protection Agency to set national ambient air quality standards for ozone, oxides of nitrogen, particulate matter, and sulfur oxides. The agency is mandated to work with state and local governments to reduce the release of other air pollutants classified as toxic air pollutants. Bernard Jacobson, Ph.D. u
For Further Information Beeson, W. L., D. E. Abbey, and S. F. Knutsen. “LongTerm Concentrations of Ambient Air Pollutants and Incident Lung Cancer in California Adults.” Environmental Health Perspectives 106 (1998): 813-822. Cohen, A. J., and C. Arden Pope III. “Lung Cancer and Air Pollution.” Environmental Health Perspectives 103, suppl. 8 (1995): 219-224. Jacobson, M. Z. Atmospheric Pollution. New York: Cambridge University Press, 2002. Krzyzanowski, M., B. Kunnadibbert, and J. Schneider, eds. Health Effects of Transport-Related Air Pollution. Geneva, Switzerland: World Health Organization, 2005. McGranahan, G., and F. Murray. Air Pollution and Health in Developing Countries. London: Earthscan, 2003. Pluschke, P., ed. Indoor Air Pollution. New York: Springer, 2004. Pope, C. Arden, III, et al. “Lung Cancer, Cardiopulmonary Mortality, and Long-Term Exposure to Fine Particulate Air Pollution.” Journal of the American Medical Association 287 (2002): 1132-1141. Ramachandran, G. Occupational Exposure Assessment for Air Contaminants. New York: CRC Press, 2005. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Eleventh Report on Carcinogens. Research Triangle Park, N.C.: Author, 2005. u
Other Resources
U.S. Environmental Protection Agency Pollutants/Toxics: Air Pollutants http://www.epa.gov/ebtpages/pollairpollutants.html World Health Organization Air Pollution http://www.who.int/topics/air_pollution/en/ See also Arsenic compounds; Bronchoalveolar lung cancer; 1,3-Butadiene; Cigarettes and cigars; Coke oven emis41
Alcohol, alcoholism, and cancer sions; Dioxins; Lung cancers; Occupational exposures and cancer; Polycyclic aromatic hydrocarbons; Radon; Smoking cessation; Soots; Tobacco-related cancers; Wood dust.
u Alcohol, alcoholism, and
cancer Category: Carcinogens and suspected carcinogens Definition: Alcohol is a chemical that is generated during fermentation of sugar. Ethyl alcohol is the specific chemical that is generally referred to as alcohol. Alcohol is the most commonly used intoxicating agent around the world. Alcoholism (also called alcohol-dependence syndrome) is a phenomenon of continuous intake of alcohol, with a compulsive need to consume it. Alcohol has been linked to several cancers but a direct causal relationship between the two has not been established. Alcohol as carcinogen: Intake of alcohol is considered a risk factor for developing various kinds of cancers, and therefore, alcohol has been classified as a carcinogen. Ethyl alcohol, the form in which alcohol is commonly consumed, undergoes an array of metabolic changes when ingested. The main enzymes that are involved in metabolism of alcohol are alcohol dehydrogenase and aldehyde dehydrogenase. A small amount (approximately 10 percent) is metabolized by microsomal cytochrome P4502E1 (CYP2E1). Alcohol dehydrogenase converts about 80 percent of ethanol to acetaldehyde. Acetaldehyde is a mutagen and a carcinogen and is considered a risk factor in many cancers of the upper gastrointestinal tract. Acetaldehyde is implicated in a variety of processes such as inflammation of the tracheal epithelium, delaying of cell cycle progression, induction of apoptosis, chromosomal damages and aberrations, and sister chromatid exchanges. Much of the carcinogenic effect of alcohol is attributed to this single metabolite. Direct association between the concentration of acetaldehyde in saliva and development of cancer has been reported. Acetaldehyde covalently bonds with deoxyribonucleic acid (DNA) and forms structures called DNA-adducts. The most common DNA-acetaldehyde adduct is N2-ethyl-dG, which is not mutagenic. Acetaldehyde also induces the formation of the mutagenic DNA adduct called Cr-PdG (alpha-methylgamma-hydroxy-1, N2-propano-2′-deoxyguanosine). Polyamines are one of the basic molecules essential for cells and are implicated in cell growth and differentiation, nucleic acid synthesis, and protection against oxidative 42
Salem Health: Cancer damage. Polyamines facilitate acetaldehyde-induced formation of Cr-PdG adducts. Cr-PdG adducts are highly mutagenic and interfere with DNA replication and repair, inducing cancer formation. Polyamines also react with acetaldehyde and form crotonaldehyde, which is highly carcinogenic. Response to alcohol is individualistic and differs among people and races. This is because of polymorphisms in the genes for the enzymes alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). Presence of the ALDH2*1/2 allele significantly increases the risk of upper aerodigestive tract cancer. In addition to these enzymes, oral bacteria also generate acetaldehyde. High amounts of acetaldehyde are detected in saliva after alcohol consumption. Saliva is directly in contact with the upper aerodigestive tract, and this contact is considered a possible mechanism for its carcinogenic effects. Alcohol and breast cancer: Alcohol is one of the most ancient intoxicants known to humankind. Consuming one or two drinks a day is not just common but is also a social custom in many cultures. However, research suggests that even one or two drinks a day could put women at a greater risk for developing breast cancer. A study conducted at the
Alcohol has been linked to several cancers, although a direct causal relationship has not been established. (PhotoDisc)
Salem Health: Cancer
How Much Is Too Much? The risk for cancers of the mouth, esophagus, pharynx, larynx, and liver in men and women and breast cancer in women increases after about two drinks per day for men and one per day for women. One drink is defined as 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of 80proof liquor. The risk for liver cancer goes up significantly after five or more drinks per day. Source: National Cancer Institute
National Cancer Institute tested postmenopausal women for differences in hormone levels after alcohol consumption (15 or 30 grams of alcohol per day) for eight weeks. Results showed a significant elevation of estrone sulfate (an estrogen metabolite) and the hormone DHEAS (dehydroepiandrosterone sulfate). DHEAS is secreted by the adrenal glands, and increased levels of DHEAS indicate induction of a process called adrenal steroidogenesis, reflecting stimulation of the hypothalamic-pituitaryadrenal axis in the brain as a response to alcohol consumption. Alcohol and liver cancers: Excessive consumption of alcohol leads to alcohol liver disease. One type of alcohol liver disease is called alcoholic cirrhosis of the liver, a condition in which normal liver tissue is completely destroyed. Cirrhosis of the liver is considered the primary risk factor for development of hepatocellular carcinoma (liver cancer). Even though alcohol does not seem to cause liver cancer directly, there is a strong association between alcohol and liver cancer.
Aleukemia all cancer-related deaths are caused by chronic alcohol consumption. Education to make people aware of the link between alcohol consumption and cancer should aid in prevention of such cancers. Geetha Yadav, Ph.D. u
For Further Information Cho, Chi Hin, and Vishnudutt Purohit, eds. Alcohol, Tobacco, and Cancer. New York: Karger, 2006. Dorgan, J. F., et al. “Serum Hormones and the AlcoholBreast Cancer Association in Postmenopausal Women.” Journal of the National Cancer Institute 93 (2001): 710-715. Seitz, H. K., B. Maurer, and F. Stickel. “Alcohol Consumption and Cancer of the Gastrointestinal Tract.” Digestive Diseases 23 (2005): 297-303. Seitz, H. K., and F. Stickel. “Molecular Mechanisms of Alcohol-Mediated Carcinogenesis.” Nature Reviews 7 (2007): 599-612. Yirmiya, Raz, and Anna N. Taylor, eds. Alcohol, Immunity, and Cancer. Boca Raton, Fla.: CRC Press, 1993.
u
Other Resources
American Cancer Society Alcohol and Cancer http://www.cancer.org/docroot/PRO/content/ PRO_1_1x_Alcohol.pdf.asp?sitearea=PRO National Cancer Institute Alcohol Consumption http://progressreport.cancer.gov/doc_detail .asp?pid=1&did=2007&chid=71&coid=706&mid= See also Esophageal cancer; Gastrinomas; Gastrointestinal cancers; Hepatomegaly; Laryngeal cancer; Liver cancers; Pancreatic cancers; Pancreatitis.
Alcohol and other cancers: Drinking two or more drinks per day increases the risk of oral and upper gastrointestinal tract (GI) cancers in both men and women. Alcoholrelated cancers include those of the mouth, esophagus, and larynx. Drinking alcohol together with smoking increases the risk of developing cancer more than drinking alone. Alcohol is addictive, and alcoholism leads to enhanced tolerance levels, loss of control, cravings for alcohol, and an inability to stop drinking even when people wish to stop or need to stop for their health. Evidence shows that the nutritional status of the body is also negatively affected by alcohol.
Related conditions: Acute and chronic myelogenous leukemia (AML and CML), acute and chronic lymphatic leukemia (ALL and CLL)
Perspectives and progress: According to World Health Organization statistics, alcohol is responsible for about 1.8 million deaths a year, and alcohol-related cancer is the most common cause of these deaths. Some 3.6 percent of
Definition: Aleukemia describes a condition in which a patient has a normal or reduced white blood cell count. Leukemia cells are present in the bone marrow. Leukemia cells may also be present in the blood. Aleukemia may be
u Aleukemia Category: Diseases, symptoms, and conditions Also known as: Aleukemic myelosis, aleukemic leukemia
43
Alkaline phosphatase test (ALP)
Salem Health: Cancer
present in any of the four major types of leukemia: AML, CML, ALL, and CLL.
u Alkaline phosphatase test
Risk factors: The risk factors are the same as those for leukemia. The risks include age, genetic diseases, prolonged exposure to some chemicals such as benzene, chemotherapies used to treat other forms of cancer, and exposure to high doses of radiation or tobacco smoke.
Category: Procedures Also known as: ALKP, alk phos, alkaline phosphatase total
Etiology and the disease process: Aleukemias start when there is damage to the deoxyribonucleic acid (DNA) of blood cells. Normal cell development is interrupted, causing a decrease of mature cells and an increase in immature cells. Incidence: Aleukemia is present at the start of about 25 to 30 percent of acute leukemias. It is more prevalent in hairy cell leukemia, which is a slow-growing subtype of CLL. Symptoms: There may be no symptoms present. Patients may experience fatigue, weight loss, easy bruising, fever, and infections. Screening and diagnosis: No specific screening test exists for aleukemia. A low white blood cell count found when a complete blood count (CBC) is done as part of a routine exam or in response to symptoms may lead to further testing and diagnosis. Diagnosis is made by the examination of blood smears and bone marrow for the presence of leukemia cells. Staging is not done for any of the leukemias except CLL. The staging of CLL is based on imaging studies, blood tests, and bone marrow examination. The stages, ranging from Stage 0 to IV, are based on the involvement of lymph nodes, spleen, and liver, and decreasing numbers of red blood cells. The other forms of leukemia are classified by cell type. Treatment and therapy: Treatment depends on the type of cell involved and the classification or staging level. In leukemias that progress slowly, treatment may not start until the disease is more advanced. Prognosis, prevention, and outcomes: Prognosis depends on the type of cell involved and the rate of progression. No method of prevention exists. Treatment may slow the progress of the disease or cause complete remission. Some types of leukemia may not respond to treatment. Wanda E. Clark, M.T. (ASCP) See also Acute lymphocytic leukemia (ALL); Acute myelocytic leukemia (AML); Anemia; Antiandrogens; Blood cancers; Chronic lymphocytic leukemia (CLL); Chronic myeloid leukemia (CML); Eosinophilic leukemia; Fanconi anemia; Leukemias. 44
(ALP)
Definition: Alkaline phosphatase (ALP) is an enzyme that helps in the process of digestion and bone development. All tissues contain ALP. Higher concentrations are found in the liver, bone, kidney, and intestines. Various processes within the tissues release ALP into the blood. By measuring ALP blood levels, doctors can determine the presence of liver and bone disease, including cancer. ALP levels are determined by testing serum or plasma on an automated chemistry analyzer. Cancers diagnosed: Cancers of the bone, renal cells, liver, gallbladder, and bile ducts Why performed: The test is done as a part of a chemistry or liver panel to detect liver or bone disease. Once a diagnosis has been made and treatment started, the test may be done to determine if treatment is effective or if disease has progressed or returned. Patient preparation: The patient may be asked not to eat or drink or take certain medications for six to twelve hours prior to the test. Steps of the procedure: A small sample of blood is collected from a vein and placed in a tube. In children, blood may be obtained from a capillary in the heel or finger. After the procedure: A small gauze or cotton ball is applied at the site of needle insertion. The patient is asked to apply pressure. The person collecting the blood observes the site for bleeding and may apply a bandage. The bandage may usually be removed in thirty to sixty minutes. Risks: Risks from the procedure include bleeding, bruising, hematoma (bleeding under the skin), fainting, lightheadedness, or the need for multiple needle sticks to obtain a sample. Results: Normal ALP levels vary by the patient’s sex and age and by the analyzer used. Each laboratory establishes a set of normal ranges based on this information. The physician receives a report of the test results with the normal values established by the testing laboratory. Elevated levels indicate the possibility of liver or bone disease, including the presence of a tumor. The test does not distinguish from which tissue the increased amount of alkaline phosphatase comes. The physician may order
Salem Health: Cancer
Alkylating agents in chemotherapy reactive compounds containing alkyl groups. They are employed as antineoplastics, drugs that kill neoplasms (cancerous tumor cells) by interfering with their deoxyribonucleic acid (DNA) and cell division.
other blood tests, including an alkaline phosphatase isoenzyme test that determines if the increased ALP comes from bone, liver, or intestine. Other procedures such as X rays may also be ordered. Following cancer treatment, ALP levels are expected to decrease. If levels remain high or increase, then some cancer may remain or has returned. Wanda E. Clark, M.T. (ASCP)
Cancers treated: Various, especially slow-growing cancers such as solid tumors and leukemias Subclasses of this group: Alkyl sulfonates, ethyleneimines and methylmelamines, nitrogen mustards, nitrosoureas, platinum compounds, triazenes
See also Immunocytochemistry and immunohistochemistry; Paget disease of bone; Placental alkaline phosphatase (PALP).
Delivery routes: These drugs are administered both intravenously and orally in capsule and tablet form, on an inpatient, outpatient, and at-home basis, depending on the specific drug, type of cancer, and its location and aggressiveness. When possible, these drugs are best delivered to the tumor site to limit damage to normal cells.
u Alkylating agents in
chemotherapy Category: Chemotherapy and other drugs ATC code: 101A
How these drugs work: One of the oldest classes of chemotherapeutic drugs, alkylating agents were discovered during World War II when physician Cornelius P. Rhoads drew a connection between the lowered white
Definition: Alkylating neoplastic agents form a class of chemotherapeutic drugs, all of which consist of highly
Common Alkylating Agents Subclass
Delivery Mode
Cancers Treated
Altretamine Hexalen (hexamethylmelamine)
Ethylenimines
Oral
Ovarian cancer
Busulfan
Alkyl sulfonates
Oral, IV
Chronic myelogenous leukemia, other blood cancers
Platinum compounds
IV
Ovarian carcinoma
Drug
Brands
Carboplatin (CBDCA)
Paraplatin
Carmustine (BCNU)
BiCNU, Nitrosoureas Gliadel Wafer
IV
Brain tumors, multiple myeloma, Hodgkin disease, non-Hodgkin lymphoma, malignant melanoma, breast cancer, gastrointestinal cancers, Ewing sarcoma, and Burkitt lymphoma; applied topically for mycosis fungoides
Chlorambucil
Leukeran
Nitrogen mustards
Oral
Chronic lymphocytic leukemia, some non-Hodgkin lymphomas, advanced Hodgkin disease
Cisplatin (CDDP)
Platinol-AQ
Platinum compounds
IV
Metastatic testicular tumors, metastatic ovarian tumors, advanced bladder carcinoma
Cyclophosphamide (CTX)
Cytoxan
Nitrogen mustards
Oral, IV
Lymphomas, multiple myelomas, leukemias, mycosis fungoides, neuroblastoma, ovarian carcinoma, retinoblastoma, breast cancer
Dacarbazine (DTIC)
DTIC-Dome
Triazenes
IV
Melanoma, Hodgkin disease
Ifosfamide (isophosphamide)
Ifex
Nitrogen mustards
IV
Germ cell testicular cancer, sarcomas
(continued on page 46)
45
Alkylating agents in chemotherapy
Salem Health: Cancer Side effects: Although alkylating agents are more toxic to cancer cells than to normal cells, these drugs are nonspecific. That is, they target normal as well as cancerous tissue, so they exhibit the “Janus effect”: They kill both bad and good cells. Therefore they have toxic side effects, depending on the specific drug, its dosage, the duration of administration, and the individual patient’s physical condition and attitude. Common side effects include depressed blood cell counts, tiredness and fatigue, diarrhea, alopecia (hair loss), nausea and vomiting, infertility (both amenorrhea in women and impaired spermatogenesis in men), damage to intestinal mucosa, exfoliation of the bladder epithelium resulting in fluid retention, and in extreme cases cardiotoxicity, which would mitigate the chemotherapy regimen. In addition, some alkylating agents increase the risk of future malignancies, such as acute myeloid leukemia, which may emerge years after treatment. Christina J. Moose, M.A.
blood cell counts in six hundred sailors (who had been exposed to mustard gas during the sinking of the Liberty in 1943) and the possibility that the nitrous mustards could be adopted for use in leukemia patients. It was later observed that alkylating agents substitute alkyl groups for the hydrogen groups in the DNA of tumor cells. The alkyl groups cross-link guanine nucleobases in the double-helix strands of DNA, which makes it impossible for the two DNA strands to uncoil and separate in preparation for replication. As a result, these drugs prevent tumor cells from dividing during mitosis, stopping the cells’ growth. They may also stimulate the natural process of cell death (apoptosis). Because DNA is more actively replicated and transcribed in rapidly dividing cancer cells than in normal cells, these drugs are more toxic to tumor tissue than to normal tissue. Alkylating agents are also known to add methyl or alkyl groups onto any of the four nitrogenous bases found in DNA(adenine, guanine, cytosine, thymine), frequently altering the base-pairing relationships and leading to new mutations.
Common Alkylating Agents (continued)
46
Drug
Brands
Subclass
Delivery Mode
Lomustine (CCNU)
CeeNU
Nitrosoureas
Oral
Brain tumors, Hodgkin disease, bronchogenic carcinoma, non-Hodgkin lymphomas, malignant melanoma, breast cancer, renal cell carcinoma, carcinoma of the GI tract
Mechlorethamine (nitrogen mustard)
Mustargen
Nitrogen mustards
IV
Hodgkin disease, lymphosarcoma, chronic myelocytic or chronic lymphocytic leukemia; polycythemia vera; mycosis fungoides, bronchogenic carcinoma, non-Hodgkin lymphomas, malignant melanoma, breast cancer, renal cell carcinoma, carcinoma of the GI tract; applied topically for mycosis fungoides
Melphalan (L-PAM)
Alkeran
Nitrogen mustards
Oral, IV
Multiple myeloma, ovarian carcinoma
Oxaliplatin (oxalatoplatin, oxalatoplatinum)
Eloxatin, Transplatine
Platinum compounds
IV
Advanced ovarian cancer; may be effective for head and neck cancers, skin cancer, lung cancers, and non-Hodgkin lymphomas
Procarbazine
Matulane, Natulane
Hydrazine derivatives
Oral
Hodgkin disease and other lymphomas, brain tumors, skin cancer, lung cancer, multiple myeloma, mycosis fungoides
Cancers Treated
Streptozocin
Zanosar
Nitrosoureas
IV
Pancreatic islet cell cancer
Temozolomide
Temodar
Triazenes
Oral
Brain tumors (astrocytomas)
Thiotepa
Thioplex
Ethylenimines
IV, spinal injection, bladder infusion
Bladder cancer, ovarian cancer, breast cancer, lymphomas, bronchogenic carcinoma, and metastatic pleural, pericardial, and peritoneal cancers
Salem Health: Cancer
Alopecia
u For Further Information Chabner, Bruce A., and Dan L. Longo, eds. Cancer Chemotherapy and Biotherapy: Principles and Practice. Philadelphia: Lippincott Williams & Wilkins, 2006. Fischer, David S., et al. The Cancer Chemotherapy Handbook. 6th ed. St. Louis: Mosby, 2003. Panasci, Lawrence C., and Moulay A. Alaoui-Jamali, eds. DNA Repair in Cancer Therapy. Totowa, N.J.: Humana Press, 2004. Podolsky, M. Lawrence. Cures out of Chaos. Newark, N.J.: Harwood Academic, 1997. Skeel, Roland T. Handbook of Cancer Chemotherapy. 6th ed. Philadelphia: Lippincott Williams & Wilkins, 2003. u
Other Resources
National Cancer Institute Drug Information Summaries http://www.cancer.gov/cancertopics/druginfo/ alphalist See also Antineoplastics in chemotherapy; Bis(chloromethyl) ether and technical-grade chloromethyl methyl ether; 1,4-Butanediol dimethanesulfonate; Carcinogens, known; Carcinogens, reasonably anticipated; Chemotherapy; Chlorambucil; 1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea (MeCCNU); Cyclophosphamide; Infertility and cancer; Mustard gas; Sterility; Thiotepa.
u Alopecia Category: Diseases, symptoms, and conditions Also known as: Alopecia disseminata, alopecia universalis, alopecia totalis, baldness, hair loss, acomia, pelade Related conditions: Anagen effluvium, telogen effluvium Definition: Alopecia is abnormal loss of hair, a common side effect of treatments for cancers, including chemotherapy and radiation therapy. There are many types of alopecia, with many causes, including certain skin cancers and other types of cancer that spread to the skin, although marked hair loss from skin cancer is extremely rare. Risk factors: Chemotherapy for any cancer greatly increases the risk of alopecia, and radiation therapy increases the risk of hair loss from the irradiated area. Etiology and the disease process: Each human hair grows from a hair follicle, an elongated pouch formed during fe-
Chemotherapy has caused this woman to lose her hair. (© Lisa F. Young/Dreamstime.com)
tal development by growth of the upper part of the skin, the epidermis, down into the lower part, the dermis. The lower part of the follicle, the hair bulb, contains the germinal matrix, the cells that form the hair. Each hair goes through a three-phase growth cycle: anagen, or active growth; catagen, or regression; and telogen, or resting. When the telogen phase for each hair is complete, a new anagen phase begins. Human hairs complete their recurring growth cycle, as old hairs are pushed out by new hairs, in random order. At any given time, about 85 percent of hairs are in the anagen, or active growth phase. Chemotherapeutic agents target rapidly reproducing cells, like cancer cells. Unfortunately, these agents do not know the difference between a cancer cell and the rapidly reproducing cells of the germinal matrix in a hair bulb. They stop cell division, or mitosis, in matrix cells, just as they do in cancer cells. The anagen phase comes to a stop, and in many cases, all the hair that is in the anagen phase is shed. Hair lost through chemotherapy almost always regrows, because the hair follicle is left intact. Radiation therapy also stops the reproduction of rapidly dividing cells, but in higher doses, 47
Alpha-fetoprotein (AFP) levels radiation can damage the hair follicles it touches, preventing regrowth of hair. Incidence: At least some degree of hair loss is likely with many forms of chemotherapy. Certain drugs or combinations of drugs are virtually certain to cause some degree of hair loss. A few drugs cause nearly complete hair loss. Symptoms: Symptoms of alopecia related to cancer range from temporary thinning or breakage of a small patch of hair to loss of hair all over the body (alopecia disseminata, alopecia universalis, alopecia totalis), and hair loss can be temporary or permanent, depending on the cause. Screening and diagnosis: Diagnosis of chemotherapyrelated alopecia follows visible hair loss within days or weeks of administration of chemotherapeutic drugs. Treatment and therapy: Therapies for alopecia caused by chemotherapy include administration of vitamins, minerals, or omega-3 and omega-6 fatty acids—substances that promote healthy hair. The benefit of these therapies on cancer-related hair loss is still being researched, and consumption of some vitamins and minerals may reduce the effectiveness of chemotherapy, so any treatment for hair loss during therapy should be approved by the treating physician. Treatment for cancer-caused alopecia includes treatment for the underlying cancer, which may include surgery or chemotherapy. Again, noticeable hair loss from cancer itself is extremely rare. Prognosis, prevention, and outcomes: The prognosis for alopecia caused by chemotherapy depends on the chemicals used, the dosage, and the frequency of treatment. More intensive treatment is likely to cause more extensive hair loss. Whatever the amount or type of hair loss from chemotherapy, the prognosis is eventual regrowth of hair. Patchy regrowth may begin before chemotherapy is completed, an average of three to five months after initial hair loss from the first treatment. Because chemotherapy disrupts the matrix from which the hair is formed, including the melanocytes, or cells that give hair its color, regrown hair may differ in color or texture from the original hair. There has been some limited success in preventing scalp hair loss from chemotherapy through use of scalp cooling or a hairline tourniquet during administration of the chemotherapy. These, however, have been successful with only certain chemical agents. Their use has been questioned by some oncologists because, while they protect scalp follicles from damage, they also protect any cancer cells present in the scalp. Research trials are being conducted on other treatments that may reduce hair loss from chemotherapy. The prognosis for alopecia caused by radi48
Salem Health: Cancer ation therapy depends on the dosage of radiation. High doses usually cause permanent hair loss to the irradiated area; low doses more often cause temporary, local hair loss. Cathy Anderson, R.N., B.A. u
For Further Information Bleiker, T. O., N. Nicolaou, J. Traulsen, and P. E. Hutchinson. “‘Atrophic Telogen Effluvium’ from Cytotoxic Drugs and a Randomized Controlled Trial to Investigate the Possible Protective Effect of Pretreatment with a Topical Vitamin D3 Analogue in Humans.” British Journal of Dermatology 153, no. 1 (2005): 103-112. Jothilakshmi, P. K., A. J. Watson, and E. Jude. “Acute Alopecia Due to Metformin Treatment for Polycystic Ovarian Syndrome.” Journal of Obstetrics and Gynaecology 26, no. 6 (2006): 584-585. Wang, J., Z. Lu, and J. L. Au. “Protection Against Chemotherapy-Induced Alopecia.” Pharmaceutical Research 23, no. 11 (2006): 2505-2514. Wyatt, A. J., G. D. Leonard, and D. L. Sachs. “Cutaneous Reactions to Chemotherapy and Their Management.” American Journal of Clinical Dermatology 7, no. 1 (2006): 45-63.
u
Other Resources
Chemotherapy.com http://www.chemotherapy.com Healthline http://www.healthline.com WebMD http://www.webmd.com See also Alkylating agents in chemotherapy; Chemotherapy; Cyclophosphamide; Paraneoplastic syndromes; Radiation therapies; Self-image and body image; Side effects.
u Alpha-fetoprotein (AFP) levels Category: Procedures Also known as: Total AFP, AFP-13 percent, alphafetoglobulin, αFP, AFP tumor marker Definition: Alpha fetoprotein (AFP) is a protein produced by fetal tissue and by tumors. There are several forms of AFP. The test for AFP generally measures total AFP. The test is performed on serum or plasma on an automated chemistry analyzer.
Salem Health: Cancer Cancers diagnosed: Cancers of the liver, testes, and ovaries Why performed: The AFP test is done to detect and monitor cancers of the liver, testes, and ovaries. Physicians may order the test for patients with chronic liver disease because of the high risk of developing liver cancer. Because AFP is also produced by a fetus, AFP levels are generally higher in pregnant women. A test for AFP done on pregnant women is not done to detect a tumor but is used with other data to detect possible abnormalities in the developing fetus. Patient preparation: No special preparation is necessary. Steps of the procedure: A small sample of blood is collected from a vein and placed in a tube. In children, blood may be obtained from a capillary in the heel or finger. After the procedure: A small gauze or cotton ball is applied at the site of needle insertion. The patient is asked to apply pressure. The person collecting the blood observes the site for bleeding and may apply a bandage. The bandage may usually be removed in thirty to sixty minutes. Risks: Risks include bleeding, bruising, hematoma (bleeding under the skin), fainting, light-headedness, or the need for multiple needle sticks to obtain a sample. Results: Normal AFP levels vary by the patient’s sex and age and by the analyzer used. Each laboratory establishes normal ranges based on this information. The physician receives a report of the test results with the normal values established by the testing laboratory. AFP decreases at birth, and adult levels are normally low. Elevated levels are present in liver cancer and in some cancers of the testes and ovaries. Generally, higher levels of AFP indicate a larger tumor. The test is not considered specific for diagnosis, but it is an indicator that a tumor may be present. Physicians may order imaging studies and additional laboratory tests to determine the presence of a tumor. Some physicians order a test called AFP-13 percent, as 13 is one of the forms of AFP that make up the total. An increased percentage of AFP-13 to total AFP indicates an increased risk of developing liver cancer or a poorer prognosis. AFP levels usually return to normal within a month of treatment. Wanda E. Clark, M.T. (ASCP) See also Ataxia telangiectasia (AT); Beckwith-Wiedemann syndrome (BWS); Germ-cell tumors; Pathology; Placental alkaline phosphatase (PALP); Proteomics and cancer research; Testicular cancer; Yolk sac carcinomas.
Alveolar soft-part sarcomas
u Alveolar soft-part sarcomas Category: Diseases, symptoms, and conditions Also known as: Nonrhabdomyosarcoma soft-tissue sarcomas, ASPS Related conditions: Soft-tissue sarcomas Definition: Alveolar soft-part sarcoma is a slow-growing, malignant tumor that develops in deep soft tissues and muscles, most often in the thighs and buttocks. It is also found in the arm, chest, bladder, abdomen, and—in children—the head and neck. It gets its name from the way the tumor cells are clustered, resembling alveoli, or the air sacs of the lungs. Risk factors: No risk factors are known, and alveolar softpart sarcoma is nonhereditary. Etiology and the disease process: The disease’s etiology is murky. Early development of alveolar soft-part sarcoma appears to be linked to a genetic mutation involving the separation of a gene from chromosome 17 and its attachment to the X chromosome. A wealth of blood vessels allows tumor cells to enter the bloodstream and spread to other areas, usually the lungs and brain. Childhood alveolar soft-part sarcoma appears to have a different, and generally less aggressive, biology. Incidence: Alveolar soft-part sarcoma is rare, with 40 to 80 new cases annually in the United States. About half of alveolar soft-part sarcoma patients are between the ages of fifteen and twenty-nine, and women generally outnumber men, especially among younger patients. Symptoms: Common symptoms include a soft, painless lump, soreness, reduced range of motion, and numbness. Because alveolar soft-part sarcoma grows slowly in deep, elastic tissues, patients often do not notice symptoms until the cancer is advanced or has spread. Screening and staging: Diagnostic procedures include laboratory tests and imaging studies such as computed tomography (CT) scans, magnetic resonance imaging (MRI), and bone scans. A biopsy is required, however, to confirm alveolar soft-part sarcoma. Tumors are staged based on size, grade, and degree of spread: • Stage I: Low grade, with little potential for spreading • Stages II and III: High grade, with increased potential for spreading • Stage IV: Metastasis to distant organs Other criteria are typically used for staging pediatric alveolar soft-part sarcoma. 49
Amenorrhea Treatment and therapy: Surgical removal of the tumor and surrounding tissue is the primary treatment. Radiation therapy may be used before to shrink the tumor and after to kill any remaining cells, although it is used in children only if surgery alone is ineffective. Chemotherapy is not generally beneficial. Other therapies are under study. Prognosis, prevention, and outcomes: The five-year survival rate for patients with localized tumors is around 80 percent. If the disease has metastasized, the rate drops to 20 percent. However, long-term survival is possible even with spread because alveolar soft-part sarcoma grows slowly. The prognosis for children is considerably better, as their tumors are generally smaller and localized. Alveolar soft-part sarcoma can recur more than ten years after initial diagnosis, so long-term follow-up is recommended. Judy Majewski, M.S. See also Dermatofibrosarcoma protuberans; Ewing sarcoma; Fibrosarcomas, soft-tissue; Hemangiosarcomas; Liposarcomas; Mesenchymomas, malignant; Rhabdomyosarcomas; Sarcomas, soft-tissue; Synovial sarcomas.
u Amenorrhea Category: Diseases, symptoms, and conditions Also known as: Primary amenorrhea, secondary amenorrhea, absent periods, absent menses, absent menarche Related conditions: Pregnancy, menopause, pituitary or gynecologic tumors Definition: Amenorrhea is the absence of menstruation, whether temporary or permanent. Amenorrhea is normal prior to puberty, during pregnancy and lactation, and after menopause. Amenorrhea may also occur as the symptom of a variety of abnormal conditions, including pituitary or gynecologic tumors, and is an expected result of many chemotherapeutic cancer drugs. Primary amenorrhea is the absence of menarche, the initial menstrual period, in women age sixteen and older. Menarche occurs normally in women between the eleventh and seventeenth year. The average age of menarche in the United States is 12.8 years. Secondary amenorrhea is absence of menses for three months in a woman with previously normal menstruation and for nine months in a woman with oligomenorrhea, which is infrequent periods and fewer than the normal eleven to thirteen a year. 50
Salem Health: Cancer Risk factors: Both primary and secondary amenorrhea can be influenced by a host of other factors, some of which include immunodeficiency, anorexia nervosa, congenital abnormalities of the reproductive tract, obesity, diabetes, dietary restriction, starvation, metabolic disorders, drugs, and excessive physical exercise. Amenorrhea can also signal a pituitary or a gynecologic tumor, and it is a common and even expected result of chemotherapy or radiation treatment for cancer. Etiology and the disease process: Amenorrhea is often due to the absence or change in hormones produced in the hypothalamus, the pituitary gland, or the ovaries (the triad that directs reproduction), and it can result from an abnormality in the outflow tract. In primary amenorrhea, in the presence of secondary sex characteristics and a uterus, the most common cause is outflow tract obstruction with a transverse vaginal septum or imperforate hymen, both easily correctable. However, primary amenorrhea can also have a genetic cause. The most common cause of secondary amenorrhea is pregnancy during a woman’s reproductive years. Secondary amenorrhea may also be related to lifestyle choices. Athletes and ballet dancers who train vigorously often experience missed periods. Stress, obesity, and starvation can also result in secondary amenorrhea. In these cases, women stop menstruating because the ovaries do not produce enough estrogen in a cyclic manner to cause the uterine lining to thicken and shed normally. If pregnancy is not the cause, the physician may test the patient’s levels of hormones produced by the thyroid and the pituitary glands. When amenorrhea is accompanied by elevated levels of prolactin, galactorrhea, headaches, or visual disturbances, a pituitary tumor may be the cause. Adenomas are the most common cause of anterior pituitary dysfunction. Gynecological tumors such as ovarian cancer must also be ruled out in the presence of amenorrhea. Cancer treatments such chemotherapy and radiation are often associated with amenorrhea. The greater the dose of the chemotherapeutic agent, the greater the chance of amenorrhea. Studies linking particular cancer treatments to the incidence of amenorrhea remain incomplete, but two drugs particularly linked to amenorrhea are doxorubicin and cyclophosphamide. Incidence: In the United States, the incidence of primary amenorrhea is 2.5 percent. The incidence of secondary amenorrhea is between 1 and 4 percent. Rarely, the cause of amenorrhea is a tumor of the pituitary. The true incidence of pituitary adenomas is difficult
Salem Health: Cancer to know with certainty because they are often asymptomatic; autopsy estimates range from 2.7 to 27 percent. Symptoms: The first sign of primary amenorrhea is the absence of menses. If the cause of absence of flow is an anomaly of the outflow tract of the blood, the patient may experience cramping and severe abdominal pain. In the case of secondary amenorrhea, other that the absence of menstruation, symptoms may include: • galactorrhea, in which case the breasts produce milk in a woman who is not pregnant or breastfeeding • headache or reduced peripheral vision as a potential sign of an intracranial tumor • hirsutism, or increased hair growth in a male pattern caused by excess androgen • vaginal dryness, hot flashes, night sweats, or disordered sleep, suggesting ovarian insufficiency or premature ovarian failure (premature menopause) • excessive weight gain or loss • anxiety Screening and diagnosis: With primary amenorrhea and the absence of secondary sex characteristics, the physician may order an ultrasound to determine if a uterus is present and measure the levels of two hormones produced by the anterior pituitary: the follicle stimulating hormone (FSH), which stimulates growth of the follicle in the ovary, and luteinizing hormone (LH), which triggers ovulation. Very low levels suggest that the gonads, or sex glands, have failed to develop or begin functioning. Karyotyping to study the chromosome arrangement may reveal a genetic reason for the absence of menarche. An example is Turner syndrome, which is a congenital endocrine disorder caused by failure of the ovaries to respond to pituitary hormone stimulation. In addition to primary amenorrhea and failure of sexual maturation, the physical examination may note short stature. About onethird of the patients show webbing of the neck, marled cubitus valgus (a deformity of the arm in which the forearm deviates laterally), and developmental disabilities. Often genetic studies reveal the presence of only 45 chromosomes, the second X chromosome being absent. Treatment and therapy: A thorough medical history often reveals the cause of amenorrhea, which can then be corrected by surgery, medication, or lifestyle changes. Secondary amenorrhea may be caused by some medications such as phenothiazines, some narcotics, and any condition related to pituitary insufficiency or thyroid dysfunction. For cases due to lifestyle choices, reducing the amount or intensity of exercise and maintaining a healthy
Amenorrhea weight should correct hormone levels and result in a return to regular periods. If is determined to be a symptom of a pituitary or gyencologic tumor, the patient will undergo tests for malignancy and follow-up treatment and therapy indicated for the particular cancer diagnosed. Prognosis, prevention, and outcomes: Most cases of amenorrhea are treatable, although some resulting from genetic conditions cannot be corrected. In women with low thyroid-stimulating hormone (TSH), or hypothyroidism, which is more often associated with hypermenorrhea or oligomenorrhea, the menstrual cycle is often returned to normal following hormone replacement therapy. If a pituitary tumor is causing the amenorrhea, these tumors are rare and often asymptomatic, seldom resulting in death. They are typically slow growing and benign. However, the numerous hormones produced in the pituitary orchestrate many bodily functions, so patients with these tumors may face a lifetime of hormone replacement and long-term follow-up care. Jane Adrian, M.P.H., Ed.M., M.T. (ASCP) u
For Further Information Bell, Ruth, et al. Changing Bodies, Changing Lives: A Book for Teens on Sex and Relationships. 3d ed. New York: Times Books, 1998. Hobart, Julie A., and Douglas R. Smucker. “The Female Athlete Triad.” American Family Physician 61, no. 11 (June 1, 2000). Master-Hunter, Tarannum, and Diana L. Heiman. “Amenorrhea: Evaluation and Treatment. ” American Family Physician 73, no. 8 (April 15, 2006). Slap, Gail B. “Amenorrhea.” In The Gale Encyclopedia of Childhood and Adolescence, edited by Jerome Kagan. Detroit: Gale, 1998.
u
Other Resources
American College of Obstetricians and Gynecologists http://www.acog.org American Society for Reproductive Medicine http://www.asrm.org See also Alkylating agents in chemotherapy; Chemotherapy; Endometrial cancer; Infertility and cancer; Neuroendocrine tumors; Ovarian cysts; Sterility. 51
American Association for Cancer Research (AACR)
u American Association for
Cancer Research (AACR) Category: Organizations Definition: Founded in 1907, the American Association for Cancer Research (AACR) is a nongovernmental organization of physicians, scientists, and advocates seeking to overcome the burden of cancer through research and dissemination of information. With more than 24,000 members in more than sixty countries, it is one of the largest organizations of its kind. Funding research: The AACR does not conduct cancer research itself but instead acts as a base of financial support for researchers. There are two basic types of support provided by the organization: direct research funding and scholarly or travel grants. As of 2007, the annual budget of the AACR was approximately $3.65 million. Approximately 69 percent of that went to funding research, while 15 percent went to education programs, and the remaining 16 percent was required for operational expenses. The AACR has provided more than $16 million dollars in research funding since 1993. The AACR provides three major grants that directly fund cancer research. The Jeannik M. Littlefield-AACR Grants in Metastatic Colon Cancer Research provide awards ranging from $500,000 to $1 million; four of these grants were given in 2007. The BCRF-AACR Grants for Translational Breast Cancer Research provide awards up to $250,000; three of these grants were given in 2007. The Avon Foundation-AACR International Scholar Awards in Breast Cancer Research provide up to $100,000; twelve of these grants were awarded in 2007. The AACR also has four other grants that range from $30,000 to $50,000. All of these awards pay for expenses such as laboratory equipment, materials, salaries, and limited travel. The other type of grant that the AACR provides helps students and scientists attend the many workshops and conferences offered by the AACR and other cancer research organizations. These types of grants may cover travel expenses, housing, and registration fees. Without such grants, many researchers, especially those who are younger or are just beginning to build a reputation in the field, would not be able to attend these collaborative events. Publications: Because dissemination of information is of vital importance, both to researchers seeking to make scientific progress and to the doctors and patients seeking treatment options, the AACR publishes five journals and one magazine. Each of these journals is peer-reviewed, 52
Salem Health: Cancer and together they contain approximately 23,000 pages each year. The AACR’s earliest journal, Cancer Research, was first published in January of 1949. It is the most highly quoted cancer journal worldwide. It accepts work from all areas of cancer research and is published bimonthly. Clinical Cancer Research focuses specifically on innovative clinical research, especially that which bridges the gap between laboratory research and clinical application. It began in January of 1995 and is also published on a bimonthly basis. Cancer Epidemiology, Biomarkers and Prevention was first published in November of 1991 and is published monthly. The journal focuses on the causes of cancer and cancer prevention. The AACR’s newest journals, Molecular Cancer Therapeutics and Molecular Cancer Research, were first published in 2001 and 2002, respectively. These journals focus on cancer research developments in molecular biology and are published on a monthly basis. CR magazine, which stands for “collaborations, results,” is intended not only for research scientists and physicians but also for people who have cancer, survivors of cancer, and anyone who is affected by the disease. The AACR hopes to help create community and camaraderie among people affected by cancer, providing the emotional support that many patients and family members need. The editorial board for the magazine is made up of cancer research scientists, cancer advocates, and cancer survivors. It began publication in the spring of 2006 and is published quarterly. CR magazine also provides podcasts of cancer news stories on its Web site. Events: To facilitate communication among scientists, the AACR holds numerous workshops, meetings, and conferences. The Annual Meeting of the AACR is the largest annual meeting in the field and is regarded by many cancer researchers as the most important. In 2007, it hosted more than 16,000 cancer scientists at the Los Angeles Convention Center. For five days, these scientists attended forty-six symposia, twenty forums, sixty-nine sessions, and more than forty minisymposia. Almost six thousand abstracts were presented at the seven poster sessions. The AACR publishes the proceedings of its annual meeting and also makes them available on its Web site, along with audio recordings and Webcasts from the event. In addition to the annual meeting, the AACR holds several large conferences and around a dozen smaller conferences. The larger conferences usually have between 500 and 3,000 attendees and focus on such topics as racial and ethnic disparities in cancer, molecular diagnostics, and cancer prevention. Smaller conferences usually attract be-
Salem Health: Cancer tween 150 and 400 people, and the topics tend to cover a great variety of special subjects, such as oncogenomics or proteomics in cancer research. The AACR also aids younger cancer researchers by organizing educational workshops throughout the year. These workshops are designed to provide opportunities for young investigators to develop essential research skills. Robert Bockstiegel, B.S. u For Further Information Jeffries, Lee P., ed. Leading Topics in Cancer Research. New York: Nova Science, 2007. Martakis, Ignatius K., ed. Cancer Research at the Leading Edge. New York: Nova Science, 2007. Pereira, Larissa S., ed. Cancer Research Perspectives. New York: Nova Science, 2008. u
Other Resources
American Association for Cancer Research http://www.aacr.org American Society of Clinical Oncology http://www.asco.org Association of American Cancer Institutes http://www.aaci-cancer.org See also American Cancer Society (ACS); American Institute for Cancer Research (AICR); Dana-Farber Cancer Institute; Duke Comprehensive Cancer Center; Fox Chase Cancer Center; Fred Hutchinson Cancer Research Center; Jonsson Comprehensive Cancer Center (JCCC); M. D. Anderson Cancer Center; Mayo Clinic Cancer Center; Memorial Sloan-Kettering Cancer Center; National Cancer Institute (NCI); National Science Foundation (NSF); Prevent Cancer Foundation; Robert H. Lurie Cancer Center.
u American Cancer Society
(ACS) Category: Organizations Also known as: American Society for the Control of Cancer Definition: The American Cancer Society (ACS) is an organization that provides cancer information, aids cancer patients, and collects and contributes funds for cancer research. History: Several New York City physicians established the American Society for the Control of Cancer (ASCC),
American Cancer Society (ACS) the ACS’s predecessor, in 1913. At that time, approximately 75,000 people in the United States died of cancer each year. ASCC leaders strove to educate people, including medical professionals, regarding cancerous conditions and treatments. The ASCC published articles in both mainstream and professional periodicals. During the mid-1930’s, ASCC Women’s Field Army volunteers distributed cancer information directly to people and collected funds for the organization’s work. By 1938, approximately 150,000 people were affiliated with the ASCC. After World War II, the renamed American Cancer Society (ACS) embraced research to control cancer. The ACS introduced its list of seven cancer warnings in 1947. Services and procedures performed: The ACS emphasizes cancer prevention, mitigating physical and emotional pain, and survival. The society strives to decrease cancer occurrence and death rates. ACS funds from donors advance cancer research, create educational material, staff the National Cancer Information Center, provide such support services as housing near cancer centers for patients and people accompanying them, and publicize issues relevant to cancer control. The ACS Web site posts cancer information, and the organization distributes printed and visual media to individuals and health centers. The ACS’s Cancer Survivor Network enables people affected by cancer to communicate. The ACS seeks donors, ranging from individuals to corporations. Fund-raisers include the ACS’s Relay for Life. A board of directors oversees national ACS activities, including distribution of fellowships and grants. Divisions and local units also conduct ACS work. By 2006, about three million volunteers, representing both medical professionals and people from other walks of life, participated in providing ACS services. Research: The ACS invests the most private funds for oncology investigations in the United States. ACS leaders support innovative research seeking to identify causes of cancer and to improve prevention and treatment methods. By the early twenty-first century, the ACS had invested $3 billion for researchers to pursue investigations. As of 2007, the ACS awarded peer-evaluated projects $130 million yearly. ACS-supported achievements created better screening techniques such as the prostate-specific antigen (PSA) test. The ACS funded research evaluating the use of Pap smears to detect cervical cancer and mammograms to detect breast cancer. Treatment methods also benefited from ACS financial support. Funded by the ACS, Sidney Farber studied the use of aminopterin to accomplish remission of 53
American Institute for Cancer Research (AICR) cancer, enabling chemotherapy to become a viable method to treat many cancers. ACS-supported researchers focusing on pediatric oncology developed more effective methods to combat leukemia in children. Investigators used ACS research money to study genes associated with cancer. An ACS-financed study linked cigarettes and cancer. ACS research funds contributed to creation of anticancer pharmaceuticals. Education: The ACS creates and distributes educational information to enhance people’s awareness of cancer issues. The society stresses preventing cancers by embracing healthy behaviors. The ACS urges people to seek cancer screening to detect cancers and seek treatment expeditiously to aid survival. The society’s information is incorporated in health lessons taught in many U.S. schools. ACS advertisements in various media promote colorectal and breast cancer screening and stopping smoking. The ACS publishes three journals for medical professionals, educational guides devoted to specific cancers, and books for patients’ children and caregivers. The society’s cookbook has appeared in several editions as new information regarding nutritional aspects of cancer prevention is determined. The ACS distributes Cure: Cancer Updates, Research & Education. The society supports workshops and conferences where medical professionals learn about current oncology information and methods. Advocacy: In 2007, the ACS devoted $15 million to advertisements for print and television commercials stressing how lack of insurance affects cancer detection and treatment. The ACS allied with other health groups and the American Association of Retired Persons (AARP) to promote better health care access. The nonpartisan Cancer Action Network (CAN) complements the ACS, conducting lobbying, which the ACS cannot pursue. CAN’s political work includes securing nonsmoking areas, preparing voter guides, and sponsoring a hotline to contact politicians. Elizabeth D. Schafer, Ph.D. u For Further Information American Cancer Society. The American Cancer Society’s Healthy Eating Cookbook: A Celebration of Food, Friends, and Healthy Living. 3d ed. Atlanta: American Cancer Society, 2005. Herdman, Roger, and Leonard Lichtenfeld, eds. Fulfilling the Potential of Cancer Prevention and Early Detection: An American Cancer Society and Institute of Medicine Symposium. Washington, D.C.: National Academies Press, 2004.
54
Salem Health: Cancer Ross, Walter S. Crusade: The Official History of the American Cancer Society. New York: Arbor House, 1987. Stein, Kevin, et al. “The American Cancer Society’s Studies of Cancer Survivors.” American Journal of Nursing 106, no. 3 (March, 2006): 83-85. u
Other Resources
American Cancer Society http://www.cancer.org American Cancer Society Cancer Action Network http://www.acscan.org Cure: Cancer Updates, Research, and Education http://www.curetoday.com See also American Association for Cancer Research (AACR); American Institute for Cancer Research (AICR); Dana-Farber Cancer Institute; Duke Comprehensive Cancer Center; Fox Chase Cancer Center; Fred Hutchinson Cancer Research Center; Jonsson Comprehensive Cancer Center (JCCC); M. D. Anderson Cancer Center; Mayo Clinic Cancer Center; Memorial Sloan-Kettering Cancer Center; National Cancer Institute (NCI); National Science Foundation (NSF); Prevent Cancer Foundation; Robert H. Lurie Cancer Center.
u American Institute for Cancer
Research (AICR) Category: Organizations Definition: The American Institute for Cancer Research (AICR) is a private charity that sponsors research into the relationship between diet and cancer and works to disseminate findings about that relationship. History: Before the 1980’s, most cancer research was focused on diagnosis and treatment of the disease. Many scientists believed that cancer operated like a virus that affected cell metabolism, and they focused on early intervention and chemotherapy as their main strategies. The AICR was established in 1982 around the principle that cancer is preventable and that the disease is not random but is affected by lifestyle choices. At the time of its founding, this principle was not widely accepted. Later that same year however, the National Academy of Sciences published a report entitled Diet, Nutrition, and Cancer, and this document became the initial basis for the AICR’s cancer education program. In 1997, the AICR collaborated with the World Cancer
Salem Health: Cancer
American Institute for Cancer Research (AICR)
Research Fund (WCRF), based in the United Kingdom, to publish a 670-page report called Food, Nutrition, and the Prevention of Cancer: A Global Perspective. The report was the work of sixteen scientists from eight countries, who spent three years reviewing studies on diet and cancer. It was developed with participation from experts at the National Cancer Institute and the World Health Organization and was peer-reviewed. The report indicated that between 30 and 40 percent of all cancers could be directly linked to lifestyle choices such as food, drink, exercise, and overall health. The AICR produced more than 30,000 copies of the report and freely distributed it to cancer researchers and politicians. In 1999 the AICR published Stopping Cancer Before It Starts, a book that brought the message of the report to the public. The AICR began to expand more rapidly after the publication of these works. Private donations, the primary source of funding for the organization, increased both in number and size. As of 2007, more than 12 million Americans had made a donation to the organization, which had a total annual revenue exceeding $38 million and had contributed more than $82 million to research projects.
AICR Recommendations for Cancer Prevention
Educating the public: Spreading the message that people can lower their risk of cancer is a major part of the AICR’s program. In 2006, approximately $20 million, over 50 percent of the organization’s annual budget, went to educational activities. One of the ways the AICR fulfills its mission is through a free quarterly newsletter, which the AICR sends to more than 1.5 million homes. The newsletter provides meal-planning suggestions, recipes, and basic nutritional health information. The organization also produces more than seventy brochures, covering a wide array of topics within the subject of nutrition and cancer. Its latest series, The New American Plate, encourages people to fill two-thirds of their plate with fruits, vegetables, and grains, and keep protein to one-third or less. The AICR has also produced public service announcements, which have been carried by hundreds of television stations across the United States. Newspapers and magazines have also been a resource for the AICR. The organization also maintains a Web site and a national nutrition hotline to provide more in-depth information about ways that people can reduce their risk of cancer. The institute also hosts educational seminars and an annual conference. These educational seminars are offered free of charge and presented by registered dieticians. As of 2007, more than 41,000 people had attended a seminar, and they had been offered in more than 133 cities. The AICR annual research conference is becoming a major event in the field of cancer research, as the 2005 con-
• • • •
Eat mostly plant-based foods, limit consumption of red meat (beef, pork, and lamb), and avoid processed meats. Engage in physical activity every day for at least thirty minutes. Maintain a healthy weight throughout life, preferably as lean as possible without being underweight. Do not smoke or chew tobacco.
ference hosted more than four hundred participants and speakers from twenty-five universities and research facilities. Research grants: The AICR works to contribute funding to scientists in the field of cancer research who focus on the connection between cancer and diet. Approximately 14 percent of the annual budget goes to funding proposed research. To decide which proposals to fund, the institute follows a set of grant review process standards, established by the National Cancer Institute. Proposals are reviewed by a panel of experts on the basis of scientific merit. Final decisions about funding are made by the AICR Board of Directors. The AICR Investigator Initiated Grants Program awards up to $75,000 per year for up to two years to be used for research into either diet and cancer or physical activity and cancer. The AICR Post Doctoral Awards Program is intended for less established researchers and provides up to $38,000 per year for up to two years. The AICR also provides matching funds grants. The institute also supports the Marilyn Gentry Fellowship Program at the University of North Carolina at Chapel Hill School for Public Health, department of nutrition. The fellowship is named after AICR president Marilyn Gentry and is intended to support researchers as they transition from postdoctoral work into assistant professorships. Robert Bockstiegel, B.S. u
For Further Information American Institute for Cancer Research. Diet and Health Recommendations for Cancer Prevention: Healthy Living and Lower Cancer Risk. Washington, D.C.: Author, 2006. _______. The New American Plate Cookbook: Recipes for a Healthy Weight and a Healthy Life. Berkeley: University of California Press, 2005. 55
4-Aminobiphenyl Weldon, Glen, ed. Dietary Options for Cancer Survivors: A Guide to Research on Foods, Food Substances, Herbals, and Dietary Regimens That May Influence Cancer. Washington, D.C.: American Institute for Cancer Research, 2002. u
Other Resources
American Institute for Cancer Research http://www.aicr.org American Society of Clinical Oncology Http://www.asco.org Association of American Cancer Institutes http://www.aaci-cancer.org See also American Association for Cancer Research (AACR); American Cancer Society (ACS); Dana-Farber Cancer Institute; Duke Comprehensive Cancer Center; Fox Chase Cancer Center; Fred Hutchinson Cancer Research Center; Jonsson Comprehensive Cancer Center (JCCC); M. D. Anderson Cancer Center; Mayo Clinic Cancer Center; Memorial Sloan-Kettering Cancer Center; National Cancer Institute (NCI); National Science Foundation (NSF); Prevent Cancer Foundation; Robert H. Lurie Cancer Center.
u 4-Aminobiphenyl Category: Carcinogens and suspected carcinogens RoC status: Known human carcinogen since 1980 Also known as: 4-Biphenylamine, p-aminobiphenyl, para-aminobiphenyl, p-aminodiphenyl Related cancers: Bladder cancer, liver cancer Definition: 4-Aminobiphenyl, an aromatic amine, occurs as a colorless to yellowish brown crystalline solid that turns purple in air and has an floral odor. Exposure routes: When heated, 4-aminobiphenyl emits toxic fumes. For the general public, exposure to 4-aminobiphenyl comes from inhalation of tobacco smoke. Occupational exposure occurs from inhalation by laboratory personnel who are doing research with 4-aminobiphenyl. When most of the 4-aminobiphenyl was disposed of by injection into underground wells in the late 1980’s, small amounts of it were released into the air, subjecting some individuals to possible contamination. Where found: 4-Aminobiphenyl is a by-product of tobacco smoke and is found as a contaminant in diphenylamine. Its use is confined to laboratory research, although 56
Salem Health: Cancer it may still be found in some dyes, particularly in cosmetics and drugs that contain yellow dye number 1 and in rubber compounds that were manufactured before the mid1950’s. At risk: Scientists and laboratory technicians who work where 4-aminobiphenyl is used in research as a chemical antioxidant have a high risk for 4-aminobiphenyl contamination. Because 4-aminobiphenyl is generated in tobacco smoke, people who smoke are at high risk for contamination. The general public is at risk for contamination from secondhand tobacco smoke. Etiology and symptoms of associated cancers: Inhalation of 4-aminobiphenyl can produce headaches, lethargy, urinary burning, and blood in the urine (hematuria). When metabolized, it can be activated by liver enzymes to form adducts with blood serum proteins, particularly hemoglobin and albumin. Hemoglobin adducts are associated with an increased risk for liver cancer. In some cases, 4-aminobiphenyl can undergo additional metabolism to form reactive compounds that are transported to the bladder, where they bind to deoxyribonucleic acid (DNA) molecules. In laboratory tests on cultured human cells, 4-aminobiphenyl caused genetic damage that included cell transformation and inhibition of DNA repair. 4-aminobiphenyl can cross the human placenta and has been detected in fetal blood. History: 4-Aminobiphenyl was commercially produced in the United States from the early 1930’s until the mid1950’s. It was used in the detection of sulfates, in the production of azo dyes and yellow-dye stuffs, and as an antioxidant in the production of rubber. There are still a few companies in the United States that manufacture 4-aminobiphenyl for use in laboratory research. Alvin K. Benson, Ph.D. See also Bladder cancer; Cigarettes and cigars; Diethanolamine (DEA); Liver cancers; Tobacco-related cancers.
u Amputation Category: Procedures Definition: Surgical removal of all or part of a limb as a result of peripheral vascular disease, trauma, tumor, infection, or congenital anomaly. Cancers treated: Soft-issue neoplasias (malignant fibrous histiocytoma, fibrosarcoma, rhabdomyosarcoma, synovial sarcoma); bone malignancies (osteosarcoma, chondrosarcoma, adamantinoma, Ewing sarcoma)
Salem Health: Cancer
Amputation
Why performed: Amputations are performed to remove extremities that are severely diseased, injured, or no longer functional. Amputation has five goals: removal of all diseased tissue; relief of pain; proper wound healing; prevention of metastatic spread of tumor cells; and construction of a stump that will permit useful function. Amputation as a musculoskeletal procedure is often accomplished as an alternative to limb salvage and should be considered a reconstructive maneuver. Because of the psychological implications and the alteration of body self-image with amputation, a multidisciplinary team approach should be taken to return the patient to a maximum level of independent function. The process should be considered the first step in the rehabilitation of the patient rather than a failure of treatment. Epidemiologic data on the incidence of amputation in the United States from 1993 to 2003 show that the number of lower-extremity amputations increased 14 percent, from 99,522 to 123,379 cases. Average hospital charge for this procedure increased 40 percent, from $24,332 to $34,046. Nearly two-thirds of amputations are performed in individuals with diabetes, even though these individuals represent only 6 percent of the entire population. Patient preparation: Amputation and subsequent healing depend on several factors, including vascular inflow, nutrition, and an adequate immune system. Prior to surgery, patients should be evaluated regarding these parameters. Patients with malnutrition or immune deficiency have a high rate of wound breakdown or infection. A serum albumin level below 3.5 grams per deciliter (g/dl) indicates a malnourished patient. An absolute lymphocyte count below 1,500 cubic millimeters is a sign of immune deficiency. If possible, amputation should be delayed in patients until these values can be improved by nutritional support. In severely affected patients, nasogastric or percutaneous gastric feeding tubes are necessary. Oxygenated blood is a prerequisite for wound healing. A hemoglobin level of more than 10 g/dl is required. Doppler ultrasonography has been used to measure vascular inflow and to predict the success of wound healing. An absolute Doppler pressure of 70 millimeters of mercury (mm Hg) and an ischemic index of 0.5 or greater are necessary at the surgical site. The transcutaneous partial pressure of oxygen (Tcp02) is now regarded as the gold standard in the measurement of vascular inflow. Values greater than 40 mm Hg correlate with acceptable healing rates. Steps of the procedure: With regard to tumor stage and desired functional outcome, there are a variety of surgical procedures pertaining to upper-limb, lower-extremity, or
Treatment of some cancers involves amputation, which requires the patient to learn new living skills. (Digital Stock)
axial skeletal amputation. Patients with musculoskeletal neoplasms face new choices in treatment with the development of limb salvage techniques and adjuvant chemotherapy and radiation therapy. If an amputation is chosen, then the incision must be planned carefully to achieve the appropriate surgical margin. These surgical margins are characterized by the relationship of the surgical incision to the lesion, to the inflammatory zone surrounding the lesion, and to the anatomic compartment in which the lesion is located. The four types of surgical margins include the following: • intralesional: the surgical incision enters the lesion • marginal: the surgical incision enters the inflammatory zone but not the lesion • wide margin: the incision enters the same anatomic compartment of the lesion but is outside the inflammatory zone • radical: the incision remains outside the anatomic compartment 57
Amyloidosis After the procedure: A variety of wound care methods are used after amputation, including rigid dressings, soft dressings, controlled environment chambers, air splints, and skin traction. The use of an immediate postoperative prosthesis (IPOP) has been shown to be effective in decreasing the time to limb maturation and definitive prosthetic fitting. Rehabilitation and prosthetic fitting remain the primary postoperative goals. Risks: The amputee is at risk for deep vein thrombosis (15 percent) and pulmonary embolism (2 percent). Prolonged postoperative immobilization, stagnation of blood due to ligation of large veins, delayed prosthetic fitting, and inactivity increase the overall risk of thromboembolism (clot). Approximately 80 to 90 percent of amputees experience some episodes of phantom limb pain, which are often severe but infrequent. Other major complications include failure of wound healing, infection, postoperative edema, joint contractures, and dermatological problems such as skin irritation as a result of improper prosthetic fit, breakdown over stump margins, and episodes of contact dermatitis. Results: There is an ongoing controversy when comparing limb salvage to amputation with regard to energy expenditure to ambulate, quality-of-life measures, and the performance of activities of daily living. Studies suggest that functional outcomes are comparable with either limb salvage or amputation. Overall survival remains comparable with either treatment. With some tumors, amputation may achieve better local disease control. Both treatment groups report qualityof-life problems involving employment, health insurance, social isolation, and poor self-esteem. John L. Zeller, M.D., Ph.D. u
For Further Information Bone, M., P. Critchley, and D. Buggy. “Gabapentin in Postamputation Phantom Limb Pain: A Randomized, Double-Blind Placebo-Controlled, Cross-Over Study.” Regional Anesthesia and Pain Medicine 27, no. 5 (2002): 481. Doherty, Gerard M., and Lawrence W. Way, eds. Current Surgical Diagnosis and Treatment. 12th ed. New York: Lange Medical Books/McGraw-Hill, 2006. Menendez, L. R., ed. Orthopaedic Knowledge Update: Musculoskeletal Tumors. Rosemont, Ill.: American Academy of Orthopedic Surgeons, 2002. Peabody, T. D., et al. “Evaluation and Staging of Musculoskeletal Neoplasms.” The Journal of Bone and Joint Surgery: American Volume 80, no. 8 (1998): 1204. Skinner, Harry B., ed. Current Diagnosis and Treatment 58
Salem Health: Cancer in Orthopedics. 4th ed. New York: Lange Medical Books/McGraw-Hill, 2006. u
Other Resources
American Academy of Orthopedic Surgeons http://www.aaos.org American College of Surgeons http://www.acs.org See also Bone cancers; Fibrosarcomas, soft-tissue; Hyperthermic perfusion; Juvenile polyposis syndrome; Limb salvage; Liposarcomas; Lymphangiosarcomas; Mastectomy; Neuroectodermal tumors; Occupational therapy; Orthopedic surgery; Sarcomas, soft-tissue; Surgical oncology; Synovial sarcomas; Veterinary oncology.
u Amyloidosis Category: Diseases, symptoms, and conditions Also known as: AL amyloidosis, immunoglobulin lightchain amyloidosis, primary amyloidosis Related conditions: Multiple myeloma Definition: Amyloidoses are a class of illnesses in which fibrillar protein deposits form throughout the body. Immunoglobulin-related (AL) amyloidosis, a disorder sometimes caused by cancerous antibody-secreting plasma cells, results when misfolded antibody chains form deposits that impair function of the heart, kidneys, and other organs. Risk factors: There are no known risk factors. Etiology and the disease process: In a minority of patients with multiple myeloma, antibody fragments that are produced by malignant plasma cells form insoluble fibrillar protein deposits. Deposits can form in many organs but are most often found in the kidney, heart, liver, and peripheral and autonomous nervous systems. These deposits ultimately lead to death, most commonly via heart disease and renal failure. Incidence: The overall incidence of AL amyloidosis is approximately 1 in 100,000 people per year. Men are more likely than women to develop AL amyloidosis. Approximately 15 percent of patients with multiple myeloma develop AL amyloidosis, but cases of myeloma-associated amyloidosis make up a small fraction of AL amyloidosis cases. Symptoms: Symptoms depend on the organs involved and vary among patients. Common symptoms include periph-
Salem Health: Cancer eral edema, proteinuria, hepatomegaly, hypotension, shortness of breath, irregular heartbeat, purpura, macroglossia, carpal tunnel syndrome, and peripheral neuropathy. Screening and diagnosis: Many amyloidoses are diagnosed by Congo Red staining of tissues biopsied from subcutaneous fat pads, rectal mucosa, bone marrow, or other sources. Once diagnosis of amyloidosis is established, a free light chain blood test is performed to confirm immunoglobulin chains as the cause of amyloid deposits. Treatment and therapy: Current treatments for amyloidosis parallel those used for multiple myeloma. Melphalan plus predisone reduces the number of malignant plasma cells and levels of circulating immunoglobulin light chains. This is often followed by autologous stem cell transplantation, aimed at rebuilding healthy bone marrow. In some patients, treatment results in a temporary resorption of amyloid fibrils and improvement in organ function. The malignant plasma cells are not completely eradicated, however, and remission is the usual course. IDOX (4′deoxy-4′-iododoxorubicin), a drug that binds to amyloid fibrils and promotes their disassembly, has shown promise in early trials. Prognosis, prevention, and outcomes: Prognosis for patients with AL amyloidosis depends on which organs are affected. Patients with cardiac involvement have the worst prognosis, while patients with involvement limited to other organs have longer median survival times. There is no known way to prevent amyloidosis. Kyle J. McQuade, Ph.D. See also Bone marrow transplantation (BMT); Crohn disease; Orbit tumors; Paraneoplastic syndromes; Stem cell transplantation.
Anal cancer
Stage at Diagnosis and Five-Year Relative Survival Rates for Cancer of the Anus, 1996-2004 Stage Localizeda Regionalb Distantc Unstaged
Individuals Diagnosed (%) Survival Rate (%) 49 32 10 10
81.7 61.1 2.8 57.6
Source: Data from National Cancer Institute, Surveillance Epidemiology and End Results, Cancer Stat Fact Sheets, 2008 a Cancer still confined to primary site b Cancer has spread to regional lymph nodes or directly beyond the primary site c Cancer has metastasized
Risk factors: There are several risk factors for anal cancer, including cigarette smoking and anal receptive sexual intercourse. Infection with the human papillomavirus (HPV16), the sexually transmitted disease that causes genital warts, can cause anal squamous intraepithelial lesions (ASIL), which may develop into anal cancer. People with a suppressed immune system from cancer, cancer treatments, organ transplantation, HIV, or AIDS have an increased risk of anal cancer. The number of people with both HIV and anal cancer is rising. Etiology and the disease process: Researchers do not know the exact cause of the genetic changes that make healthy cells turn into anal cancer cells, although multiple risk factors have been identified. The anal cancer cells multiply and form masses or tumors.
Related conditions: Anorectum cancer, anal squamous intraepithelial lesions (ASIL), human papillomavirus (HPV), human immunodeficiency virus (HIV), acquired immunodeficiency syndrome (AIDS)
Incidence: Anal cancer is a rare form of cancer; however, the number of new cases began to increase in the early 1980’s. The incidence of anal cancer is 1 in 100,000 people. New cases in 2007 in the United States were estimated to reach 4,650. Anal cancer occurs more frequently in women than in men. Women are more likely to develop cancer in the anal canal. Men are more likely to develop cancer tumors on the outside of the anus. Anal cancer occurs most frequently in adults in their early sixties, at a median age of sixty-one years.
Definition: Anal cancer is a rare cancer that forms in the anus, which is at the end of the rectum. The anus is about 1.5 inches long and contains sphincter muscles that control bowel movements. Stool passes through the anus as it leaves the body.
Symptoms: Anal cancer may not cause symptoms. Bleeding from the anus is a common early sign. This type of cancer may cause pain, itching, abnormal anal discharge, and changes in the diameter of stools. A mass or growth may develop in the anus. Nearby lymph nodes may
u Anal cancer Category: Diseases, symptoms, and conditions Also known as: Cancer of the anus, anal canal cancer
59
Anal cancer
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be swollen. The anus may feel unusually full. Screening and diagnosis: Screening tests for anal cancer are recommended for people with a high risk of anal cancer. Women should receive anal cancer screening as part of a yearly exam. Annual anal cancer screening is recommended for men after the age of fifty. Anal cancer is diagnosed with a series of tests and procedures. A digital rectal exam (DRE) is used to check for lumps, masses, or growths in the anus. Endoscopy, using an anoscope or rigid protosigmoidoscopy, allows inspection of the interior anal canal. An anoscope is a thin tube with a viewing instrument and light that is inserted into the anus. A protosigmoidoscope is longer and allows sections of the colon to be viewed as well. Ultrasound, computed tomography (CT) scans, positron emission (PET) scans, and magnetic resonance imaging (MRI) scans are used to provide images of the anal structures and to help determine if the cancer has spread. Fine needle aspiration and sentinel lymph node biopsy are used to obtain cells for examination to confirm if cancer is present. Staging is used to identify cancer growth and metastasis, plan treatment, and predict recovery. Fortunately, anal cancer rarely metastasizes. • Stage I: Anal cancer is 2 centimeters (cm) or less. • Stage II: Anal cancer is larger than 2 cm, is confined to the anus, and has not spread beyond the anus. • Stage IIIA: Anal cancer is any size with spread to nearby lymph nodes or close areas, such as the bladder, urethra, or vagina. • Stage IIIB: Anal cancer is any size with spread to nearby lymph nodes and close areas, or it has spread to lymph nodes in the pelvis. • Stage IV: Anal cancer has spread to distant locations in the body. Treatment and therapy: Chemoradiation is the treatment of choice for anal cancer. External radiation, brachytherapy, or both may be used. Chemotherapy 5-FU and Mutamycin (mitomycin) may be used in combination with radiation or surgery. Surgery is used for patients with residual anal cancer and includes local resection or abdominoperineal resection (APR). Prognosis, prevention, and outcomes: Anal cancer screening, HPV testing, HIV testing, quitting smoking, 60
Cancer of the anus. (BSIP/Photo Researchers, Inc.)
knowing the STD status of sexual partners before intercourse, and not participating in anal sex may help prevent anal cancer. Condoms may reduce the risk of HPV and HIV, but they are not a guarantee. HPV vaccination is available for girls and women. Many cases of anal cancer that are detected and treated early can be cured. However, anal cancer may recur even with treatment. It was estimated that 690 men and women with anal cancer would die in the United States in 2007, a rate of 0.2 per 100,000 people. Mary Car-Blanchard, O.T.D., B.S.O.T. u
For Further Information Cranston, R. D., et al. “The Prevalence, and Predictive Value, of Abnormal Anal Cytology to Diagnose Anal Dysplasia in a Population of HIV-Positive Men Who Have Sex with Men.” International Journal of STD and AIDS 18, no. 2 (February, 2007): 77-80. Das, P., C. H. Crane, and J. A. Ajani. “Current Treatment for Localized Anal Carcinoma.” Current Opinions in Oncology 19, no. 4 (July, 2007): 396-400. Meyer, J., B. Czito, F. F. Yin, and C. Willett. “Advanced Radiation Therapy Technologies in the Treatment of Rectal and Anal Cancer: Intensity-Modulated Photon Therapy and Proton Therapy.” Clinical Colorectal Cancer 6, no. 5 (January, 2007): 348-356. Uronis, H. E., and J. C. Bendell. “Anal Cancer: An Overview.” Oncologist 12, no. 5 (May, 2007): 524-534.
Salem Health: Cancer u
Androgen drugs
Other Resources
American Cancer Society How Is Anal Cancer Diagnosed? Http://www.cancer.org/docroot/CRI/content/CRI_ 2_4_3X_How_Is_Anal_Cancer_Diagnosed_47.asp National Cancer Institute Anal Cancer Treatment http://www.cancer.gov/cancertopics/pdq/treatment/ anal/patient See also Abdominoperineal resection (APR); Anoscopy; Colostomy; Computed tomography (CT) scan; Digital rectal exam (DRE); Endoscopy; Gastrointestinal cancers; Gastrointestinal oncology; Infectious cancers; Risks for cancer; Sexuality and cancer; Sigmoidoscopy.
u Androgen drugs Category: Chemotherapy and other drugs ATC code: G03B Definition: Androgens are steroid hormones produced by the adrenal glands and testes or ovaries, responsible for male sex characteristics in the body. Testosterone, an endogenous androgen, is converted to estrogen by the enzyme aromatase. Androgenic agents can be used in the treatment of breast cancer. Cancers treated: Metastatic hormone-responsive breast cancer in postmenopausal women, or in premenopausal women who have undergone ovary ablation Subclasses of this group: Anabolic steroids, alkylated androgens, testosterone esters Delivery routes: Administered orally as tablets or capsules, or by intramuscular injection How these drugs work: Testosterone esters are lipophilic compounds that, when dissolved in oil, are administered via intramuscular injection. Alkylated androgens can be
given orally as their metabolic deactivation is hindered by the alkyl group at the 17α position. The mechanism of action for androgenic agents in breast cancer has not been fully established, though they are believed to block the growth of estrogen-dependent tumors by inhibiting aromatase activity. Older drugs such as calusterone underwent clinical trials in the 1960’s and 1970’s, with response rates of approximately 20 percent. Androgen drugs are not considered first-line therapy for breast cancer, as they are more toxic than other hormonal agents in use and response rates remain low. Androgens, when used, are frequently given in combination with aromatase inhibitors to inhibit the production of estrogen in vivo. Side effects: Androgens are male sex hormones and can cause masculinizing effects in women, including deepening voice, hirsutism, acne, and clitoral enlargement. Alkylated androgens are less potent than testosterone and hence possess a lower risk of these side effects, but liver toxicity, cholestatic hepatitis, and jaundice can occur at relatively low doses. Androgen therapy should be discontinued following abnormal liver function tests until the cause has been determined. Androgen therapy in patients with preexisting cardiac, renal, or hepatic disease increases the risk of edema and progression to congestive heart failure. In such cases, dosing should be discontinued and administration of a diuretic considered. Breast cancer patients undergoing androgen therapy are at increased risk of bone breakdown and reabsorption, leading to hypercalcemia. If this occurs, then drug therapy should be discontinued and the patient evaluated, as hypercalcemia may also indicate the progression of bone metastases. Karen M. Nagel, Ph.D. See also Amenorrhea; Antiandrogens; Appetite loss; Bisphenol A (BPA); Breast cancer in men; Chemoprevention; Endocrine cancers; Fanconi anemia; Granulosa cell tumors; Hormonal therapies; Myelofibrosis; Receptor analysis; Tumor flare.
Androgen Drugs for Breast Cancer Treatment Drug
Brands
Subclass
Delivery Mode
Testolactone Testosterone enanthate Fluoxymesterone Methyltestosterone
Teslac Delatestryl Androxy, Halotestin, Ora-Testrylm Android-F, Hysterone Tested, Virilon, Android-10, Methitest
Anabolic steroid Testosterone ester Alkylated androgen Alkylated androgen
Oral Intramuscular Oral Oral
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Anemia
Salem Health: Cancer
u Anemia Category: Diseases, symptoms, and conditions Also known as: Low red blood cell count, erythropenia, iron-poor blood Related conditions: Cytopenia Definition: Anemia is a low number of red blood cells, decreased volume of red blood cells, or a reduced concentration of hemoglobin. Risk factors: For anemia of cancer, risk is associated with the type of cancer, stage of disease, and treatment regimen. Etiology and the disease process: Anemia may be caused by deficiencies of vitamin B12, folic acid, or iron; antibody formation; kidney failure; lead poisoning; bone-marrow dysfunction; chemotherapy; or radiation therapy. It can also result from infiltration of bone marrow by leukemia or lymphomas or from internal bleeding or excessive blood loss from repeated blood sampling. Anemias caused by deficiencies in folic acid, vitamin
B12, and iron are generally known as nutritional anemias. In these forms of anemia, the endogenous hormone erythropoietin, responsible for red blood cell production, appears to be present in adequate amounts. Patients with cancer, however, can be anemic because of deficiencies in these nutrients. The anemia of cancer, a subset of anemia of chronic disease, is marked by reduction in the amount of the hormone erythropoietin found in the circulation, suppression of bone marrow function, disturbances in iron metabolism, and activation of the inflammatory and immune systems in response to the insult of cancer that activates hormones, which in turn decrease the production of endogenous erythropoietin. Another form of anemia is aplastic anemia, which may be caused by chemotherapy, radiation therapy, or drugs. In the normal state of health, endogenous erythropoietin is released by peritubular cells in the kidney cortex when specialized cells sense hypoxia (low oxygen content of the blood). In the bone marrow, erythropoietin stimulates the proliferation and differentiation of primitive cells (that is, progenitor cells) that will mature and differentiate
Numerous types of anemia exist.
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Anemia
into red blood cells. As the cells mature and differentiate, they synthesize hemoglobin, the iron-containing pigment that is responsible for carrying oxygen to all cells in the body and carrying carbon dioxide away from cells.
sions. In cases of severe anemia, however, transfusions are routinely used because it takes several days for the erythropoiesis-stimulating proteins to increase red blood cell count and hemoglobin concentration.
Incidence: It is estimated that the frequency of severe anemia, marked by a hemoglobin concentration less than 8 grams per deciliter (g/dl) across a broad range of cancers, is 5 to 20 percent, and that of mild anemia, marked by a hemoglobin concentration of 8 to 11 g/dl, is 25 to 45 percent.
Prognosis, prevention, and outcomes: The prognosis for anemia depends greatly on the type of anemia. For anemia of cancer, anemia may be directly related to prognosis and survival. Research suggests that it may be important to maintain hemoglobin concentration at a high level to decrease the effects of hypoxia, especially during treatment. Because chemotherapy and radiation therapy target rapidly dividing cells, both cancer cells and bone marrow cells, it is difficult to prevent anemia due to treatment without reducing the efficacy of treatments. Also, the anemia of cancer involves endogenous inflammatory and immune functions, which cannot be prevented. Proper nutrition may be useful in preventing anemia caused by deficiencies in folic acid, iron, and vitamin B12. MaryAnn Foote, M.S., Ph.D.
Symptoms: Symptoms of anemia can include fatigue, pale skin (including nail beds and the lining of the eyelids), dizziness, chills, shortness of breath, rapid pulse, and chest pains. Screening and diagnosis: A blood test can measure the hemoglobin concentration, or hematocrit; hemoglobin concentration is generally used, as it is more accurate than hematocrit. Other tests that are often done at the same time are red blood cell indices, which include red blood cell count, mean corpuscular volume (MCV), mean corpuscular hemoglobin concentration (MCHC), and mean corpuscular hemoglobin (MCH). Iron parameters, which include serum iron, total iron-binding capacity, percent transferrin saturation, and serum ferritin, are measured. A test for occult blood in the stool as a possible source of blood loss is often done, particularly in the setting of gastrointestinal cancers. A normal red blood cell count is 3.5 to 5.0 × 1012/liter for women and 4.3 to 5.9 × 1012/liter for men. Hematocrit, the measure of the volume of red blood cells as a percentage of the total blood volume, is 37 to 47 percent for women and 45 to 57 percent for men. Normal concentration of hemoglobin is 14 to 17.5 g/dl for men and 12 to 16 g/dl for women. Treatment and therapy: While anemia of cancer can be treated with transfusions of packed red blood cells, the standard of care at most cancer treatment centers is the use of recombinant human erythropoiesis-stimulating proteins such as epoietin alfa (Epogen or Procrit) or darbepoietin alfa (Aranesp). The recombinant human erythropoiesisstimulating proteins are given as injections three times a week to once every three weeks depending on the patient’s needs and type of recombinant protein used. The use of these recombinant proteins allows oncologists the option of not using red blood cell transfusions, with their small but inherent risks of autoimmunization and infection. The possibility of failure of bone marrow or stem cell transplantation increases with the number of previous transfu-
u
For Further Information Crawford, C., et al. “Relationship Between Changes in Hemoglobin Level and Quality of Life During Chemotherapy in Anemic Cancer Patients Receiving Erythropoietin Therapy.” Cancer 95 (2002): 888-895. Molineux, G., M. A. Foote, and S. G. Elliott, eds. Erythropoietins and Erythropoiesis: Molecular, Cellular, Preclinical, and Clinical Biology. Basel, Switzerland: Birkhäuser, 2003.
u
Other Resources
Anemia.com http://www.anemia.com MedlinePlus Anemia http://www.nlm.nih.gov/medlineplus/anemia.html See also Acute lymphocytic leukemia (ALL); Acute myelocytic leukemia (AML); Angiogenesis inhibitors; Antifungal therapies; Aplastic anemia; Blood cancers; Bone marrow transplantation (BMT); Chronic lymphocytic leukemia (CLL); Chronic myeloid leukemia (CML); Colony-stimulating factors (CSFs); Fanconi anemia; Hairy cell leukemia; Hematologic oncology; Hemolytic anemia; Stem cell transplantation; Thrombocytopenia; Transfusion therapy; Waldenström macroglobulinemia (WM); Young adult cancers. 63
Angiogenesis
u Angiogenesis Category: Cancer biology Also known as: Blood vessel formation Definition: Angiogenesis is the formation of new blood vessels. It is a perfectly normal process in a developing or growing body, and during a woman’s reproductive years, it enables the menses and pregnancy. In addition, angiogenesis maintains health by developing a new blood supply in injured tissue, controlling inflammation, and even healing fractures of the bone. In health, the body controls angiogenesis, but in cancer, the body loses control. Angiogenesis is thought to be a process by which a cancer obtains its blood supply from its host. Without vascularization—the provision of blood vessels—no tissue in the body can live. Nearly every cancer known is associated with pathological angiogenesis. Relation of angiogenesis to cancer. In one way, a cancerous tumor is like any other bodily structure: Its survival de-
Tumor angiogenesis. (©ISM/Phototake—All rights reserved)
64
Salem Health: Cancer pends on the provision of oxygen and nutrients and the removal of waste. Cancerous tumors differ from normal tissue in that they tend to spread, or metastasize, without regard to normal borders between different tissues such as muscle, cartilage, and bone. Blood supply to a tumor enables it to spread. For its support and ability to grow, in effect the cancer must persuade the body to build vessels to and throughout the tumor, something that seems counterintuitive. In fact, the body contains defenses against this. As cancer develops, however, these defenses are short-circuited. The way the tumor fools its host into cooperation is chemically—with proteins and enzymes found naturally in the body but used by the tumor to its advantage. Proteins that induce growth are known as growth factors. Researchers have shown evidence that one chemical secreted by tumors, vascular endothelial growth factor (VEGF), in effect attracts blood vessels. Induced by growth factors and possibly hormones, new blood vessels actually sprout from existing vascular tracts into and around the cancer. Researchers also report that breast cancer cells produce interleukin-8 (IL-8), a protein that normally attracts white blood cells to injuries and inflammation, but which is also known to be angiogenic. Other researchers, exploring the role of certain enzymes in regulating angiogenesis in breast cancer, are focusing on the extracellular matrix, noncellular material that surrounds any tissue (picture the stuffing around mattress springs) and common not only to normal tissues but also to tumor cells. In addition to taking up space between cells (including cartilage, tendon, ligament, and bone), the extracellular matrix performs a critical function. Under normal circumstances after adulthood, the extracellular matrix prevents unauthorized (non-injury-related) angiogenesis and cell movement. Cancer short-circuits that inhibitory function. Compared with normal breast cells, some breast cancer cells have higher levels of two enzymes that degrade heparin, an important component of the extracellular matrix. A weakened and degraded extracellular matrix might well enable abnormal cell movement and angiogenesis. Not every researcher, however, is convinced that tumors depend on angiogenesis. Citing the “immature” vasculature of some tumors—meaning that the blood vessels are not as well organized as in normal body tissues— and the lack of consistent evidence from clinical trials, they question cancer’s angiogenesis dependency. Those who support the connection counter that cancer growth is by its very nature not only disorganized—it is growing a tumor rather than a kidney or a pancreas—but also, relative to other tissues, new in origin. Because cancer’s
Salem Health: Cancer
Angiogenesis
Known Angiogenic Growth Factors
• • • • • • • • • • •
Angiogenin Angiopoietin-1 Del-1 Fibroblast growth factors: acidic (aFGF) and basic (bFGF) Follistatin Granulocyte colony-stimulating factor (G-CSF) Hepatocyte growth factor (HGF) /scatter factor (SF) Interleukin-8 (IL-8) Leptin Midkine Placental growth factor
• • • • • • • • •
Platelet-derived endothelial cell growth factor (PD-ECGF) Platelet-derived growth factor-BB (PDGF-BB) Pleiotrophin (PTN) Progranulin Proliferin Transforming growth factor-alpha (TGF-alpha) Transforming growth factor-beta (TGF-beta) Tumor necrosis factor-alpha (TNF-alpha) Vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF)
Source: The Angiogenesis Foundation
growth, unlike that of healthy tissue, is continual, its vasculature might be expected to remain immature. Preventing cancer-related angiogenesis: If tumors do require angiogenesis to survive and spread, then it seems logical to discourage angiogenesis. Inhibitors of angiogenesis were first discovered in 1975 and since then have been detected in such diverse natural sources as tree bark, green tea, fungi, shark cartilage and muscle, sea coral, and various herbs. Ways to prevent or change the process of angiogenesis being investigated include blocking the chemical signals from the tumor, making these signals less effective; preventing the breaching of the extracellular matrix; and after a tumor has already been supplied with blood vessels, causing the vessels to normalize, or stop supplying the tumor. Another area being researched targets oncogenes, genes that cause normal cells to become cancerous and also, it is believed, activate the angiogenesis switch. Researchers are developing antioncogene drugs. Angiogenesis inhibitors, while promising, have yet to be proven as efficacious treatments, in part because of the complexity and diversity of the tumors themselves. What works for one tumor may not work for another. Another complication of agents that inhibit angiogenesis is the chaos they could produce in inflammation control and healing. Nevertheless, the possibility of inhibiting angiogenesis only where it is needed, with very targeted inhibitors and perhaps with the assistance of other drugs such as paclitaxel (Taxol) and cyclophosphamide (Cytoxan, Neosar) and such COX-2 inhibitors as celecoxib (Celebrex) and thalidomide, all of which interfere with angiogenesis, remains an attractive investigative path. Research and clinical trials are ongoing. Jackie Dial, Ph.D.
u
For Further Information Chan, David. Breast Cancer: Real Questions, Real Answers. New York: Marlowe & Company, 2006. Firedewald, Vincent, M. D. Buzdar, and Michael Bokulich. Ask the Doctor: Breast Cancer. Kansas City, Mo.: Andrews McMeel, 1997. Link, John. Breast Cancer Survival Manual: A Step-byStep Guide for the Woman with Newly Diagnosed Breast Cancer. 4th ed. New York: Holt, 2007.
u
Other Resources
American Cancer Society http://www.cancer.org Angiogenesis Foundation About Angiogenesis http://www.angio.org/understanding/ understanding.html MayoClinic.com Angiogenesis Inhibitors: New Cancer Drugs Stop Tumor Growth http://www.mayoclinic.com/health/angiogenesis/ CA00079 National Breast Cancer Foundation http://www.nationalbreastcancer.org See also Angiogenesis inhibitors; Bioflavonoids; Biological therapy; BRAF gene; Bronchoalveolar lung cancer; Cancer biology; Cartilage supplements; Chemotherapy; Gene therapy; Genetics of cancer; Hereditary leiomyomatosis and renal cell cancer (HLRCC); HIV/AIDS-related cancers; Human growth factors and tumor growth; Im65
Angiogenesis inhibitors munotherapy; Kidney cancer; Matrix metalloproteinase inhibitors; Oral and oropharyngeal cancers; Phenolics; Robert H. Lurie Cancer Center; Sarcomas, soft-tissue.
u Angiogenesis inhibitors Category: Chemotherapy and other drugs Definition: Angiogenesis inhibitors prevent the formation of new blood capillaries formed by the process called angiogenesis. As a result, cancer tumors are starved and die. Cancers treated: Multiple myeloma, mantle cell lymphoma, metastatic colorectal cancer, advanced renal cancer, gastrointestinal stromal tumors Delivery routes: Delivered intravenously on an inpatient basis (Velcade, Avastin) or orally in tablet (Sutent, Nexavar) and capsule (Thalomid) forms on an at-home basis How these drugs work: Angiogenesis is critical to normal growth, providing a network of new blood capillaries
Salem Health: Cancer that deliver oxygen and nutrients to developing tissues. Once formed, capillaries do not increase in size or number, because the endothelial cells that line them do not divide. In some normal conditions (wound repair, menstruation), however, they do. Tumors require a constant supply of newly formed blood capillaries in order to grow. Early in the angiogenesis process, tumors secrete “growth factors,” which signal the endothelial cells to proliferate. The new capillaries attach themselves to the tumor and deliver oxygen and nutrients. This blood supply also allows tumor cells to spread to other areas of the body (metastasize), a process that is a major cause of cancer deaths. Some scientists have long hypothesized that attacking angiogenesis might be a powerful tool in preventing tumor growth. Removing the blood supply might prevent the growth of new tumor cells and cause the tumors to grow more slowly or become smaller. In 1971, Dr. Judah Folkman, of Children’s Hospital in Boston, published a paper proposing the hypothesis that all tumor growth is angiogenesis-dependent. This founded the field of angiogenesis research and its control, a field of investigation that is now studied by many scientists.
A mouse with lung cancer, left, was treated with angiogenesis inhibitors in an experiment by Judah Folkman. Twelve days later, the tumor in the mouse, right, showed substantial improvement. (AP/Wide World Photos)
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Salem Health: Cancer
Angiogenesis inhibitors
Angiogenesis Inhibitors Drug
Brands
Subclass
Delivery Mode
Cancers Treated
Bevacizumab
Avastin
Monoclonal antibody
IV
Metastatic colorectal cancer
Bortezomib
Velcade
Dipeptide boronic acid analogue
IV
Multiple myeloma, mantle cell lymphoma
Sorafenib tosylate
Nexavar
Bi aryl urea
Oral
Advanced renal cell carcinoma
Sunitinib malate
Sutent
Malate salt of an indolinone-based tyrosine kinase inhibitor
Oral
Advanced kidney cancer, gastrointestinal stromal tumors
Thalidomide
Thalomid
Glutamic acid derivative
Oral
Multiple myeloma
In December, 2006, the United States’ National Cancer Institute (NCI) listed thirty angiogenesis inhibitors undergoing clinical trials. By 2007, the U.S. Food and Drug Administration (FDA) had approved five angiogenesis inhibitors for use in cancer treatment: Velcade, Avastin, Nexavar, Sutent, and Thalomid. Velcade was approved in 2003 for the treatment of multiple myeloma patients who had received at least two prior therapies with anticancer drugs and had demonstrated disease progression on the last therapy. It was approved in 2005 for multiple myeloma patients who had received one prior therapy and in 2006 for mantle cell lymphoma in patients who had received one prior therapy. Velcade interrupts various cell-signaling pathways critical to angiogenesis. Avastin was approved in 2004 to treat metastatic colorectal cancer. It is believed to act by attaching to a protein growth factor active in angiogenesis. When the growth factor is bound to Avastin, it cannot carry out its function in the angiogenesis process. Avastin enhances the effects of standard chemotherapy but does not appear to be effective when given alone to patients with colorectal cancer. Nexavar was approved in 2005 to treat adults with advanced renal cell carcinoma, an aggressive form of the disease and the most common of kidney cancers. It has not been studied in children. Nexavar is a small molecule, and as such, it enters endothelial cells and inhibits enzymes involved in intercellular signaling linked to cell division; it also acts by binding to vascular endothelial growth factor. Sutent was approved in 2006 for the treatment of gastrointestinal stromal tumors and advanced kidney cancer. Sutent is also a small molecule that enters tumor cells and prevents angiogenesis and cell proliferation by blocking the signaling activity of several growth factors. Thalomid (thalidomide) was approved in 2006 for the treatment of newly diagnosed multiple myeloma, in combination with the chemotherapy drug dexamethasone.
Thalidomide’s activity depends on its ability to block the growth factor signals necessary for angiogenesis. In 1994, Folkman and coworkers published a paper providing evidence that thalidomide is an angiogenesis inhibitor. Its ability to block the development of new blood vessels likely caused the limb malformations in babies of mothers who took the drug as a sedative during pregnancy. Both men and women taking the drug for cancer treatment are required to use contraception to avoid pregnancy. Side effects: The side effects of angiogenesis inhibitors depend on the medication. Some of the more common angiogenesis inhibitors have the following side effects: • Velcade: Fatigue, nausea, diarrhea, anorexia, constipation, thrombocytopenia, peripheral neuropathy, pyrexia, vomiting, and anemia • Avastin: High blood pressure, fatigue, blood clots, diarrhea, decreased white blood cells, headache, appetite loss, and mouth sores • Nexavar: Rash, diarrhea, high blood pressure, and redness, pain, swelling, or blisters on the palms of the hands or soles of the feet • Sutent: Diarrhea, skin discoloration, mouth irritation, weakness, altered taste, fatigue, high blood pressure, bleeding, swelling, and hypothyroidism • Thalomid: Somnolence, constipation, neuropathy, venous thromboembolism, and rash Bernard Jacobson, Ph.D. u
For Further Information D’Amato, R. J., M. S. Loughnan, E. Flynn, and J. Folkman. “Thalidomide Is an Inhibitor of Angiogenesis.” Proceedings of the National Academy of Sciences 91 (1994): 4082-4085. Davis, D. W., R. S. Herbst, and J. L. Abbruzzese, eds. Antiangiogenic Cancer Therapy. New York: CRC Press, 2007. 67
Angiography Folkman, J. “Tumor Angiogenesis: Therapeutic Implications.” New England Journal of Medicine 285 (1971): 1182-1186. Forough, R., ed. New Frontiers in Angiogenesis. New York: Springer, 2006. Sieman, D. W., ed. Vascular-Targeted Therapies in Oncology. Hoboken, N.J.: Wiley, 2006. Skinard, E. T., ed. New Research on Angiogenesis Inhibitors. Hauppage, N.Y.: Nova Science, 2006. u
Other Resources
Food and Drug Administration http://www.fda.gov National Cancer Institute Drug Information Summaries http://www.cancer.gov/cancertopics/druginfo/ alphalist See also Angiogenesis; Biological therapy; Chemotherapy; Oral and oropharyngeal cancers; Sarcomas, softtissue.
u Angiography Category: Procedures Also known as: Arteriography, angiogram, arteriogram Definition: Angiography is a general term for a minimally invasive imaging technique that uses real-time X rays and a special dye to see inside blood vessels, lymph nodes, and certain glands deep inside the body. The dye, known as a contrast medium, is injected into the body to highlight the vessels, lymph nodes, glands—and cancerous tumors— and make them easier to see. The contrast medium is a low-dose radioactive compound known as a radioisotope. The image created by the X ray is called an angiogram. Cancers diagnosed or treated: Cancers of the lymphatic system, the digestive system, the lungs, the brain, and certain glands Why performed: Doctors use angiography to detect and directly examine cancerous tumors and to show the blood flow to a tumor. A direct real-time view of a tumor and blood flow helps doctors diagnose and treat the cancer. With angiography, doctors can determine a tumor’s size, appearance, and relationship to nearby organs and tissues; whether the tumor is growing or extending into nearby parts of the body; and whether cancer cells are spreading to other parts of the body. In some cases, doctors use the procedure to deliver medicine to a tumor. 68
Salem Health: Cancer Patient preparation: Patient preparation varies slightly depending on the part of the body to be examined and whether the patient is already in the hospital (inpatient) or having the procedure done and then returning home the same day (outpatient). Nurses help the inpatient prepare. Outpatients stay several hours in a recovery room before going home. Most outpatients receive a mild sedative to help them relax during the procedure. The test may take up to several hours. Generally, patients should not eat or drink anything for eight hours before the procedure. Patients should tell their doctors if they are pregnant or breast-feeding; which medications they are taking, including aspirin; if they have any bleeding problems or are taking blood-thinning medications; if they have allergies to any substances or medications; if they suffer from asthma; if they have a history of kidney problems or diabetes; if they have blockage of the blood vessels caused by atherosclerosis (hardening of the arteries), high blood pressure, or aging; and if they think they will find it difficult to lie still during the procedure. Steps of the procedure: A team of technicians and nurses led by a radiologist (a doctor who diagnoses diseases by studying X rays and other images) conducts the procedure. The procedure takes place in the radiology laboratory of a medical center. The patient wears a hospital gown and receives a mild sedative but remains awake. The patient lies supine on a table much like an operating table. The surgeon makes a small incision near a blood vessel in the neck, chest, groin, or arm. Using real-time X rays displayed on a video screen for guidance, the surgeon then inserts a thin, flexible tube called a catheter into the vessel. The surgeon guides the catheter through the blood vessels until the tip reaches the area to be studied. Once the catheter is placed in the exact spot, the radiologist injects the dye. The dye travels through the catheter and to the blood vessels, making the target easier to see in the X ray. A round cylinder or rectangular box, known as a fluoroscope, takes the pictures. It moves both above and beneath the patient. After the procedure: After the test, a nurse applies a pressure bandage at the site where the catheter was inserted. Some patients feel tenderness or soreness at the site. Depending on where the catheter was inserted, the patient may have to remain in bed—in the hospital or at home— from several hours up to a day. The patient receives pain medicine if needed. Some people experience a headache, flushing of the face, or a salty or metallic taste in the mouth after the dye is inserted, but these feelings disappear quickly. Doctors generally recommend that patients drink extra fluids to help pass the dye from the body.
Salem Health: Cancer
Angiosarcomas
Risks: Angiography is a very common test. Both the X ray and the dye are safe. The exposure to radiation is low. There are, nevertheless, some small risks. There is a remote chance that a person may react to the contrast agent, or dye. Common contrast agents are iodine, barium, and gadolinium. In addition, patients may feel a slight burning sensation when the doctor injects the dye or some discomfort at the site where the catheter is inserted. Patients do not feel the catheter inside the body. There is a small risk of bleeding, pain, or infection at the site where the catheter is inserted. Results: The angiogram shows that there are no problems if the dye flows smoothly through the blood vessels and no tumors appear in the lymph nodes or glands studied. If the angiogram reveals that blood vessels are not in their normal position or the blood is flowing in an abnormal pattern, then a tumor may be present. Doctors will then conduct additional tests. Wendell Anderson, B.A. u
For Further Information Icon Health. Angiogram: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. San Diego, Calif.: Author, 2004.
Pagana, Kathleen Deska, and Timothy J. Pagana. Mosby’s Manual of Diagnostic and Laboratory Tests. 3d ed. St. Louis: Mosby Elsevier, 2006. Welch, H. G. Should I Be Tested for Cancer? Maybe Not and Here’s Why. Berkeley: University of California Press, 2004. See also Bile duct cancer; Chemoembolization; Embolization; Endocrinology oncology; Exenteration; Eye cancers; Gallbladder cancer; Hemangioblastomas; Hematemesis; Hemoptysis; Imaging tests; Lymphadenectomy; Lymphangiography; Pancreatic cancers; Percutaneous transhepatic cholangiography (PTHC); Testicular cancer; X-ray tests.
u Angiosarcomas Category: Diseases, symptoms, and conditions Related conditions: Soft-tissue malignancy Definition: Angiosarcomas are cancers that develop from blood vessels. Although the most common sites where they occur are the arms, legs, neck, and head, these tumors can occur anywhere on the body, most frequently on the skin or in the soft tissue. Angiosarcomas are made up of
An angiosarcoma on the knee. (©Lester V. Bergman/Corbis)
69
Anoscopy malignant cells that are rapidly proliferating and capable of extensive infiltration. Risk factors: Some risk factors have been linked with the development of angiosarcoma. Primarily, these include previous exposure to radiation therapy or chemotherapy, as well as exposure to carcinogens such as certain polyester fibers or bone wax. Etiology and the disease process: In many cases, angiosarcoma develops as a complication of a preexisting condition. For example, a radical mastectomy can lead to the development of an angiosarcoma in the soft tissue and skin of the breast. Additionally, foreign materials in the body, such as shrapnel, have resulted in angiosarcomas. Incidence: Angiosarcoma is a very rare tumor type, occurring in only 2 to 3 patients out of 1 million individuals. Nearly half of all angiosarcomas develop in the head and neck regions, but they also can occur in the soft tissue of the lower and upper extremities. Least common of all angiosarcomas are those that occur in other areas of soft tissue, such as the breast, kidney, and liver. Symptoms: Angiosarcomas in the soft tissues of the extremities may be identified as growing masses, while those that occur on the skin generally appear as blue or black nodules. Angiosarcomas that develop in other areas of soft tissue, especially within the abdominal cavity, are capable of growing quite large and often are not diagnosed until the size of the tumor begins to affect the surrounding tissues and organs. Screening and diagnosis: Diagnosis occurs by recognizing the abnormal growths within the skin or extremities of the patient. Angiosarcomas within the abdominal cavity may remain undiagnosed until related symptoms become apparent, such as neuronal symptoms occurring from compression of the lumbar or pelvic nerves. Treatment and therapy: Surgery and radiation therapy are common methods to treat angiosarcomas. Depending on the location, chemotherapy may also be used in combination with these other strategies. The most common chemotherapeutic agent to treat angiosarcoma is Adriamycin (doxorubicin). Prognosis, prevention, and outcomes: Angiosarcomas are aggressive tumors that have a tendency to spread rapidly and frequently reoccur, even after treatment. The reported five-year survival rate for these patients is only 20 percent. Lisa M. Cockrell, B.S. 70
Salem Health: Cancer See also Accelerated partial breast irradiation (APBI); Endotheliomas; Fibrosarcomas, soft-tissue; Hemangiosarcomas; Liver cancers; Lymphangiosarcomas; Sarcomas, soft-tissue; Veterinary oncology.
u Anoscopy Category: Procedures Definition: Anoscopy is the examination of the anus, anal canal, and lower end of the rectum with an endoscope. Cancers diagnosed: Anal cancer, rectal cancer, cancer of an unknown primary site Why performed: Anoscopy is a diagnostic procedure to evaluate the presence of hemorrhoids, anal fissures, abscess, inflammation, tumors (malignant and benign), foreign bodies, infection such as condyloma or warts caused by human papillomaviruses (HPV), and anal squamous skin lesions associated with the human immunodeficiency virus (HIV). Patient preparation: The patient is instructed to clear stool from the rectal vault. A laxative, enema, or other preparation may be necessary for complete emptying of the rectum. For pediatric patients, their parents should be counseled on proper preparations for the procedure so that the patients’ anxiety may be reduced. In emergency cases, preparation for the procedure may not be possible. Steps of the procedure: The patient is asked to use a medical examination gown and to remove underwear. The position during the examination is either bending forward over the examining table or lying on the examination table on the patient’s left or right side with both lower limbs drawn up to the chest. The doctor performs a digital rectal examination wherein a gloved, lubricated index finger is inserted into the rectum to check for abnormalities and structures that can block visualization; the prostate is also examined in male patients. The external area of the anus is examined prior to the anoscope insertion. The doctor then uses the anoscope, a tubular instrument with a light source, to view the anus, anal canal, and lower rectum. The anoscope is lubricated prior to its insertion into the anus and anal canal; the patient may be asked to “bear down” during the insertion, as during a bowel movement. During the procedure, the patient may feel some pressure and the urge to defecate. A biopsy may be obtained during the procedure, as needed. The doctor slowly withdraws the anoscope as the anal canal is viewed carefully.
Salem Health: Cancer After the procedure: Patients can return to normal activities. If a biopsy was taken, then the patient may be instructed to have a sitz bath daily to relieve mild pain. Risks: No significant risk is associated with anoscopy. A small amount of bleeding and mild pain may occur if the patient has hemorrhoids or if a biopsy was obtained. Results: Normal results will show no structural or color abnormalities. Abnormal findings include hemorrhoids, fissures, infections, abscess, inflammation, or tumors. Miriam E. Schwartz, M.D., M.A., Ph.D., and Colm A. Ó’Moráin, M.A., M.D., M.Sc., D.Sc. See also Anal cancer; Hemorrhoids.
u Anthraquinones Categories: Complementary and alternative therapies; chemotherapy and other drugs Definition: Anthraquinones form a group of anticancer agents derived from plant products. Anthraquinones naturally occur in some plants, such as aloe, senna, rhubarb, Cascara buckthorn, and sheep sorrel. Indian rhubarb root (Rheum palmatum) contains several anthraquinones. Sheep sorrel (Rumex acetosella) contains several types of anthraquinones. Subclasses of this group are emodin, aloe emodin, and anthraquionone derivatives. A number of conventional chemotherapeutic agents, such as Adriamycin (doxorubicin), are derivatives of anthraquinones. Cancers treated or prevented: Prostate cancer, breast cancer, non-Hodgkin lymphoma, acute leukemia Delivery routes: Anthraquionones are typically consumed as a mixture of several botanicals, such as in a tea, although intravenous administration has been used in the past. How these drugs work: Anthraquionones are ingredients in herbal mixtures such as Essiac or Flor-Essence that are typically consumed as a tea. The primary herbs in these botanical mixtures, rhubarb and sheep sorrel, are thought to contain anthraquionones. Such herbal extracts have been in use as a cancer treatment since the 1920’s, when they were popularized by a Canadian nurse, Rene Caisse, who obtained the recipe from a woman who claimed that it cured her breast cancer. Caisse opened a clinic and treated patients for more than forty years. After her death, researchers at Memorial Sloan-Kettering in New York tested her product, with inconclusive results. Anthraquionones are alleged to have anti-inflamma-
Anthrax tory effects and cytotoxic effects against tumor cells. Proponents claim that they strengthen the immune system, reduce tumor size, and improve and prolong the lives of people with many types of cancer. Although they have been shown to have tumor inhibition properties, they have been shown to stimulate tumor cell growth as well. Anthraquinones have been shown to stimulate various cytokines that are important in tumor cell defense, including IL-1, IL-6, and TNF. In experimental settings, anthraquinones have been shown to potentiate the action of Adriamycin (doxorubicin), a widely used chemotherapy drug, but the clinical significance of this action is unknown. Anthraquionone derivatives, such as Adriamycin and mitoxantrone, have been shown to be effective as chemotherapeutics. Side effects: Natural anthraquinones and their derivatives have laxative properties. Therefore, a side effect associated with anthraquionones is diarrhea as well as hyperkalemia as a result of chronic diarrhea. They have also been reported to cause nausea, vomiting, and contact dermatitis. A principal danger of this and other unconventional therapies is that they may delay diagnosis and conventional treatment of serious disease. C. J. Walsh, Ph.D. See also Essiac; Green tea; Herbs as antioxidants.
u Anthrax Category: Chemotherapy and other drugs Definition: Anthrax (from the Greek word for coal, anthrako, for the characteristic black skin lesions seen in cutaneous anthrax) is an often fatal infectious disease caused by the bacterium Bacillus anthracis. This bacterium is particularly virulent because it is surrounded by a coating that prevents the immune system from killing it and it secretes a toxin lethal to certain white blood cells (macrophages). Anthrax toxin, the key virulent component of B. anthracis, is currently being studied for use as targeted biological therapy for drug-resistant tumors. B. anthracis is sensitive to a number of antibiotics, including doxicyclin, and fluoroquinolones. Most people, however, do not have preexisting immunity to anthrax because it is not a routine immunization—with the exception of some U.S. military personnel. Cancers treated: Melanoma, breast cancer, colon cancer Delivery routes: Injection 71
Antiandrogens
Salem Health: Cancer
How this substance works: Anthrax infection begins when the spores of the bacteria are inhaled or come into contact with the skin. Anthrax toxin, produced by the bacteria, is the primary virulent factor. The toxin is activated by furin, a protein found in all living cells. Anthrax toxin may be genetically engineered to eschew furin and instead target only cells with high levels of urokinase, a protein produced prolifically by human tumor cells. The anthrax toxin contains three proteins that are innocuous when separate but work together to create a lethal environment for cells. Protective antigen (PA) is an anthrax protein that adheres to a host cell surface and bores a hole into it. The other A number of Bacillus anthracis bacteria. (Centers for Disease Control and Prevention) two proteins released by the bacteria, edema factor (EF) and lethal factor (LF), are too large to penetrate the outside of the cell unblocking the effect of androgens, which are hormones reless PA chaperones them inside. For cellular intoxication, quired for the development and survival of both normal PA is always needed; once inside the cell, only EF or LF is and cancerous prostate cells. needed to speed up the reactions that ultimately lead to rendering inactive parts of the immune system and finally Cancers treated: Prostate cancer to cell suicide (apoptosis). The term “anthrax lethal toxin,” Subclasses of this group: Nonsteroidal antiandrogens when used in cancer therapy research, refers to the combiand synthetic steroids nation of PA and LF. PA is the substance in the anthrax vaccine. Delivery routes: Administered orally as either capsules or Cancer researchers hope to harness the cellular suicide tablets, can be taken on an at-home basis caused by the anthrax toxin to prevent tumors from growing and spreading. In animal studies, the toxin both destroyed How these drugs work: Androgens are male hormones, tumor cells and prevented vascularization of tumors— which include testosterone, dehydroepiandrosterone, and which typically need a lot of nutrients, via vascularization, dihydrotestosterone. Androgens bind to androgen recepto grow. The bioengineered anthrax toxin has not been tors on the surface of prostate cells and turn on signaling shown to damage deoxyribonucleic acid (DNA) or prepathways involved in cellular development and survival vent cell growth in normal cells, common occurrences in and normal prostate function. Most prostate cancers, howtraditional chemotherapy. ever, are also dependent on androgen signaling. Therefore, without it, tumors may stop growing. Side effects: The potential side effects of anthrax therapy Nonsteroidal antiandrogens and synthetic steroids comare not yet known. pete with natural androgens for binding sites on androgen Pamela Richardson, M.S. receptors, thereby blocking the activity of the natural anSee also Biological therapy; Clinical trials. drogens. Synthetic steroids can also act on the hypothalamus in the brain to reduce the production of testosterone. Although antiandrogens inhibit androgen activity, blood levels of testosterone and other androgens may still be u Antiandrogens high, which could promote cancer cell growth. Therefore, antiandrogens are commonly used in combination with Category: Chemotherapy and other drugs other drugs that lower androgen levels, such as luteinizing ATC code: 102BB, G03HA hormone-releasing hormone agonists, which can stop tesDefinition: Antiandrogens are a class of drugs used to tosterone production. Antiandrogens may also be combined with inhibitors of the 5-α reductase enzyme, which treat prostate cancer. They can cause tumor cell death by 72
Salem Health: Cancer
Antidiarrheal agents
Common Antiandrogens for Prostate Cancer Treatment Drug
Brands
Subclass
Delivery Mode
Bicalutamide Cyproterone acetate Flutamide Nilutamide
Casodex Androcur, Climen Eulexin Anandron, Nilandron
Nonsteroidal antiandrogen Synthetic steroid Nonsteroidal antiandrogen Nonsteroidal antiandrogen
Oral Oral Oral Oral
block the conversion of testosterone into dihydrotestosterone. Dihydrotestosterone is thought to be a more potent and active androgen than testosterone. Side effects: Because antiandrogens affect the prostate, they may cause low sperm counts or reduce fertility. Other common side effects include diarrhea, hot flashes, liver toxicity, constipation, decreased appetite, nausea or vomiting, and flulike symptoms. Long-term treatment may also cause osteoporosis, in which bones become weakened. There are also some drug-specific side effects. For example, nilutamide can temporarily cause the eyes to become light sensitive and take longer to adjust to changes in light and dark settings. Flutamide is also associated with the rare side effects of dizziness, fainting, and severe headaches. Elizabeth A. Manning, Ph.D. See also Antiestrogens; Breast cancer in men; Breast cancers; Chemoprevention; Hormonal therapies; Immunotherapy; Tumor flare.
u Antidiarrheal agents Category: Chemotherapy and other drugs ATC code: AO7DA Definition: Antidiarrheal agents are a class of drugs used for the treatment or symptomatic relief of diarrhea. Cancers treated: Antidiarrheal agents are typically used to treat diarrhea associated with carcinoid tumors, colon cancer, lymphoma, thyroid cancer, pancreatic cancer, and pheochromocytoma, as well as cancer treatment-induced diarrhea, caused by such treatments as chemotherapy, radiation therapy, surgery, and bone marrow transplantation. Other causes of diarrhea in patients with cancer include anxiety and stress associated with the diagnosis. For these patients, antidiarrheal agents may be used in combination with antianxiety drugs.
Patients who have diarrhea with a different underlying cause should receive treatment specific to the cause. For example, those who have diarrhea caused by Clostridium difficile should be treated with the antibiotic metronidazole. Antidiarrheal agents may be administered as adjunct therapy after the initiation of antibiotic therapy. Subclasses of this group: Adsorbents, bulk-forming agents, opioids, piperidine derivatives, synthetic octapeptides, mucosal prostaglandin inhibitors Delivery routes: Administered orally in tablet, caplet, capsule, suspension, and liquid form at home or in the hospital; octreotide is administered by subcutaneous injection or by continuous intravenous (IV) infusion while the patient is hospitalized How these drugs work: Adsorbents bind with intestinal contents, increasing their density. Adsorbents such as kaolin and charcoal may inhibit the absorption of other antidiarrheals, making them ineffective. Bulk-forming agents treat diarrhea by absorbing water within the bowel and producing a formed stool. Mucosal prostaglandin inhibitors stimulate the absorption of fluid and electrolytes through the intestinal wall. They also reduce intestinal inflammation and motility by inhibiting prostaglandin synthesis. Moreover the mucosal prostaglandin inhibitor bismuth subsalicylate is thought to have antimicrobial action against Escherichia coli, a bacterium that causes diarrhea. Opioids bind to receptor sites in the intestinal tract, slowing intestinal motility. Synthetic octapeptides inhibit the release of serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide, slowing intestinal motility. Piperidine derivatives reduce peristolic activity by acting directly on the intestinal wall muscles. The reduction in peristolic activity delays intestinal content transit time, increases fecal density, and reduces fluid and electrolyte loss. Side effects: Side effects vary according to the drug class. Adsorbents such as bismuth subsalicylate may cause temporary darkening of the tongue and stools. Bulk-forming agents such as polycarbophil may cause abdominal dis73
Antidiarrheal agents
Salem Health: Cancer
Common Antidiarrheal Agents Drug (Other Names) Brands
Subclass
Delivery Mode Conditions Treated
Aspirin
Bayer aspirin, Ecotrin, Empirin, Halfprin, Norwich Extra Strength
Mucosal prostaglandin inhibitor
Oral
Radiation therapy-induced diarrhea
Bismuth subsalicylate
Bismatrol, Bismatrol Extra, Kaopectate, Extra strength Kaopectate, Pepto-Bismol, PeptoBismol Maximum Strength, Pink Bismuth
Adsorbent, mucosal prostaglandin inhibitor
Oral
Diarrhea associated with colon cancer; lymphoma; thyroid cancer; pancreatic cancer; pheochromocytoma; cancer treatment (antibiotic therapy, bone marrow transplantation, chemotherapy, radiation therapy)
Charcoal
Charcoal Plus DS, CharcoCaps
Adsorbent
Oral
Diarrhea associated with colon cancer; lymphoma; thyroid cancer; pancreatic cancer; pheochromocytoma; cancer treatment (antibiotic therapy, bone marrow transplantation, chemotherapy, radiation therapy)
Difenoxin hydrochloride and atropine sulfate
Motofen
Opioid
Oral
Diarrhea associated with colon cancer; lymphoma; thyroid cancer; pancreatic cancer; pheochromocytoma; cancer treatment (antibiotic therapy, bone marrow transplantation, chemotherapy, radiation therapy)
Diphenoxylate hydrochloride and atropine sulfate
Logen, Lomanate, Lomotil, Lonox
Opioid
Oral
Diarrhea associated with colon cancer; lymphoma; thyroid cancer; pancreatic cancer; pheochromocytoma; cancer treatment (antibiotic therapy, bone marrow transplantation, chemotherapy, radiation therapy)
comfort, bloating, dependence (with prolonged use), increased flatus, and intestinal blockage. Mucosal prostaglandin inhibitors such as aspirin may cause allergic reaction, bruising, gastrointestinal bleeding, hearing loss, hepatitis, itching, low platelet count, nausea, prolonged bleeding time, ringing in the ears, and rash. Opioids such as diphenoxylate hydrochloride and atropine sulfate may cause abdominal discomfort, allergic reaction, blurred vision, confusion, dizziness, dry mouth, dry skin, euphoria, headache, inability to urinate, increased heart rate, itching, loss of appetite, nausea, pancreatitis, rash, respiratory depression, restlessness, sedation, swollen gums, and vomiting. Piperidine derivatives such as loperamide may cause abdominal pain, distention or discomfort; allergic reaction; constipation; dizziness; dry mouth; drowsiness; fatigue; nausea; rash; and vomiting. 74
The synthetic octapeptide, octreotide, may cause abdominal discomfort, arrhythmias, backache, blurred vision, burning or pain at the injection site, cold symptoms, fat malabsorption, flatulence, flulike symptoms, flushing, gallbladder problems, hair loss, hyperglycemia, hypoglycemia, hypothyroidism, joint pain, low heart rate, nausea, pancreatitis, redness at the injection site, swelling, urinary tract infection, and vomiting. Collette Bishop Hendler, R.N., M.S. u
For Further Information Drug Facts and Comparisons 2008. 62d ed. St. Louis: Wolters Kluwer Health, 2008. Karch, Amy M. 2008 Lippincott’s Nursing Drug Guide. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2008.
Salem Health: Cancer
Antiestrogens
Common Antidiarrheal Agents (continued) Drug (Other Names) Brands
Subclass
Delivery Mode Conditions Treated
Kaolin and pectin
Kao-Spen, Kapectolin, KP
Adsorbent
Oral
Diarrhea associated with colon cancer; lymphoma; thyroid cancer; pancreatic cancer; pheochromocytoma; cancer treatment (antibiotic therapy, bone marrow transplantation, chemotherapy, radiation therapy)
Loperamide
Imodium, Imodium A-D, Piperidine derivative Kaopectate II Caplets, Maalox Anti-Diarrheal Caplets, Pepto Diarrhea Control
Oral
Diarrhea associated with colon cancer; lymphoma; thyroid cancer; pancreatic cancer; pheochromocytoma; cancer treatment (antibiotic therapy, bone marrow transplantation, chemotherapy, radiation therapy)
Octreotide
Sandostatin, Sandostatin LAR
Synthetic octapeptide
Subcutaneous injection, IV
Diarrhea associated with colon cancer; lymphoma; thyroid cancer; pancreatic cancer; pheochromocytoma; cancer treatment (antibiotic therapy, bone marrow transplantation, chemotherapy, radiation therapy)
Paregoric
Camphorated Tincture of Opium
Opioid
Oral
Diarrhea associated with colon cancer; lymphoma; thyroid cancer; pancreatic cancer; pheochromocytoma; cancer treatment (antibiotic therapy, bone marrow transplantation, chemotherapy, radiation therapy)
Polycarbophil
Equalactin, Fiberall, FiberCon, Fiber-Lax, Konsyl Fiber, Mitrolan, Phillips’ Fibercaps
Bulk-forming agent
Oral
Diarrhea associated with colon cancer; lymphoma; thyroid cancer; pancreatic cancer; pheochromocytoma; cancer treatment (antibiotic therapy, bone marrow transplantation, chemotherapy, radiation therapy)
Nursing 2008 Drug Handbook. Philadelphia: Lippincott Williams & Wilkins, 2008.
mone-sensitive breast cancers because of their ability to inhibit estrogen-stimulated cancer growth.
See also Antinausea medications; Chemotherapy; Colorectal cancer; Crohn disease; Diarrhea; Enteritis; Gastrointestinal complications of cancer treatment; Inflammatory bowel disease; Laxatives; Side effects; Symptoms and cancer.
Cancers treated: Breast cancer
u Antiestrogens Category: Chemotherapy and other drugs ATC code: 102BA Definition: Antiestrogens interfere with the function of estrogen receptors. They are used in the treatment of hor-
Subclasses of this group: Selective estrogen receptor modulators (SERMs), estrogen receptor downregulators Delivery routes: Administered either intramuscularly or orally in capsule, tablet, or solution form on an inpatient, outpatient, or at-home basis How these drugs work: In 1962, ICI Pharmaceuticals synthesized the antiestrogen tamoxifen, what they hoped to be a new oral contraceptive. Although tamoxifen did not prove effective as a contraceptive, the discovery of hormone receptors in breast tissue by Elwood V. Jensen in 1966 led some researchers to believe that tamoxifen could 75
Antifungal therapies
Salem Health: Cancer
Common Antiestrogens for Breast Cancer Treatment Drug
Brands
Subclass
Delivery Mode
Fulvestrant Raloxifene Tamoxifen Toremifene
Faslodex Evista Nolvadex, Soltamox Fareston
Estrogen receptor downregulators SERMs SERMs SERMs
Intramuscular Oral Oral Oral
be a therapeutic option in hormone-sensitive breast cancer. Clinical research in the early 1970’s produced evidence that tamoxifen was effective in advanced breast cancers, and by the 1980’s it became the treatment option of choice for hormone-sensitive breast cancers in pre- and postmenopausal women as well as men. Later it was approved for use in reducing the risk of breast cancer in patients who are susceptible to the disease. Tamoxifen is a selective estrogen receptor modulator (SERM), a subclass of antiestrogens that act by binding to and changing estrogen receptors, resulting in both estrogenic and antiestrogenic effects depending on cell type. Antiestrogenic effects result in a slowing of cancer cell cycling and impaired deoxyribonucleic acid (DNA) replication. Estrogen receptor downregulators are used as a second-line treatment in hormone-sensitive breast cancer and act similarly to SERMs in that they antagonize the estrogen receptors of breast cells. These drugs, however, are pure estrogen receptor antagonists: Independent of cell type, they completely degrade the estrogen receptor, resulting in a total loss of transcriptional activity in cancer cells.
u Antifungal therapies
Side effects: Common side effects of antiestrogens are menopausal symptoms (hot flashes, night sweats), vaginal discharge, vaginal irritation, vaginal bleeding, gastrointestinal (GI) symptoms (nausea and vomiting, constipation, diarrhea), fatigue, muscle cramps, joint pain, and thromboembolism. Although tamoxifen inhibits estrogen receptors in breast cells, it is a partial agonist in the endometrium and can cause endometrial changes, such as endometrial cancer, polyps, endometriosis, uterine fibroids, and ovarian cysts. Amber L. Fields, M.S.
Delivery routes: Antifungal agents can be administered orally in capsules, tablets, or liquid suspension or vaginally by vaginal tablet. The can be administered in the hospital or at home. Some antifungal agents are administered by intravenous (IV) infusion while the patient is hospitalized. As the patient’s condition improves, IV infusions may be administered at home or in an outpatient treatment center.
See also Antiandrogens; Breast cancer in men; Breast cancers; Chemoprevention; Ductal carcinoma in situ (DCIS); Estrogen receptor downregulator (ERD); Estrogenreceptor-sensitive breast cancer; Fertility drugs and cancer; Hormonal therapies; Hormone receptor tests; Hormone replacement therapy (HRT); Isoflavones; Mastectomy; Phytoestrogens; Progesterone receptor assay; Receptor analysis; Soy foods. 76
Category: Chemotherapy and other drugs ATC code: J02 Definition: Antifungal therapies form a class of antiinfective drugs that are effective against fungi such as Aspergillus, Candida, Cryptococcus, Fusarium, and Scedosporium apiospermum. Cancers treated: Antifungal agents are used to treat fungal infections that develop in patients with any type of cancer. Fungal infections commonly occur in patients with acute lymphoblastic leukemia and acute myelocytic and monocytic leukemia. Antifungal agents are also used to prevent fungal infections in patients who have undergone bone marrow or stem cell transplantation. Subclasses of this group: Polyene antibiotics, echinocandins, bis-triazole derivatives, fluorinated pyrimidines, synthetic triazoles, imidazole derivatives, polyene macrolides
How these drugs work: Polyene antibiotics bind to components of the fungal cell membrane and alter the cell’s permeability, causing fungal cell death. Echinocandins work by inhibiting an enzyme that is essential to the fungal cell wall. Bis-triazole derivatives inhibit the fungal cytochrome P-450 and weaken the fungal cell wall, causing fungal cell death. Fluorinated pyrimidines interfere with protein synthesis within the fungal cells, causing cell death. Synthetic triazoles inhibit fungal cell wall synthesis, causing cell wall instability and eventually cell death. Imidazole derivatives inhibit the formation of ergosterol, a
Salem Health: Cancer
Antifungal therapies
sterol necessary for fungal cell-wall synthesis. Without ergosterol, the fungal cell wall becomes permeable and unstable, causing cell death. Polyene macrolides bind to sterols, making the fungal cell wall permeable. This increased permeability allows intracellular components to leak from the fungal cell, causing fungal cell death. Side effects: Side effects vary according to the antifungal agent. The amphotericans are potent antifungals that have toxic side effects, including kidney and liver failure. Side effects that may occur with antifungal agents include abdominal pain, abnormal dreams, allergic reaction, anemia, anxiety, back pain, bacterial bloodstream infection, bloody nose, bloody urine, blurred vision, cardiac arrest, chest pain, chills, cholestatic jaundice, confusion, constipation, cough, cytomegalovirus (CMV) infection, diar-
rhea, dyspepsia, edema, elevated sodium levels, enlarged breasts with tenderness, epigastric pain, fatigue, flushing, hives, gum disease, gastrointestinal bleeding, hallucinations, headache, heart failure, herpes simplex infection, hypotension, hyperglycemia, hypertension, hyperventilation, infection, insomnia, impotence, itching, light sensitivity, low calcium levels, low magnesium levels, low phosphorus levels, low potassium levels, low white blood cell count, loss of appetite, mouth ulceration, muscle aches, nausea, nervousness, petechiae, pulmonary edema, rash, respiratory failure, rhinitis, rigors, severe depression, severe vaginal bleeding, shortness of breath, sinusitis, sore throat, suicidal tendencies, sweating, taste perversion, upper respiratory tract infection, urinary tract infection, vomiting, and weakness. Collette Bishop Hendler, R.N., M.S.
Common Antifungal Agents Drug (Other Names) Brands
Subclass
Delivery Mode Conditions Treated
Amphotericin B cholesteryl sulfate complex
Amphotec
Polyene antibiotic
Continuous or Invasive aspergillosis in patients with cancer intermittent IV (especially those with acute leukemia) who cannot infusion tolerate amphotericin B deoxycholate
Amphotericin B desoxycholate
Polyene Amphocin, Amphotericin B antibiotic for injection, Fungizone
IV infusion
Prevention of fungal infection in bone marrow transplant patients; treatment of systemic infections caused by histoplasmosis, coccidioidomycosis, blastomycosis, cryptococcosis, disseminated candidiasis, aspergillosis, phycomycosis, zygomycosis, or meningitis in patients with cancer
Amphotericin B lipid complex
Abelcet
Polyene antibiotic
IV infusion
Fungal infections including Aspergillus and Candida in cancer patients who cannot tolerate amphotericin B desoxycholate
Amphotericin B liposomal
AmBisome
Polyene antibiotic
IV infusion
Suspected fungal infections in patients with low white blood cell count and fever; fungal infections caused by Aspergillus, Candida, or Cryptococcus species in cancer patients who cannot tolerate amphotericin B desoxycholate
Anidulafungin
Eraxis
Echinocandin IV infusion
Bloodstream infection and intra-abdominal abscess or peritonitis caused by Candida in patients with cancer
Caspofungin
Cancidas
Echinocandin IV infusion
Bloodstream infection and intra-abdominal abscess or peritonitis or pleural space infections caused by Candida in patients with cancer; aspergillosis in cancer patients who cannot tolerate all forms of amphotericin B (continued on page 78)
77
Antimetabolites in chemotherapy
Salem Health: Cancer
Common Antifungal Agents (continued) Drug (Other Names) Brands
Subclass
Delivery Mode Conditions Treated
Fluconazole
Diflucan
Bis-triazole derivative
Oral, IV infusion
Prevention of candidiasis in bone marrow transplant patients; cryptococcal meningitis or oropharyngeal, vulvovaginal, or systemic candidiasis
Flucytosine (5-FC, 5-fluorocytosine)
Ancobon
Fluorinated pyrimidine
Oral
Bloodstream infection, endocarditis, urinary tract infection, or lung infection caused by Candida or Cryptococcus in patients with cancer; meningitis caused by Cryptococcus in patients with cancer
Itraconazole
Sporanox
Synthetic triazole
Oral, IV infusion
Aspergillosis, oropharyngeal and esophageal candidiasis, blastomycosis, or nonmeningeal histoplasmosis in patients with cancer
Ketoconazole
Nizoral
Imidazole derivative
Oral
Oral candidiasis, systemic candidiasis, coccidioidomycosis, blastomycosis, histoplasmosis, chromomycosis, paracoccidioidomycosis, and severe dermatophyte infections that do not respond to other therapy in patients with cancer
Micafungin sodium
Mycamine
Echinocandin IV
Prevention of Candida infection in stem cell transplant patients and treatment of esophageal candidiasis
Nystatin
Mycostatin, Nilstat, Nystex
Polyene macrolide
Oral, vaginal
Intestinal, oral, or vaginal candidiasis in patients with cancer
Posaconazole
Noxafil
Triazole derivative
Oral
Prevention of Aspergillus and Candida infections in cancer patients
Voriconazole
Vfend
Synthetic triazole derivative
Oral, IV infusion
Candida infections of the bloodstream, esophagus, kidney, abdomen, bladder wall, wound, and skin in patients with cancer. Aspergillosis and serious infections caused by Fusarium and Scedosporium apiospermum in patients with cancer who cannot tolerate other antifungal therapy.
u For Further Information Drug Facts and Comparisons 2008. 62d ed. St. Louis: Wolters Kluwer Health, 2008. Karch, Amy M. 2008 Lippincott’s Nursing Drug Guide. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2008. Nursing 2008 Drug Handbook. Philadelphia: Lippincott Williams & Wilkins, 2008.
See also Aflatoxins; Candidiasis; Infection and sepsis; Neutropenia; Side effects.
78
u Antimetabolites in
chemotherapy Category: Chemotherapy and other drugs ATC code: 101B Definition: Antimetabolites are drugs that interfere with deoxyribonucleic acid (DNA) replication processes in cells. These agents have a structure very similar to that of some of the components involved in the synthesis of nucleotides, the structural units of DNA. This similarity causes the cell to mistake the antimetabolite for a natural component, allowing the drug to effectively inhibit nucleotide synthesis. Nucleotide synthesis and subsequent DNA replication are processes that a cell must undergo before it can divide, and therefore quickly growing tumor cells are
Salem Health: Cancer particularly susceptible to interference with DNA replication. Further, inhibiting DNA replication triggers the activation of death-promoting pathways in these cells, causing the antimetabolite to decrease the tumor size. Cancers treated: Many solid tumors, including breast, colon, lung (small-cell and non-small-cell), ovarian, and head and neck cancers; several leukemias and lymphomas, including acute lymphocytic leukemia, indolent B-cell lymphoma, and non-Hodgkin lymphoma Subclasses of this group: Folic acid antagonists, pyrimidine antagonists, purine antagonists, sugar-modified analogs, ribonucleotide reductase inhibitors Delivery routes: Intravenous (IV), oral, intra-arterial (into an artery), intrathecal (into the spinal canal) How these drugs work: The development of antimetabolite therapy was based on the understanding of the importance of DNA replication in cell division and proliferation. Antimetabolites inhibit DNA replication through one or both of two mechanisms. First, these drugs can inhibit the synthesis of nucleotides, the structural molecules that make up the DNA strand. The four nucleotides that are used to replicate DNA are divided into two categories. The two purine nucleotides are adenine and guanine, while the two pyrimidines are cytosine and thymine. With the exception of thymine, these nucleotides also serve as the structural units for ribonucleic acid (RNA). In RNA, thymine is replaced with another nucleotide, uracil. When the synthesis of these molecules is inhibited, the cellular pool of nucleotides is reduced, limiting the ability of the cell to synthesize new DNA strands. The second mechanism of action is the actual incorporation of the antimetabolite into the DNA itself. It is known that the enzymes responsible for DNA replication can mistake the agents for DNA nucleotides, but the direct consequences of this mistaken identity are as of yet unknown. There are four main subclasses of antimetabolites: folic acid antagonists, pyrimidine and purine antagonists, sugar-modified analogs, and ribonucleotide reductase inhibitors. Folic acid (folate) antagonists are thought to act primarily through inhibition of the dihydrofolate reductase (DHFR) enzyme. DHFR functions to change the structure of folic acid, also known as vitamin B9, allowing it to be used in various metabolic processes that result in the formation of nucleotides. Inhibition of DHFR therefore reduces the production of many of the nucleotides essential for DNA replication. Methotrexate is the prototypical folate antagonist, and it has been successfully used as an anticancer drug in the clinic for decades. One of the reasons that methotrexate is so efficacious is that once it en-
Antimetabolites in chemotherapy ters the cell, it is chemically modified in such a way that it is unable to exit the cell. This causes the intracellular concentration of methotrexate to remain very high. Pyrimidine and purine antagonists target tumor cells via a dual mechanism of action-inhibition of nucleotide synthesis and incorporation into DNA. To inhibit nucleotide synthesis, pyrimidine antagonists can directly inhibit the thymidylate synthase protein, a critical enzyme in the formation of the thymine nucleotide. When thymidylate synthase mistakes pyrimidine antagonists for their natural substrate, the agent inhibits and traps the enzyme in the middle of the catalysis reaction. A stable complex of the enzyme and drug are formed, decreasing the number of enzymes available for the further formation of thymine. Because there is a relatively small concentration of thymine normally in the cell, reducing these pools can drastically inhibit DNA synthesis. The most common pyrimidine antagonists, fluoropyrimidines, have also been found to incorporate into DNA and RNA, replacing the nucleic acids thymine and uracil, respectively. This incorporation occurs at a relatively low level, however, and is not thought to be the primary cause for cell death. Fluoropyrimidines, especially 5-fluorouracil, are used to treat many commonly occurring cancers, including colorectal, breast, gastric, pancreatic, and head and neck tumors. Compared with pyrimidine antagonists, purine antagonists incorporate more readily into nucleic acids. Purine antagonists also inhibit the synthesis of nucleic acids. Each purine antagonist may inhibit purine synthesis at different points along the metabolic pathway, but their effects are perhaps most notable on the enzymes PRPP amidotransferase and IMP dehydrogenase. Purine antagonists are considered to be self-limiting, meaning that the biochemical effects produced by the agent can antagonize each other. For example, when purine synthesis is inhibited, total DNA replication is reduced, thereby diminishing the potential for incorporation of the drug into the DNA. The main purine antagonists are mercaptopurine and thioguanine, and they are used primarily to treat leukemia, especially in children. Sugar-modified analogs were discovered in screening programs established after the clinical success of pyrimidine and purine antagonists was established. Widely used in leukemia therapy, the sugar-modified analog cytarabine was isolated from a species of sponge from the Caribbean Sea. It is characterized by a modification of the sugar moiety, not the base portion, of the nucleotide analog. Unlike the other pyrimidine and purine antagonists, which can affect both DNA and RNA, cytarabine almost exclusively affects DNA. The primary mechanism of action of cytarabine is incorporation into the DNA in place of the 79
Antimetabolites in chemotherapy
Salem Health: Cancer
cytosine nucleotide. The other main sugar-modified analog, fludarabine, has a modification in both the base and sugar moiety. Hydroxyurea is the prototypical ribonucleotide reduc-
tase inhibitor. The enzyme ribonucleotide reductase has a global effect on all DNA synthesis, as it is the enzyme responsible for converting the precursor ribonucleoside diphosphates to deoxyribonucleotide diphosphates.
Common Antimetabolites
80
Drug (Other Names)
Brands
Subclass
Delivery Mode
Cancers Treated
Azacytidine (Aza-C, 5-AC)
Vidaza
Pyrimidine antagonist
IV
Chronic myelocytic leukemia
Capecitabine Xeloda (prodrug of fluorouracil)
Pyrimidine antagonist
Oral
Metastatic colorectal cancer, metastatic breast cancer
Chlorodeoxyadenosine (CdA)
Cladribine, Leustatin
Purine antagonist
IV
Indolent B-cell lymphocytic leukemia (especially hairy cell leukemia); may have activity in chronic lymphocytic leukemia and non-Hodgkin lymphoma
Cytarabine (ara-C)
Cytosar-U, DepoCyt
Sugar-modified analog
IV, intrathecal, subcutaneous
Acute nonlymphocytic leukemia, advanced non-Hodgkin lymphoma, chronic myelocytic leukemia, meningeal leukemia
Fludarabine (F-ara-A)
Fludara
Sugar-modified analog
IV, oral
Refractory chronic lymphocytic leukemia, non-Hodgkin lymphoma
Fluorodeoxyuridine (FdUrd, 5-FUdR, FdUMP)
FUDR, Floxuridine
Pyrimidine antagonist
Hepatic arterial infusion
Cancer of the gastrointestinal tract, especially tumors that have metastasized to the liver
Fluorouracil (FUra, 5-FU)
Adrucil
Pyrimidine antagonist
IV
Many solid cancers, including colorectal, breast, head and neck, gastric, and pancreatic tumors
Gemcitabine
Gemzar
Pyrimidine antagonist
IV
Locally advanced or metastatic lung cancer, pancreatic cancer, ovarian cancer, metastatic breast cancer
Hydroxyurea (HU, hydroxycarbamide)
Droxia, Hydrea
Ribonucleotide reductase inhibitors
oral
Chronic myelocytic leukemia, head and neck cancer, cervical cancer, ovarian cancer, melanoma
Mercaptopurine (MP, 6-MP)
Purinethol
Purine antagonist
Oral
Acute lymphocytic leukemia
Methotrexate (MTX, amethopterin)
Trexall, Rheumatrex
Folic acid antagonist
Oral, IV, intra-arterial, intrathecal
Breast cancer, bone cancers including osteogenic sarcoma, acute lymphocytic leukemia, head and neck cancer, bladder cancer, and several other solid tumors including lung, uterine, and cervical cancer
Pentostatin (2′-deoxycoformycin, dCF)
Nipent
Purine antagonist
IV
Indolent B-cell lymphocytic leukemia (especially hairy cell leukemia); may have activity in chronic lymphocytic leukemia
Thioguanine (TG, 6-TG)
Thioguanine Tabloid
Purine antagonist
Oral
Acute nonlymphocytic leukemia
Tiazofurin
Riboxamide
Purine antagonist
IV
Currently in clinical testing for several leukemias, especially chronic myelocytic leukemia
Salem Health: Cancer Side effects: In general, antimetabolites are more toxic to cells that are actively dividing, compared to cells that are not. Because tumor cells rapidly proliferate, antimetabolites can target these cells quite effectively. The drugs cannot differentiate, however, between cancer cells and rapidly dividing healthy cells, such as those that occur in the bone marrow, the lining of the gastrointestinal tract, and hair follicles. Therefore, most side effects induced by these drugs are dependent on which normal cells are affected. Methotrexate toxicity is mainly confined to the bone marrow and the gastrointestinal tissue lining. The side effects that can result in systemic therapy with pyrimidine and purine antagonists are mainly bone marrow suppression, although gastrointestinal toxicity can occur. Fluoropyrimidines, in particular, induce nausea, vomiting, anorexia, and diarrhea. Lisa M. Cockrell, B.S. u For Further Information Jackman, Ann L., ed. Antifolate Drugs in Cancer Therapy. Totowa, N.J.: Humana Press, 1999. Kantarjian, Hagop M., et al. The MD Anderson Manual of Medical Oncology. New York: McGraw-Hill, 2006. Kufe, Donald W., et al., eds. Holland Frei Cancer Medicine 7. 7th ed. Hamilton, Ont.: BC Decker, 2006. Pratt, William B., et al. The Anticancer Drugs. 2d ed. New York: Oxford University Press, 1994. Rustum, Youcef M., ed. Fluoropyrimidines in Cancer Therapy. Totowa, N.J.: Humana Press, 2003. Skeel, Roland T. Handbook of Cancer Chemotherapy. 7th ed. Philadelphia: Lippincott Williams & Wilkins, 2007. u
Other Resources
National Cancer Institute Drug Information Summaries http://www.cancer.gov/cancertopics/druginfo/ alphalist See also Antineoplastics in chemotherapy; Chemotherapy.
u Antinausea medications Category: Chemotherapy and other drugs ATC code: A04A Definition: Antinausea agents, or antiemetics, encompass a range of drug classes that act on the peripheral and central nervous systems to prevent nausea and vomiting. In patients with cancer, antiemetics are used to control acute, delayed, and anticipatory nausea and vomiting that result from chemotherapy.
Antinausea medications Cancers treated: Indirectly used in the treatment of many cancers to control nausea and vomiting associated with many chemotherapy regimens Subclasses of this group: Serotonin-3 antagonists, substituted benzamides, corticosteroids, pheothiazines, benzodiazepines, butyrophenones, cannabinoids, neurokinin-1 antagonists Delivery routes: Administered to inpatients and outpatients as oral tablets, capsules, or liquids; as intravenous or intramuscular solutions; or as rectal suppositories How these drugs work: Nausea and vomiting, or emesis, are the most common chemotherapy-associated toxicities, affecting more than 75 percent of patients, especially with the development of combination regimens. The effective use of antinausea agents to improve chemotherapy tolerance is one of the most important advances of supportive cancer care. Among the first of agents to deter emesis was metoclopramide, a substituted benzamide that acts as a dopamine receptor antagonist and, at higher doses, as an additional serotonin receptor antagonist. Although the exact mechanisms of nausea and vomiting reflexes have not been determined, neurotransmitter blockade at dopaminergic, serotonergic, neurokinin-1, and other receptors in the central nervous system or peripherally in the gastrointestinal tract successfully controls the reactions. Like metoclopramide, phenothiazines such as chlorpromazine and butyrophenones such as haloperidol also prevent nausea and vomiting by dopaminergic blockade. Dopamine antagonism from these three subclasses provides relief of moderate emesis. The more newly developed serotonin-3 (5HT-3) receptor antagonists work peripherally, especially in the small intestine, and are extremely effective for the treatment and prevention of acute emesis. Ondansetron, granisetron, and dolasetron are equivalent in efficacy and may provide total receptor blockade, as evidenced by their dose-related efficacy plateaus. Palonsetron, a newer agent, is longer acting than others in the subclass. Because acute emesis is associated with peripheral control and delayed emesis is associated with central control, 5HT-3 antagonists are more effective in treating acute nausea and vomiting, which occurs in the first twenty-four hours after chemotherapy is administered. Benzodiazepines such as lorazepam have some antiemetic activity by blocking cortical input to the emetic center but are more useful for their sedative and anxiolytic effects, which make the agents ideal for combination regimens. In addition, these drugs induce retrograde amnesia, which is successful in preventing anticipatory nausea and 81
Antinausea medications
Salem Health: Cancer
Common Antinausea Agents Drug
Brands
Subclass
Delivery Mode
Type of Nausea Treated
Aprepitant
Emend
Neurokinin-1 receptor antagonist
Oral
Delayed prophylaxis, primarily (combined with corticosteroid)
Chlorpromazine, prochlorperazine, promethazine
Thorazine, Compazine, Phenergan
Phenothiazines
Oral, IV, rectal
Mild-to-moderate acute (combined with corticosteroid or 5HT-3 antagonist); breakthrough
Dexamethasone, methylprednisolone
Decadron, Medrol, MethaPred
Corticosteroids
Oral, IV
Mild-to-moderate acute as monotherapy; moderate-to-severe acute when combined with 5HT-3 antagonist; delayed prophylaxis when combined with NK-1 inhibitor; delayed postchemotherapy when combined with substituted benzamide; anticipatory
Cannabinoids
Oral
Anticipatory, breakthrough, or refractory nausea and vomiting
Dronabinol Haolperidol, droperidol
Haldol, Inapsine
Butyrophenones
Oral, IV, intramuscular
Mild-to-moderate acute (not recommended agents because of toxicities)
Lorazepam
Ativan
Benzodiazepine
Oral, IV, intramuscular
Anticipatory or breakthrough
Metoclopramide
Reglan
Substituted benzamide
Oral, IV
Acute or anticipatory (not as first-line agent); delayed when combined with corticosteroid
Ondansetron, granisetron, dolasetron, palonosetron
Zofran, Kytril, Anzemet,
Serotonin-3 receptor antagonists
Oral, IV
Uncontrolled mild, moderate, or severe acute; Moderate-to-severe acute (combined with corticosteroid); Delayed (less effective than NK-1 inhibitor)
vomiting that may occur with repeat chemotherapy administration. Neurokinin-1 (NK-1) receptors are more recently studied targets of nausea mechanisms; the only currently approved agent in the NK-1 antagonist class is aprepitant. Because NK-1 mediates substance P activation of NK-1 receptors in the brainstem, aprepitant’s NK-1 receptor antagonism is useful for the treatment of delayed emesis, which is more centrally mediated. Although its efficacy alone is not yet confirmed, aprepitant successfully prevents acute and delayed nausea and vomiting when combined with serotonin antagonists and corticosteroids. Corticosteroids, especially dexamethasone, methylprednisolone, and prednisone, have a confirmed effect, alone or in combination, against moderate nausea and vomiting, despite an unknown mechanism of action and a lack of receptor blockade. Corticosteroids are often the second drug in a combination regimen with dopamine, serotonin, or NK-1 receptor antagonists. Lastly, cannabinoids such as dronabinol act centrally 82
with psychotropic activity to provide limited but affirmed antinausea activity. They can be used for patients with moderate emesis and poor tolerance or response to other agents or for patients who need control of breakthrough pain. Side effects: Each subclass of antinausea agents is associated with different side effects; successful combination regimens provide greater efficacy without overlapping drug toxicities. Metoclopramide side effects are primarily related to dopamine antagonism and include extrapyramidal reactions, including acute dystonic reactions. Akathisia, or restlessness, is common and may persist for hours. Drowsiness and diarrhea are also possible. Phenothiazines and butyrophenones also cause dopaminerelated drowsiness, diarrhea, and extrapyramidal reactions. In addition, constipation, dizziness, and hypotension have been noted. Lorazepam is associated with sedation in addition to amnesia, confusion, transient enuresis, and blurred vision. Serotonin antagonists all have similar side effects
Salem Health: Cancer of mild to moderate headache in 20 to 30 percent of patients and mild, uncommon occurrences of constipation or diarrhea. Corticosteroids may cause insomnia, hyperglycemia, gastrointestinal upset, and, rarely, psychosis. NK-1 antagonism leads to fatigue, dizziness, headache, and gastrointestinal disturbances. Side effects of dronabinol include dysphoria, hallucinations, dizziness, dry mouth, sedation, and disorientation. Nicole M. Van Hoey, Pharm.D. u For Further Information Grunberg, S. M. “Antiemetic Activity of Corticosteroids in Patients Receiving Cancer Chemotherapy: Dosing, Efficacy, and Tolerability Analysis.” Annals of Oncology 18, no. 2 (February, 2007): 233-240. Jordan, K., H. J. Schmoll, and M. S. Aapro. “Comparative Activity of Antiemetic Drugs.” Critical Reviews in Oncology/Hematology 61, no. 2 (February, 2007): 162175. Roila, F., S. Fatigoni, and G. Ciccarese. “Daily Challenges in Oncology Practice: What Do We Need to Know About Antiemetics?” Annals of Oncology 17, suppl. 10 (September, 2006): 90-94.
See also Chemotherapy; Gastrointestinal complications of cancer treatment; Nausea and vomiting; Topoisomerase inhibitors.
u Antineoplastics in
chemotherapy Category: Chemotherapy and other drugs ATC code: 101 Also known as: Chemotherapeutic agents, antitumor compounds, cytotoxic antibiotics Definition: Antineoplastics are anticancer drugs used to treat malignancies and cancerous growths. Cancers treated: Various types of cancers Subclasses of this group: Alkylating agents, antimetabolites, mitotic inhibitors, topoisomerase inhibitors, cytotoxic antibiotics Delivery routes: Oral, intravenous, intramuscular, or subcutaneous injection How these drugs work: Antineoplastics are chemicals used to treat cancer and inhibit tumor cell growth. The term “neoplastic” refers to cancer cells, so the term “antineoplastic” literally means “anticancer cell.” Antineo-
Antineoplastics in chemotherapy plastic agents are used to stop tumor development or prevent the spread of cancer and to relieve some symptoms associated with cancer or to prolong patient survival. Antineoplastics are also sometimes referred to as chemotherapeutic agents, antitumor compounds, or cytotoxic antibiotics. The first antineoplastic agents were used in the 1940’s and either were made from synthetic chemicals or were derived from natural plants. More than fifty antineoplastic agents are approved by the Food and Drug Administration (FDA) for use in the United States. There are several major categories of antineoplastic agents based on their origins, chemical structures, and the how they work. These classifications include alkylating agents, antimetabolites, cytotoxic antibiotics, mitotic inhibitors, and topoisomerase inhibitors. Antineoplastic agents inhibit tumor cell growth using different mechanisms, with many affecting deoxyribonucleic acid (DNA) synthesis and interfering with cell division. Others work by altering immune function or affecting hormonal status of tumors. Antineoplastic drugs are either cycle specific or non-cycle specific, with cycle specific drugs acting only during certain phases of the cell cycle while non-cycle specific drugs may act during any cell cycle phase. The largest group of antineoplastic compounds is the alkylating agents, which were among the first anticancer drugs used. These compounds are the most commonly used agents in chemotherapy. Alkylating agents work by cross-linking DNA and preventing DNA bases from pairing up correctly, which interferes with DNA synthesis. Categories of alkylating agents include busulfans, alkylating-like drugs, nitrogen mustards, ethylenimines, and nitrosureas. Nitrogen mustards comprise the largest group of alkylating drugs and are particularly useful for treating neoplasms that increase white blood cells, such as lymphomas and leukemias, because they result in leukopenia. Unlike most other types of antineoplastic agents, nitrosureas can cross the blood-brain barrier and thus are useful for treating brain tumors. Also included among the alkylating agents are the metal salts, such as carboplatin and cisplatin. Other examples of alkylating agents include chlorambucil, cyclophosamide, and thiotepa. Antimetabolites work by interfering with cancer cell metabolism. Antimetabolites are analogs of normal metabolites (nucleic acids) and act by replacing natural substances. Since these compounds structurally resemble DNA base pairs, they become incorporated into DNA, thus interfering with DNA synthesis. Antimetabolites are cell-cycle specific and attack cells only during certain cell cycle phases. Most antimetabolites are preferentially effective against cells that are actively synthesizing DNA. 83
Antineoplastics in chemotherapy
Salem Health: Cancer
Antimetabolites are classified by the metabolite that they affect and include folic acid, purine, and pyrimidine analogs. All these compounds function by interfering with DNA synthesis in some way, either by directly inhibiting important enzymes or by being converted into substances that impair DNA synthesis. Methotrexate, a folic acid analog, inhibits an enzyme necessary for regeneration of intermediates required for DNA synthesis. Pyrimidine and purine analogs are converted into compounds that inhibit enzymes involved in DNA synthesis. 5-Fluorouracil and cytarabine are examples of pyrimidine analogs. Purine analogs include 6-mercaptopurine and pentostatin. Some antineoplastic drugs are considered antimitotics or mitotic inhibitors and bind to tubulin, preventing polymerization of microtubules necessary for mitotic spindle formation. This prevents mitosis and arrests cells during metaphase. Many of the vinca alkaloids function as mitotic inhibitors. Topoisomerase inhibitors interfere with
DNA synthesis by disrupting the function of the enzymes topoisomerases I and II, which are important in tubulin formation. Topoisomerases control the structure of DNA necessary for replication, and compounds that inhibit these enzymes work by preventing DNA from being unwound, a step required for DNA synthesis. Topoisomerase inhibitors include ironotecan, topotecan, etoposide, and teniposide. Many antineoplastic compounds are derived from plants and are known as natural products. They vary mechanistically, with some functioning as alkylating agents, some inhibiting mitosis, and some affecting enzymes important in DNA synthesis. The vinca alkaloids, made from the periwinkle plant (Catharanthus rosea), and the taxanes, made from the Pacific yew tree (Taxus), work as mitotic inhibitors by disrupting microtubule formation. Podophyllotoxins, derived from the mayapple plant (Podophyllum peltatum), and camptothecans, from the Asian “Happy
Common Antineoplastic Agents
84
Drug (Other Names)
Brands
Subclass
Delivery Mode
Cancers Treated
Asparaginase
Elspar
Miscellaneous
IV, intramuscular, subcutaneous
Acute lymphoblastic leukemia
Bleomycin
Blenoxane
Cytotoxic antibiotic
IV
Testicular cancer, squamous cell carcinoma, Hodgkin disease
Busulfan
Busulfex
Alkylating agent
Oral, IV
Chronic myelogenous leukemia, other blood cancers
Carboplatin (CBDCA)
Paraplatin
Alkylating agent
IV
Ovarian carcinoma
Cisplatin (CDDP)
Platinol-AQ Alkylating agent
IV
Testicular, ovarian, and bladder cancers
Chlorambucil
Leukeran
Alkylating agent
IV, oral
Leukemias, lymphomas, various cancers, Hodgkin disease
Cyclophosphamide (CTX)
Cytoxan
Alkylating agent
IV, oral
Leukemias, lymphomas, ovarian and breast cancers
Cytarabine (Ara C)
Cytostar-U
Antimetabolite
IV, subcutaneous
Leukemias, non-Hodgkin lymphoma
Dactinomycin (actinomycin D)
Cosmogen
Cytotoxic antibiotic
IV
Testicular carcinomas, sarcomas, other solid tumors
Doxorubicin Adriamycin, Cytotoxic (hydroxyldaunorubicin) Rubex antibiotic
IV
Leukemias, Hodgkin lymphoma, bladder cancer, breast cancer, other solid tumors
Etoposide
Etophos, Vepesid
Mitotic inhibitor
Oral, IV
Leukemias, lymphomas, lung, ovarian, and testicular cancers
5-fluorouracil (5-FU)
Adrucil
Antimetabolite
IV
Colon, rectal, breast, stomach, pancreatic cancers
Ifosfamide (isophosphamide)
Ifex
Alkylating agent
IV
Germ-cell testicular cancer, sarcomas
Salem Health: Cancer
Antineoplastics in chemotherapy
Tree” (Camptotheca acuminate), function as topoisomerase inhibitors. Most of these compounds are effective against tumor cells during various cell cycle phases. Another category of antineoplastics includes the antitumor or cytotoxic antibiotics, many of which are produced by species of the soil fungus Streptomyces. There are several cytotoxic antibiotics, such as Dactinomycin (actinomycin D), bleomycin, and doxorubicin. Cytotoxic antibiotics generally act during various phases of the cell cycle. Dactinomycin works by binding to DNA and preventing ribonucleic acid (RNA) synthesis, an important step in making proteins. Doxorubicin works by causing DNA to uncoil, which prevents the cell from reproducing. Bleomycin acts by fragmenting DNA. There are also many compounds that do not fit into these categories but are still useful antineoplastic agents, such as hormones, enzymes, and reagents used in immunotherapy. Hormones work by altering the cellular envi-
ronment, making it unfavorable for tumor growth. Enzymes, such as L-asparaginase, break down substances such as asparagine that tumor cells need for survival. Mitotane is a chemical related to the insecticide dichlorodiphenyl-trichloroethane (DDT) and interferes with the formation of adrenocortical steroids, with selective cyototoxic effects toward cells of the adrenal cortex. Other compounds include retinoids, such as bexarotene and tretinoid. Side effects: Antineoplastic compounds can destroy normal cells as well as neoplastic cells, although generally antineoplastic agents have greater effects on tumor cells because they grow rapidly. Many side effects associated with antineoplastic agents occur because of their effects on normal cells, especially those that divide rapidly, such as the cells of hair follicles, ovaries, testes, and blood-forming organs. Hair loss is common as a result of effects on
Common Antineoplastic Agents (continued) Drug (Other Names)
Brands
Subclass
Delivery Mode
Cancers Treated
Irinotecan
CPT-11
Topoisomerase inhibitor
IV
Metastatic colorectal cancer, bowel cancer
Mercaptopurine (6-MP)
Purinethol
Antimetabolite
Oral
Leukemia
Methotrexate (amethopterin)
Rheumatrex Antimetabolite
Oral, IV, subcutaneous
Acute lymphoblastic leukemia
Mitomycin (mitomycin C)
Mutamycin
Cytotoxic antibiotic
IV
GI, bladder, and breast cancers
Mitotane (o,p’-DDD)
Lysodren
Miscellaneous
Oral
Adrenocortical carcinoma
Oxaliplatin (oxalatoplatin)
Eloxatin, Alkylating agent Transplatine
IV
Advanced ovarian cancer, head and neck cancers
Pentostatin (deoxycoformycin)
Nipent
Antimetabolite
IV
Leukemias
Tenisopide
Vumon, VM-26
Mitotic inhibitor
IV
Leukemias, lymphomas, neuroblastoma
Thiotepa
Thioplex
Alkylating agent
IV, spinal injection
Bladder cancer, ovarian cancer, breast cancer, lymphomas
Topotecan
Hycamtin
Topoisomerase inhibitor
IV
Ovarian, small-cell lung cancers
Vincristine
Mitotic inhibitor Oncovin, Cytocristin, Vincristine sulfate
IV
Non-Hodgkin lymphoma, leukemias, smallcell lung cancer, cervical and breast cancers
Vinorelbine
Navelbine
IV
Leukemia, lymphoma, melanoma, breast and lung cancers
Mitotic inhibitor
85
Antioxidants hair follicles. Anemia, immune system impairment, and clotting problems result from adverse effects on bloodforming organs, which lead to decreased red blood cell, white blood cell, and platelet numbers. Nausea and vomiting are among the most common adverse side effects. Other side effects may include blood in the urine, diarrhea, fever or chills, cough, wheezing, shortness of breath, unusual bruising, problems with urination, dizziness, irregular heartbeat, skin rash, fatigue, loss of taste, headache, swelling, allergic reactions, or body aches. C. J. Walsh, Ph.D. u
For Further Information Clinical Pharmacology Made Incredibly Easy. 3d ed. Philadelphia: Lippincott Williams & Wilkins, 2008. Dawson, James S., Magali N. F. Taylor, and Peter J. W. Reide. Pharmacology. Philadelphia: Elsevier Health Sciences, 2002. Portable Pathophysiology. Philadelphia: Lippincott Williams & Wilkins, 2007. Skidmore-Roth, Linda. Mosby’s 2007 Nursing Drugs Reference. St. Louis: C. V. Mosby, 2006. Vardanyan, Ruben, and Victor Hruby. Synthesis of Essential Drugs. Philadelphia: Elsevier, 2006. u
Other Resources
Cancer Backup General Information on Chemotherapy http://www.cancerbackup.org.uk/Treatments/ Chemotherapy/Generalinformation/Overview MedlinePlus http://www.nlm.nih.gov/medlineplus/ druginformation.html National Cancer Institute Drug Information Summaries http://www.cancer.gov/cancertopics/druginfo/ alphalist See also Alkylating agents in chemotherapy; Chemotherapy; Immunotherapy; Proteasome inhibitors.
u Antioxidants Category: Lifestyle and prevention; complementary and alternative therapies Definition: Antioxidants are a class of compounds that help prevent damage to deoxyribonucleic acid (DNA), cellular proteins, and cell membranes by combining with 86
Salem Health: Cancer potentially damaging molecules called free radicals and neutralizing them. The body naturally makes many antioxidants, while others are found in fruits, vegetables, and grains. Antioxidants are also produced synthetically as dietary supplements. Cancers treated or prevented: Antioxidants are used to treat most types of cancer, although their effectiveness is questionable. They are usually taken for cancer prevention, although the link between antioxidant consumption and cancer prevention in humans is not proven. Delivery routes: Oral, as tablets, caplets, capsules, powder, or tea; some fruits and vegetables are high in antioxidants How these compounds work: Free radicals are formed during normal cellular metabolism. Free radicals are compounds that are unstable because they contain an unpaired electron. This unpaired electron causes the free radical to react with other molecules in order to gain another electron, creating an electron pair and a more stable molecule. The process of gaining an electron is called oxidation. Antioxidants in the body react with free radicals and make them harmless to cells. Cells naturally make many antioxidants such as glutathione and coenzyme Q10 (ubiquinone). When the number of free radicals exceeds the antioxidants available to neutralize them, however, the body develops a condition called oxidative stress. Oxidative stress appears to make cells especially susceptible to damage. Free radical formation and oxidation are normal processes. Oxidation and oxidative stress, however, are thought to contribute to aging, as well as to cancer, cardiovascular disease, and other chronic diseases. In the absence of adequate antioxidant compounds, free radicals most often combine with and damage DNA, cellular proteins, and molecules in cell membranes. This damage can cause gene mutations and change cellular metabolism, which may lead to cancer and other diseases. Exposure to ultraviolet (UV) light, radiation, cigarette smoke, and other known carcinogens increases the number of free radicals that are formed, suggesting another link between free radicals, oxidative stress, and cancer. In theory, increasing the amount of antioxidants in the body should decrease the amount of damage to DNA and cells and reduce the risk of cancer. Antioxidants have been shown to prevent or slow the development of some cancers in cell cultures grown in the laboratory and in some animal studies. The results in human studies have been mixed. Despite claims by some manufacturers of antioxidant dietary supplements, no clear link between antioxidant
Salem Health: Cancer
Antioxidants
consumption and cancer prevention or treatment has been established in humans. The role of antioxidants in the prevention and treatment of cancer is of high interest to research scientists. Many clinical trials are being conducted, and there is no cost for qualified individuals to participate in a clinical trial. The body makes some antioxidants, but others must be acquired through diet. Common antioxidants that the body does not make include vitamins A, C, and E, carotenoids, and flavonoids. Selenium is a mineral that is not strictly an antioxidant but is essential to many antioxidant reactions and often classed with the antioxidants. Coenzyme Q10 and glutathione are antioxidants naturally produced by the body that are also manufactured sold as high-dose supplements. Vitamin A (retinol) is a fat-soluble vitamin found in liver, egg yolks, whole milk, and dairy products made with whole milk. It is also sold as a dietary supplement and is included in most multivitamin tablets and in special antioxidant formulations such as ACE, a combination of vitamins A, C, and E. Vitamin Ais essential to health, but its role in cancer prevention and treatment is unclear. All-trans-retinoic acid (ATRA, Vesanoid) is a pharmaceutical drug that is a derivative of vitamin A. It is successfully used to treat promyelocytic leukemia and is being studied in Berries contain flavonoids, a group of antioxidant compounds. (U.S. Deindividuals with breast and skin cancers. To date, partment of Agriculture) however, vitamin A alone has not shown the same cancer-reducing effects as ATRA. min C has very strong antioxidant activities. Nevertheless, Alpha-carotene, beta-carotene, beta-cryptoxanthin, lumultiple human studies have failed to find a significant tein, zeaxanthin, and lycopene are all carotenoids that link between cancer prevention and vitamin C intake. show antioxidant activity in laboratory tests. These comVitamin E is a group of related compounds, the most pounds are found in red, yellow, and orange plants such as active of which is alpha-tocopherol. Vitamin E is a fatcarrots, cantaloupe, mango, and tomato. Beta-carotene soluble vitamin with antioxidant properties. It is found in and lycopene are also sold as dietary supplements either olive, sunflower, and safflower oils and in many nuts. The individually or in combination with other antioxidants. In role of vitamin E in cancer prevention is controversial. In the body, carotenoids are converted into vitamin A. An ex2004, researchers at The Johns Hopkins University Mediamination of twenty-one studies relating lycopene concal School did a meta-analysis of nineteen clinical trials sumption and prostate cancer found that men with the that included more than 136,000 individuals. This analysis highest lycopene intake had a modest decrease in the incishowed that taking more than 400 international units (IU) dence of prostate cancer. The role of carotenoids in cancer prevention is actively being studied. of synthetic vitamin E daily increased the chance of dying Vitamin C (ascorbic acid) is a water-soluble vitamin by about 4 percent. This amount is less than the safe daily found in citrus fruits. For centuries, it has been known that upper limit of 1,500 IU recommended by the United States vitamin C is essential for preventing the disease scurvy. Institute of Medicine for adults age nineteen and older. Dietary supplements of vitamin C are often promoted as a The Johns Hopkins analysis has been criticized because it preventive or treatment for the common cold, although did not differentiate between individuals taking different clinical studies have not proved its effectiveness. Vitaforms of vitamin E, such as the dietary supplement alpha87
Antiperspirants and breast cancer tocopherol acetate. This is a significant criticism because different forms of vitamin E have different activity levels in the body. Flavonoids are a group of antioxidant compounds found primarily in brewed tea, red wine, dark chocolate, apples, berries, and citrus fruits. These compounds have antioxidant activity. Traditional Chinese medicine has promoted the health effects of green tea for centuries, and recent studies show that dark (bitter) chocolate in small quantities may promote heart health, but the role of flavonoids in cancer prevention is unclear. Selenium is a mineral found in fish, shellfish, grains, Brazil nuts, and many vegetables that are grown in selenium-rich soils. By itself, selenium is not an antioxidant, but it plays a critical role in antioxidant activity and is often classified with the antioxidants that must be acquired through diet. Selenium deficiency has been linked to increases in colorectal, lung, and prostate cancers. Increased selenium intake in people who are not selenium deficient, however, does not decrease the risk of developing cancer. Additionally, selenium is toxic in large doses. Coenzyme Q10 and glutathione are the main antioxidants made by the body. They are also sold as dietary supplements. Studies of individuals who supplemented their diet with synthetic coenzyme Q10 or glutathione found no evidence that these supplements protected against cancer. Individuals who maintain a healthy weight and eat a diet low in fats and high in fruits, vegetables, and whole grains develop cancer at a lower rate than individuals who eat a more traditional American diet high in fat and low in fruits and vegetables. The American Cancer Society and the National Cancer Institute recommend that individuals meet as many of their vitamin, mineral, and antioxidant needs as possible by eating a healthy, varied diet rather than by taking dietary supplements. As of 2008, neither organization recommended the use of antioxidant supplements to treat or prevent cancer. Side effects: In 2007, a peer-reviewed meta-analysis of antioxidant studies was published in the Journal of the American Medical Association. Researchers looked at the data from sixty-eight clinical trials involving 232,606 individuals. They found that taking dietary supplements of vitamin A, beta-carotene, and vitamin E increased the risk of death from all causes by 5 percent. This increase was not seen in individuals who took vitamin C dietary supplements. The study did not look at individuals who increased their intake of these antioxidants through diet. Martiscia Davidson, A.M.
88
Salem Health: Cancer u
For Further Information DeCava, Judith A. The Real Truth About Vitamins and Antioxidants. 2d ed. Fort Collins, Colo.: Selene River Press, 2006. Frei, Balz, ed. Natural Antioxidants in Human Health and Disease. San Diego, Calif.: Academic Press, 2006. Panglossi, Harold V., ed. Antioxidants: New Research. New York: Nova Science, 2006. Quillin, Patrick. Beating Cancer with Nutrition. 4th ed. Tulsa, Okla.: Nutrition Times Press, 2005.
u
Other Resources
American Cancer Society Antioxidants and Cancer: The Jury’s Still Out http://www.cancer.org/docroot/NWS/content/ NWS_2_1x_Antioxidants_and_Cancer_The_ Jurys_Still_Out.asp MedlinePlus Antioxidants http://www.nlm.nih.gov/medlineplus/ antioxidants.html National Cancer Institute Antioxidants and Cancer Prevention: Fact Sheet http://www.cancer.gov/cancertopics/factsheet/ antioxidantsprevention See also Beta-carotene; Bioflavonoids; Carotenoids; Chemoprevention; Coenzyme Q10; Complementary and alternative therapies; Curcumin; Dietary supplements; Essiac; Free radicals; Fruits; Garlic and allicin; Green tea; Herbs as antioxidants; Isoflavones; Lutein; Lycopene; Nutrition and cancer prevention; Phenolics; Phytoestrogens; Resveratrol; Wine and cancer.
u Antiperspirants and breast
cancer Category: Social and personal issues Definition: Breast cancer is a cancer of the breast tissue, more common among women than men. In the United States, breast cancer is the third most common cause of death in women. Antiperspirants have been studied for a possible link to breast cancer. Looking at the link: Antiperspirants and deodorants are common over-the-counter cosmetics that are used to significantly reduce perspiration and to control body odor. Most commercially available antiperspirants contain alu-
Salem Health: Cancer
Antiperspirants and breast cancer
minum or aluminum-zirconium salts or complexes. These aluminum complexes react with salts in the sweat and form a plug that blocks the sweat duct. As a result, the duct cannot release liquid sweat. Blockage of a number of sweat ducts minimizes the sweat produced by underarms. The plugs are removed over time when the skin sloughs them off naturally. During the past decade, there have been numerous reports on the Internet and in the news claiming that underarm deodorant or antiperspirant use increases the risk of breast cancer, especially in women. However, there is no conclusive scientific evidence linking underarm antiperspirant use and subsequent development of breast cancer. Although there are no published scientific reports delineating a possible mechanism by which the use of underarm antiperspirants could cause breast cancer, public concern regarding this issue persists. Studies that looked at the correlation between antiperspirant use and the development of breast cancer have not been conclusive. The results of a 2002 study investigating the relationship between underarm antiperspirant use and breast cancer did not show an increased risk for women who reported regularly using underarm antiperspirants or deodorant. However, a 2003 study that examined the frequency of underarm shaving and antiperspirant or deodorant use among 437 breast cancer survivors found that those who shaved frequently and used these products were diagnosed with breast cancer at an earlier age. In addition, the study found that those who started the shaving and antiperspirant or deodorant use earlier than sixteen years of age were diagnosed at an earlier age with breast cancer than those who started these habits later in life. These results suggest, though not conclusively, that there could be a link between underarm hygiene habits and breast cancer.
More research is needed in this area to enable women to make informed choices.
Aluminum: Aluminum salts or complexes are one of the major constituents of many commercial antiperspirants and deodorants. Estrogen is a naturally occurring female hormone that is known to promote the growth and division of breast cells. Aluminum salts are classified as metalloestrogens (metals with estrogen hormone-like properties). Research studies have shown that aluminum salts cause an increase in estrogen-related gene expression in human breast cancer cells grown in the laboratory. However, this result has not yet been translated into human breast cancer cells in the body. Aluminum was detected at varying concentrations in human breast cancer tissue from one study of women with breast cancer. The source of the aluminum was not conclusively established, and hence a definite correlation between aluminum from antiperspirants and breast cancer cannot be made from this study.
u
Parabens: Esters of the chemical p-hydroxybenzoic acid are commonly called parabens and are used as preservatives in antiperspirants and many other skin-care cosmetics. Research has demonstrated that parabens possess estrogenic properties both in laboratory-grown cells and in cells within the body (in vitro and in vivo). Scientists have put forth the hypothesis that parabens can be absorbed by breast tissue from topical application of cosmetics such as antiperspirants and could accumulate there, causing the development and spread of breast cancer. A 2004 study that detected parabens in breast tumor tissue partially proved the hypothesis that parabens can accumulate in breast tissue. However, the study did not prove that the accumulated parabens caused breast cancer. Moreover, the study did not prove that the parabens originated from the antiperspirants. It also did not involve an analysis of healthy breast tissue for parabens and hence did not prove that parabens were found only in cancerous tissue and not in healthy tissue. More specific well-designed research is needed to address the absorption of parabens by the skin and objectively evaluate whether they increase the risk of breast cancer. The rising incidence of breast cancer in younger women combined with the fact that it is a major killer of women in the United States makes it a major public health issue. Considering the fact that a majority of young women use antiperspirants and deodorants, the importance of wellfunded, case-controlled research investigations to conclusively establish the proposed link between their use and breast cancer development cannot be overemphasized. Lalitha Krishnan, Ph.D. For Further Information “Antiperspirants Don’t Cause Breast Cancer.” Harvard Women’s Health Watch 10, no. 5 (2003): 7. Harvey, P. W., and D. J. Everett. “Significance of the Detection of Esters of P-hydroxybenzoic Acid (Parabens) in Human Breast Tumours.” Journal of Applied Toxicology 24 (2004): 1-4. McGrath, K. G. “An Earlier Age of Breast Cancer Diagnosis Related to More Frequent Use of Antiperspirants/ Deodorants and Underarm Shaving.” European Journal of Cancer Prevention 12, no. 6 (2003): 479-485. Mirick, D. K., S. Davis, and D. B. Thomas. “Antiperspirant Use and the Risk of Breast Cancer.” Journal of the National Cancer Institute 94, no. 20 (2002): 15781580. Surendran, A. “Studies Linking Breast Cancer to Deodor89
Antiviral therapies
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ants Smell Rotten, Experts Say.” Nature Medicine 10, no. 3 (2004): 216.
u Antiviral therapies
Other Resources
Category: Chemotherapy and other drugs ATC code: J05
American Cancer Society Antiperspirants and Breast Cancer Risk http://www.cancer.org/docroot/MED/content/ MED_6_1x_Antiperspirants.asp?sitearea=PED National Cancer Institute Antiperspirants/Deodorants and Breast Cancer: Questions and Answers http://www.cancer.gov/cancertopics/factsheet/Risk/ AP-Deo See also Carcinogens, known; Carcinogens, reasonably anticipated; Diethanolamine (DEA).
Definition: Antiviral agents are used to treat infections caused by viruses. In patients with cancer, they are also used in combination with other medications to treat human papillomavirus (HPV)-positive cervical cancer and head and neck squamous cell cancer. Antiviral agents known as protease inhibitors, nucleoside reverse transcriptase inhibitors, and nonnucleoside reverse transcriptase inhibitors are indicated for human immunodeficiency virus (HIV) infection. Cancers treated: Cervical cancer, head and neck cancers, HIV infection and opportunistic viral infections associated with all types of cancer. (continued on page 92)
Common Antiviral Agents Drug (Other Names)
Brands
Subclass
Delivery Mode Conditions Treated
Abacavir sulfate
Ziagen
Nucleoside reverse transcriptase inhibitor
Oral
Human immunodeficiency (HIV) infection in patients with Kaposi sarcoma, other opportunistic cancers
Acyclovir, acyclovir sodium
Zovirax
Synthetic purine nucleoside
Oral, IV
Varicella and herpes zoster in cancer patients
Adefovir dipivoxil
Hepsera
Acyclic nucleotide analog Oral
Chronic hepatitis in cancer patients
Amantadine hydrochloride
Symmetrel
Synthetic cyclic primary amine
Oral
Prevention or treatment of influenza A in cancer patients
Amprenavir
Agenerase
Protease inhibitor
Oral
Kaposi sarcoma for treatment of HIV infection
Atazanavir sulfate
Reyataz
Protease inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Cidofovir
Vistide
Nucleotide analog
IV
Cytomegalovirus (CMV) retinitis
Darunavir ethanolate
Prezista
Protease inhibitor
Oral
Kaposi sarcoma for treatment of HIV infection
Delavirdine mesylate
Resciptor
Nonnucleoside reverse transcriptase inhibitor
Oral
Kaposi sarcoma for treatment of HIV infection
Didanosine (ddl)
Videx, Videx EC
Nucleoside reverse transcriptase inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Efavirenz
Sustiva
Nonnucleoside reverse transcriptase inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers (continued)
90
Salem Health: Cancer
Antiviral therapies
Common Antiviral Agents (continued) Drug (Other Names)
Brands
Subclass
Delivery Mode Conditions Treated
Emtricitabine
Emtriva
Nucleoside reverse transcriptase inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Enfuvirtide
Fuzeon
Fusion inhibitor
Subcutaneous injection
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Entecavir
Baraclude
Guanosine nucleoside analog
Oral
Chronic hepatitis B in patients with cancer
Famciclovir
Famvir
Synthetic acyclic guanine Oral derivative
Acute herpes zoster infection and recurrent genital herpes in patients with cancer
Fosamprenavir calcium Lexiva
Protease inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Foscarnet sodium Foscavir (phosphonoformic acid)
Pyrophosphate analog
IV
CMV retinitis in patients with cancer
Gangciclovir
Cytovene
Synthetic purine Oral, IV nucleoside guanine analog
CMV retinitis in patients with cancer
Indinavir sulfate
Crixivan
Protease inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Lamivudine
Epivir
Nucleoside reverse transcriptase inhibitor
Oral
HIV infection in patients with Kaposi sarcoma and other opportunistic cancers; chronic hepatitis B infection in cancer patients
Lopinavir and ritonavir
Kaletra
Protease inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Nelfinavir mesylate
Viracept
Protease inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Nevirapine
Viramune
Nonnucleoside reverse transcriptase inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Oseltamivir phosphate
Tamiflu
Selective neuraminidase inhibitor
Oral
Prevention and treatment of influenza infection
Ribavirin
Copegus, Rebetol, Synthetic nucleoside Ribaspheres, Virazole
Oral, inhalation
Chronic hepatitis infection
Ritonavir
Norvir
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Protease inhibitor
(continued on page 92)
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Antiviral therapies
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Common Antiviral Agents (continued) Drug (Other Names)
Brands
Subclass
Delivery Mode Conditions Treated
Saquinavir mesylate
Invirase
Protease inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Stavudine (2,3 didehydro3deoxythymidine, d4T)
Zerit, Zerit XR
Nucleoside reverse transcriptase inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Tenofovir disoproxil fumarate
Viread
Nucleoside reverse transcriptase inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Tipranavir
Aptivus
Protease inhibitor
Oral
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Valacyclovir hydrochloride
Valtrex
Synthetic purine nucleoside
Oral
Herpes zoster and genital herpes in cancer patients
Valganciclovir
Valcyte
Synthetic nucleoside
Oral
CMV retinitis in cancer patients
Zanamivir
Relenza
Selective neuraminidase inhibitor
Inhalation
Prevention and treatment of influenza virus A and B
Zidovudine (azidothymidine, AZT)
Retrovir
Nucleoside reverse transcriptase inhibitor
Oral, IV
HIV infection in patients with Kaposi sarcoma, other opportunistic cancers
Subclasses of this group: Nucleotide analogs, purine nucleoside analogs, acyclic guanine derivatives, pyrophosphate analogs, purine nucleoside guanine derivatives, protease inhibitors, nucleoside reverse transcriptase inhibitors, nonnucleoside reverse transcriptase inhibitors Delivery routes: Administered orally in the form of capsules, tablets, and solutions at home or in the hospital; some also administered in the hospital by intravenous (IV) infusion or subcutaneous injection How these drugs work: The first successful antiviral drug, acyclovir, was discovered in the 1960’s for the treatment of herpesvirus infection. The increased incidence of HIV infection in the 1980’s initiated the development of a variety of antiviral agents that are available today. Antiviral agents work in a variety of ways depending on the drug type. Some competitively inhibit an enzyme located on the viral deoxyribonucleic acid (DNA) chain, halting growth of the viral DNA. Some work on viral ribonucleic acid (RNA), preventing the virus from penetrating healthy cells. Others inhibit viral nucleic acid synthesis by interacting directly with the DNA enzymes. Protease inhibitors 92
inhibit the enzyme needed for viral replication. Reverse transcriptase inhibitors also inhibit viral replication after incorporating themselves into the viral DNA. Side effects: The most common side effects associated with antiviral therapy include gastrointestinal symptoms such as anorexia, abdominal pain, diarrhea, dyspepsia, flatulence, nausea, and vomiting. Other side effects that may occur with antiviral therapy include headache, dizziness, insomnia, depression, suicidal ideation, peripheral neuropathy, weakness, rash, sweating, back pain, chest pain, fever, muscle ache, pneumonia, weight loss, anxiety, elevated or decreased blood pressure, pancreatitis, tremor, cough, shortness of breath, chills, low white blood cell count, low platelet count, anemia, hypoglycemia, seizures, hepatitis, and liver toxicity. Collette Bishop Hendler, R.N., M.S. u
For Further Information Drug Facts and Comparisons 2008. St. Louis: Wolters Kluwer Health, 2008. Lorigan, Paul, ed. Lung Cancer. Dana-Farber Cancer Institute Handbook. New York: Mosby Elsevier, 2007.
Salem Health: Cancer Nursing 2008 Drug Handbook. Philadelphia: Lippincott Williams & Wilkins 2008. See also Antidiarrheal agents; Antifungal therapies; Aplastic anemia; Herpes simplex virus; Herpes zoster virus; Infection and sepsis; Leukoencephalopathy; Viral oncology; Virus-related cancers.
u Anxiety Category: Social and personal issues Definition: Anxiety encompasses a complex set of behavioral, cognitive, and physiological responses to a perceived threat. Symptoms of anxiety include apprehension or fearfulness toward a future event or outcome, physical signs (such as muscle tension, elevated heart rate, breathing changes, and sweating), and often concern about the meaning or implications of the anxious reaction itself. Description of the problem: A key feature of anxiety is the perception of an imminent or future threat, regardless of the accuracy of the perception. Although it is easy to imagine exaggerated or unrealistic appraisals of threat in many circumstances, in the case of cancer, anxiety is a normal and expected reaction to a true threat—a serious and often life-threatening disease. Therefore, distinguishing a normal anxious reaction from a pathological one is difficult in cancer patients as well as in their caregivers and loved ones. Excessive anxiety is a marker of poor coping among cancer patients and warrants further evaluation. Vital to the assessment of clinically significant anxiety is the extent to which anxiety meaningfully impairs the ability to function. For example, extreme anxiety may prevent an otherwise able patient or loved one from continuing to work, or it may interfere with medical care when a patient’s fearful avoidance prevents or delays receipt of tests or treatments. The American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders: DSM-IV-R (4th rev. ed., 2000) recognizes several distinct types of anxiety disorders, including generalized anxiety disorder, panic disorder, specific phobia, social phobia, obsessivecompulsive disorder, and post-traumatic stress disorder. Anxiety may also be a prominent feature of depression or an adjustment disorder (a short-term psychological reaction to a stressful event), both of which are common among cancer patients. The experience of being a cancer patient can contribute to the development of anxiety disorders in several ways.
Anxiety For example, a patient may develop a phobia of particular objects or procedures such as needles or diagnostic tests that were associated with highly stressful experiences. After cancer care, some patients may experience symptoms of post-traumatic stress disorder, characterized by recurrent intrusive memories and flashbacks, avoidance of reminders of stressful events, and hyperarousal symptoms such as sleep difficulties and irritability. Anxiety may also have origins in medical causes such as certain types of tumors or physiological side effects from some treatments. Prevalence: Not surprisingly, research suggests that the vast majority of cancer patients experience anxiety at some point during their illness. Far fewer develop clinical anxiety disorders. Although several studies have suggested an increased prevalence of anxiety disorders among cancer patients, others suggest little or no difference in this prevalence when cancer patients are compared with the
While receiving chemotherapy, a young boy plays a virtual reality game in an effort to distract him from the treatment and relieve his anxiety. (AP/Wide World Photos)
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APC gene testing general population. Reported rates of anxiety disorders are usually lower when assessed using formal diagnostic criteria and range from 10 to 30 percent. Assessment: In the clinical setting, anxiety is most commonly assessed face to face by a primary care provider or by a provider with special expertise in mental health, such as a psychiatrist or a clinical psychologist. The assessment is usually in the form of an interview to establish the nature, duration, and severity of symptoms according to established criteria, whether according to the diagnostic standards set out by the American Psychiatric Association or some other diagnostic system. Numerous standardized questionnaires are also available to measure anxiety in clinical and research settings. These questionnaires ask respondents to self-report the frequency or severity of various symptoms commonly associated with anxiety. Examples of anxiety assessment questionnaires that have been used with cancer patients include the Beck Anxiety Inventory, the State-Trait Anxiety Inventory, and the Hospital Anxiety and Depression Scale. Treatment and therapy: Anxiety related to medication or disease is usually first treated by managing the underlying condition causing symptoms. However, in many cases, anxiety is treated as a condition in its own right. Effective interventions for anxiety include both medical and psychological treatment options. Medical management of anxiety usually entails treatment with an anxiolytic (antianxiety) or antidepressant medication, the latter particularly when signs of a depressed mood are present. The most commonly prescribed anxiolytic medications belong to the class of drugs known as benzodiazepines, which includes clonazepam (Klonopin), alprazolam (Xanax), and diazepam (Valium). Commonly prescribed antidepressants include selective serotonin reuptake inhibitors (SSRIs) such as paroxetine and sertraline (Zoloft), serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine (Effexor) and duloxetine (Cymbalta), and to a lesser extent tricyclic antidepressants such as imipramine (Tofranil) and clomipramine (Anafranil). Psychological treatments include individual psychotherapy (talk therapy), group therapy, family therapy, and certain mind-body interventions. In particular, research heavily supports the efficacy of cognitive-behavioral therapy, which encompasses a variety of therapeutic techniques. Broadly speaking, the goals of cognitive-behavioral therapy for anxiety are to guide patients toward a more balanced and rational appraisal of their concerns and to encourage behaviors that reduce or neutralize anxieties rather than exacerbate them. Other frequently used thera94
Salem Health: Cancer peutic approaches include training in relaxation techniques, mindfulness meditation, and hypnosis. Biofeedback may also be effective in helping patients recognize and manage physical symptoms of anxiety by, for example, reducing muscle tension and cardiovascular reactivity to stress. Andrea Bradford, M.A. u
For Further Information American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-IV-TR. 4th rev. ed. Washington, D.C.: Author, 2000. Antony, Martin M., Susan M. Orsillo, and Lizabeth Roemer, eds. Practitioner’s Guide to Empirically Based Measures of Anxiety. New York: Kluwer Academic/Plenum, 2001. Baum, Andrew, and Barbara L. Andersen, eds. Psychosocial Interventions for Cancer. Washington, D.C.: American Psychological Association, 2001.
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Other Resources
American Psychiatric Association http://www.psych.org American Psychological Association http://www.apa.org Anxiety Disorders Association of America http://www.adaa.org National Cancer Institute Anxiety Disorder http://www.cancer.gov/cancertopics/pdq/ supportivecare/anxiety See also Counseling for cancer patients and survivors; Depression; End-of-life care; Grief and bereavement; Living with cancer; Medical marijuana; Pain management medications; Palliative treatment; Psycho-oncology; Psychosocial aspects of cancer; Relationships; Self-image and body image; Sexuality and cancer; Side effects; Stress management; Support groups; Survivorship issues.
u APC gene testing Category: Procedures Also known as: Adenomatosis polyposis coli gene testing Definition: The APC gene is a tumor-suppressor gene that is often mutated in colorectal and other cancers. Most mutations leading to colorectal cancer occur spontaneously in
Salem Health: Cancer
Aplastic anemia
the digestive tracts of affected individuals, but approximately 5 percent of cases result from inherited mutations in APC. Testing for mutations in APC usually involves determining the deoxyribonucleic acid (DNA) sequence of a patient’s APC gene, but other screens are sometimes used.
See also Adenomatous polyps; Colorectal cancer; Desmoid tumors; Gardner syndrome; Genetic counseling; Genetic testing; Hereditary cancer syndromes; Hereditary polyposis syndromes; Tumor markers; Turcot syndrome.
Cancers diagnosed: Familial adenomatous polyposis, familial colon cancer
u Aplastic anemia
Why performed: Testing for mutations in the APC gene is performed to diagnose familial adenomatous polyposis (FAP), an inherited condition in which precancerous polyps form in the colon. Although these polyps are initially benign, they may develop into cancer if untreated. The DNA of patients exhibiting symptoms of FAP is sequenced to confirm diagnosis and to characterize the mutation in APC. Because FAP is an inherited disorder, genetic testing is often done in relatives of those afflicted with FAP in order to determine whether prophylactic treatment is required.
Category: Diseases, symptoms, and conditions Also known as: Bone marrow failure
Patient preparation: Patients considering genetic testing may meet with a genetic counselor to discuss the benefits and risks of the test and the significance of negative, positive, and inconclusive tests. The material required for genetic testing is obtained from a blood sample. Steps of the procedure: Blood samples are sent to a clinical laboratory that offers APC screening. DNA is purified from the blood sample, and the DNA that encodes for APC is amplified by polymerase chain reaction (PCR) and sequenced using standard, automated methods. After the procedure: The patient may consult with a physician or genetic counselor to discuss the implications of the test results.
Related conditions: Thrombocytopenia (low platelet count), neutropenia (low white count) Definition: The bone marrow is responsible for producing all of the blood cells in the body. Aplastic anemia is a lifethreatening condition caused when the bone marrow stops producing enough new cells to create new blood cells. The typical life span of red blood cells is 120 days, platelets about 6 days, and white blood cells about 1 day. The bone marrow needs to produce cells continuously to replace the dying cells. Aplastic anemia can be acquired or hereditary. The more common acquired aplastic anemia can be a temporary condition caused by exposure to toxic chemicals, pesticides, and benzenes. Common causes for the cancer patient are chemotherapy and radiation. Hereditary aplastic anemia is rare and can be associated with Fanconi anemia, Shwachman-Diamond syndrome, and dyskeratosis congenita. Etiology and the disease process: Although the cause of most aplastic anemia is unknown, those cases induced by chemotherapy and radiation result from the therapy’s suppression of bone marrow function. The bone marrow is not able to manufacture the cells that are needed to create red blood cells, platelets, and white blood cells.
Risks: Complications from drawing blood are rare but may include pain, bleeding, hematoma, or infection. Because the information obtained from APC screening may have dramatic psychological effects, it is essential that patients be offered genetic counseling.
Incidence: Aplastic anemia is a rare condition with only about 500 to 1,000 new cases each year in the United States. Of patients who are diagnosed with aplastic anemia, 20 percent have an inherited disorder as well.
Results: Sequence analysis allows clinicians to identify the specific DNA mutation(s) present in a FAP patient. Once the mutation has been identified, close relatives can be screened to determine if they share the FAP-causing mutation. Patients who do not carry the mutation are at no greater risk for colon cancer than the general population. Colectomy (surgical resection of the colon) and other prophylactic treatment are recommended for individuals who carry cancer-causing mutations in the APC gene. Kyle J. McQuade, Ph.D.
Symptoms: The signs and symptoms of aplastic anemia may be seen immediately or can be slow to develop and be dependent on the blood counts themselves. Common symptoms include fatigue, dizziness, an irregular heart rate, fevers, frequent infections, frequent nose bleeds, oozing gums, blood in the stool, bruising, difficulty in stopping bleeding from a cut, and petechiae (similar to a red pinpoint rash, located on the arms, legs, and trunk). Patients may also complain of severe shortness of breath even while at rest. 95
Aplastic anemia
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can be given to help the bone marrow release immature red blood cells from the bone marrow to mature and become functioning red cells. Not all forms of aplastic anemia will respond to growth factors. Platelet transfusions will help the patient be able to form clots to stop bleeding. White blood cells are not typically transfused because of their short life span; however, they may be given to patients who have a severe infection. Patients with a low white blood cell count may receive filgrastim, a white blood cell growth factor, to stimulate the release of the immature white blood cells so that they can mature and fight off infections. Like the red cell growth factor, filgrastim may not be applicable for all forms of aplastic anemia. This pinpoint rash on the palm of the hand is a symptom of aplastic anemia. (Custom Patients may receive medications such Medical Stock Photo) as antithymocyte globulin (ATG), cyclosporine, and methylprednisolone. TradiScreening and diagnosis: Aplastic anemia is typically tional therapy consists of the patient taking all three medifound when patients complain of fatigue to their physications. It may take a few months before an improvement cians. The physical assessment includes looking for pale in blood counts is apparent. Patients may say that they are or yellow-tinted skin; listening to the heart, lungs, and feeling better before their counts actually reflect an imbreathing patterns; feeling the liver and spleen for enlargeprovement. Antibiotics and antivirals may also be given to ment; and checking for signs of bleeding. The physician prevent infection. may also assess the patient’s environment to determine Bone marrow transplants are more commonly used whether exposure to toxic chemicals or other triggers has with younger patients to replace damaged bone marrow. occurred. Diagnostic testing includes analysis of blood, Research is ongoing to develop additional treatments for urine, and stool samples, and bone marrow aspiration and aplastic anemia. biopsy. The patient may also have images taken (X rays, Prognosis, prevention, and outcomes: Historically computed tomography scans, and ultrasound) to look for aplastic anemia has had a poor prognosis. However, great enlarged organs. Once testing is complete, the aplastic strides have been made on the treatments available for anemia is staged according to how many cells are seen in aplastic anemia, and modern therapy has cured or manthe bone marrow. The three stages are moderate, severe, or aged the disease in many patients. Treatment can be effecvery severe. tive but may take months before results are seen. Patients may also need to try different therapies to find one that Treatment and therapy: The treatment for aplastic aneworks for them. Some forms of aplastic anemia can be premia depends on the severity and the patient’s symptoms. vented by avoiding exposure to toxins, radiation, and medThe patient’s overall health also determines what type of ication, but other forms cannot be prevented. treatment can be tolerated. Moderate aplastic anemia is not Katrina Green, R.N., B.S.N., O.C.N. treated, but the physician keeps a close eye on the blood counts and the patient’s symptoms. If the aplastic anemia is caused by chemotherapy or radiation, the patient is treated with transfusions and growth factors. Transfusions of red blood cells and platelets are the most common. Red blood cell transfusions help raise the hematocrit and hemoglobin, which improves the anemia symptoms. Epoietin alfa, a red blood cell growth factor, 96
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For Further Information Klag, Michael J, ed. Johns Hopkins Family Health Book. New York: HarperCollins, 1999. Schrezenmeier, Hubert, and Andrea Bacigalupo, eds. Aplastic Anemia: Pathophysiology and Treatment. New York: Cambridge University Press, 2000.
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Other Resources
Aplastic Anemia & MDS International Foundation http://www.aplastic.org National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov See also Anemia; Bone marrow transplantation (BMT); Fanconi anemia; Hairy cell leukemia; Hematologic oncology; Leukemias; Leukopenia; Myelodysplastic syndromes; Neutropenia; Transfusion therapy.
u Appendix cancer Category: Diseases, symptoms, and conditions Also known as: Carcinoid tumor, colonic adenocarcinoma, mucinous cyst adenocarcinoma, signet-ring cell adenocarcinoma Related conditions: Appendicitis, peritoneal carcinomatosis, disseminated peritoneal adenomucinosis Definition: Appendix cancer is a cancerous tumor in the appendix, the pouchlike, thin tube with a closed end that is located in the lower right quadrant of the abdomen. The appendix, also called the vermiform appendix because its appearance is wormlike, is attached to the cecum, the first section of the large intestine, close to where it joins with the small intestine. It is not known to have a significant function in the body but may play a role in the immune system. Cancerous tumors that originate in the appendix are part of the larger grouping of colorectal or gastrointestinal cancers. Types of appendix cancer include carcinoid tumor, mucinous cyst adenocarcinoma, colonic-type adenocarcinoma, and signet-ring cell adenocarcinoma. Risk factors: Because appendix cancer is not common, no specific risk factors have been identified. However, risk factors for colorectal cancers in general include a diet high in red meat, lack of exercise, obesity, and cigarette smoking. Etiology and the disease process: The cause of appendix cancer is unknown. It often goes undiagnosed until it causes appendicitis or the appendix ruptures. In a majority of patients, appendix tumors spread in a process called peritoneal seeding, in which multiple, initially small, tumors are produced throughout the abdominal cavity. Lowgrade tumors grow more slowly and are generally less invasive, whereas high-grade tumors are faster growing and considerably more invasive.
Appendix cancer Incidence: Cancer that starts in the appendix, or primary appendix cancer, is uncommon. Therefore, these cancers are usually included in the statistical data for colorectal cancer. and actual incidence rates are not available. One estimate is that about 1 percent of colorectal cancer cases in the United States are primary appendix cancer, with about 1,100 new cases diagnosed in 2007. About 66 percent of appendix tumors are carcinoid tumors, 20 percent are mucinous cyst adenocarcinoma, and 10 percent are colonic-type adenocarcinoma. Signet-ring cell adenocarcinoma, which is very rare, is an aggressive cancer that is more difficult to treat than other adenocarcinomas. Symptoms: People with appendix cancer may not experience symptoms until the disease is far advanced. The first reported symptoms are typically those of appendicitis, which include fever, pain in the lower right quadrant of the abdomen, nausea, and vomiting. Other symptoms may include bowel changes, abdominal bloating, pelvic pain, infertility, and an increase in waistline size, with possible navel protrusion. Some people experience no symptoms at all, and the cancer is found incidentally during surgery for another condition such as ovarian tumors. Screening and diagnosis: There are no screening tests for appendix cancer. Most often it is found during surgery for another abdominal condition, either when a biopsy is performed on the tissue that has been removed or when the surgeon observes abnormalities or tumors in the abdomen. Computed tomography scanning, magnetic resonance imaging, and ultrasound can be performed if appendix cancer is suspected or to determine the extent of the cancer’s spread. Radionuclide scanning is performed to determine the spread of a carcinoid tumor. No standard staging system exists for appendix cancer. Instead, appendix tumors are usually classified by whether the cancer is confined to the appendix or has spread and how far: to distant organs or only to nearby tissues. Treatment and therapy: The treatment of appendix cancer depends on the type of tumor, its size, and whether the cancer has spread. Surgery to remove the tumor along with nearby blood vessels, lymph nodes, and part of the large bowel is the most common treatment for tumors that are low grade and slow growing. Currently, the most effective treatment for higher-grade, more aggressive tumors and tumors that have seeded the abdomen is a procedure called cytoreductive or debulking surgery. During this procedure, the surgeon removes as much of the cancer in the abdomen as possible. When complete, it means that all visible tumors were removed; when incomplete, it means 97
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Stage at Diagnosis and Relative Survival Rates for Appendix Cancer, 1988-2001 Survival Rates (%) Stage Stage I Stage II Stage III Stage IV
1-Year
5-Year
10-Year
97.4 92.6 87.2 65.9
89.9 73.9 48.3 25.4
83.2 63.9 37.0 16.2
Source: Data from L. A. G. Ries et al., eds., Cancer Survival Among Adults: U.S. SEER Program, 1988-2001—Patient and Tumor Characteristics, NIH Pub. No. 07-6215 (Bethesda, Md.: National Cancer Institute, 2007)
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Other Resources
American Cancer Society http://www.cancer.org Appendix Cancer (Appendiceal Carcinoma) & Peritoneal Surface Malignancy http://www.appendix-cancer.com Cancer.Net http://www.cancer.net/portal/site/patient See also Carcinoid tumors and carcinoid syndrome; Continuous hyperthermic peritoneal perfusion (CHPP); Small intestine cancer; Stomach cancers.
u Appetite loss that some tumors could not be removed. This surgery is typically combined with intraoperative hyperthermic intraperitoneal chemotherapy; a high concentration of a chemotherapy solution is instilled in the abdomen during surgery. The solution, heated to just above normal body temperature, has been found to be effective because it destroys cancer cells and tumors that are too small to be seen and also because it can reach all surfaces in the abdomen. Postoperative intraperitoneal chemotherapy is also used in some cases. Prognosis, prevention, and outcomes: The prognosis for appendix cancer varies greatly and depends on several factors, including the type of tumor, whether it has spread, and how it is treated. Complete cytoreductive surgery combined with intraoperative hyperthermic intraperitoneal chemotherapy has been found to be effective in increasing survival rates, especially with mucinous cyst adenocarcinoma. Appendix cancer has no known method of prevention. Dorothy P. Terry, R.N. u
For Further Information Carmignani, C. P., and P. H. Sugarbaker. “Synchronous Extraperitoneal and Intraperitoneal Dissemination of Appendix Cancer.” European Journal of Surgical Oncology 30, no. 8 (October, 2004): 864-868. Holland, Jimmie C., and Sheldon Lewis. The Human Side of Cancer. New York: HarperCollins, 2000. Sugarbaker, Paul H. “New Standard of Care for Appendiceal Epithelial Neoplasms and Pseudomyxoma Peritonei Syndrome?” Lancet Oncology 7, no. 1 (January, 2006): 69-76. 98
Category: Diseases, symptoms, and conditions Also known as: Anorexia Related conditions: Cachexia Definition: Loss of appetite in cancer patients, referred to by medical professionals as anorexia, may result from either the cancer itself or the treatments used to combat the disease. Cancer-related anorexia is associated with weight loss and has been shown to correlate with a poorer outcome and a lower quality of life. Risk factors: Those with cancer and undergoing chemotherapy for cancer are at risk. Etiology and the disease process: Because many cancer treatments affect not only cancer cells but also healthy cells, several unwanted side effects may result. For instance, chemotherapy may reduce the turnover of taste receptor cells in the tongue, which may alter the flavor of food. Additional damage to other cell types in the mouth may result in sores, gum disease, dry mouth, and sore throat. Cells in the digestive tract may also be injured, resulting in abnormal gut motility and difficulty swallowing. Together, these effects may change the way food tastes and decrease the desire to eat. Emotional side effects, such as fear and depression, as well as psychological effects, such as food aversion, can also contribute to the loss of appetite. Furthermore, many cancer patients with anorexia report early satiety, meaning that they feel full after eating only a small amount of food. Biological causes for cancer-related anorexia also exist. Cytokines released by tumor cells or produced by immune cells in response to cancer may affect the central nervous system and the gastrointestinal tract to promote
Salem Health: Cancer appetite loss. Specifically, the central nervous system is responsible for controlling food intake and energy homeostasis, while effects on the gastrointestinal tract can influence feelings of fullness. Examples of cytokines that may affect appetite include tumor necrosis factor-alpha (TNF-α), C-reactive protein, interleukin-1 beta (IL-1 beta), IL-6, and tumor-derived lipid mobilizing factor (LMF). However, there is some conflicting data as to whether blood levels of these cytokines correlate with, or are responsible for, the loss of appetite. Incidence: In general, approximately 25 percent of cancer patients report loss of appetite. The incidence can be as high as 90 percent for patients with advanced cancers. However, different types of cancers tend to have different rates of anorexia. For example, approximately 60 to 80 percent of patients with cancers of the lung, stomach, pancreas, or esophagus have significant weight loss caused, in part, by anorexia. However, loss of appetite is not as frequent in patients with breast or prostate cancer. Treatment and therapy: Cancer-related anorexia may be managed by either changing eating habits or taking medication. There are several dietary suggestions for cancer patients who struggle with loss of appetite. Liquid or powdered meal replacements as well as juice, soups, and milkbased drinks or shakes may be used in place of solid food to provide nutrients. Eating several small meals or snacks instead of three large meals per day may also be more feasible for patients with cancer-related anorexia. Additionally, drinking a glass of wine or exercising regularly may also stimulate the appetite. However, patients should consult with their doctors before consuming alcohol or beginning an exercise regimen. The pharmacological treatment of cancer-related anorexia can be broadly divided into three groups: appetite stimulants, anticatabolic agents, and anabolic agents. Examples of appetite stimulants include progestational agents (such as megestrol acetate and medroxyprogesterone), which can improve caloric intake. Corticosteroids (such as prednisolone and methylprednisolone) may improve appetite because of their inhibition of prostaglandin metabolism and IL-1 signaling. Cyproheptadine, an antihistamine, is also a serotonin antagonist, and its effects on this neurotransmitter in the brain can also promote an increase in appetite. A more controversial appetite stimulant is cannabis (marijuana), as it can stimulate CB1 receptors in the brain to enhance appetite. Anticatabolic agents, which inhibit the production or activity of appetite-decreasing cytokines, are also important in combating cancer-related anorexia. Examples include thalidomide (a potent inhibitor of TNF-α produc-
Appetite loss tion) and eicosapentaenoic acid (an inhibitor of adenylate cyclase activity and tumor-derived LMF activity). Anabolic agents such as oxandrolone and fluoxymesterone have been studied as well, and they may build lean tissue mass by increasing muscle protein synthesis. The hormone androgen may also be useful in cancer patients (except for those with hormone-dependent tumors) as it can promote muscle growth and strength and may also induce the secretion of leptin, a hormone produced by adipose tissue to stimulate appetite. Prognosis, prevention, and outcomes: Generally appetite loss resolves itself when its underlying cause is remedied. Although appetite loss can interfere with the healing process, it does not usually cause death in patients with early-stage cancers. However, cancer-related anorexia is often associated with cachexia, a wasting syndrome characterized by not only the loss of appetite but also weight loss, breakdown of muscle tissues, depletion of reserves within fat (adipose) tissue, fatigue, and weakness. In advanced-stage cancer, the cancer anorexia-cachexia syndrome is observed in about 80 percent of patients and is one of the most frequent causes of death. u
For Further Information Behl, D., and A. Jatoi. “Pharmacological Options for Advanced Cancer Patients with Loss of Appetite and Weight.” Expert Opinion on Pharmacotherapy 8, no. 8 (June, 2007): 1085-1090. Perboni, S., and A. Inui. “Anorexia in Cancer: Role of Feeding-Regulatory Peptides.” Philosophical Transactions of the Royal Society B: Biolocial Sciences 361, no. 1471 (July 29, 2006): 1281-1289. Poole, K., and K. Froggatt. “Loss of Weight and Loss of Appetite in Advanced Cancer: A Problem for the Patient, the Carer, or the Health Professional?” Palliative Medicine 16, no. 6 (November, 2002): 499-506. Rubin, H. “Cancer Cachexia: Its Correlations and Causes.” Proceedings of the National Academy of Sciences of the United States of America 100, no. 9 (April 29, 2003): 5384-5389.
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Cancer.Net Appetite Loss http://www.ascocancerfoundation.org/patient/ Diagnosis+and+Treatment/Treating+Cancer/ Managing+Side+Effects/Appetite+Loss 99
Arsenic compounds National Cancer Institute Eating Hints for Cancer Patients: Before, During, and After Treatment http://cancer.gov/cancertopics/eatinghints/page3 Elizabeth A. Manning, Ph.D. See also Antidiarrheal agents; Cachexia; End-of-life care; Gastrointestinal cancers; Gerson therapy; Living with cancer; Medical marijuana; Pain management medications; Palliative treatment; Side effects; Taste alteration; Weight loss.
u Arsenic compounds Category: Carcinogens and suspected carcinogens RoC status: Known human carcinogen since 1980 Also known as: Arsenic pentoxide, arsenic trioxide, arsenic acid Related cancers: Lung cancer, bladder cancer, liver cancer, kidney cancer, prostate cancer, colon cancer, certain types of skin cancer Definition: Arsenic occurs in small concentrations in earth and minerals. Leaching effects of water and wind erosion continuously release trace amounts, which can be transported over long distances via windblown dust, surface water, and groundwater flow. Inorganic arsenic compounds are naturally occurring combinations of arsenic and oxygen, sulfur, or chlorine. These and the complex minerals they are associated with are generally water soluble and occur as white, odorless solids. They typically have high melting and boiling points and can be extremely toxic, even fatal, if inhaled or ingested in large quantities. Exposure routes: Arsenic compounds in the form of dust and fumes can be absorbed through dermal layers of the skin or can be inhaled and absorbed in respiratory passageways. Arsenic can be ingested orally as a contaminant in food or water. Where found: Arsenic is a naturally occurring material in soil and water and also in various ores, especially copper and lead. Therefore, arsenic compounds are found throughout the environment. Arsenic naturally combines with other naturally occurring elements including sulfur, oxygen, and chlorine to create relatively stable inorganic arsenic compounds. Often the most concentrated environmental forms of arsenic are released into the atmosphere via volcanoes and mineral and ore erosion. Because arsenic compounds cannot be destroyed, a fairly constant 100
Salem Health: Cancer level of toxic inorganic compounds of arsenic always exists in the environment, either in soil, water, or as airborne particulate matter. Because most arsenic compounds are soluble in water, airborne arsenic may be transported great distances before being removed via precipitation to return to soil and water. At risk: Compounds of inorganic arsenic are used in the manufacture of semiconductors and as a wood preservative. They are also used in making special glass. People involved in these industries are especially at risk because of direct occupational exposure. Because many arsenic compounds occur in ores, people who work in metal smelters are often exposed to higher levels of arsenic. Similarly, carpenters and contractors and others may be exposed to the fumes of burning wood treated with an arsenic preservative or inhale sawdust from treated wood. The most common arsenic poisoning incidents occur among workers involved in the production of arsine, an extremely toxic gas produced by combining arsenic and hydrogen. Finally, people who live in areas with high levels of arsenic in rock or in water are at greater risk. Etiology and symptoms of associated cancers: Studies conducted on humans testing positive for high levels of inorganic arsenic compounds show significant correlations with various cancers, including skin, liver, lung, and bladder cancer. Studies show an especially strong positive correlation between an increase in toxicity levels of arsenic in air, soil, and water and an increase in nonmelanoma skin cancer. Internal cancers, including liver, kidney, and bladder cancer, probably result from exposure to arsenic via ingestion of food and liquid contaminated with high levels of inorganic arsenic and its compounds. As plants fairly readily absorb inorganic arsenic and its compounds, plants in habitats with high levels of arsenic will be contaminated with higher than normal amounts of this highly toxic mineral. Digestion of plant food in the gastrointestinal tract increases exposure to and absorption of certain arsenic compounds, which then are carried to the liver, kidney, aorta, and skin before they are transferred to the bladder for excretion. Note that this list of exposed organs equates to the more common types of arsenic-induced cancers. The two most common types of nonmelanoma skin cancers associated with toxic arsenic levels are basal cell carcinoma and squamous cell carcinoma. Basal cell carcinoma begins in the lowest layer of the epidermis, called the basal cell layer. It is highly unusual for a basal cell cancer to spread to lymph nodes or to distant parts of the body. However, if a basal cell cancer is left untreated, it can grow into nearby areas and invade the bone or other tissues be-
Salem Health: Cancer neath the skin. Squamous cell carcinomas tend to be more aggressive than basal cell cancers. They are more likely to invade fatty tissues just beneath the skin, and slightly more likely to spread to lymph nodes or distant parts of the body, although this is still uncommon. Symptoms include changes in skin texture, size, or color, and the area may become sore or ooze. Very high levels of arsenic exposure and absorption via all routes may lead to a decrease in blood cell production, lymphatic cancer, brain damage, and, in women, infertility and miscarriages. History: In industry, inorganic arsenic compounds were used as pesticides as early as the middle of the nineteenth century. Within the next century, however, use of such compounds was curbed because of noticeable environmental effects. The most common use for inorganic arsenic since the 1980’s is in wood preservation. Pressuretreated wood is made by immersing wood in chromated copper arsenate (CCA) or applying it to the wood under pressure. The arsenic component helps protect the treated wood from weather damage, insects, and decay. CCA is no longer used for residential projects but is used for industrial building. Although the United States has not produced arsenic since 1985, it is still the world’s leading arsenic consumer. This puts people at risk in nontraditional ways. For example, people with decks and other housing structures constructed with preserved wood are automatically at increased risk of arsenic exposure, as are farmers who used arsenic-containing pesticides. In medicine, diseases such as syphilis and psoriasis, leukemia, and asthma were commonly treated with inorganic arsenic solutions until the 1970’s. Even in the twenty-first century, it is still used as an antiparasitic agent in veterinary medicine, especially in many countries outside the United States. Continued use of arsenic in all its forms has actually increased environmental levels in soil, water, and air—-a trend that is likely to continue with increased industrial demands for this highly valuable but also highly toxic mineral. Dwight G. Smith, Ph.D. u
For Further Information Battacharyua, Prosun, et al., eds. Biogeochemical Interactions, Health Effects, and Remediation. Vol. 9 in Arsenic in Soil and Groundwater Environment. Cambridge, Mass.: Elsevier, 2007. Frost, Floyd J. Cancer Risks Associated with Elevated Levels of Drinking Water Arsenic Exposure. Washington, D.C.: AWWA Research Foundation and U.S. Environmental Protection Agency, 2004.
Arterial embolization Naidu, R., et al., eds. Managing Arsenic in the Environment: From Soil to Human Health. Enfield, N.H.: CSIRO and Science, 2006. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Eleventh Report on Carcinogens. Research Triangle Park, N.C.: Author, 2005. u
Other Resources
National Library of Medicine Environmental Health and Toxicology: Enviro-Health Links—Arsenic and Human Health http://sis.nlm.nih.gov/enviro/arsenicandhumanhealth .html See also Basal cell carcinomas; Bowen disease; Chewing tobacco; Cigarettes and cigars; Coke oven emissions; Fibrosarcomas, soft-tissue; Free radicals; Hemangiosarcomas; Hepatomegaly; Liver cancers; Lung cancers; Melanomas; Nickel compounds and metallic nickel; Occupational exposures and cancer; Pesticides and the food chain; Soots; Squamous cell carcinomas.
u Arterial embolization Category: Procedures Also known as: Transarterial bland embolization, transarterial chemotherapy, transarterial chemo embolization (TACE) Definition: Arterial embolization is the intentional blockage of an artery, thus depriving a tumor of a blood supply, oxygen, and nutrients. In some cases, embolization is used to deliver drugs or other chemotherapeutic agents via blood vessels to induce the cytotoxicity of tumors. Cancers treated: Hepatocellular carcinoma, tongue carcinoma Why performed: In patients whose cancer is significantly advanced and for whom surgical options cannot be considered, or in conditions of metastasis outside the liver and inadequate hepatic reserves, arterial embolization is preferred as a viable alternative. This option is generally chosen when the tumor is greater than 4 centimeters in size and there are multiple lesions. Arterial embolization takes advantage of the fact that the liver receives its blood supply from two main sources, the hepatic artery and hepatic portal vein, and that the major supplier of blood to liver is the hepatic artery. During the embolization procedure, the hepatic artery is blocked. Embolization may be combined 101
Artificial sweeteners with chemotherapy or radiotherapy to enhance the effects of treatments. Patient preparation: Patients are briefed on all the steps and options involved in the procedure. A hospital stay is generally required. Patients receive intravenous sedation to cause numbness and to mitigate pain. Steps of the procedure: During the procedure, an angiographic catheter is introduced in the branches of the hepatic artery. Usually a dye is injected for contrast and to acquire images. The hepatic artery is then blocked with occluding agents such as polyvinyl alcohol beads, which are transported to terminal hepatic arteries and occlude the vessels. The liver can still be healthy and functional using a blood supply derived from the alternative route of portal veins. In cases where arterial embolization is combined with chemotherapy (as in transarterial chemo embolization, or TACE), an anticancer drug (such as doxorubicin) is injected through the catheter and then the artery is blocked. Pressure is applied to prevent bleeding after the procedure is performed. Sometimes radiotherapy is combined with arterial embolization. After the procedure: An overnight stay in the hospital may be required. Generally, patients are advised to take adequate rest and avoid strenuous activities for at least twenty-four hours. The procedure may be repeated every six to eight weeks. Risks: Total liver failure, although not common, is a risk associated with this procedure. Side effects termed “embolization syndrome,” including nausea, abdominal pain, and mild fever, may ensue. Results: Increasing evidence shows that this procedure increases the rates of survival in liver cancer patients. In cases where it is combined with chemotherapy, recovery is expedited as a result of the presence of increased and prolonged concentrations of drugs around tumors. Geetha Yadav, Ph.D. See also Carcinoid tumors and carcinoid syndrome; Chemoembolization; Embolization; Hereditary leiomyomatosis and renal cell cancer (HLRCC); Hereditary nonVHL clear cell renal cell carcinomas; Hereditary papillary renal cell carcinomas; Kidney cancer; Leiomyomas; Living will; Urinary system cancers; Virus-related cancers.
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u Artificial sweeteners Category: Lifestyle and prevention Also known as: Aspartame, saccharin Definition: Artificial sweeteners are nonnutritive chemical substances that have virtually no or very low caloric value and are used as substitutes in food products for natural sweeteners such as sugar and honey. Artificial sweeteners are commonly used for controlling weight and insulin levels. Government-approved artificial sweeteners: Artificial sweeteners are nonnutritive in nature since they provide no calories or energy to the body. There are five artificial sweeteners—aspartame (NutraSweet, Equal), saccharin (Sweet’N Low, Sweet Twin, Necta Sweet), acesulfame K (Sunnet, Sweet One), neotame, and sucralose (Splenda)— approved for use in the United States by the U.S. Food and Drug Administration (FDA). Two artificial sweeteners that the FDAhas not approved are alitame and cyclamate. Aspartame is two hundred times sweeter than sugar and was approved for use as a general-purpose sweetener in all foods and drinks in 1996. Saccharin is two hundred to seven hundred times sweeter than sugar. It is used as a tabletop sweetener and in soft drinks and chewing gum. Acesulfame K was first approved by the FDA as a tabletop sweetener and is about two hundred times sweeter than sugar. Neotame, which is about seven thousand to fourteen thousand times sweeter than sugar, was approved in 2002 as a general-purpose sweetener in a wide variety of food products. Sucralose is the only artificial sweetener that has three chlorine atoms in its chemical structure and is six hundred times sweeter than sugar. It was approved in 1998 for use in food products, such as beverages, chewing gum, and frozen desserts. Sucralose was approved by the FDAas a general-purpose sweetener in all foods in 1999. Metabolism: Sucrose, the chemical entity in natural table sugar, binds to special receptor proteins in the taste buds. This binding initiates a cascade of events that finally results in a signal sent to the brain that causes the sensation of sweet taste. Additionally, sugar is a carbohydrate that is metabolized by the body to provide calories. Artificial sweeteners have a greater affinity for the receptor proteins and work by binding two hundred to fourteen hundred times more strongly to the receptor proteins than sucrose. As a result of their stronger binding capacity, the artificial sweeteners are needed in much lower quantities than sugar to produce the same degree of sweetness. The artificial sweeteners are either excreted by the body or converted to by-products with little or no caloric
Salem Health: Cancer output. Saccharin, sucralose, and acesulfame K are excreted unchanged by the body and do not provide any calories. The enzymes in the body hydrolyze neotame and produce methanol as a by-product. Aspartame is broken down in the body to produce methanol and the amino acids aspartic acid and phenylalanine and very few calories compared with sugar. Methanol is further degraded to formaldehyde in the body. Both methanol and formaldehyde are toxic to human beings at high doses. People with the genetic disease phenylketonuria (PKU) lack the enzyme that breaks down phenylalanine. Because phenylalanine is produced as a by-product of aspartame digestion, people with PKU should not ingest aspartame. Foods containing aspartame must carry a label warning consumers with PKU that the product is a source of phenylalanine. Cancer risk: Questions regarding the risk of cancer associated with the consumption of artificial sweeteners arose when early studies indicated that saccharin caused bladder cancer in test animals. Subsequent epidemiological studies of groups of people did not find a definitive correlation between saccharin use and bladder cancer. There are two more controversial reports on the correlation between aspartame use and cancer. One study found more lymphomas and leukemias in rats fed very high doses of aspartame while the other study did not find a link between aspartame use and cancer. Artificial sweeteners are regulated by the Food and Drug Administration. Before artificial sweeteners can be launched in the U.S. market, the FDA reviews numerous safety studies conducted with them, including the studies that assess their potential cancer risk. The reviews have not conclusively demonstrated any strong positive correlation between various cancers and artificial sweetener use. Studies continue to be conducted, and the FDA will continue to review and evaluate the results. Artificial sweeteners are beneficial for people with diabetes and for people on weight-loss plans. The effects of their long-term use on weight-maintenance and cancer risk are controversial because they are not clearly understood. In the light of insufficient experimental data and all the controversy swirling around the use of artificial sweeteners, moderation should be the watchword for everyone using them. Lalitha Krishnan, Ph.D. u
For Further Information Abegaz, E. M. “Aspartame Not Linked to Cancer.” Environmental Health Perspectives 115, no. 1 (January, 2007): A16-17. Gallus, S., et al. “Artificial Sweeteners and Cancer Risk in
Asbestos a Network of Case-Control Studies.” Annals of Oncology 18, no. 1 (January, 2007): 40-44. Lim, U., et al. “Consumption of Aspartame-Containing Beverages and Incidence of Hematopoietic and Brain Malignancies.” Cancer Epidemiology Biomarkers and Prevention 15 (September, 2006): 1654-1659. Soffritti, Morando, et al. “First Experimental Demonstration of the Multi-potential Carcinogenic Effects of Aspartame Administered in the Feed to Sprague-Dawley Rats.” Environmental Health Perspectives 114, no. 3 (March, 2006): 379-385. u
Other Resources
Green Facts http://www.greenfacts.org/en/aspartame/artificialsweeteners.htm MayoClinic.com Artificial Sweeteners: A Safe Alternative to Sugar http://www.mayoclinic.com/health/diabetes-diet/ NU00592 National Cancer Institute Artificial Sweeteners and Cancer: Questions and Answers http://www.cancer.gov/cancertopics/factsheet/Risk/ artificial-sweeteners See also Dietary supplements; Nutrition and cancer prevention; Obesity-associated cancers; Weight loss.
u Asbestos Category: Carcinogens and suspected carcinogens RoC status: Known human carcinogen since 1980 Also known as: Chrysotile, actinolite, amosite, anthophyllite, crocidolite, tremolite Related cancers: Pleural and peritoneal mesothelioma, gastrointestinal cancers, laryngeal cancer, possibly kidney and other cancers Definition: Asbestos refers to six naturally occurring fibrous silicate minerals: the serpentine mineral chrysotile and the amphibole minerals actinolite, amosite, anthophyllite, crocidolite, and tremolite. The fire-resistant properties of these minerals have been known since antiquity. Their fibers are released into the environment from both natural and human sources and are found in indoor and outdoor air, soil, drinking water, food, and even some medicines. Although there are a variety of forms of asbes103
Asbestos tos, some more associated with cancer than others, all forms of asbestos share a common characteristic: Because asbestos consists of silica crystals, the fibers are inherently irritating to human tissue. Exposure routes: Inhalation and ingestion Where found: Materials for roofing, thermal and electrical insulation, cement pipe and sheets, flooring, gaskets, friction materials, coatings, plastics, textiles, paper, and other products At risk: Workers in asbestos mining and milling, shipyards, building demolition, insulation, brake repair, and asbestos abatement, and their families Etiology and symptoms of associated cancers: Several asbestos-related conditions are nonmalignant, including asbestos warts (callus-like growths that form when asbestos fibers become embedded in the skin), asbestosis, pleural plaques, pleural thickening, and pleural effusions (the collection of fluid around the lung a few years after asbestos exposure). Inhaled or ingested asbestos fibers lead to the two most serious asbestos-related disorders: the noncancerous asbestosis, in which scarred and increasingly stiff lung tissue progressively reduces breathing capacity, and the cancer known as malignant mesothelioma. These diseases may take years or decades to develop, although there have been cases of adolescents developing mesothelioma within only a few months of initial asbestos exposure.
Salem Health: Cancer Malignant mesothelioma takes two main forms: pleural mesothelioma, in which tumors form on the outer lining of the lungs, and peritoneal mesothelioma, in which tumors form on the peritoneum, the sac containing the abdominal organs. Both have a high mortality rate because mesothelioma is rarely detected in its early stages; the average age of diagnosis is sixty. Symptoms—chest pain, cough, weight loss, and shortness of breath—are often attributed to more common diseases such as asthma. As the cancer spreads, lung capacity is diminished, and the patient eventually succumbs to the inability to take in sufficient oxygen, if not to the failure of other organs after the cancer metastasizes. Asbestos exposure has also been associated with cancers of the stomach, liver, and other organs. Researchers have observed digestive-tract cancers in workers exposed to crocidolite, amosite, and chrysotile, although study results are inconsistent. An excess of laryngeal cancer has been reported in shipyard workers, chrysotile miners, insulation workers, and others exposed to asbestos. People living near asbestos factories or mines or living with asbestos workers have also developed mesothelioma; however, there is no clear association between cancer risk and exposure to asbestos in drinking water. Smokers who are also exposed to asbestos are at a synergistically (rather than additively) greater risk of developing lung cancer.
History: In the 1930’s, researchers established that asbestos presented especially high risks of causing lung diseases in miners, shipyard workers, and others who either manufactured or worked with materials incorporating asbestos, such Asbestosis: Most Frequently Recorded Occupations as insulation. It soon became evident on Death Certificate that exposure to minute amounts of asbestos could lead to asbestos-related Occupation Number of Deaths Percent disorders. Miners’ spouses developed Plumbers, pipefitters, and steamfitters 238 8.3 mesothelioma after being exposed to Managers and administrators 129 4.5 asbestos through doing laundry, for exElectricians 125 4.4 ample, while children became victims Carpenters 120 4.2 through exposure to their parents’ work Insulation workers 108 3.8 clothes in the home. Laborers, except construction 95 3.3 In the United States, asbestos was Supervisors, production occupations 85 3.0 one of the first hazardous air pollutants Welders and cutters 78 2.7 regulated by the Clean Air Act of 1970. Janitors and cleaners 74 2.6 The first lawsuits resulting from occuTruck drivers 66 2.3 All other occupations 1,639 57.3 pational exposures began in the late Occupation not reported 102 3.6 1960’s and increased in 1973 when the Total 2,859 100.0 Fifth Circuit Court of Appeals applied strict liability in Borel v. Fibreboard Source: Multiple cause of death data from the National Center for Health Statistics Paper Prods. Corp. (493 F.2d 1076). In Note: U.S. residents age fifteen and over, selected states and years, 1990-1999. 1976, Congress passed the Toxic Sub-
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Ascites Bowker, Michael. Fatal Deception: The Untold Story of Asbestos—Why It Is Still Legal and Still Killing Us. Emmaus, Pa.: Rodale, 2003. Harris, L. V., and I. A. Kahwa. “Asbestos: Old Foe in Twenty-First Century Developing Countries.” Science of the Total Environment 307, nos. 1-3 (2003): 1-9. Institute of Medicine of the National Academies. Board on Population Health and Public Health Practices. Committee on Asbestos: Selected Health Effects. Asbestosis: Selected Cancers. Washington, D.C.: National Academies Press, 2006. Pass, Harvey I. One Hundred Questions and Answers About Mesothelioma. Sudbury, Mass.: Jones & Bartlett, 2004. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Eleventh Report on Carcinogens. Research Triangle Park, N.C.: Author, 2005. u
Other Resources
’Lectric Law Library A History of Asbestos Use and Asbestos Litigation http://www.lectlaw.com/files/med40.htm National Toxicology Program http://ntp.niehs.nih.gov An X ray of a lung showing cancer caused by asbestos. (James Cavallini/Photo Researchers, Inc.)
stances Control Act, which imposed regulations regarding asbestos, including a requirement that asbestos abatement occur in schools. The International Labour Organization’s Asbestos Convention of 1986 mandated that national laws should “prescribe the measures to be taken for the prevention and control of, and protection of workers against, health hazards due to occupational exposure to asbestos.” The widespread use of asbestos fibers in multiple applications means that exposure remains a concern in the twenty-first century. Although asbestos is no longer as widely used in industry, which has reduced exposure in the workplace, people still risk asbestos exposure when engaging in home improvement projects as they rip out old flooring or replace ceiling tiles. Christina J. Moose, M.A. u
For Further Information Bartrip, Peter. Beyond the Factory Gates: Asbestos and Health in Twentieth Century America. New York: Continuum, 2006.
See also Air pollution; Bronchoalveolar lung cancer; Cancer clusters; Carcinomatosis; Epidermoid cancers of mucous membranes; Free radicals; Head and neck cancers; Kidney cancer; Laryngeal cancer; Lung cancers; Mesothelioma; Occupational exposures and cancer; Risks for cancer; Sarcomas, soft-tissue; Statistics of cancer; Throat cancer; Urinary system cancers.
u Ascites Category: Diseases, symptoms, and conditions Also known as: Peritoneal cavity fluid or peritoneal fluid excess, hydroperitoneum, abdominal dropsy, peritoneal carcinomatosis, malignant ascites Related conditions: Late-stage cancer or liver disease, associated with ovarian, endometrial, breast, gastrointestinal (stomach, colon, pancreatic) cancer Definition: Ascites is an abnormal accumulation of excess fluid in the abdominal (peritoneal) cavity that causes swelling or bloating. In late-stage cancer, tumor cells may be isolated from the fluid. Ascites can also occur with liver disease. 105
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Risk factors: Ascites is not uncommon in cancer patients; 15 to 50 percent develop this condition at some time during their illness. Ascites is most common in patients with ovarian cancer but may also be present in patients with uterine, breast, colon, stomach, and pancreatic cancers. Liver involvement with cancer can increase the problem with ascites. Noncancerous conditions that can result in ascites include hepatitis, kidney failure, heart failure, and constrictive pericarditis (inflammation of the sac around the heart). Etiology and the disease process: A lining of tissue, the peritoneum, supports the organs in the abdomen and covers the peritoneal cavity. Normally a small amount of body fluid lubricates this cavity and is kept in correct proportion by a pressure gradient. The liver stores blood and fluid depending on the pressure in the venous and arterial blood system. Under normal conditions, the lymphatic system drains 80 percent of the peritoneal fluid, so minimal accumulation occurs. When pathological or disease conditions
occur, the fluid accumulates and edema settles in the peritoneal cavity. In malignant ascites, a tumor may obstruct the lymphatic system so that drainage cannot occur. Liver involvement can cause a backup of fluid into the peritoneal cavity. In severe cases of ascites, gallons of liquid can fill the peritoneal cavity, pressing on the diaphragm (the muscles that separate the chest from the abdomen and allow a person to breathe). Ascites is not actually a disease but a symptom of some pathological condition within the body. Some of the conditions that can result in ascites include cirrhosis of the liver (80 percent of ascites cases), pancreatic ascites, chylous ascites (a symptom of lymphoma), and cancer. Renal and endocrine ascites occur in rare instances. Incidence: Approximately 10 percent of all cases of ascites occur in cancer patients. As many as half of all cancer patients will experience ascites. About 30 percent of all ovarian cancer patients have ascites, with as many as 60 per-
Abdomen distended by ascites. (Custom Medical Stock Photo)
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Salem Health: Cancer cent presenting with ascites at death. Most cases result from disease that starts in the peritoneum or spreads from other body organs (metastasis). Symptoms: Mild ascites may not be noticeable or present any symptoms. As the disease progresses, the abdomen can become more distended and swollen to the point of discomfort and pain. The patient may experience a feeling of heaviness. The patient may have trouble sitting, walking, or moving around. Fluid buildup may cause indigestion, nausea, or vomiting. The patient may experience diminished appetite with weight loss and general fatigue. When the fluid becomes excessive, the patient may have weight gain and shortness of breath. Some patients complain of swelling in the legs and ankles or experience hemorrhoids. Changes may occur in the navel as fluid collects. The severity of symptoms depends on the progression of the disease.
Ashkenazi Jews and cancer the problem. Generally, unless the cause is corrected, the fluid will return after draining with paracentesis. In fact, rapid reduction through the draining of fluid can result in rapid reaccumulation of fluid. Removing more than five liters at one time can result in hypotension, shock, and death. Robert W. Koch, D.N.S., R.N. u
For Further Information Ginès, Pere, et al., eds. Ascites and Renal Dysfunction in Liver Disease: Pathogenesis, Diagnosis, and Treatment. 2d ed. Malden, Mass.: Blackwell Publishing, 2005. Hawkins, Rebecca. “Clinical Focus: Ascites.” Clinical Journal of Oncology Nursing 5, no. 1 (January/February, 2001).
u
Other Resources
Screening and diagnosis: Diagnosis is confirmed using a physical exam and patient history along with X rays, ultrasound, computed tomography, or paracentesis with fluid analysis (removing fluid through a thin needle into the abdomen). Simple measuring of abdominal girth can provide a baseline for continued assessment.
Cancer.Net Fluid in the Abdomen or Ascites http://www.cancer.net/patient/Diagnosis+and+ Treatment/Treating+Cancer/Managing+Side+Effects/ Fluid+in+the+Abdomen+or+Ascites+-+ASCO+ curriculum#mainContent idmainContent
Treatment and therapy: Treatment is targeted to the symptoms and to improve quality of life. One approach is to reduce sodium and fluid intake to decrease fluid buildup. Another is the use of diuretic drugs that promote removal of fluid through the kidneys as urination. Caution must be taken in the use of diuretics as the patient may experience hypovolemia (a drop in circulating blood volume through large loss of blood or fluid) with a severe drop in blood pressure or a potassium imbalance that can threaten the regular beat of the heart. If discomfort is severe, a therapeutic paracentesis can be performed by the health care provider. This procedure drains fluid from the abdomen through a thin needle inserted into the peritoneal cavity. This procedure is generally performed with a local anesthesia. Rarely, surgery to shunt the fluid away from the abdominal cavity (peritoneovenous shunt) or specific chemotherapy may help. Repeated paracentesis as can be tolerated by the patient may be the only effective approach long term. Few alternative or complementary approaches are effective for ascites. Diet can be modified to minimize sodium intake. The patient should consume potassium-rich foods such as low-fat yogurt, cantaloupe, or baked potatoes to assist with proper heart function.
MedlinePlus Ascites http://www.nlm.nih.gov/medlineplus/ency/article/ 000286.htm
Prognosis, prevention, and outcomes: The prognosis for ascites depends on the underlying cause and intensity of
See also Cytology; Gallbladder cancer; Gastrointestinal cancers; Hepatomegaly; Krukenberg tumors; Mesothelioma; Paracentesis; Peritoneovenous shunts; Ultrasound tests.
u Ashkenazi Jews and cancer Category: Social and personal issues Also known as: German or Eastern European Jews Definition: Although the major cancer risk factors in all populations are socioeconomic status, diet, lifestyles, and environment (which Jews in general share with other ethnic and racial groups), Ashkenazi Jews, originally from central, northern, and Eastern Europe, have some specific gene mutations that increase their susceptibility to certain forms of cancer. Description of the population: In the ninth or tenth century, Ashkenazi (meaning “German” in Hebrew) Jews began settling in northern France and western Germany. Toward the beginning of the sixteenth century, their com107
Ashkenazi Jews and cancer munity became centered in Poland-Lithuania. For centuries the religious and political isolation of the Ashkenazim (plural of Ashkenazi) within the larger host communities ensured their genetic purity, all the more so as they tended to intermarry. This means that the term “Jewish,” in addition to religious and cultural denotations, can also refer to a common biological background distinct from that of others. There are about 10 million Jews in the world, the majority of whom are Ashkenazi rather than Sephardic Jews. Sephardic Jews, also known as Spanish or Oriental Jews, hail from Spain, Portugal, and North Africa and are in a minority in the United States as in most parts of the world. Although American Jews, mostly Ashkenazim, are generally health conscious and respect medical science and its providers so that they tend to practice preventive health care, they are nevertheless more affected by certain disorders than members of other ethnic groups. Cancer researchers, starting in the 1990’s, began to discover that specific gene mutations leading to cancers of the breast, ovaries, colon, and rectum were more prevalent among Ashkenazi Jews than in the population at large. This suggested a genetic origin. Cancers of genetic origin: Ashkenazi Jews can trace their roots back to a small number of founders—several hundreds or thousands of them—who originally lived in a confined environment and tended to intermarry. Geneticists theorize that if even just a few of these founders had a gene mutation, this mutation would have been amplified in later generations of Ashkenazim, largely because of intermarriage. This theory is confirmed by the fact that people of Ashkenazi Jewish descent have a higher incidence of a number of specific mutations, including those that increase the risk of developing certain types of cancer. Such childhood neurological dysfunctions as Tay-Sachs disease and Bloom syndrome are caused by gene mutations and are more prevalent among Ashkenazi Jews. Breast and ovarian cancer: Isolated in 1994, BRCA1 is a major gene that, when one of its two copies is inherited in an altered form, predisposes individuals to breast (and ovarian) cancer. BRCA1 (for breast cancer 1) was found in 1 percent of the general Jewish population (mostly Ashkenazim) in the United States compared with 0.1 to 0.6 percent in Americans at large. Soon another breast cancer gene, BRCA2 (for breast cancer 2), was also discovered to have greater prevalence among the Ashkenazim, bringing the overall risk factor among them even higher. Three distinct mutations in the BRCA1 and BRCA2 genes were found in 1 out of 40 Ashkenazi Jewish women, increasing their odds of getting breast or ovarian cancer. When these 108
Salem Health: Cancer mutated genes are inherited from both parents rather than one, the risk of the disease is increased even further. Astudy by the Journal of the American Medical Association (JAMA) published in June, 2007, pointed out that in the case of breast cancer, the gene mutation may have originated from a woman’s father rather than from her female antecedents. Half of genetic mutations for breast cancer are inherited from a father, not a mother. However, unless the father has female relatives with breast cancer, the faulty gene may have passed down unnoticed and without causing cancer (because breast cancer among men is rare). Accordingly, when a woman has few aunts or older sisters, a gene mutation can hide in a family tree so that it appears that her breast or ovarian cancer struck out of nowhere when it really originated from a mutation handed down by her father. A woman with breast cancer who has a BRCA1 or BRCA2 gene mutation has a four times greater chance of developing cancer in the other breast and a ten times greater risk of developing ovarian cancer than a woman with breast cancer who has no BRCA gene alteration. This finding argues that women at greater risk, such as the Ashkenazim, should have genetic testing because three commonly used predictive methods do not accurately estimate the genetic breast cancer risk without a family history of such carcinomas. However, Orthodox Jewish rabbis may oppose genetic testing on the grounds that it might cause couples to refrain from marriage and procreation. It must be borne in mind, too, that the Ashkenazim, like others, are subject to breast cancer risks independent of genetic causes. Colorectal cancer: Ashkenazi Jews have a lifetime risk of colorectal cancer of 9 to 15 percent, one of the highest in the world, compared with 5 to 6 percent for non-Ashkenazi populations. Although rare in the general population, the A636P mutation is detected in up to 7 percent of Ashkenazi Jews with early-onset colorectal cancer. Hereditary nonpolyposis colorectal cancer (HNPCC) is a dominantly inherited syndrome attributable to mutations in one of several deoxyribonucleic acid (DNA) mismatch repair genes, most commonly MLH1 and MSH2. Although rare in the general population, among Ashkenazi Jews, the MSH2 mutation is found to a greater degree with early-onset colorectal cancer and may account for up to one-third of HNPCC. Pancreatic and other cancers: Pancreatic cancer is the most fatal of all gastrointestinal cancers. Its survival rate of only 1 to 3 percent in the West disproportionately affects the Ashkenazim. Approximately 5 to 10 percent of this cancer shows familial clustering, and there are no pan-
Salem Health: Cancer creatic cancer screening programs with acceptable sensitivity and specificity. Men who inherit the altered BRCA1 gene are slightly more at risk to experience prostate cancer as well. Similarly, carcinomas of the stomach and nonHodgkin lymphoma have a higher incidence among the Ashkenazim. Interpreting statistics: Although Ashkenazi Jews have one of the highest lifetime colorectal cancer risks of any ethnic group in the world, carcinoma of the uterine cervix occurs very infrequently among them, and lung cancer among the Ashkenazim is also low, probably because of decreased tobacco use. The interpretation of statistics that portray variations in the incidence of cancer in any ethnic or religious group, including Ashkenazi Jews, must be carefully evaluated in view of the greater picture. Peter B. Heller, Ph.D. u
For Further Information Brandt-Rauf, Sherry I., et al. “Ashkenazi Jews and Breast Cancer: The Consequences of Linking Ethnic Identity to Genetic Disease.” American Journal of Public Health 96, no. 11 (2006): 1979-1988. Goodman, Richard, and Arno G. Motulsky, eds. Genetic Diseases Among Ashkenazi Jews. New York: Raven Press, 1979. Kedar-Barnes, I., and P. Rozen. “The Jewish People: Their Ethnic History, Genetic Disorders, and Specific Cancer Susceptibility.” Familial Cancer 3, nos. 3/4 (2004): 193-199. Kolata, Gina. “Using Genetic Tests: Ashkenazi Jews Vanquish a Disease.” The New York Times, February 18, 2003, Sec. F, pp. 1, 6. Lippe, Scott D. “Ashkenazi Jews and Colon Cancer.” American Journal of Gastroenterology 94, no. 10 (1999): 3085. Locker, G. Y., and H. T. Lynch. “Genetic Factors and Colorectal Cancer in Ashkenazi Jews.” Familial Cancer 3, nos. 3/4 (2004): 215-221. Lynch, H. T., et al. “Cancer in Jews: Introduction and Overview.” Familial Cancer 3, nos. 3/4 (2004): 177192. _______. “Familial Pancreatic Carcinoma in Jews.” Familial Cancer 3, nos. 3/4 (2004): 233-240. Mahowald, Mary B. “Ethnicity, Cultural Differences, and Sex Selection.” In Genes, Women, Equality. New York: Oxford University Press, 2000. Vadlamani, Lalit, et al. “Colorectal Cancer in RussianSpeaking Jewish Emigrés: Community-Based Screening.” American Journal of Gastroenterology 96, no. 9 (2001): 2755-2760.
Asian Americans and cancer u
Other Resources
Genetics Home Reference http://ghr.nlm.nih.gov National Cancer Institute Cancer Risk in Ashkenazi Jews Who Carry a Specific Mutation in a Gene Previously Associated with Colon Cancer http://www.cancer.gov/newscenter/Ashkenaziestimating-risk-colon-QA See also BRCA1 and BRCA2 genes; Ethnicity and cancer; Family history and risk assessment; Fanconi anemia; Geography and cancer; Hairy cell leukemia; Pancreatic cancers; Rectal cancer.
u Asian Americans and cancer Category: Social and personal issues Definition: Cancer is one of the leading causes of death in Asian Americans. Cancer kills more Asian American women than women of any other ethnicity in the United States. Asian Americans have higher incidence and mortality rates for certain cancers, with wide disparities between Asian ethnic groups. Overall, there are disproportionately high rates of liver, breast, cervical, and lung cancer in the largest Asian American and Pacific Islander groups. Description of the population: There are approximately 11.9 million Asian Americans living in the United States, and more than twenty-five Asian ethnicities are represented. Asian Americans and Pacific Islanders refer to people who originate in many countries and represent myriad ethnicities. Major ethnic groups included by the U.S Census Bureau are Chinese, Japanese, Korean, Malayan, Mien, Cambodian, Indonesian, Burmese, Bhutanese, Bangladeshi, Filipino, Hmong, Sikh, Sri Lankan, Laotian, Pakistani, Nepalese, Thai, Vietnamese, Tongan, Samoan, Marianan, Guamanian, and Chuukese. Cancer statistics are very limited in some Asian American and Pacific Islander ethnic subgroups. In fact, many of the statistics represent cancer incidence and mortality only in Chinese, Vietnamese, Filipino, Korean, Japanese, Tongan, and Samoan peoples; national statistics on Mien and Hmong are scarce. Asian Americans and Pacific Islanders are considered a health disparity population, which is defined as “a population displaying a significant disparity in the overall rate of disease incidence, prevalence, morbidity, mortality or sur109
Asian Americans and cancer vival rates in the population as compared to the health status of the general population,” according to the Minority Health and Health Disparities Research and Education Act of 2000. Incidence, death, and survival statistics: Asian Americans and Pacific Islanders have the fourth highest incidence rates of cancer of all ethnicities (329.3 per 100,000 people for men and 263.9 per 100,000 for women). The most common cancers in Asian American and Pacific Islander women are breast (79.7 per 100,000), colorectal (32.1 per 100,000), and lung (26.9 per 100,000). The highest cancer incidences in Asian American and Pacific Islander men are prostate (79.8 per 100,000), lung (49.7 per 100,000), and colorectal (42.0 per 100,000). Vietnamese women have the highest rates of cervical cancer. The rates are not only the highest of all Asian American and Pacific Islander groups, but five times higher than the rates for white women. Vietnamese men
Cancer kills more Asian American women than women of any other ethnicity in the United States. (PhotoDisc)
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Salem Health: Cancer have incidence and death rates from liver cancer that are seven times higher than those of white men. Native Hawaiians have the second highest all-site cancer mortality (207.2 per 100,000), while African Americans have the highest rates (209.8 per 100,000). Asian American and Pacific Islander men and women have the highest incidence rates of stomach cancer (9.3 per 100,000 for women and 17.5 per 100,000 for men) and intrahepatic bile duct cancer (11.0 per 100,000 for women and 20.1 per 100,000 for men) of all ethnicities. Breast cancer is the leading cause of cancer deaths in Asian American and Pacific Islander women, and Koreans have the highest incidence and mortality from stomach cancer. Lung cancer rates are 18 percent higher for Southeast Asians than whites. Japanese have the highest incidence and mortality rates for stomach and uterine cancers, while Koreans have the lowest colorectal cancer screening rates. Hmong have elevated rates of multiple cancers, including liver, cervical, nasopharyngeal, leukemia, and nonHodgkin lymphoma. Risk statistics: Socioeconomic status, hepatitis B infection, tobacco use, language barriers, and low rates of participation in cancer screening are major challenges. Recent immigrants who are monolingual have difficulty accessing medical care. Further, the concept of disease prevention is alien to many who had limited or no access to medical care in their native countries. Most Asian American subgroups are diagnosed with cancer at a more advanced stage than whites. A cancer diagnosis is frightening for most people, regardless of ethnicity. Adding to the challenge in Asian American and Pacific Islander groups are cultural beliefs promoting fear of cancer. A cancer diagnosis can result in ostracism, loss of friendships, and being regarded as the carrier of bad luck. These common occurrences prevent many Asian Americans from seeking early medical attention and participating in cancer prevention screening. Smoking is relatively common in Asian Americans and Pacific Islanders (17.8 percent of men and 4.8 percent of women). Immigrants arrive in the United States with smoking habits in place. Social and work formalities override concerns about lung cancer. Also, commercial advertising for tobacco products is great in stores that serve a large Asian American and Pacific Islander customer base. Hepatitis B infection is widespread in China and Southeast Asia, so it is also present in immigrants from these areas. An infected person might not have symptoms for decades. Infection is most commonly transmitted at childbirth, when the infant is exposed to the infected mother’s
Salem Health: Cancer
Asian Americans and cancer
Top Ten Cancer Sites: Incidence and Death Rates for Asian Americans and Pacific Islanders, 2004 Incidence Cancer Site Prostate Female breast Lung and brochus Colon and rectum Corpus and uterus Liver and intrahepatic bile duct Stomach Non-Hodgkin lymphoma Thyroid Ovary
Rate per 100,000 People 79.8 79.7 36.7 36.4 15.6 13.5 12.8 11.9 9.1 8.7
Death Cancer Site Lung and brochus Female breast Prostate Colon and rectum Liver and intrahepatic bile duct Pancreas Stomach Ovary Non-Hodgkin lymphoma Leukemias
Rate per 100,000 People 26.3 12.6 11.4 11.2 10.2 7.7 7.0 4.6 4.5 3.8
Source: U.S. Cancer Statistics Working Group, United States Cancer Statistics: 1999-2004 Incidence and Mortality Web-Based Report (Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention and National Cancer Institute, 2007)
blood. Other routes of transmission include drug use (sharing needles) and tattoos. Although the hepatitis B vaccine is effective in preventing infection, in many Asian countries the vaccine is expensive and not always available at rural clinics. Very limited public health education exists in many Asian countries. People are unaware of the association between chronic hepatitis B infection and liver cancer and do not know that infection can be asymptomatic and that treatment is available. Asian American and Pacific Islander women have very low participation rates for mammography, Pap smears, and performance of breast self-exams. Participation has increased with awareness based on language-appropriate information regarding availability of Medicare coverage for screening, centers where native languages are spoken, and ways to prevent and detect cancer in its early stages. Perspective and prospects: Screening, early detection of cancer, and treatment are the core approach to dealing effectively with cancer, regardless of the person’s race or ethnicity. However, achieving this goal within myriad Asian American and Pacific Islander groups involves enormous complexity. Asian Americans born in the United States and those with higher levels of education and jobs providing medical insurance are more likely to be aware of and participate in prevention and early cancer screening practices. Hawaiians and Pacific Islanders have more dietary and obesity-related medical issues than Vietnamese and Chinese. Hmong and Mien communities maintain health beliefs that do not easily blend with West-
ern medicine. Physical isolation and language barriers among immigrants are persistent challenges. Modifiable behaviors and factors that lead to higher rates of certain cancers in Asian American and Pacific Islander communities include hepatitis B infection (liver cancer), tobacco use (lung and bronchial cancers), and low participation in cancer screenings such as Pap smears (cervical cancer), mammography testing (breast cancer), and fecal occult blood testing, colonoscopy, and bariumcontrast X ray (colorectal cancer). High-fat diets, certain environmental exposures including radiation, and genetic factors also are known to increase the risk of certain cancers. Organizations such as the Asian American Network for Cancer Awareness, Research and Training (AANCART), have been major sources of data on cancer incidence and mortality in specific Asian American communities. Clearly, health education that is culture- and languageappropriate plays a major role in prevention and early detection of cancer in all Asian American communities. Distrust of Western medicine is a major barrier in Hmong and some other groups. Language-appropriate materials stressing mammograms, fecal occult blood tests, prostatespecific antigen (PSA) tests, and Pap testing must be widely distributed within Asian American communities, followed up by health workers who are able to explain the role of screening and early detection. There are no studies indicating that Asian Americans have a genetic predisposition for any particular cancer. Therefore, economic and cultural disparities are the main issues facing anyone 111
Astrocytomas
Salem Health: Cancer
intent on lowering cancer rates in these communities. Bilingual community health workers have had success in reaching many immigrant populations. University medical centers and public health departments in cities with large Asian American communities have been addressing specific issues such as hepatitis B antigen/antibody screening, identification and treatment of individuals with chronic hepatitis B, Vietnamese-language cervical cancer screening programs, and antismoking programs. The greatest challenge continues within monolingual communities. Janet R. Green, M.S.P.H. u
For Further Information Haynes, M. Alfred, and Brian D. Smedley, eds. The Unequal Burden of Cancer: An Assessment of NIH and Research Programs for Ethnic Minorities and the Medically Underserved. Washington, D.C.: National Academy Press, 1999. Smedley, Brian D., Adrienne Y. Steth, and Alan P. Nelson eds. Unequal Treatment: Confronting Racial and Ethnic Disparities in Health Care. Washington D.C.: National Academy Press, 2003. Wong, S. T., et al. “Disparities in Colorectal Cancer Screening Rates Among Asian Americans and NonLatino Whites.” Cancer 104, no. 12 (2005): S2,940S2,947. u
Stanford School of Medicine—Asian Liver Center http://liver.stanford.edu Vietnamese Community Health Promotion Project— University of California, San Francisco http://www.suckhoelavang.org/main.html See also Chewing tobacco; Choriocarcinomas; Ethnicity and cancer; Krukenberg tumors; Statistics of cancer; Stomach cancers.
u Astrocytomas Category: Diseases, symptoms, and conditions Also known as: Gliomas Related conditions: Primary brain tumors Definition: Astrocytomas, the most common gliomas, are primary malignant brain tumors that can occur in most parts of the brain and occasionally in the spinal cord. As the name implies, astrocytomas are derived from astrocytes—nonneural support cells of the central nervous system. The types of astrocytomas based on clinical pathology include pilocytic astrocytoma, fibrillary astrocytoma, anaplastic astrocytoma, and glioblastoma multiforme. Because astrocytomas are primary brain tumors formed in the brain, they rarely spread to other parts of the body;
Other Resources
American Cancer Society http://www.cancer.org Asian American Cancer Support Network http://www.aacsn.org Asian American Network for Cancer Awareness, Research and Training (AANCART). http://www.aancart.org Asian American Pacific Islander Health Foundation http://www.apiahf.org Centers for Disease Control and Prevention Highlights in Minority Health and Health Disparities http://www.cdc.gov/omhd National Cancer Institute SEER Cancer Statistics Review 1975-2005 http://seer.cancer.gov/csr/1975_2005 112
An MRI of the brain of a man with a cerebellar glioma. The tumor appears in bright contrast to the surrounding brain tissue. (Simon Fraser/Photo Researchers, Inc.)
Salem Health: Cancer however, they usually grow rapidly and invade surrounding normal brain tissue and therefore are life-threatening. Risk factors: Brain tumors are caused by mutated or missing genes that result in abnormal cells. High-dose ionizing radiation used over time to treat brain tumors may on occasion cause secondary tumors. Exposure to certain chemicals such as pesticides, petrochemicals, and formaldehyde, and to electromagnetic fields over time increase the risk of developing astrocytomas. Etiology and the disease process: Generally, malignant brain tumors are caused by changes in genetic structure due to inherited or environmental factors. It was thought that only 5 percent of primary brain tumors, including astrocytomas, are inherited; however, one study has shown that 80 percent of patients with grade IV astrocytoma (glioblastoma multiforme) had anomalous copies of chromosome 7. Familial clustering of gliomas is also associated with defined inherited tumor syndrome, including Li-Fraumeni syndrome, Turcot syndrome, and the neurofibromatosis I syndrome. Incidence: Gliomas of both benign and malignant tumors account for 45 to 50 percent of all primary brain tumors; grade I and II astrocytomas account for 25 to 30 percent of all gliomas. Approximately 13,000 people in the United States die of malignant brain tumors every year, which represents about 2 percent of all cancer-related deaths. Symptoms: Various symptoms may occur with astrocytomas, which depend largely on the location and size of the tumor. Seizure, focal neurologic deficits such as weakness or speech problems, and headaches are common symptoms. The headaches that are associated with brain tumors are typically worse in the morning and accompanied by vomiting. Sometimes increased pressure on the brain tissue can cause blurred, double, or even loss of vision. Behavioral changes may also follow with changes in mood and general state of well-being. Screening and diagnosis: Methods of screening and diagnosing astrocytomas include computed tomography (CT) scans, magnetic resonance imaging (MRI), angiograms, X rays of the head and skull, and biopsies. Other brain scans, such as magnetic resonance spectroscopy (MRS), single-photon emission computed tomography (SPECT), or positron emission tomography (PET), provide a gauge of brain activity and blood flow. Brain tumors are graded based on the following criteria: mitotic index (growth rate), vascularity (blood supply), presence of necrotic center, invasive potential (border distinctness), and similarity to normal cells.
Astrocytomas
Relative Survival Rates for Astrocytomas, 1988-2001 Years 1 2 3 5 8 10
Survival Rate (%) 62.3 48.4 42.7 35.8 30.7 27.8
Source: Data from L. A. G. Ries et al., eds., Cancer Survival Among Adults: U.S. SEER Program, 1988-2001—Patient and Tumor Characteristics, NIH Pub. No. 07-6215 (Bethesda, Md.: National Cancer Institute, 2007)
Accordingly, astrocytomas can be graded into four levels. Pilocytic astrocytoma are grade I tumors that are slow growing and do not invade the surrounding normal tissue, and are commonly diagnosed in children and young adults. Low-grade astrocytomas, including fibrillary or protoplasmic astrocytomas, are grade II tumors that grow slightly faster than grade I tumors and are invasive, with high incidence in the cerebrums of young adults and in the brain stems of children. Anaplastic astrocytomas are grade III, malignant and invasive tumors that occur in the same location as the low-grade astrocytomas and have a high recurrence rate. Glioblastomas multiforme are grade IV, a malignant type that is by far the most common glioma: Approximately 50 percent of astrocytomas are glioblastomas. The common sites of tumors are cerebral hemispheres in adults and the brain stem in children, and they typically contain more than one cell type. Treatment and therapy: Treatment options differ according to size, grade, and location of the tumor. Tumors may be removed by craniotomy, an open-skull procedure. They may also be removed by ultrasonic aspiration, in which ultrasonic waves fragment the tumors, which are then aspirated. Alternatively, stereotactic radiosurgery may be performed with a Gamma Knife on benign, malignant, or metastatic tumors that are around 4 centimeters (cm) in size. Chemotherapy may be used as a primary therapy in young children or as an adjuvant after tumor removal with radiosurgery. For pilocytic and fibrillary astrocytomas, complete resection of the tumor is achieved; however, if excision is not possible because of the tumor’s location, chemotherapy is indicated in young children and radiotherapy in adults. The treatment options for anaplastic astrocytoma and glioblastoma multiforme include total re113
Ataxia telangiectasia (AT) section followed by radiotherapy and chemotherapy after surgery. Prognosis, prevention, and outcomes: The prognosis and outcome of astrocytomas largely depend on the age of the patient, histological features of the tumor, and degree of neurologic or functional impairment. In low-grade astrocytomas, the mean survival time after surgery is six to eight years with the prognosis depending on whether the tumor undergoes progression to a malignant phenotype. Complete recovery is possible in pilocytic astrocytoma if total resection is achieved, while fibrillary astrocytomas show frequent recurrence. In patients with anaplastic astrocytomas and glioblastoma multiforme, the extent of resection is a prognostic factor; generally, younger patients below the age of forty-five have a better prognosis. Bagirathy Ravishankar, Ph.D. u For Further Information Arjona, D., et al. “Early Genetic Changes Involved in Low-Grade Astrocytic Tumor Development.” Current Molecular Medicine 6 (September, 2006): 645-650. Compostella, A., et al. “Prognostic Factors for Anaplastic Astrocytomas.” Journal of Neuro-Oncology 81 (February, 2007): 295-303. Miller, C. R., and A. Perry. “Glioblastoma.” Archives of Pathology and Laboratory Medicine 131 (March, 2007): 397-406. Robins, H. Ian, et al. “Therapeutic Advances for Glioblastoma Multiforme: Current Status and Future Prospects.” Current Oncology Reports 9, no. 1 (2007): 66-70. Szeifert, G., et al. “The Role of the Gamma Knife in the Management of Cerebral Astrocytomas.” Progress in Neurological Surgery 20 (2007): 150-163. u
Other Resources
Mayo Clinic Gliomas http://www.mayoclinic.org/glioma/astrocytomas.html Neurosurgery Today Astrocytoma Tumors http://www.neurosurgerytoday.org/what/patient_e/ tumors.asp See also Brain and central nervous system cancers; Cell phones; Craniotomy; Gamma Knife; Gliomas; Oligodendrogliomas; Spinal axis tumors.
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u Ataxia telangiectasia (AT) Category: Diseases, symptoms, and conditions Also known as: A-T, Louis-Bar syndrome, BoderSedgwick syndrome Related conditions: Nijmegen breakage syndrome Definition: Ataxia telangiectasia (AT) is a rare primary immunodeficiency disease that causes ataxia (Greek for “lack of order”), or uncoordinated movements. This symptom is caused by dysfunction of the central nervous system that coordinates movement. Telangiectasias are small, red spider veins caused by dilation of blood vessels. In AT these appear in the eyes, cheeks, and other skin surfaces. Risk factors: AT is caused by mutations in the ATM gene (ataxia telangiectasia, mutated) located on chromosome 11q22-23, which codes for a 370kDa protein kinase. The ATM gene is 150kb with 66 exons. Etiology and the disease process: The ATM protein kinase responds to double-stranded deoxyribonucleic acid (DNA) breaks, by autophosphorylation to an active form. This active ATM kinase is involved in the assembly of a multiprotein complex that helps the cell respond to DNA damage. ATM is also involved in triggering the accumulation of the tumor-suppressor protein p53 that is a master control switch to prevent cells from dividing. If the ATM protein is lacking, there is a delay in the accumulation of p53, so the cell continues to divide without DNA repair and increases the chances of mutations leading to cancer. Incidence: AT is a rare recessive genetic disease with an incidence of 1 in 40,000 to 1 in 100,000. Symptoms: AT symptoms include neurodegeneration, causing uncoordinated movements; immunodeficiency, such as a lack or reduced level of immunoglobulin A (IgA), immunoglobulin E (IgE), and immunoglobulin G2 (IgG2); extreme sensitivity to ionizing radiation; and an increased risk of cancer. Telangiectasias are not always present. Those with AT have frequent sinus and respiratory infections and can have recurring severe lung infections. The neurological problems result in delayed development of motor skills and poor balance, which are typically noted by two years of age. As the neurological degeneration continues, with progressive loss of muscle control, patients usually require a wheelchair for mobility in their teenage years. Slurred speech is generally present by age ten. AT patients also may have mild diabetes mellitus, premature gray hair, difficulty swallowing, and de-
Salem Health: Cancer layed physical and sexual development. Their intelligence quotient (IQ) is normal. People with AT have an increased risk of developing cancer, especially leukemia and lymphoma. Other cancers, such as stomach, brain, ovary, skin, liver, larynx, and breast, are also associated with AT. Screening and diagnosis: Ataxia, uncoordinated movements, is typically the symptom noted first. Telangiectasia may or may not be observed. Lab tests show a low lymphocyte count, especially of T and B lymphocytes. A screen of serum immunoglobulins may show low levels of IgA, IgG2, immunoglobulin G4 (IgG4), and IgE. Magnetic resonance imaging (MRI) and computed tomography (CT) scans may show cerebellar atrophy. Those with AT also have elevated levels of alpha-fetoprotein and carcinoembryonic antigen in the serum. The size of the thymus may be examined by X rays. A molecular diagnosis of AT includes sequencing of the ATM gene or examining closely linked markers if there is a family history of the disease. A test of protein function or a cytogenetic test to look for specific breakpoints can also be done. Treatment and therapy: There is no specific treatment for AT; rather the specific symptoms are treated. Antibiotics are given to control infections. Gamma-globulin injections can help the dysfunctional immune system. Physical, occupational, and speech therapy can be of benefit. Because of the sensitivity to ionizing radiation, AT patients with cancer should not receive radiation therapy. They should not have unnecessary X rays for screening tests. Prognosis, prevention, and outcomes: There is no cure for ataxia telangiectasia. Life expectancy varies, but often those with AT die in their twenties, although some live to their forties. Almost half of AT deaths are due to lung infections. If the frequent infections can be controlled, about 20 percent of those with AT die from cancer. About 28 percent of AT deaths are due to both pulmonary infections and malignancies. The parents of an AT child can have molecular diagnoses to assess their risk of having another child with AT. If both parents are carriers of a mutated ATM gene, there is a 25 percent risk of having a child with AT. Prenatal testing can be done to determine if the fetus has AT. There are suggestions that those who are carriers of a mutant ATM gene may be at a greater risk of developing cancers, especially leukemia and lymphoma, so more frequent cancer screenings may be beneficial to carriers. There is evidence that ATM mutations are breast cancer susceptibility alleles. AT is a rare disease, but the study of the ATM gene has led to a better understanding of how the cell responds to double-stranded DNA damage. Susan J. Karcher, Ph.D.
Autologous blood transfusion u
For Further Information Ahmed, M., and N. Rahman. “ATM and Breast Cancer Susceptibility.” Oncogene 25 (2006): 5906-5911. Andreassen, C. N. “Can Risk of Radiotherapy-Induced Normal Tissue Complications Be Predicted from Genetic Profiles?” Acta Oncologica 44 (2005): 801-815. Lavin, M. F., and S. Kozlov. “ATM Activation and DNA Damage Response.” Cell Cycle 6, no. 8 (2007): 931942. Lee, Y., and P. J. McKinnon. “Responding to DNA Double Strand Breaks in the Nervous System.” Neuroscience 145 (2007): 1365-1374. McKinnon, P. J. “ATM and Ataxia Telangiectasia.” EMBO Reports 5 (2004): 772-776. Niida, H., and M. Nakanishi. “DNA Damage Checkpoints in Mammals.” Mutagenesis 21 (2006): 3-9. Shiloh, Y. “The ATM-Mediated DNA-Damage Response: Taking Shape.” Trends in Biochemical Sciences 31 (2006): 402-410. u
Other Resources
National Cancer Institute Ataxia Telangiectasia: Fact Sheet http://www.cancer.gov/cancertopics/factsheet/ ataxiaqa National Institute of Neurological Disorders and Stroke Ataxia Telangiectasia Information Page http://www.ninds.nih.gov/disorders/a_t/a-t.htm See also Family history and risk assessment; Genetic testing; Nijmegen breakage syndrome.
u Autologous blood transfusion Category: Procedures Also known as: Preoperative autologous blood donation (PABD), intraoperative blood salvage, postoperative blood salvage, acute normovolemic hemodilution (ANH) Definition: Autologous blood transfusion is the collecting and reinfusing of a patient’s own blood. Collection is done before surgery and/or during or after the surgical procedure. Cancers treated: All types of cancer, based on the physician’s decision Why performed: Autologous blood transfusion is performed to replace blood lost as a result of surgery. 115
Axillary dissection Patient preparation: A physician evaluates the patient to determine whether autologous transfusion is appropriate. The decision is based on established standards. The criteria that the physician uses include the likelihood of the patient needing blood during or after surgery, the type of cancer, and other medical conditions that the patient has. There must also be an autologous donor/transfusion program available to the patient, adequate time to collect blood prior to surgery, and equipment available for the collection and reinfusion of blood during surgery. Steps of the procedure: The physician writes an order for autologous transfusion. For preoperative autologous blood donation (PABD), the patient donates one or more units of blood at a blood donor center. The donor center staff attaches special labels to the unit of blood indicating it is for a specific patient. Blood collected prior to surgery is stored for up to forty-two days, separately from other blood. Two systems are available for the collection and reinfusion of blood during surgery. One system is semiautomated: Blood is collected, washed, and transfused to the patient. The other system is a suction system that collects the blood and returns it to the patient without washing. The patient is constantly monitored by anesthesia staff. In acute normovolemic hemodilution, blood is removed, and, at the same time, a solution to maintain fluid volume is infused. The blood is collected into blood bags and may be stored for up to twenty-four hours if properly refrigerated. The patient is monitored by anesthesia staff during surgery and by nursing staff after surgery. Postoperative blood salvage is not usually used for cancer patients. After the procedure: Following the donation of blood prior to surgery, the donor center staff gives the patient refreshments and observes the patient for any signs of an adverse reaction. During and following the transfusion of autologous blood, anesthesia staff or a nurse monitors the patient for any signs of an adverse reaction. Risks: The risks of PABD are infusion of the wrong unit of blood, which is very low. The risks of intraoperative blood salvage include reinfusing cancer cells and the reduction of platelets and other clotting factors. The risks of acute normovolemic hemodilution include a reduction of hemoglobin and oxygen-carrying capacity and the dilution of clotting factors. Results: Ideally, autologous blood transfusion results in a decrease in blood loss and a better surgical outcome. Wanda E. Clark, M.T. (ASCP) See also Transfusion therapy. 116
Salem Health: Cancer
u Axillary dissection Category: Procedures Also known as: Axillary lymph node dissection Definition: Axillary dissection is a surgical procedure carried out to remove and examine underarm lymph nodes through an incision in the armpit region (axilla). Cancers treated: Carcinoma of the breast, melanoma Why performed: For persons with operable breast cancer or melanoma, axillary dissection is used to determine whether cancer has spread beyond the primary tumor. Because these primary tumor cells usually infiltrate axillary lymph nodes before invading distant organs, physicians recommend that nodes be removed and examined histologically for the absence or presence of malignant cells. The results will guide the treatment course. Patient preparation: A few days before surgery, the patient undergoes a blood test, chest X ray, and electrocardiogram in order to assess general health. To avoid excessive bleeding, any blood-thinning medications are usually suspended at this time. Patients are cautioned not to eat or drink in the eight hours before surgery and, on admission to the hospital, are asked to sign an informed consent form. Steps of the procedure: The operation, performed under general anesthesia, lasts up to two hours. The surgeon makes an incision under the arm and removes a section of fat that contains a cluster of lymph nodes. The incision is sutured, and a drain is generally inserted to remove excess fluid. After the procedure: Most patients remain in the hospital overnight, longer if complications develop. Nurses monitor the patient until the anesthetic wears off and vital signs stabilize. The drain may be left in place until the first follow-up visit. Postoperative measures include medication to relieve pain, preventive care to avoid infection at the incision site, the use of compression bandages to reduce fluid retention, and stretching exercises to rehabilitate arm movement. No heavy lifting is allowed during the recovery period of up to six weeks. Risks: The most common complications of axillary dissection are numbness under the arm, swelling of the arm (lymphedema) with feelings of tightness and reduced range of motion, and infection at the incision site. Results: Before proceeding with an axillary dissection, the surgeon may decide to biopsy the sentinel lymph node (the very first node that drains fluid from the tumor). If no cancer cells are found, then no other nodes or only a few
Salem Health: Cancer adjacent key nodes are removed. If tumor cells are detected, however, then a more extensive axillary dissection is performed to excise six to ten nodes or more. The greater the number of cancerous nodes, the less favorable is the prognosis for survival. Anna Binda, Ph.D. See also Breast cancers; Cutaneous breast cancer; Lobular carcinoma in situ (LCIS); Lumpectomy; Lymphedema; Mastectomy; Melanomas; Mucinous carcinomas; Sentinel lymph node (SNL) biopsy and mapping.
u Azathioprine Category: Carcinogens and suspected carcinogens RoC status: Known human carcinogen since 1985 Also known as: Azasan, Imuran Related cancers: Non-Hodgkin lymphoma, cancers of the skin and liver Definition: Azathioprine is a drug prescribed for transplant patients and those whose immune systems attack their own tissues, but long-term usage causes cancer. Exposure routes: Ingestion, intravenous injection, and inhalation Where found: The drug is found in hospitals, used for transplant and autoimmune disease patients, and in manufacturing plants that make and package the drug. At risk: Patients who take azathioprine and workers who manufacture it. Etiology and symptoms of associated cancers: In the liver, azathioprine is converted to 6-mercaptopurine, which inhibits deoxyribonucleic acid (DNA) synthesis. This suppresses the immune system but can also cause a dangerous decrease in the number of white blood cells (leukopenia)
Azathioprine and platelets (thrombocytopenia), increased risk of infection and bleeding, gastrointestinal disturbances, and liver damage. The substance 6-mercaptopurine also inserts between adjacent nucleotide bases in DNA molecules and causes mutations that lead to various types of cancer. Azathioprine increases the risk of developing squamous cell carcinoma, a type of skin cancer that appears as persistent wartlike growths, scaly patches, or open sores that crust over and bleed; non-Hodgkin lymphoma, a blood-based cancer of white blood cells called T cells, the most common symptoms of which are painless swelling of the neck, or underarm lymph nodes, unexplained fever, loss of weight and appetite, itchy skin with reddened patches, and constant fatigue; and cancer of the bile ducts or hepatobiliary carcinomas, whose symptoms include jaundice, itching, stomach pain, weight loss, and fever. History: The pioneer of liver transplantation, Sir Roy Yorke Calne, first used azathioprine to prevent organ rejection in liver transplant patients. Azathioprine was the standard antirejection drug in the 1970’s for organ transplants and was later enlisted to treat patients who suffer from diseases that result when the immune system attacks the patient’s own body (autoimmune diseases). Several epidemiological studies have shown that transplant patients who took azathioprine were at a high risk for different types of tumors. Other patients who took azathioprine but were not transplant patients, including those with rheumatoid arthritis, systemic lupus, inflammatory bowel disease, and certain skin and renal diseases, have also shown higher incidences of such malignancies, but not as high as those observed in transplant patients, since the dosages to treat autoimmune diseases are lower than those used for transplant patients. Mycophenolate mofetil, which is not as carcinogenic, is gradually replacing azathioprine as the antirejection drug of choice. Michael A. Buratovich, Ph.D. See also Crohn disease; Myasthenia gravis; Pancolitis.
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Bacillus Calmette Guérin (BCG)
u Bacillus Calmette Guérin
(BCG) Category: Chemotherapy and other drugs ATC code: 103AX03 Also known as: BCG Live, Pacis BCG Live, TICE BCG Definition: Bacillus or bacille Calmette Guérin (BCG) solution is an immunotherapeutic agent containing live, weakened bacteria. It is currently approved by the U.S. Food and Drug Administration (FDA) as a primary therapy for carcinoma in situ of the urinary bladder. The BCG solution for bladder cancer contains water, saline, and a freeze-dried and live (but avirulent) strain of Mycobacterium bovis, an organism that causes tuberculosis in cattle. The BCG vaccine is used throughout the world to immunize humans against tuberculosis, with varying rates of efficacy; the BCG vaccine is not routinely administered in the United States. BCG is named for the two Pasteur Institute researchers who discovered the vaccine against human tuberculosis: physician Léon Charles Albert Calmette (1863-1933) and bacteriologist Jean-Marie Camille Guérin (1872-1961). Cancers treated: Superficial or early-stage bladder cancer in which tumors have not entered the muscle layer of the bladder wall Delivery routes: Instillation How this substance works: Generally BCG treatment follows surgery to remove tumors from the surface (epithelium) of the inside of the bladder (lumen). A health care provider inserts a catheter to deliver the BCG solution to the bladder. The solution remains in the bladder for at least two hours. The millions of M. bovis bacteria in BCG solution stimulate the immune system to seek out and destroy cancer cells. Patients usually have a series of weekly instillations over a number of months followed by maintenance instillations, depending on the treatment plan. The exact mechanism of action of the BCG solution is unknown. It is thought that certain proteins in the bacteria adhere to the urothelium or lining of the bladder wall. The urothelium then releases a number of cytokines or inflammatory substances that alert the immune system that a pathogen is present. The bacteria may also enter the cancer cells and break down proteins to display on the cancer cell surface, thus flagging it for destruction by the immune system. Approximately 70 percent of patients respond to initial treatment, and 75 percent of those patients remain free of 118
Salem Health: Cancer bladder cancer for more than five years. Because BCG contains live bacteria, patients with compromised immune systems should not be treated with BCG solution. Patients should also not take antibiotics, which would kill the live bacteria and prevent effective treatment. Side effects: Most patients (80 to 90 percent) who receive successive treatments with BCG solution experience one or more side effects, including the urgent need to urinate, blood in the urine, pain during urination, fatigue, nausea, chills, and a low-grade fever that lasts twenty-four to seventy-two hours. Pamela Richardson, M.S. See also Biological therapy; Bladder cancer; Immunocytochemistry and immunohistochemistry; Immunotherapy.
u Bacteria as causes of cancer Category: Carcinogens and suspected carcinogens Also known as: Helicobacter pylori, Salmonella typhi, Streptococcus bovis, Chlamydophila (previously Chlamydia) pneumoniae Related cancers: Gastrointestinal cancers, lung cancer Definition: Although no bacterium has been shown to be absolutely responsible for causing cancer, very strong evidence implicates two types of bacteria in the process of cancer formation, and less convincing evidence implicates others. Each of these types of bacteria has been shown to cause a persistent (chronic) infection in which the organisms are in contact with the tissue over a long period of time. During that time, genes for cell division and other cell maintenance functions, the same ones that are damaged by other known chemical and physical carcinogens, are damaged by the metabolic and toxic products produced by these bacteria. Equally important are immune system defenses and additional genetic and environmental factors that make only certain individuals susceptible to these organisms. The two types of bacteria are Helicobacter (associated with gastric cancer) and Salmonella typhi (gallbladder cancer). Additional bacteria probably associated with different cancers include Streptococcus bovis (colorectal cancer), Chlamydophilia pneumoniae (lung cancer), strains of Escherichia coli (colorectal cancer associated with Crohn disease and ulcerative colitis), and different types of oral streptococci (oral cancers). Exposure routes: Ingestion and inhalation Where found: Infected and uninfected persons carrying certain bacteria; contaminated water, air, and surfaces
Salem Health: Cancer At risk: Genetically susceptible individuals specific to each type of bacteria Etiology and symptoms of associated cancers: Cancer caused by H. pylori is characterized by tumors in the protective layer of mucus in the stomach, including the immune tissue. Continued high incidence of stomach cancer in areas of Asia suggests that a diet high in salted, smoked, and pickled foods is a contributory factor. Transmission of H. pylori is thought to be by the fecal-oral route. The second strongest case for bacterial causation of cancer involves S. typhi and its role in causing cancer of the gallbladder. It has been known since the famous case of Typhoid Mary that survivors (or carriers without symptoms) of typhoid fever carry S. typhi for at least a year and can transmit the pathogen in their feces. The organism resides in the gallbladder during that entire time, thus fulfilling one of the conditions necessary to cause cancer (long exposure). Cancer formation in the gallbladder is frequently associated with gallstone formation (solid deposits of cholesterol or calcium salts). Symptoms that may indicate a diseased gallbladder include chronic indigestion, upper abdominal pain, nausea and vomiting, and fever. All of these symptoms may also be associated with additional gastrointestinal problems, so they are not definitive for gallbladder problems, including gallbladder cancer. Associated risk factors include cholelithiasis (especially untreated symptomatic chronic gallstones), obesity, reproductive factors, environmental exposure to toxic chemicals, congenital malformation of bile ducts, and chronic infections affecting the gallbladder. The most significant risk factor for those cancers associated with S. typhi appears to be chronic infection of the gallbladder. Data show that patients with chronic infections with this organism are eight times more likely to have cancer of the gallbladder than those who had acute infections in which the organisms were cleared from their body. Genetic susceptibility of American Indians and Mexican Americans, especially women (in all populations), to gallbladder cancer suggest that these groups are predisposed to develop it primarily or secondarily due to an increased incidence of cholesterol gallstones. A secondary pathway of cancer development revolves around congenital malformation of the bile duct, and is seen primarily in people from Japan, Korea, and possibly China. History: The first indication that a relationship existed between bacteria and cancer occurred in 1951, when researchers found that patients frequently had both infective endocarditis (infection of the heart) and colonic carcinoma. It took until 1974 to identify S. bovis as the bacte-
Bacteria as causes of cancer rium associated with the colonic cancer and bacteremia (bacteria in blood). It is known today that S. bovis is a natural inhabitant of the human gastrointestinal tract and causes both endocarditis and bacteremia. Patients having colon carcinoma frequently also harbor S. bovis, and these cancerous lesions may develop years after having endocarditis or bacteremia. Further research has focused on the bacteria naturally found in the gastrointestinal tract and their ability to metabolize nutrients into carcinogens. Experiments done using gastrointestinal flora from rats determined that metabolic products are mutagenic (cause mistakes in deoxyribonucleic acid, or DNA). The fact that germ-free rats did not develop tumors as frequently as normal animals was also significant in defining the relationship between diet and gastrointestinal flora. Data from later experiments have suggested that the presence of microorganisms as a causative agent for cancer formation may be more complicated than first thought. Conflicting reports suggest that the presence of H. pylori is both detrimental and beneficial in the development of esophageal cancer. The ability to use the presence of microorganisms as an indication that cancer may also be present (in situations in which the cancer is not easily diagnosed at an early stage) is being examined. This is the case with oral tumors and specific oral bacteria. Therefore, the precise relationship between microorganisms and different types of cancer is still unclear and remains to be determined. Steven A. Kuhl, Ph.D. u
For Further Information Hope, Mari, et al. “Sporadic Colorectal Cancer: Role of the Commensal Microbiota.” FEMS Microbiology Letters 244 (2005): 1-7. Lax, Alistair, and Warren Thomas. “How Bacteria Could Cause Cancer: One Step at a Time.” Trends in Microbiology 10 (2002): 293-299. Mager, Dixie. “Bacteria and Cancer: Cause, Coincidence, or Cure? A Review.” Journal of Translational Medicine 4 (2006): 14.
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Other Resources
Centers for Disease Control and Prevention Helicobacter pylori http://www.cdc.gov/ncidod/aip/research/hp.html National Cancer Institute H. pylori and Cancer: Fact Sheet http://www.cancer.gov/cancertopics/factsheet/ HPylori 119
Barium enema
Salem Health: Cancer
See also Achlorhydria; Alcohol, alcoholism, and cancer; Diverticulosis and diverticulitis; Esophagitis; Ethnicity and cancer; Helicobacter pylori; Infectious cancers; Mucosa-associated lymphoid tissue (MALT) lymphomas; Poverty and cancer; Prostatitis; Risks for cancer; Stomach cancers; Virus-related cancers.
u Barium enema Category: Procedures Also known as: Lower gastrointestinal (GI) series, single-contrast barium enema, double-contrast barium enema, air contrast barium enema Definition: A barium enema involves the insertion of barium sulfate, a radiopaque contrast medium, into the colon, the first section of the large intestine. This procedure is used with X rays as a diagnostic and screening test for colon cancer, colorectal cancer, and colon polyps, growths that are sometimes a precursor to colon cancer.
A barium enema is an outpatient procedure that is performed at a hospital radiology department or an outpatient radiology center. A barium enema does not require anesthesia, and patients are awake. A single-contrast barium enema takes about forty-five minutes, and a doublecontrast study takes about an hour to complete. Patients disrobe and wear an examination gown for the procedure. Steps of the procedure: Patients lie on an X-ray table. An X ray is taken before the barium is inserted. Patients lie on their side for the barium insertion process. Awell-lubricated plastic tube is gently inserted through the anus and into the rectum. Barium is slowly poured through the tube to fill the colon. The barium is monitored on a barium fluoroscope monitor. A balloon at the end of the enema tube is inflated to keep the barium in the colon. Patients may receive medication to relieve cramping. X rays are taken from a variety of angles. Patients are asked to change positions, and the X-ray table may be tilted. Pressure may be applied to the patient’s abdomen to help move the barium through the colon.
Cancers diagnosed: Colon cancer, colorectal cancer, colon polyps Why performed: A barium enema with X rays is used to screen for and help diagnose colon cancer, colorectal cancer, and colon polyps. The American Cancer Society recommends screening beginning at the age of fifty, earlier for people with risk factors. Barium sulfate shows up on X rays and highlights the shape of the colon better than X rays alone. A single-contrast barium enema uses barium sulfate that is inserted into the colon. A double-contrast barium enema involves inserting barium into the colon, emptying the colon, and then expanding the colon with air. The barium remains on the lining of the colon, and the air expands the folds of the colon to allow a better view. Patient preparation: Patients consume a clear liquid diet for one to three days before the test. Patients are instructed to consume large amounts of water and to use laxatives and enemas on the day before the test. An enema may be repeated on the day of the test to make sure the bowel is clear of stool and gas. For women, a pregnancy test may be used to ensure that the patient is not pregnant. Patients should tell their doctor if they have a latex allergy. 120
An X ray of the abdomen (frontal view), showing cancer of the left descending colon, after a barium enema. (©ISM/Phototake—All rights reserved)
Salem Health: Cancer At the end of the procedure, the enema tube is gently removed. Patients empty the barium from the colon by using a bedpan or going to the bathroom. After the barium is removed, a few final X rays are taken. For a double-contrast barium enema, the colon is drained of barium. The colon is then filled with air, and X rays are taken. When the procedure is complete, the enema tube is removed, and patients empty the colon of barium. Afew final X rays are taken. After the procedure: Patients should drink plenty of fluids to help remove the barium from their bodies. Bowel movements will contain barium for one to two days following the tests. The barium may make bowel movements appear pink or white in color.
Barium swallow European Journal of Radiology 61, no. 3 (March, 2007): 382-387. Rosman, A. S., and M. A. Korsten. “Meta-analysis Comparing CT Colonography, Air Contrast Barium Enema, and Colonoscopy.” American Journal of Medicine 120, no. 3 (March, 2007): 203-210. See also Adenomatous polyps; Barium swallow; Colon polyps; Colonoscopy and virtual colonoscopy; Colorectal cancer screening; Crohn disease; Diverticulosis and diverticulitis; Gallium scan; Imaging tests; Medicare and cancer; Ovarian cancers; Pancolitis; Premalignancies; Small intestine cancer; X-ray tests.
Risks: A barium enema is a low-risk procedure. Occasionally, the barium may harden, resulting in constipation. Drinking extra fluids and using a laxative may relieve constipation. In rare cases, the bowel may become inflamed or perforated. Patients should contact their doctor if they experience bleeding, severe pain, fever, or no bowel movements within two days of the procedure.
u Barium swallow
Results: The X-ray films are read by a radiologist. The ordering doctor may review the films as well. A healthy colon and rectum are free of abnormal growths or polyps. Any abnormalities, such as cancer or precancerous tissues, are visible on the films. Abnormal results are followed with colonoscopy. Mary Car-Blanchard, O.T.D., B.S.O.T.
Definition: A barium swallow is a diagnostic test in which the patient ingests barium sulfate, a radiopaque contrast medium. It is used with X rays to detect mouth, throat, vocal cords, esophagus, stomach, and small intestine cancers.
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For Further Information Etzioni, D. A., et al. “Measuring the Quality of Colorectal Cancer Screening: The Importance of Follow-Up.” Diseases of the Colon and Rectum 49, no. 7 (July, 2006): 1002-1010. Fenton, J. J., et al. “Delivery of Cancer Screening: How Important Is the Preventive Health Examination?” Archives of Internal Medicine 167, no. 6 (March 26, 2007): 580-585. Jimbo, M., et al. “Effectiveness of Complete Diagnostic Examination in Clinical Practice Settings.” Cancer Detection and Prevention 30, no. 6 (2006): 545-551. Pickhardt, P. J. “The Natural History of Colorectal Polyps and Masses: Rediscovered Truths from the Barium Enema Era.” American Journal of Roentgenology 188, no. 3 (March, 2007): 619-621. Rollandi, G. A., E. Biscaldi, and E. DeCicco. “Double Contrast Barium Enema: Technique, Indications, Results, and Limitations of a Conventional Imaging Methodology in the MDCT Virtual Endoscopy Era.”
Category: Procedures Also known as: Barium swallow X ray, barium swallow exam, barium swallow test, barium meal, doublecontrast barium swallow, upper gastrointestinal (GI) series, esophagraphy, esophagogram, esophagram
Cancers diagnosed: Oral cavity (mouth) cancer; oropharyngeal (throat) cancer; vocal cord cancer, including laryngeal and hypopharyngeal cancer, glottic cancer, supraglottic cancer, subglottic cancer; esophageal cancer; stomach cancer; stomach polyps, which may precede stomach cancer; small intestine cancer, including carcinoid tumors, gastrointestinal stromal tumors, lymphomas, and adenocarcinoma Why performed: A barium swallow with X rays is performed to help diagnose cancer of the mouth, throat, vocal cords, esophagus, stomach, and small intestine. When swallowed, barium sulfate shows up on X rays and highlights the linings of the above-mentioned structures. A double-contrast barium swallow involves swallowing substances that create air in the stomach to expand it, allowing a better view. Patient preparation: Patients may be placed on a restricted diet a few days before the test. Patients should not eat, drink, chew gum, or smoke after midnight before the test. Patients receive instructions from their doctors about swallowing medications. The stomach needs to be empty for the procedure. In some cases, the stomach contents are removed through a tube placed in the nose. For women, a 121
Barium swallow
Salem Health: Cancer taken. Then, patients drink sixteen to twenty ounces of barium sulfate. The barium sulfate is mixed in a thick drink that may have flavor added to it; otherwise, the drink is described as tasting chalky. The examination table may be tilted or pressure may be applied to the patient’s abdomen to help spread the barium. The barium is viewed on a barium fluoroscope monitor as it travels through the upper digestive tract. Still X-ray images can be taken at any time. Patients may need to drink more barium sulfate as the test progresses. For a double-contrast barium swallow, the patient swallows baking soda crystals. The baking soda creates gas, and the air expands the stomach. Additional images are taken, and the patient is repositioned or the examination table is tilted as necessary. After the procedure: Patients should drink plenty of fluids to help remove the barium from their bodies. Patients can eat a regular diet unless instructed otherwise. Bowel movements will contain barium for one to two days following the tests. The barium may make bowel movements appear white, gray, or pink in color.
Extended, infiltrating, and mild stenosing esophageal cancer are revealed by a barium X ray. (©ISM/Phototake—All rights reserved)
pregnancy test may be performed to ensure that the patient is not pregnant. Abarium swallow is an outpatient procedure that is performed at a hospital radiology department, outpatient radiology center, or doctor’s office. The test does not require anesthesia, and patients are awake. A barium swallow usually takes from thirty to sixty minutes, depending on the extent of the procedure. Patients disrobe and wear a gown for the test. Patients need to remove metal objects that may interfere with the X rays, including glasses, dentures, and jewelry. Steps of the procedure: The patient’s vital signs are taken before the test and monitored during the test. Patients may sit, stand, or lie on an X-ray table for the procedure. Patients may be secured to the X-ray table if it is tilted to allow images to be taken from various angles. X rays of the patient’s heart, lungs, and abdomen are 122
Risks: A barium swallow is considered a low-risk procedure. The radiation exposure is low, but it carries a small risk of cancer. Patients may be allergic to the flavorings that are mixed with the barium drink. Occasionally, the barium may harden, resulting in intestinal blockage or constipation. Patients should contact their doctor if they have not had a bowel movement within one to two days of the procedure. Results: The X-ray films are read by a radiologist. The ordering doctor may review the films as well. The linings of healthy structures are free of abnormal growths or polyps. Any abnormalities, such as cancer or precancerous tissues, appear as growths or polyps. Mary Car-Blanchard, O.T.D., B.S.O.T. u
For Further Information Drop, A., et al. “The Modern Methods of Gastric Imaging.” Annales Universitatis Mariae Curie-Skuodowska 59, no. 1 (2004): 373-381. Gore, R. M., et al. “Upper Gastrointestinal Tumours: Diagnosis and Staging.” Cancer Imaging 29, no. 6 (December, 2006): 213-217. Hosaka, K. “Radiological Investigation of the Mucosae Around Early Gastric Cancers.” Journal of Gastroenterology 41, no. 10 (October, 2006): 943-953. Kunisaki, C., et al. “Outcomes of Mass Screening for Gastric Carcinoma.” Annuals Surgical Oncology 13, no. 2 (February, 2006): 221-228.
Salem Health: Cancer Levine, M. S., and S. E. Rubesin. “Diseases of the Esophagus: Diagnosis with Esophagography.” Radiology 237, no. 2 (November, 2005): 414-427. Pasuawski, M., J. Zuomaniec, E. Ruci½ska, and W. Koutyk. “Synchronous Primary Esophageal and Gastric Cancers.” Annales Universitatis Mariae Curie-Skuodowska 59, no. 1 (2004): 406-410. Summers, D. S., M. D. Roger, P. L. Allan, and J. T. Murchison. “Accelerating the Transit Time of Barium Sulphate Suspensions in Small Bowel Examinations.” European Journal of Radiology 62, no. 1 (April, 2007): 122-125. See also Diarrhea; Esophageal cancer; Gastrointestinal cancers; Gastrointestinal complications of cancer treatment; Imaging tests; Laryngeal cancer; Laryngectomy; Small intestine cancer; Stomach cancers; Throat cancer; Upper gastrointestinal (GI) series; X-ray tests.
u Barrett esophagus Category: Diseases, symptoms, and conditions Also known as: Barrett’s esophagus, Barrett’s metaplasia, Barrett’s mucosa, Barrett’s syndrome, columnar epithelium lined lower oesophagus (CELLO), columnar-lined esophagus Related conditions: Esophageal adenocarcinoma, gastroesophageal reflux disease (GERD), hiatal hernia
Barrett esophagus people with GERD, some of the acid of the stomach leaks into the esophagus, possibly because of a weakness in the sphincter. In about 10 to 15 percent of these people, the acid changes the color and makeup of the cells lining the esophagus. These cells are much like cells in the intestines; they are darker than the normal esophagus tissue and more resistant to stomach acid. Rarely, Barrett esophagus cells develop into a precancerous state called dysplasia. Dysplasia, in some cases, then develops into esophageal cancer. Incidence: About 700,000 adults in the United States have Barrett esophagus. It is very uncommon in children; the average age of diagnosis is sixty. It is twice as common in men as in women. Caucasians and Hispanics are more likely to develop this condition than those of other ethnic backgrounds. Symptoms: Symptoms include chronic heartburn, chronic acid reflux, trouble swallowing or a feeling that something is stuck in the throat, weight loss, spitting up food, excessive burping, hoarseness, sore throat, and bleeding. Sometimes people with chronic heartburn will get some relief from their symptoms when they develop Barrett esophagus. The intestinal metaplasia may help protect the esophagus from the stomach acid because those cells are normally found in the intestines and are better able to withstand stomach acid. Screening and diagnosis: Adults over the age of forty who have had chronic heartburn or acid reflux may be
Definition: Barrett esophagus is a condition in which some of the cells lining the esophagus (tube that carries food to the stomach) are replaced with a different type of cell similar to those lining the intestines, a process called intestinal metaplasia. Rarely, these cells develop into cancer of the esophagus (esophageal adenocarcinoma). This condition is named after Norman Barrett, who first described it in 1957. Risk factors: Developing Barrett esophagus is linked to chronic heartburn and another common condition called gastroesophageal reflux disease (GERD). However, the chances of heartburn or GERD developing into Barrett esophagus are very small. Sometimes people who develop GERD have a part of the stomach that bulges through the diaphragm (hiatal hernia). This kind of hernia may trap acid in the esophagus and cause more damage, eventually leading to GERD and progressing into Barrett esophagus. Etiology and the disease process: Normally, a round muscle (sphincter) near the bottom of the esophagus keeps stomach acid from washing back up into the esophagus. In
Barrett esophagus has produced two areas of dysplasia. (Custom Medical Stock Photo)
123
Basal cell carcinomas screened with an endoscopy to see whether they have Barrett esophagus. However, screening for this disease is not commonly recommended as an endoscopy is expensive and the rate of discovering the condition is very low. People who have no symptoms should not have an endoscopy just to see if they have this condition. Barrett esophagus can be diagnosed only by performing a biopsy on suspected tissue. There is no staging for Barrett esophagus. Treatment and therapy: Treatment for Barrett esophagus involves avoiding further damage. Therapies that keep the acid in the stomach from moving up into the esophagus may include antacid-type medications or other medications that stop stomach acid production. Lifestyle changes, such as losing weight, stopping smoking, and avoiding certain foods, also help. Other ways to keep the acid in the stomach include eating smaller meals more often, wearing loose-fitting clothing, waiting two to three hours after eating before lying down, and elevating the head of the bed 8 to 10 inches. A type of surgery that reinforces the sphincter that keeps acid in the stomach may also help. There is no cure for Barrett esophagus other than surgically removing the esophagus. This type of surgery is only performed on those who have already developed esophageal adenocarcinoma or are at very high risk for developing it. With this surgery, the affected part of the esophagus is removed, and the stomach is brought up and attached to the nonaffected part of the esophagus. Possible treatments for removing Barrett esophagus cells are being investigated. These include various ways of destroying those cells with lasers or chemicals. However, removing the cells has not yet been proven to reduce the risk of Barrett esophagus recurring or developing into esophageal cancer. Removing the Barrett esophagus cells is usually recommended only when a patient has highly developed precancerous or already cancerous cells. Prognosis, prevention, and outcomes: Barrett esophagus may not cause any problems or symptoms in those who have it. It is only significant because it is a precursor to esophageal adenocarcinoma, but even those who have Barrett esophagus have a less than 1 percent chance of developing this type of cancer. Those who have been diagnosed with Barrett esophagus should be screened regularly, every one to three years, to ensure that the cells are not developing into cancer. Some ways of attempting to prevent further damage to the esophagus are to eat a diet low in fat and high in fruits, vegetables, and fiber. Avoiding smoking and maintaining a healthy weight may also help. Marianne M. Madsen, M.S. 124
Salem Health: Cancer u
For Further Information Parker, James, and Philip M. Parker, eds. The Official Patient’s Sourcebook on Barrett’s Esophagus: A Revised and Updated Directory for the Internet Age. San Diego, Calif.: Icon Health, 2004. Shalauta, Saad R. “Barrett’s Esophagus.” American Family Physician 69, no. 9 (May 1, 2004): 2113-2118. Sharma, Prateek, and Richard E. Sampliner, eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2d ed. Malden, Mass.: Blackwell, 2006. u
Other Resources
Barrett’s Oesophagus Foundation http://www.barrettsfoundation.org.uk MedicineNet.com Barrett’s Esophagus http://www.medicinenet.com/barretts_esophagus/ article.htm National Digestive Diseases Information Clearinghouse Barrett’s Esophagus http://digestive.niddk.nih.gov/ddiseases/pubs/barretts See also Esophageal cancer; Esophagectomy; Esophagitis; Histamine 2 antagonists; Premalignancies; Upper gastrointestinal (GI) endoscopy.
u Basal cell carcinomas Category: Diseases, symptoms, and conditions Also known as: Basal cell cancer, BCC Related conditions: Basal cell epitheliomas Definition: Basal cell carcinoma is a cancer in which the cancerous cells resemble the basal cells of the epidermis, the outer layer of the skin. It is the most common type of skin cancer. Risk factors: Exposure to ultraviolet light is the primary risk factor. People with light skin and eyes are more susceptible because they have less melanin, the pigment that colors skin and blocks the sun’s radiation. People who are exposed to more ultraviolet light because they work outdoors or use tanning booths are also at greater risk. Children are particularly susceptible to skin damage from the sun because they burn more readily. Arsenic exposure, usually from contaminated drinking water, is another risk factor.
Salem Health: Cancer
Basal cell carcinomas
Etiology and the disease process: Basal cell carcinomas are thought to begin in the upper part of the skin, the epidermis, or in a hair follicle. The basal cell layer forms the base of the epidermis. Basal cells continually divide to form new cells of skin, hair, or glands. They become cancerous when something disrupts their deoxyribonucleic acid (DNA) instructions for making normal new cells. The most common cause is ultraviolet radiation, probably UVB. These rays can hit the nuclei of skin cells and damage chromosomes or DNA. The body repairs most of the damage to chromosomes, but cells that are not repaired can begin to divide wildly and become cancer cells, which destroy surrounding cells or tissues. Basal cell carcinomas are slow growing and rarely spread to other parts of the body. If left untreated, however, they can do extensive damage to surrounding tissue. Incidence: Basal cell carcinoma is the most common skin cancer in the United States, making up about 75 percent of skin cancers. Nearly a million new cases are reported each year, and about 90 percent of those are attributed to solar radiation, although some cases occur in skin rarely exposed to the sun. Men are at higher risk than women, probably because they have, in the past, worked outdoors more. Basal cell carcinoma is more common in adults than in children, and the elderly are the most likely candidates, as these cancers can take twenty to fifty years to manifest after radiation exposure. Symptoms: The most common symptom of basal cell carcinoma is a skin lesion, which is a superficial growth or a sore that does not heal. There are many types of basal cell carcinoma and nearly as many types of lesions. Lesion size varies from a few millimeters to several centimeters, and some lesions are larger than they appear on the skin because they invade underlying tissues. The lesions are usually painless, though the surrounding skin can become irritated and tender. Some lesions are flat, reddish or crusty patches that can be mistaken for psoriasis or eczema. The color and appearance of lesions varies widely, from white or yellow and scarlike to pink, red, tan, brown, or black. Lesions are often waxy or translucent in appearance, and many are described as pearly. Some lesions are smooth and symmetrical, while others have irregular borders or a bumpy surface with superficial blood vessels. Other lesions have rolled edges with a crater in the middle. Many lesions bleed easily. Screening and diagnosis: The U.S. Preventive Services Task Force evaluated routine screening for skin cancers in 2001 and did not find evidence to recommend whole-body
A patient with basal cell carcinoma. (Custom Medical Stock Photo)
skin examination for skin cancer, so health care providers look for skin cancers as circumstances allow or warrant. The diagnosis of basal cell carcinoma is made by histologic, or microscopic, examination of lesional cells from a sample of the lesion or from examination of the entire lesion. The type and variety of cancer are determined by the makeup and differentiation of cells. Treatment and therapy: The most common treatment for basal cell carcinoma is surgical excision, or removal, of the lesion. Some normal tissue is taken all around the lesion so that the physician can be sure no cancer cells are left. Mohs surgery, which allows for better margin control, is the treatment of choice for sclerosing basal cell carcinoma. Other treatments include curettage and electrodesiccation, or scraping of the lesion and destroying the remaining tissue with electric current; cryosurgery, or freezing with liquid nitrogen; topical chemotherapy; radiation; laser surgery; and photodynamic therapy, in which a 125
Beckwith-Wiedemann syndrome (BWS) sensitizer is absorbed into the lesion, which is then exposed to a laser beam. Prognosis, prevention, and outcomes: The cure rate is about 85 to 99 percent for primary tumors. One variant of basal cell carcinoma, called sclerosing, morpheaform, or infiltrating, is more likely to recur after treatment. This variant, which usually resembles a scar, is more difficult to treat because it grows in thin strands that may be missed in the tissue sample. Though death from basal cell carcinoma is extremely rare, untreated lesions can cause extensive damage and disfigurement, sometimes requiring skin grafts or reconstructive surgery. Early detection and treatment give the best outcomes. Basal cell carcinoma is also highly preventable through avoidance of excessive sun exposure, particularly in childhood. Childhood exposure to ultraviolet radiation can result in skin cancer that appears decades later. Limiting sun exposure, using sunscreen, and wearing sun-protective clothing and hats are useful methods of preventing damage to the skin from ultraviolet light. Cathy Anderson, R.N., B.A. u For Further Information Burns, C. A., and M. D. Brown. “Imiquimod for the Treatment of Skin Cancer.” Dermatology Clinics 23, no. 1 (2005): 151-164. Neale, R. E., et al. “Basal Cell Carcinoma on the Trunk Is Associated with Excessive Sun Exposure.” Journal of the American Academy of Dermatology 56, no. 3 (2007): 380-386. Noble, J. Textbook of Primary Care Medicine. 3d ed. St. Louis: Mosby, 2001.
u
Other Resources
Medem Medical Library http://www.medem.com Skin Cancer Foundation http://www.skincancer.org See also Arsenic compounds; Bowen disease; Choriocarcinomas; Dermatology oncology; Electroporation therapy; Exenteration; Eye cancers; Eyelid cancer; Lip cancers; Medulloblastomas; Melanomas; Mohs surgery; Moles; Neuroectodermal tumors; Radical neck dissection; Skin cancers; Squamous cell carcinomas; Sunlamps; Turcot syndrome; Vulvar cancer. 126
Salem Health: Cancer
u Beckwith-Wiedemann
syndrome (BWS) Category: Diseases, symptoms, and conditions Also known as: Wiedemann-Beckwith syndrome, exomphalos-macroglossia-gigantism (EMG) syndrome Related conditions: Hemihypertrophy (enlargement of one side of the body); hypoglycemia (low blood sugar); exomphalos (a protrusion of the umbilicus) or other abdominal wall defects such as umbilical hernia, omphalocele, and diastasis recti; visceromegaly (enlarged organs) or enlarged tongue or skeleton; adrenal gland abnormalities such as adrenocortical cytomegaly (enlarged cells of the adrenal cortex); dysplasia of the renal medulla; and embryonal cancerous tumors (tumors that arise from embryonic or fetal tissue) such as nephroblastoma (Wilms’ tumor affecting the kidney, about 75 percent), hepatoblastoma (liver malignancy, about 1 to 11 percent), rhabdomyosarcoma (a soft-tissue tumor most commonly found in the head and neck, arms, and legs, and the renal and genital tracts, about 5 percent), and neuroblastoma (affecting primitive neuronal cells in the adrenal gland and behind the peritoneum, the serous tissue that lines the abdomen, about 4 percent) Definition: Beckwith-Wiedemann syndrome (BWS) is a congenital overgrowth disorder caused by abnormalities in the 11p15.5 region of chromosome 11. The expression of the involved chromosome is variable and the penetrance (the degree to which features or characteristics resulting from the person’s genetic makeup are seen by others) is incomplete. Penetrance is affected by either paternal or maternal transmission of information and gene control. Risk factors: De novo mutations and inheritance through familial linkage are the primary risk factors. Analysis of the chromosomes is diagnostic in familial heritance, and all show transmission through the mother. Analysis of paternally derived BWS shows duplication or trisomy of the 11p15.5 region. These multiple copies result in a varying phenotype. Thus, different patterns of inheritance have been documented. Etiology and the disease process: The overexpression of insulin-like growth factor-2 (IGF-2) is a key determinant of BWS. This overexpression occurs in the following manner. One set of chromosomes is inherited from the father, and the other is inherited from the mother. Each set of
Salem Health: Cancer chromosomes contains a gene or a set of genes responsible for the characteristics of the new individual. Often, a gene on either the maternal or paternal chromosome is expressed, while the corresponding gene on the other parent’s chromosome is silent. The expression of a gene on one parent’s chromosome and the silence of the corresponding gene on the other parent’s chromosome is termed imprinting. BWS develops when the normally expressed maternal gene is overactive. Deregulation of imprinted growth regulatory genes on chromosome 11, region 11p15.5, results in an imbalance between maternal and paternal allele expression. This region contains the genes for insulin and insulin-like growth factor-2 (IGF-2), both potent stimulators of fetal growth. This genetic aberration triggers exaggerated growth in the fetus, both in overall size as well as the enlargement of various structures and organs. Other tissues sensitive to abnormal growth factors respond by producing a high incidence of embryonal tumors and other anomalies. The loss of IGF-2 imprinting results in an overexpression of IGF-2 and leads to an enlarged body, organs, and overstimulation of embryonic tissues, which are the basis for various tumors affecting the kidneys, liver, and adrenal glands. Incidence: BWS occurs in approximately 1 in 14,000 live births in the regular population in the United States. The incidence is higher with in vitro births (assisted reproductive technology). Because of phenotypic variation, many individuals with BWS may go undiagnosed, especially if the penetrance is mild or subtle. Symptoms: Major symptoms include macroglossia (large tongue), pre- or postnatal growth greater than the ninetieth percentile, and abdominal wall defects. Minor symptoms include hypoglycemia, ear creases or helical indentations, facial nevus flammeus (port-wine stain), a large placenta at birth, and polyhydramnios (excessive amniotic fluid). Abnormalities in all body systems have been reported in association with BWS. Screening and diagnosis: Because of the high incidence of embryonal tumor formation, abdominal ultrasonographic examinations are necessary every three months, especially in the first six years of life (the period when most embryonal tumors manifest). Wilms’ tumor is rapidly progressive, and even individuals who have been examined every six months have been found to have latestage disease. Diagnosis is by imaging studies (ultrasound, magnetic resonance imaging, computed tomography, bone scans), biopsy, laboratory tests (complete blood count, blood smear, alpha-fetoprotein, tests to evaluate functioning of the involved organs).
Beckwith-Wiedemann syndrome (BWS) Staging is a process to determine whether the cancer has spread (metastasized) to other sites. Classification includes: • Stage I: The cancer can be completely removed by surgery. • Stage II: A majority of the cancer is removed by surgery with a small amount remaining at the primary site. • Stage III: The cancer has spread to the lymph nodes. • Stage IV: The cancer has spread to distant sites in the body. • Recurrent: The cancer has returned after it has been treated. Treatment and therapy: Hypoglycemia must be prevented and, if present, rapidly treated to prevent central nervous system abnormalities, especially mental retardation. Embryonic tumors require treatment (surgery, radiation, chemotherapeutic drug administration). Macroglossia is treated with surgery to ensure a patent (open) airway and normal mouth and speech development. Other anomalies are given standard treatment for the problem. Prognosis, prevention, and outcomes: Prevention requires a decision by affected individuals not to reproduce. Prenatal genetic testing is currently not available. Prenatal ultrasound examination may lead to early detection of an affected fetus. If the pregnancy is continued, medical personnel can be alerted, thus allowing prompt attention to the infant at birth to detect problems and intervene in a timely manner, hopefully preventing some complications. Prognosis depends on the range of morbidities and their management. Wanda Todd Bradshaw, R.N.C., M.S.N. u
For Further Information Cohen, M. Michael. “Beckwith-Wiedemann Syndrome: Historical, Clinicopathological, and Etiopathogenetic Perspectives.” Pediatric and Developmental Pathology 8 (2005): 287-304. Smith, Adam C., Sanaa Choufani, José C. Ferreira, and Rosanna Weksberg. “Growth Regulation, Imprinted Genes, and Chromosome 11p15.5.” Pediatric Research 61, no. 5 (2007): 43R-47R. Weksberg, Rosanna, Cheryl Shuman, and Adam C. Smith. “Beckwith-Wiedemann Syndrome.” American Journal of Medical Genetics, Part C 137C (2005): 12-23.
u
Other Resources
Beckwith-Wiedemann Syndrome Family Forum http://www.beckwith-wiedemann.info 127
Benign prostatic hyperplasia (BPH) Online Mendelian Inheritance in Man http://www.ncbi.nlm.nih.gov/sites/entrez?db=OMIM See also Adrenal gland cancers; Adrenocortical cancer; Nephroblastomas; Rhabdomyosarcomas; Wilms’ tumor.
u Benign prostatic hyperplasia
(BPH) Category: Diseases, symptoms, and conditions Also known as: Benign enlargement of the prostate (BEP), lower urinary tract symptoms (LUTS) Related conditions: Prostate cancer, urinary retention Definition: Benign prostatic hyperplasia (BPH) refers to an enlarged prostate gland. The prostate is a reproductive gland in men that produces semen, the fluid that nourishes and transports sperm. It is about the size and shape of a walnut and is located below the bladder. The gland surrounds the urethra, the tube that carries urine outside the body. The prostate grows in size in most men as they age. Risk factors: Increasing age and a family history of BPH contribute to the risk of developing this condition. Etiology and the disease process: The exact cause of BPH is unknown. It is not cancerous, nor does it increase the risk of developing prostate cancer. Incidence: Approximately 50 percent of men between the ages of fifty-one and sixty and 90 percent over age eighty develop BPH. About half of all men diagnosed with BPH have moderate to severe symptoms. Symptoms: The enlarged prostate presses down on the urethra and irritates or obstructs the bladder. Common symptoms include frequent urination two or more times per night, a sudden urge to urinate, a weak urine stream, dribbling after urinating, straining to urinate, the inability to prevent urine leakage, or the sensation that the bladder is not empty even after urinating. In extreme cases, urinary retention, the complete inability to urinate, is a problem. Screening and diagnosis: The evaluation typically consists of a complete medical history, a digital rectal exam to feel the size of the prostate, a urinalysis to check for blood or infection in the urine, a prostate-specific antigen (PSA) blood test to screen for prostate cancer, and questions to assess the severity of symptoms. Additionally, urine flow rate, a post-void residual urine test, a pressure-flow study, 128
Salem Health: Cancer an X ray of the urinary tract, or cystoscopy (a test using a scope inserted into the urethra and bladder) may be recommended. Treatment and therapy: Depending on the severity of symptoms, treatment can include lifestyle modifications, such as decreasing the intake of fluid before bedtime and limiting the consumption of alcohol and caffeine, or medication to increase urine flow. In extreme cases, surgery to remove part of the prostate may be recommended. Prognosis, prevention, and outcomes: Many men with BPH have only minor symptoms and are able to manage their discomfort with lifestyle modifications. A yearly exam is recommended to monitor symptoms and the impact of BPH on daily life. Vonne Sieve, M.A. See also Digital rectal exam (DRE); Prostate cancer; Prostate-specific antigen (PSA) test; Prostatectomy; Prostatitis; Saw palmetto; Transrectal ultrasound; Urologic oncology.
u Benign tumors Category: Diseases, symptoms, and conditions Also known as: Mass, benign neoplasm, noncancerous tumor Related conditions: Lipoma, chondroma, adenoma, hemangioma Definition: A benign tumor is a noncancerous growth that does not invade nearby tissue or spread to other parts of the body. Benign tumors are caused by cell overgrowth and are thus distinct from other tissue formations, such as cysts or abscesses. A tumor is a mass of tissue that serves no useful purpose and exists at the expense of healthy tissues. Benign tumors do not exhibit any of the three characteristics of malignant tumors: Benign tumors do not invade nearby tissues, do not metastasize, and do not grow in an unlimited, accelerated manner. Risk factors: The specific risk factors for benign tumors vary depending on the location of the tumor and the tissue type. For example, risk factors for benign breast tumors include such factors as body mass index, height, and breast size. Problems with the body’s immune system can cause tumors, both malignant and benign. Certain viruses can also play a role in tumor formation, as in cervical cancer and hepatocellular carcinoma. Exposure to loud sounds or music can increase the risk of developing benign tumors in
Salem Health: Cancer
Benign tumors
the ears, as can repeated exposure to cold water. Smoking can cause benign tumors to appear in the lower lip. Etiology and the disease process: The source of most benign tumors is a discrete population of cells that have been altered through acquired genetic defects. Such abnormal tissue masses are termed benign neoplasms. Benign tumors are usually encapsulated, meaning that they are confined to a specific, localized area and surrounded by a thin layer of tissue. This limits the growth rate and invasive potential of the tumor. In the liver, the most common benign tumors are hemangiomas. These tumors are made of abnormal blood vessels, most likely present at birth but only detected later when they cause symptoms or are identified on an ultrasound or computed tomography (CT) imBenign tumor nevus pigmented lesions. (Custom Medical Stock Photo) age obtained for another reason. Hemangiomas occur more frequently in women. Screening and diagnosis: When a tumor is found, a biInfections can cause benign tumors to appear in the larynx, opsy is performed to determine whether the tumor is bewhich can be detected by symptoms of hoarseness. nign or malignant. Although usually not life-threatening, Incidence: Benign tumors are common and usually not once diagnosed, benign tumors should be monitored regulife-threatening. However, benign tumors cause more than larly, as a benign tumor may progress and become a malig13,000 deaths annually, compared with more than 500,000 nant tumor. For instance, a colon polyp is a type of benign annual deaths due to malignant tumors. Benign tumors can tumor, but most incidences of colon cancer develop from cause serious injury or death by pressing on vital organs colon polyps. The most common benign tumors of the ear (such as the brain), tissues, or nerves in the vicinity of the occur behind the ear. They can also occur within the ear growth. Benign tumors in the kidneys can range in size canal or on the scalp and can be discovered during a roufrom 1 millimeter to several centimeters without causing tine ear examination, which includes audiometry (hearing any symptoms or requiring treatment. Benign tumors in tests) and tympanometry (middle ear testing). When lookthe lungs are relatively rare, making up only 7 to 10 pering into the ear, the doctor may observe cysts or benign tucent of all tumors in the lungs. Benign tumors in the stommors within the ear canal. ach account for 5 to 10 percent of all stomach tumors, afTreatment and therapy: Often a benign tumor will reflicting many people between the ages of forty and fifty. quire no treatment if it is located in a low-risk area where it Men are two to four times more likely to develop benign will not cause symptoms or disturb proper function of an stomach tumors compared with women. organ. If causing symptoms, benign tumors are usually Symptoms: Benign tumors may be asymptomatic or may treated by surgery. Benign tumors may also be removed cause one or more of the following symptoms depending for cosmetic reasons. The incidence of recurrence after on their location and their specific tissue type: itching, obsurgery is typically low. Chemotherapy and radiation therstruction of the intestines, bleeding or occult blood loss reapy are usually ineffective in the treatment of benign tusulting in anemia, cosmetic changes, hormonal syndromes mors. Benign tumors of the brain may be surgically recaused by hormones secreted by the tumor, compression moved to prevent harmful effects on the surrounding of the blood vessels or vital organs, and pain or dysfuncnormal brain tissue. tion induced by pressure. Benign tumors in the nose have Prognosis, prevention, and outcomes: Benign tumors the following symptoms: hard breathing, bleeding, headache, or severe eye pain and blurring. tend to grow more slowly than malignant tumors and are 129
Benzene less likely to threaten health. If a tumor is benign, the prognosis is generally very good. The situation can be more serious if the tumor is located in the brain. Michael R. King, Ph.D. u For Further Information Black, Peter McL. Living with a Brain Tumor: Dr. Peter Black’s Guide to Taking Control of Your Treatment. New York: Henry Holt, 2006. DeMonte, Franco, et al., eds. Tumors of the Brain and Spine. New York: Springer, 2007. Moore, Stephen W. Griffith’s Instructions for Patients. 7th ed. Philadelphia: Elsevier Saunders, 2005. u
Other Resources
Genetics Home Reference Benign Tumors http://ghr.nlm.nih.gov/conditionGroup=benigntumors Medline Plus Benign Tumors http://www.nlm.nih.gov/medlineplus/ benigntumors.html See also Acoustic neuromas; Adenomatoid tumors; BirtHogg-Dubé syndrome (BHDS); Brachytherapy; BRAF gene; Carcinogens, known; Carney complex; Castleman disease; Chemoprevention; Cowden syndrome; Craniopharyngiomas; Endotheliomas; Fibroadenomas; Gastrointestinal stromal tumors (GISTs); Gestational trophoblastic tumors (GTTs); Glomus tumors; Hemangioblastomas; Hystero-oophorectomy; Lacrimal gland tumors; Leiomyomas; Metastasis; Multiple endocrine neoplasia type 1 (MEN 1); Multiple endocrine neoplasia type 2 (MEN 2); Phyllodes tumors; Pineoblastomas; Radical neck dissection; Sertoli cell tumors; Tuberous sclerosis.
u Benzene Category: Carcinogens and suspected carcinogens RoC status: Known human carcinogen since 1980 Also known as: Benzol, phenyl hydride, 1,3,5cyclohexatriene Related cancers: Cancers of the blood and blood-forming organs, including acute myelogenous, monocytic, erythroblastic and lymphocytic leukemias, lymphomas, and Zymbal gland carcinomas Definition: Benzene (chemical formula C6H6) is a clear, colorless to light yellow, volatile and flammable liquid 130
Salem Health: Cancer that has an aromatic odor. It is slightly soluble in water, is sensitive to heat, and mixes easily with alcohol, ether, chloroform, acetone, carbon tetrachloride, carbon disulfide, oils, and glacial acetic acid. It forms a solid below 42 degrees Fahrenheit. In the United States, the Safe Drinking Water Act (1976) has legal control over benzene levels in drinking water, which cannot exceed 5 parts per billion (ppb). Exposure at 19,000-20,000 parts per million for five to ten minutes is fatal. Exposure routes: Inhalation, skin contact, and oral ingestion are the most toxic and dangerous routes. Where found: Benzene is an industrial chemical that is widely used as a solvent and used in inks, rubber, lacquers, paint removers, gas additives, glue backing for carpeting, high solvent paints, some furniture wax, automobile exhaust, tobacco smoke, secondhand smoke, taxidermy, firefighting, metal preparation and pouring, petroleum refining, industrial cleaning, drinking water, and closed processes to synthesize organic chemicals. It is also used to make dyes and insecticides and in the processing of numerous chemicals. At risk: Children and pregnant woman are at higher risk. However, anyone exposed to benzene is at risk. For example, the presence of benzene in gasoline makes exposure to it a risk for anyone filling an automobile gas tank. Etiology and symptoms of associated cancers: It is not clear how benzene causes damage to the blood-forming organs, which then leads to leukemias and lymphomas. Interaction between breakdown products (metabolites) is being studied as a likely cause. Exposure to as little as 1 part per million lowers white cell counts. Symptoms of leukemias and lymphomas include fever, night sweats, fatigue, bleeding and easy bruising, bone pain, frequent infections, swollen lymph nodes, and weight loss. History: Benzene is a natural component of crude oil. In 1825 Michael Faraday performed distillation experiments and extracted a gas from the oil. The gas burned, and he named it “bicarburet of hydrogen.” The chemical structure of benzene remained elusive until 1865, when Friedrich August Kekulé von Stradonitz hypothesized a hexagonal structure. Benzene was derived from the distillation of coal by A. W. Hoffman in 1846. The uses of and demand for benzene increased along with oil exploration as its usefulness in many industrial applications became apparent. Linus Pauling, the Nobel Prize-winning physicist, was
Salem Health: Cancer one of many scientists to attempt to elucidate the unique hybrid structure of benzene that was confirmed in 1931. The main use of benzene prior to World War I was in gasoline blending, as it increased octane. It was used extensively in industry in World War II, and almost all organic-chemistry-related industry involves petroleum (benzene-containing) products. Janet R. Green, M.S.P.H. See also Acute lymphocytic leukemia (ALL); Acute myelocytic leukemia (AML); Air pollution; Aleukemia; Aplastic anemia; Bioflavonoids; Blood cancers; 1,3-Butadiene; Carcinogens, known; Carcinogens, reasonably anticipated; Chlorambucil; Cigarettes and cigars; Coal tars and coal tar pitches; Coke oven emissions; Dioxins; Free radicals; Leukemias; Myelodysplastic syndromes; Myelofibrosis; Organochlorines (OCs); Phenolics; Urinary system cancers.
u Benzidine and dyes
metabolized to benzidine Category: Carcinogens and suspected carcinogens RoC status: Benzidine, known human carcinogen since 1980; dyes metabolized to benzidine, known human carcinogens since 2000 Also known as: Direct Blue 6, Direct Black 38, Direct Brown 95 Related cancers: Bladder cancer, and less frequently cancer of the stomach, liver, kidney, central nervous system, and pancreas Definition: Benzidine is an organic compound used to make dyes. It is usually found in the form of a powder that is white, reddish gray, or grayish yellow. Exposure routes: Benzidine can enter into the human body in many ways. If air containing molecules of benzidine is inhaled, the benzidine can enter into a person’s system. Benzidine can also be ingested, either directly or in contaminated drinking water. It is also possible for benzidine to enter the human body through the skin if direct contact is made with benzidine or a benzidine-based dye. Where found: For many years, benzidine was used in the production of dyes and dyeing compounds. It was also used occasionally in some clinical and laboratory settings, for example, in blood detection. Dyes that metabolize to benzidine were used in many different dyeing applica-
Benzidine and dyes metabolized to benzidine tions. Benzidine was used especially often to dye paper products, textiles, and leather goods. Plants manufacturing dyes were likely to contain large quantities of benzidine or dyes that metabolize to benzidine, as were plants that produced goods using such dyes. Beginning in the late 1970’s use of these dyes was phased out. Because of long usage, there remains the possibility of benzidine contamination in areas around plants and factories that once used benzidine or related dyes. Benzidine that is released into or makes its way into rivers or streams generally settles quickly on the bottom of the riverbed or streambed. Benzidine that was released into the environment through accidental contamination or as a waste product that ends up in the soil bonds strongly to particles found in the soil. It is not likely to seep into the groundwater and contaminate drinking water sources because of these strong bonds. Because its use in dyeing was phased out, benzidine and related dyes are used in only very small quantities in mostly research and laboratory settings in the United States. At risk: People who worked in industries that manufactured dyes or regularly used dyes in the production of other goods before the late 1970’s were at risk of exposure to high levels of benzidine and dyes that metabolize to benzidine. According to the Occupational Health and Safety Administration, in 1979 there were sixty-three separate occupations in which workers were at risk for benzidine exposure. Also at risk are people living near factories or plants that manufactured or used benzidine or benzidinebased dyes, especially if by-products of the plant were released into the air or water. Some residual benzidine may continue to exist at such locations. Benzidine and related dyes have also been identified as existing at many hazardous waste disposal sites and people who live near such areas may be at risk of exposure. Etiology and symptoms of associated cancers: Benzidine and related dyes have been shown to cause cancer in laboratory animals. Studies of humans who have a history of working with benzidine or related dyes have also shown that prolonged benzidine exposure is a significant risk factor for developing bladder cancer. Scientists do not clearly understand all the complex mechanisms involved in how benzidine causes cancer, but benzidine is believed to interfere with normal cellular processes. Bladder cancer is the cancer most commonly associated with benzidine exposure. The first signs and symptoms of bladder cancer are usually changes in bladder function or habits. This may include a person’s often feeling the urge to urinate without actually being able to do so. Needing to urinate much more frequently than usual is also 131
Benzodiazepines a possible symptom of bladder cancer, as is blood in the urine. History: Benzidine has a long history as an important industrial dye. It was first made in 1845. Its first use as a dye was in 1884, when a dye named Congo Red was created for the first time. Benzidine and related dyes were extremely useful in dyeing because of the way they adhere to cotton and cotton products. In the 1920’s some physicians and researchers began to suspect a relationship between exposure to benzidine and the development of bladder cancer. It was not until 1976, however, that major commercial production of benzidine and benzidine-based dyes ceased in the United States. There are no major manufacturers of benzidine for the purposes of dyeing or of benzidine-based dyes in the United States; however, there are still some small manufacturers of benzidine because it has some research and laboratory applications. It is considered a possible occupational carcinogen by the Occupational Safety and Health Administration. Personal protection is required for work with benzidine and related products, and it is necessary to take precautions to ensure that no benzidine is released into the environment. Benzidine is also considered a hazardous substance that requires special labeling and precautions when it is transported. Robert Bockstiegel, B.S. u For Further Information Bozzone, Donna M. Causes of Cancer. New York: Chelsea House, 2007. Pohanish, Richard P. Sittig’s Handbook of Toxic and Hazardous Chemicals and Carcinogens. 5th ed. Norwich, N.Y.: William Andrew, 2008. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Eleventh Report on Carcinogens. Research Triangle Park, N.C.: Author, 2005. Williams, Nerys R. Atlas of Occupational Health and Disease. New York: Oxford University Press, 2004. u
Other Resources
International Agency for Research on Cancer http://www.iarc.fr/index.html Occupational Safety and Health Administration http://www.osha.gov See also Carcinogens, known; Carcinogens, reasonably anticipated; Immunocytochemistry and immunohistochemistry. 132
Salem Health: Cancer
u Benzodiazepines Category: Chemotherapy and other drugs ATC code: N05BA Also known as: Alprazolam (Xanax), diazepam (Valium), lorazepam (Ativan) Definition: Benzodiazepines are a class of drugs with antianxiety, sedative, and muscle-relaxing properties. Cancers treated: Adjuvant therapy for many types of cancer Delivery routes: Orally by capsule or tablet, intramuscularly by injection How these drugs work: Benzodiazepines are a class of medications that act primarily on the gamma aminobutyric acid-α (GABA-A) receptors in the brain. Medications within the class vary according to their rapidness of onset, potency, frequency of dosing, length of effect, and halflife. They are typically used in the general medical population to alleviate anxiety or treat insomnia. Benzodiazepines are put to similar uses with cancer patients, as well as directed toward disease-specific conditions. When choosing among benzodiazepines, physicians consider the unique properties of specific medications (such as speed of onset, duration of effect, side effects), as well as patient characteristics (age, vigor, pain tolerance,
Common Benzodiazepines The following common benzodiazepines are used to treat acute mania, alcohol dependence, seizures, anxiety, insomnia, and muscular disorders. Trade Name
Generic Name
Ativan Dalmane Dormicum Halcion Klonopin Lexotanil Librium Loramet Mogadon ProSom Restoril Rohypnol Sedoxil Serax Valium Xanax
lorazepam flurazepam midazolam triazolam clonazepam bromazepam chlordiazepoxide lormetazepam nitrazepam estazolam temazepam flunitrazepam mexazolam oxazepam diazepam alprazolam
Salem Health: Cancer coping skills) and the types of cancer and treatments involved. Short-acting medications with rapid onset are often employed to treat acute anxiety, panic, and phobic responses to therapy. Longer-acting medications may be selected to assist patients engaging in painful or aversive cancer treatments (such as chemotherapy) to promote relaxation, reduce anticipatory anxiety, suppress recall of treatment, and alleviate nausea and restlessness (akisthisia). Long-acting benzodiazepines may also be employed to treat generalized anxiety and grief reactions stemming from cancer. Highly sedating benzodiazepines are often used to treat anxiety-related insomnia. Side effects: A number of side effects are associated with benzodiazepines. Long-term use can lead to drowsiness and deficits in memory, concentration, and motor coordination. Though safe for most in recommended dosages, benzodiazepines can potentially cause respiratory depression, and patients should be monitored closely as they initiate treatment. All benzodiazepines, especially those with rapid onsets and short durations of action, have the potential to cause dependence and, in rare cases in the cancer patient population, abuse. Consequently, physicians must closely supervise patients’ use of these medications. Abrupt discontinuation of benzodiazepines may cause withdrawal symptoms that, while severe, are usually managed with appropriate medical intervention. These symptoms include “rebound” anxiety, confusion, agitation, seizures, and, rarely, death. Paul F. Bell, Ph.D. See also Antinausea medications; Anxiety; Pain management medications.
u Beryllium and beryllium
compounds Category: Carcinogens and suspected carcinogens RoC status: Known human carcinogen since 2002 Also known as: Glucinium. Glucinium is a rarely used term, but it is noteworthy because, although the name describes beryllium’s tempting, sugary flavor, it does not warn of its poisonous nature, and those working with the alkaline earth metal should be cautioned. Related cancers: Lung cancer Definition: Beryllium is an alkaline earth metal found in ore deposits and in some precious stones. It was discovered in 1798 in emeralds and beryl and isolated in 1828.
Beryllium and beryllium compounds The metal did not see large-scale industrial use until the late 1950’s. In the twenty-first century, however, because of its high melting point, great elasticity, exceptional thermal conductivity, high permeability to X rays, and resistance to oxidation, beryllium finds uses across a wide range of products. Exposure routes: Inhalation of beryllium compounds that are found in dust and fumes combined with prolonged exposure elevate the risk of pulmonary disease and lung cancer. Beryllium can also enter the body through food and drinking water, but these routes seem less harmful because of its poor absorption. However, contact through abraded skin may result in local irritation, ulceration, or granulomatous growths. Where found: Beryllium has found uses across a variety of industries due to its properties as a light, high-strength metal combined with great elasticity and high melting point. A brief list includes uses in X-ray diagnostics; as a lightweight structural material required by the aerospace and missile industries; and as an alloying agent found in applications requiring high strength and first-rate electrical conductivity. Additionally, beryllium and its compounds find use in nonsparking tools, telecommunication devices, electrical contacts, nuclear reactors, ceramics, microwave equipment, communication satellites, space vehicles, aircraft, semiconductors, electrical insulators, everyday items such as golf clubs and bicycle frames, and many other applications requiring a hardening agent found in alloys such as beryllium copper. At risk: Workers experiencing chronic exposure to beryllium compounds are most at risk. This would include beryllium miners (the United States is the world’s largest producer); workers involved with beryllium alloys, ceramics, nuclear reactors, phosphorus manufacture, electronic equipment, and missiles; and garment workers exposed to beryllium dust. According to Environmental Protection Agency (EPA) estimates, work facilities in the United States release approximately 1 million pounds of beryllium and beryllium compounds into the environment annually, but the risk to the general population remains poorly understood. What is understood is that lung cancer risk rises with exposure time and beryllium dust concentration. Etiology and symptoms of associated cancers: The nonmalignant disease associated with beryllium and its compounds is called berylliosis. When exposed to high levels of beryllium, the immediate response is characterized by inflammation of the nose, larynx, trachea, bronchioles, 133
Beryllium and beryllium compounds and lungs. This is the acute form of beryllium disease and requires air levels of the metal on the order of 100 micrograms/cubic meter (mcg/m3) or more. Normally, ambient air levels are thousands of times less. As the exposure becomes more chronic, and typically from contact at much lower levels just exceeding 0.02 mcg/m3 over ten or more years, berylliosis takes the form of a granulomatous disease of the lungs and possibly other organs. Granulomas are nodular inflammatory lesions packed with immune cells (macrophages). Both the acute and chronic forms of berylliosis are usually not fatal. The beryllium lymphocyte proliferation test (BeLPT) is an effective blood test that measures beryllium sensitization. Although most people with beryllium sensitization will eventually develop berylliosis, further testing must be done to establish the individual’s disease status. This is an important diagnostic tool because chronic berylliosis is not only a serious illness but also a significant pathway to malignancy. The progression to chronic berylliosis follows a continuing, overzealous, and ultimately destructive immune response that leads to lung scarring and loss of respiratory capacity. This cascade of events is triggered by chemical messengers called cytokines, which repeatedly call in more immune cells than the lungs can process. This overzealous immune response leads to severe lung damage. The terrible number of deaths from the 1918 flu epidemic was a result of just such a cytokine storm and not from the destructive properties of the virus itself. The progression to lung cancer is not completely understood, and there is some debate over just how lung cancer arises from berylliosis, but most experts accept that chronic berylliosis is a strong marker for events leading to malignancy. History: Cancer arising from beryllium or its compounds depends on length and level of exposure. In general these exposure risks have been significantly reduced since the 1950’s, when workers might have been exposed to hundreds of times the levels found in twenty-first century working conditions. In 1991 researchers confirmed the carcinogenicity of beryllium and its compounds, and in 2002 the Department of Health and Human Services officially recognized beryllium as a carcinogen. The Occupational Safety and Health Administration (OSHA) sets permissible peak exposure limits for beryllium at 0.025 mcg/ m3; however, independent occupational health organizations are urging the reduction of these limits even further. To confuse the issue, there is even some minor debate on just how well previous data support the connection between cancer risk and beryllium exposure. 134
Salem Health: Cancer What is known is that certain factors may affect the progression of chronic beryllium disease (CBD). These factors include the individual’s work environment, the duration and intensity of exposure, and the particle size and solubility of the beryllium dust. Also the individual’s genetic makeup, lifestyle habits, and general health are contributing issues. Richard S. Spira, D.V.M. u
For Further Information American Conference of Governmental Industrial Hygienists. 1999 TLVs and BEIs: Threshold Limit Values for Chemical Substances and Physical Agents—Biological Exposure Indices. Cincinnati, Ohio: Author, 1999. American Industrial Hygiene Association. The AIHA 1998 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook. Fairfax, Va.: Author, 1998. Kelleher, P. C., et al. “Beryllium Particulate Exposure and Disease Relations in a Beryllium Machining Plant.” Journal of Occupational and Environmental Medicine 43 (2001): 238-249. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Eleventh Report on Carcinogens. Research Triangle Park, N.C.: Author, 2005. U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) on Beryllium. Washington, D.C.: National Center for Environmental Assessment, Office of Research and Development, 1999. _______. Toxicological Review of Beryllium and Compounds. Washington, D.C.: Author, 1998. U.S. Occupational Safety and Health Administration. Occupational Safety and Health Standards, Toxic and Hazardous Substances. Code of Federal Regulations 29 CFR 1910.1000. Washington, D.C.: Author, 1998.
u
Other Resources
Agency for Toxic Substances and Disease Registry ToxFAQS for Beryllium http://www.atsdr.cdc.gov/tfacts4.html U.S. Environmental Protection Agency CICAD Report on Beryllium and Beryllium Compounds http://www.inchem.org/documents/cicads/cicads/ cicad32.htm See also Carcinogens, known; Cytokines; Lung cancers.
Salem Health: Cancer
u Beta-carotene Category: Lifestyle and prevention ATC code: A11CA02 Also known as: A-Caro-25, betacarotene, carotene, carotenoid, Lumitene, retinal, retinol Definition: Beta-carotene is a member of a family of nutrients called carotenoids, which are found in many red, orange, yellow, and green fruits and vegetables (such as carrots, sweet potatoes, squash, spinach, apricots, and broccoli). The body converts beta-carotene into vitamin A, which plays a role in vision, bone development, cell division, and cell differentiation. Cancers treated or prevented: Studies have found that a diet high in fruits and vegetables containing beta-carotene reduces the risk of certain types of cancer, including those of the prostate and lung. Researchers believe that betacarotene and other antioxidants in fruits and vegetables work together to lower cancer risk.
Bethesda criteria It was thought that beta-carotene supplements might reduce the risk of certain cancers, especially lung cancer, but there is no evidence of any cancer preventive benefit when beta-carotene is taken alone in supplement form. In fact, studies have found that smokers and people who have been exposed to asbestos who take beta-carotene supplements have a significantly higher risk of developing lung cancer and of dying from their cancer than those who do not take the supplements. In addition, the National Cancer Institute’s Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (1992-2001) found that men with the highest levels of beta-carotene in their blood were at increased risk for developing more aggressive and deadly prostate cancer. Delivery routes: Oral in capsule and tablet forms. Eating five servings of fruits and vegetables daily provides 6 to 8 milligrams of beta-carotene. How this substance works: Beta-carotene is an antioxidant. It protects cells and deoxyribonucleic acid (DNA) from damage caused by unstable molecules called free radicals, which are produced during metabolic processes as cells burn up oxygen for energy. Free radicals are believed to contribute to cancer and other diseases. Vitamin A, which the body produces from beta-carotene, helps prevent the uncontrolled cell growth that occurs with cancer. Side effects: Beta-carotene may increase the risk of lung cancer or prostate cancer in people who smoke or drink alcohol heavily or who have been exposed to asbestos. It also may increase the risk of more aggressive prostate cancers. In high doses, beta-carotene may interact with some types of chemotherapy drugs or radiation. Stephanie Watson, B.S. See also Antioxidants; Carotenoids; Chemoprevention; Free radicals; Fruits; Nutrition and cancer prevention; Stomach cancers.
u Bethesda criteria Category: Procedures Definition: Bethesda criteria are a standardized set of criteria that are used to identify potential cases of hereditary nonpolyposis colorectal cancer (HNPCC), or Lynch syndrome. Carrots contain beta-carotene, among other nutrients. (U.S. Department of Agriculture)
Hereditary nonpolyposis colorectal cancer: HNPCC is an autosomal dominant disease that is characterized by early age of onset (average is before the age of forty-five), 135
Bile duct cancer tumor formation in a variety of tissues (endometrial, gastric, renal, ovarian, and skin), and microsatellite instability. HNPCC accounts for only about 3 to 5 percent of the cases of colorectal cancer, and the molecular and genetic testing that is required to diagnose this form of cancer can be quite time-consuming and costly. Therefore, it became important to set down a standardized set of criteria for identifying potential cases of HNPCC and to separate them from sporadic, noninherited forms of colorectal cancer. History: In 1997, a group of experts met at the National Institutes of Health to discuss the state of research on HNPCC. They came up with a set of criteria, the Bethesda criteria, which expanded the previous Amsterdam criteria to include extracolonic tumor formation as well as more specific histological characterization. In 2002, the criteria were further revised to define tumors that should be tested for microsatellite instability (MSI), which is the frequent mutation of repetitive deoxyribonucleic acid (DNA) sequences due to defects in the mismatch repair machinery in the cell. Criteria: Currently, the criteria for identifying a potential case of HNPCC are as follows: • Colorectal cancer diagnosed prior to age fifty • Presence of synchronous or metachronous HNPCCassociated tumors • High microsatellite instability (MSI-H) histology diagnosed prior to age sixty • One or more first-degree relatives diagnosed with an HNPCC-related tumor prior to age fifty • Colorectal cancer diagnosed in two or more first- or second-degree relatives Testing: If a patient meets the Bethesda criteria, a number of molecular and genetic tests are recommended. The ideal set of tests would include evaluation of microsatellite instability status as well as immunohistochemical analysis of tumors. In patients who show high levels of microsatellite instability and loss of expression of one or more of the DNA mismatch repair proteins, DNA sequencing of MSH2 and MLH1, the two genes most commonly mutated in HNPCC, should be performed. Patients who have mutations in either of these genes show an increased risk of developing cancer, and they should therefore undergo frequent screening. Lindsay Lewellyn, B.S. See also Ashkenazi Jews and cancer; Endometrial cancer; Ethnicity and cancer; Family history and risk assessment; MLH1 gene; MSH genes; Pancreatic cancers; PMS genes; Turcot syndrome. 136
Salem Health: Cancer
u Bile duct cancer Category: Diseases, symptoms, and conditions Also known as: Intrahepatic cholangiocarcinoma, extrahepatic cholangiocarcinoma, perihilar cancer, Klatskin tumors Related conditions: Sclerosing cholangitis, liver cancer Definition: Bile is a fluid produced by the liver that aids in the digestion of fats. Bile is transported from the liver through a series of tubes, called bile ducts, to either the gallbladder, which stores and concentrates the bile, or directly to the small intestine. Bile duct cancer forms in the inner layer of these ducts. It can develop in the smaller ducts within the liver, where it is called intrahepatic cholangiocarcinoma, or in ducts outside the liver, where it is called extrahepatic cholangiocarcinoma. Extrahepatic cholangiocarcinoma is divided into two types, depending on where the cancer originates. Perihilar cancer develops in the bile duct close to its exit point from the liver. Distal bile duct cancer develops close to where the bile duct empties into the small intestine. Approximately 95 percent of cholangiocarcinomas are adenocarcinomas. Risk factors: Conditions that irritate the bile ducts have been linked to an increased risk of developing cholangiocarcinoma. These disorders include bile duct stones, congenital bile duct cysts, viral hepatitis, sclerosing cholangitis (especially in people who smoke), and nonviral cirrhosis. Other risk factors include ulcerative colitis, liver flukes (parasites found in Asian countries), and obesity. Exposure to some chemicals, including polychlorinated biphenyls, dioxin, and Thorotrast (previously used in X-ray diagnosis), also increase the risk of developing this cancer. Etiology and the disease process: The exact cause of most cholangiocarcinomas is unknown. Patients with no known risk factors often develop this cancer. Cholangiocarcinoma is a slow-growing cancer that can remain undetected until it has reached an advanced stage. It originates in the mucosal cells that line the ducts and spreads throughout the layers of the ducts. Eventually, the ducts become blocked, preventing the flow of bile. When the cancer grows through the walls of the ducts, it can invade the liver, gallbladder, small and large intestines, and blood vessels that serve the liver. Incidence: Primary cholangiocarcinoma is a rare disease that is most common in Asian countries because of its association with liver flukes. Approximately 90 percent of cholangiocarcinomas are extrahepatic, with about 65 percent perihilar tumors and 25 percent distal cancers. About
Salem Health: Cancer
Bile duct cancer
4,000 people in the United States develop this cancer each year, most of whom are men, and about 70 percent of them are older than age sixty-five. The American Cancer Society has noted an increase in the incidence of intrahepatic cholangiocarcinoma, possibly because of improved diagnostic testing.
Relative Survival Rates for Bile Duct Cancer, 1988-2001 Survival Rates (%)
Symptoms: Most cholangiocarcinomas do not produce symptoms until they are in the advanced stages. Jaundiced and itchy skin, dark urine, and pale bowel movements may occur if the ducts become blocked and bilirubin, a chemical in bile, is forced into the blood vessels. Other symptoms include fever, bloating, loss of appetite, weight loss, and fatigue. Screening and diagnosis: There are no screening tests for cholangiocarcinoma. Diagnosis typically is made during surgery for a gallbladder disorder or during diagnostic tests for other conditions. Blood chemistry and liver function tests, though not specific for this cancer, may show abnormal results. Tumor-marker studies may show the presence of carcinoembryonic antigen and cancer antigen 19-9 (CA 19-9). Ultrasound, computed tomography scanning, magnetic resonance imaging, endoscopic retrograde cholangiopancreatography, positron emission tomography, and percutaneous transhepatic cholangiography are imaging studies used to diagnose cholangiocarcinoma, determine treatment options, and assess the spread of the disease. Biopsy and biliary brushing may be performed to obtain cells for differential testing. Staging is based on the number of tumors present and the extent of their spread to other organs. Treatment and therapy: Traditional treatment for cholangiocarcinoma includes surgery, chemotherapy, and radiation therapy. Surgery for intrahepatic cholangiocarcinoma always involves the removal of part of the liver and is a difficult procedure. In many cases, the cancer is too far advanced at the time of diagnosis for surgery to be successful or safe for the patient. Surgery for extrahepatic cholangiocarcinoma usually involves the removal of the bile duct, gallbladder, and parts of the liver and small intestine. It may also include the resection of part or all of the pancreas. When the cancer cannot be removed, symptoms may be relieved by creating a bypass around the tumor blocking the bile duct or inserting a biliary drain. Chemotherapy and radiation therapy may be used before surgery to shrink a tumor, in place of surgery when the tumor is inoperable, and after surgery to destroy cells that may have spread. Common chemotherapeutic agents used include fluorouracil, cisplatin, doxorubicin, and gemcitabine. Radiation is commonly administered in the form of
Years
Intrahepatic
Extrahepatic
1 2 3 5 8 10
27.9 19.5 8.5 4.8 3.4 3.2
43.7 25.4 17.5 12.8 9.8 9.7
Source: Data from L. A. G. Ries et al., eds., Cancer Survival Among Adults: U.S. SEER Program, 1988-2001—Patient and Tumor Characteristics, NIH Pub. No. 07-6215 (Bethesda, Md.: National Cancer Institute, 2007) Note: The median survival time for bile duct cancer is 5.6 months, for extrahepatic bile duct cancer, 9.4 months.
tiny seeds that are implanted into the duct, delivering highdose radiation directly to the tumor. Other forms of treatment that are being tested include using a person’s own immune system to fight the cancer, introducing viruses that seek out and destroy cancer cells, and photodynamic therapy, in which a special light is used to activate a drug that has been administered for the purpose of destroying cancer cells. Prognosis, prevention, and outcomes: The overall survival rate for cholangiocarcinoma is poor, with fewer than 20 percent surviving five years after diagnosis. Although there is no definitive way to prevent this disease, reducing exposure to its risk factors may prevent its development. Dorothy P. Terry, R.N. u
For Further Information Holland, Jimmie C., and Sheldon Lewis. The Human Side of Cancer. New York: HarperCollins, 2000. Souhami, Robert, and Jeffrey Tobias. Cancer and Its Management. Malden, Mass.: Blackwell, 2005. Stern, Theodore A., and Mikkael A. Sekeres. Facing Cancer: A Complete Guide for People with Cancer, Their Families, and Caregivers. New York: McGraw-Hill, 2004. u
Other Resources
American Cancer Society http://www.cancer.org 137
Bilobectomy
Salem Health: Cancer
Cancer.Net http://www.cancer.net/portal/site/patient
to be kept clean, and a gradual return to physical activity is recommended.
See also Afterloading radiation therapy; Alkaline phosphatase test (ALP); Carcinoid tumors and carcinoid syndrome; Cholecystectomy; Computed tomography (CT) scan; Endoscopic retrograde cholangiopancreatography (ERCP); Endoscopy; Gallbladder cancer; Gastrointestinal cancers; Infection and sepsis; Infectious cancers; Iridium seeds; Klinefelter syndrome and cancer; Liver cancers; Pancreatectomy; Pancreatic cancers; Percutaneous transhepatic cholangiography (PTHC).
Risks: The risks of a bilobectomy procedure are a narrowing of the bronchi (the large air passages leading from the windpipe to the lungs), scar formation, injury to nerves during surgery that may cause numbness and tingling in the chest area, and leakage of air from the surgical site with partial or complete collapse of the lung.
u Bilobectomy Category: Procedures Also known as: Lobectomy, thoracotomy Definition: A bilobectomy is a surgical procedure to remove two lobes of the lung.
Results: Surgery, including bilobectomy, is most effective for Stage I and Stage II non-small-cell lung cancer. Smoking cessation is of utmost importance to maximize surgical treatment as it improves wound healing and allows for the best outcome when additional therapies, such as radiation and chemotherapy, are used. Vicki Miskovsky, B.S., R.D. See also Bronchoalveolar lung cancer; Esophagectomy; Lobectomy; Lung cancers; Mesothelioma; Pleural effusion; Pleurodesis; Pneumonectomy; Surgical biopsies; Thoracoscopy; Thoracotomy.
Cancers treated: Various types of lung cancer Why performed: A bilobectomy is performed to remove diseased lung tissue. Patient preparation: Bilobectomy is performed under general anesthesia in a hospital with the usual preoperative preparation, such as physical examination, blood testing, and consultation with an anesthesiologist. In addition, an examination and additional lung tests will be done by a pulmonologist (a lung specialist). Steps of the procedure: The surgical procedure is performed by a thoracic surgeon making a cut in the side; the rib cage is separated or cut away to allow the lungs to be seen, and the pleura (a membrane around the lungs) is also cut away. The lung being operated on may be deflated, and the other lung continues to work with the help of a breathing tube. The lobes of the lung are pulled apart and separated, and the diseased lobes are cut free and removed. Arteries and veins that have been cut are sealed or reconnected. A drainage tube is left in the chest wall to drain or suction out fluid and air. The procedure may take from two to five hours. After the procedure: Pain medication will be used to make the patient more comfortable after the surgery. A hospital stay of about one week is to be expected; during hospitalization, breathing exercises as well as exercises for movement (range of motion) will be taught. Recovery at home can take several weeks, during which time pain medications may be used, the surgical incision site needs 138
u Bioflavonoids Category: Lifestyle and prevention Also known as: Flavonoids Definition: Flavonoids are the most common plant phenolic compounds. Their basic chemical structure consists of two benzene rings linked by a chain of three carbon atoms that can itself form a heterocyclic ring with oxygen. Variations of this chemical theme give rise to thousands of different bioflavonoids, which can be grouped in several families. Six families include bioflavonoids particularly common in the diet: flavonols, flavanols, flavonones (or flavanones), isoflavones, flavones, and anthocyanidines. Examples of bioflavonoids from each of these families are quercetin, cathechin, hesperitin, genistein, apigenin, and cyanidine, respectively. Most of the plant bioflavonoids occur as glycosides, that is, they have a sugar attached. Nutrition: The principal food sources of bioflavonoids are apples, celery, onions, green and black tea, citrus fruits, berries, soy, red wine, and cocoa. Although bioflavonoids are resistant to heat, certain food manipulations, such as the peeling of fruits or boiling, can cause some loss of their content or bioavailability. After the sugar moiety is removed by enzymes of the gastrointestinal tract, a variable portion of the ingested bioflavonoids is readily absorbed. The absorbed bioflavonoids are metabolized in the liver by conjugation with other chemical groups (for example,
Salem Health: Cancer
Biological therapy
glucuronic acid, sulfate, or methyl groups) and converted to smaller compounds.
eases, or to help lessen side effects from other cancer treatments such as chemotherapy.
Bioflavonoids and cancer: Numerous studies in experimental models, both in vivo and in vitro, have suggested that bioflavonoids have anticarcinogenic potential. As effective antioxidants, they prevent mutagenesis and tumor promotion by protecting deoxyribonucleic acid (DNA) and proteins from oxidative damage. By acting on signal transduction pathways that control the cell cycle, bioflavonoids inhibit proliferation and stimulate apoptosis, that is, programmed death, of human cancer cells. Cell cycle-related actions performed by bioflavonoids include suppressing nuclear factor kappa B activation, inhibiting mitogen-activated protein kinases, and blocking epidermal growth factor signaling. Bioflavonoids also stimulate detoxifying enzymes, such as cytochrome P450, which convert carcinogens into water-soluble compounds that can be eliminated from the body. In addition, they inhibit inflammation and angiogenesis. There is also strong scientific evidence that diets rich in fruits and vegetables protect against various forms of cancer. Some epidemiological studies have shown significant associations between high consumption of bioflavonoids and a reduced risk of certain forms of cancer, such as lung, rectal, and prostate cancers. However, several other epidemiological studies have failed to find such significant associations. Although bioflavonoids are gaining increasing acceptance as cancer-preventing agents, more consistent epidemiological data is needed before issuing specific public health guidelines. Reyniel Cruz-Aguado, Ph.D.
Cancers treated: A number of cancers, including melanoma, leukemia, breast, ovarian, colon, lung, and kidney cancers
See also Antioxidants; Beta-carotene; Carotenoids; Chemoprevention; Coenzyme Q10; Complementary and alternative therapies; Curcumin; Dietary supplements; Essiac; Free radicals; Fruits; Garlic and allicin; Green tea; Herbs as antioxidants; Isoflavones; Lutein; Lycopene; Nutrition and cancer prevention; Phenolics; Phytoestrogens; Resveratrol; Wine and cancer.
u Biological therapy Category: Chemotherapy and other drugs Also known as: Immunotherapy, biological response modifier therapy, biotherapy, biologic agents, biologic therapies, biologicals Definition: Biological therapy is an emerging, growing class of cancer drugs that work to help optimize the ability of the body’s immune system to fight cancer or other dis-
Subclasses of this group: Cytokines, monoclonal antibodies, colony-stimulating factors, antiangiogenesis agents, cancer vaccines Delivery routes: The delivery route varies depending on which biological therapy is being used. Various biological therapies may be given by mouth, by intravenous (IV) drip (infusion), by subcutaneous or intramuscular injection, or by delivery directly into a body cavity to treat a specific site. How these drugs work: The cells, antibodies, and organs of the immune system work to protect and defend the body against foreign invaders, such as bacteria or viruses. The immune system is a complex network of cells and organs that work together in a variety of ways. White blood cells are a very important part of the immune system. Lymphocytes are a type of white blood cell found in the blood and many other parts of the body that are intimately involved with the way that most biologic agents work. Types of lymphocytes include B cells, T cells, and natural killer (NK) cells. B cells mature into plasma cells that secrete proteins called antibodies, which recognize and attach to foreign substances known as antigens. Each type of B cell makes one specific antibody that recognizes one specific antigen. T cells produce proteins called cytokines, which include interferons, interleukins, and colony-stimulating factors. Cytokines are proteins that activate the immune system and that play an important role in communication between immune system cells. NK cells produce powerful cytokines that attach to and kill many foreign invaders, infected cells, and cancerous cells. Advances in techniques of molecular biology since the 1980’s have brought about a revolution in the understanding of many biological processes at a molecular level, including mechanisms involved in immunity and the pathogenesis of many diseases. In many cases, it has become possible to identify discrete specific molecular targets for therapeutic intervention and to design therapies to block or interact with those targets. At the same time, technological advances have made it possible to engineer and to produce these targeted therapeutic molecules for medical use. Physicians and researchers have found that, in addition to protecting the body against foreign invaders, the immune system might be able to differentiate between healthy 139
Biological therapy
Salem Health: Cancer
Common Biological Therapies Drug (Other Names)
Brands
Subclass
Delivery Mode Cancers Treated
Aldesleukin (interleukin-2)
Proleukin
Cytokine
Subcutaneous
Kidney cancer, melanoma
Alemtuzumab
Campath
Monoclonal antibody
IV
Chronic lymphocytic leukemia
Bacillus Calmette-Guérin vaccine
TheraCys BCG, TICE BCG
Vaccine
Introduction into bladder
Bladder cancer
Bevacizumab
Avastin
Monoclonal antibody
IV
Lung cancer, colorectal cancer
Cetuximab
Erbitux
Monoclonal antibody
IV
Head and neck cancers, colorectal cancer
Epoetin alfa, erythropoietin
Procrit
Colony-stimulating factor
Subcutaneous
Boosts red blood cell level during chemotherapy
Epratuzumab
LymphoCide
Monoclonal antibody
IV
B-cell leukemia
Filgrastim, granulocyte colony-stimulating factor
Neupogen
Colony-stimulating factor
Subcutaneous, Boosts white blood cell level during IV chemotherapy
Gemtuzumab ozogamicin
Mylotarg
Monoclonal antibody
IV
Acute myelogenous leukemia
Ibritumomab tiuxetan
Zevalin
Monoclonal antibody
IV
B-cell lymphoma
Interferon alpha-2a
Roferon-A
Cytokine
Subcutaneous
Hairy cell leukemia
Interferon alpha-2b
Intron-A
Cytokine
Subcutaneous
Melanoma, hairy cell leukemia, non-Hodgkin lymphoma, Kaposi sarcoma
Lym-1
Oncolym
Monoclonal antibody
IV
Lymphoma
Oprelvekin (interleukin-11)
Neumega
Cytokine
Subcutaneous
Boosts platelet level during chemotherapy
Panitumumab
Vectibix
Human monoclonal antibody
IV
Colorectal cancer
Quadrivalent human papillomavirus recombinant vaccine
Gardasil
Vaccine
Intramuscular
Cervical cancer
Rituximab
Rituxan
Monoclonal antibody
IV
Non-Hodgkin lymphoma
Tositumomab
Bexxar
Monoclonal antibody
IV
B-cell lymphoma
Trastuzumab
Herceptin
Monoclonal antibody
IV
Breast cancer
cells and cancer cells in the body and to eliminate cancerous ones. Biological therapies are designed to repair, stimulate, or enhance the immune system, either directly or indirectly, by assisting in the following ways: making cancer cells more recognizable by the immune system, boosting the killing power of immune system cells, changing the way in which cancer cells grow such that they act more like healthy cells, stopping the process that changes a normal cell into a cancerous cell, enhancing the body’s ability to repair or replace normal cells damaged or destroyed by other forms of cancer treatment such as chemotherapy or 140
radiation, and preventing cancer cells from spreading to other parts of the body. Biological therapies involve molecules that the body normally produces in small amounts in response to infection and disease and the use of modern recombinant deoxyribonucleic acid (DNA) technology to produce these molecules in large amounts for use in the treatment of cancers and other diseases. Molecular splicing of genes or portions of genes of interest to form DNA sequences that code for recombinant or fusion proteins is performed. These recombinant DNA sequences are spliced into plas-
Salem Health: Cancer mid vector molecules that can be introduced into host cells, which can be used in scaled-up production of large amounts of the purified recombinant or fusion protein. Important types of biological therapies are cytokines (interferons and interleukins), monoclonal antibodies, growth factors, colony-stimulating factors, antiangiogenesis agents, and cancer vaccines. Interferons were the first cytokines to be produced in the laboratory for use as biological therapies. Several types of inferons occur naturally in the body, of which interferon alpha is the most widely used in cancer treatment. Interferons can improve the immune system function against cancer cells and may in addition directly slow the growth of cancer cells or promote their development into cells with more normal behavior. There is some evidence that interferons may also stimulate NK cells and T cells, thereby boosting the immune system’s function against cancer cells. Intron A (interferon alpha) has been approved by the Food and Drug Administration (FDA) for cancer treatment; it is used for the treatment of hairy cell leukemia, melanoma, chronic myeloid leukemia, and AIDS-related Kaposi sarcoma and non-Hodgkin lymphoma. Interleukins are also cytokines that occur naturally in the body. Many types have been identified. Interleukin-2, which stimulates the growth and activity of many immune cells which can destroy cancer cells, has been the most widely studied in cancer treatment. Proleukin (interleukin-2) has been approved for use in the treatment of metastatic melanoma and metastatic renal cell carcinoma. Monoclonal antibodies are a single species of antibody that is produced in the laboratory from a single type of cell and is specific for a particular antigen. The production of monoclonal antibodies involves the creation of a hybrid cell line specific for that antibody molecule, called a hybridoma. Once produced, a hybridoma can be perpetuated in the laboratory to produce as much of the pure monoclonal antibody as desired. Monoclonal antibodies may be used in several ways. They may be used to boost the immune response to cancer cells, they may be designed to act against growth factors to inhibit the growth of cancer cells, and they may be linked to anticancer drugs, radioactive substances, or toxins to act as a vector to deliver these toxic agents directly to cancer cells. Rituxan (rituxamab) and Herceptin (trastuzumab) are examples of monoclonal antibodies that have been approved by the FDA, Rituxan for the treatment of non-Hodgkin lymphoma and Herceptin to treat metastatic breast cancer. Colony-stimulating factors (CSFs) stimulate bone marrow cells to divide and develop into white blood cells, red blood cells, and platelets. CSFs may be helpful for some patients undergoing treatment for cancer because many
Biological therapy anticancer drugs used in chemotherapy can damage the body’s ability to make these important cells in the bone marrow. Thus patients receiving chemotherapy have an increased risk of developing infections, anemia, and bleeding more easily. The dose of chemotherapy that a patient receives, and therefore the chemotherapy regimen’s effectiveness in fighting cancer, can sometimes be increased by using CSFs to eliminate or reduce the risk of infection or the need for transfusions. Neupogen (filgrastim) and Procrit (epoetin alfa) are colony-stimulating factors that the FDA has approved for use in cancer patients, Neupogen to boost the number of white blood cells during chemotherapy and Procrit to boost the number of red blood cells during chemotherapy. Antiangiogenesis agents, also called angiogenesis inhibitors, are an emerging type of biological therapy that show promise in fighting cancer. Cancer cells are rapidly dividing cells that depend on a rich network of small blood vessels to supply them with oxygen and nutrients. Tumors must generate this network of new blood vessels, a process called angiogenesis. Several types of molecules and antibodies have been shown to prevent angiogenesis and shrink tumors. Avastin (bevacizumab) is an antiangiogenic monoclonal antibody that has been approved for the treatment of lung and colorectal cancers. Cancer vaccines are another type of biological therapy being studied. Vaccines for infectious diseases work by exposing an uninfected individual to a weakened form of the infectious agent. The vaccine stimulates the immune system to mount an immune response to the agent but cannot cause the disease. The immune system produces antibodies specific to antigens present on the surface of the infectious agent. The immune system is also stimulated to produce certain types of T cells, which remember the exposure to the antigen. If the individual is subsequently challenged with the same infectious agent, then these T cells will orchestrate a quick and effective immune response, protecting the individual from contracting the disease. Cancer vaccines to treat existing cancers (therapeutic vaccines) or to protect healthy individuals from developing cancer (prophylactic vaccines) are being studied. Therapeutic vaccines may be effective in stopping the growth of existing cancer cells, in preventing cancer from recurring, or in killing existing cancer cells. Prophylactic vaccines are administered to healthy individuals to protect against cancers that are caused by viruses. Gardisil (quadrivalent human papillomavirus recombinant vaccine) is a prophylactic vaccine that has been approved by the FDA for the prevention of cervical cancer caused by human papillomavirus. Some biological therapies have been approved by the 141
Biopsy FDA for certain types of cancer, while many, still in development, are offered in clinical research studies to measure the effects of the treatment. In these cases, study results are often used as part of the FDA evaluation of the drug’s efficacy and safety. Side effects: The side effects of biological therapy regimens are variable from patient to patient. The most common side effects are a result of stimulation of the immune system and are similar to flulike symptoms, including fever, chills, body aches, nausea, vomiting, loss of appetite, and fatigue. Some patients may experience a rash or swelling at the injection site. Most side effects diminish one to two days after treatment. For patients who receive multiple doses of a biological therapy, the side effects usually lessen over time. Jill Ferguson, Ph.D. u For Further Information Kimura, F. “Molecular Target Drug Discovery.” Internal Medicine 46 (2007): 87-89. Old, L. J. “Immunotherapy for Cancer.” Scientific American 275 (1996): 136-143. Reang, P., M. Gupta, and K. Kohli. “Biological Response Modifiers in Cancer.” Medscape General Medicine 14 (2006): 33. Rosenberg, Steven A., ed. Principles and Practice of the Biologic Therapy of Cancer. 3d ed. Philadelphia: Lippincott Williams & Wilkins, 2000. Sorscher, S. M. “Biological Therapy Update in Colorectal Cancer.” Expert Opinion on Biological Therapy 7 (2007): 509-519. Zafir-Lavie, I., Y. Michaeli, and Y. Reiter. “Novel Antibodies as Anticancer Agents.” Oncogene 28 (2007): 3714-3733.
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Other Resources
American Cancer Society Immunotherapy http://www.cancer.org/docroot/CRI/content/ CRI_2_4_4X_Biological_Therapy_Immunotherapy_ 50.asp?sitearea= Emory Healthcare Biologic Therapies for Cancer Care http://healthlibrary.epnet.com/ GetContent.aspx?token=8482e079-8512-47c2-960ca403c77a5e4c&chunkiid=32583 142
Salem Health: Cancer National Cancer Institute Biological Therapy http://www.cancer.gov/cancertopics/ biologicaltherapy Stanford Comprehensive Cancer Center Biological Therapy for Cancer Treatment http://www.cancer.gov/cancertopics/ biologicaltherapy See also Anthrax; Antineoplastics in chemotherapy; Bacillus Calmette Guérin (BCG); Cancer biology; Chemotherapy; Cytokines; Gene therapy; Immune response to cancer; Immunotherapy; Medical oncology; Metastasis; Monoclonal antibodies; Nutrition and cancer treatment; Stem cell transplantation; Tumor necrosis factor (TNF); Tyrosine kinase inhibitors; Vaccines, therapeutic.
u Biopsy Category: Procedures Also known as: Tissue sampling, fine needle aspiration, needle biopsy, percutaneous biopsy, core biopsy, incisional biopsy, excisional biopsy, endoscopic or laparoscopic biopsy, surgical biopsy, open biopsy, transvenous biopsy Definition: A biopsy is the removal of a tissue sample for laboratory analysis to detect the presence of cancer cells. There are several types of biopsy procedures. The type of biopsy procedure performed is dependent on the type of cancer suspected and the area of the body being examined. In fine needle aspiration (also called needle biopsy or percutaneous biopsy), a very fine needle is inserted into the area and a sample of fluid or tissue is withdrawn through the needle into an attached syringe. This type of biopsy procedure may be used to remove tissue from an organ that is otherwise accessible only via surgery, such as the liver, pancreas, or lung. The advantage of fine needle aspiration is that it does not require a surgical incision. To place the needle accurately, ultrasound or computed tomography (CT) guidance may be used. Similar to fine needle aspiration, core biopsy uses a larger needle to withdraw a greater sample of fluid or tissue. Ultrasound or CT guidance may be used. In incisional biopsy, a scalpel or similar instrument is used to remove a portion of the suspected cancerous tissue via an incision made in the skin. Incisional biopsies are most commonly used to remove soft tissue, such as skin, connective tissue, muscle, and fat. For skin lesions, an in-
Salem Health: Cancer
Biopsy
In incisional biopsy, a scalpel is used to remove a sample of the suspected cancerous tissue through an incision made in the skin. (PhotoDisc)
cisional biopsy may be performed with a hollow, circularshaped instrument (punch biopsy), or a razor may be used (shave biopsy). Depending on the type of procedure, the patient may be under general or local anesthesia. In excisional biopsy (sometimes called open biopsy or surgical biopsy), a whole lump, tumor, or organ and a margin of normal tissue around it are removed. An excisional biopsy may be used to remove some types of tumors or suspected cancers that need to be removed entirely for an accurate diagnosis, such as the removal of lymph nodes to diagnose lymphoma accurately. General anesthesia is usually used for excisional biopsies. In endoscopic or laparoscopic biopsy, an endoscope (small camera on a thin tube) is used to view an internal area and to identify the tissue for removal. The endoscope transmits magnified images of the area onto a video monitor to guide the physician during the procedure. The endoscope can be inserted through a natural body opening, such as the throat to remove esophageal tissue, or it can be inserted through a small incision. Surgical instruments attached to the endoscope or inserted through other small in-
cisions can be used to remove the tissue. Endoscopic biopsy procedures are the most common type of biopsies. A laparoscopic biopsy procedure may be used when a tissue sample is needed from more than one area or when a larger tissue sample is needed. General or local anesthesia may be used, depending on the biopsy site. A capsule biopsy is a type of laparoscopic technique in which a patient swallows a capsule that is connected to a thin tube. X rays confirm the proper positioning of the capsule, and a syringe attached to the end of the tube is used to withdraw a tissue sample into the capsule. The capsule and tube are gently removed, and the tissue sample is taken to the laboratory for analysis. This type of biopsy procedure may be used to remove a sample of tissue from the lower gastrointestinal tract. Other biopsy procedures include colposcopic biopsies to identify and remove abnormal tissue from the cervix, transvenous biopsy to remove tissue via a catheter inserted into a vein in the neck, and bone marrow biopsy to remove a bone marrow sample through a needle inserted into the hip and withdrawn through a syringe. 143
Biopsy Cancers diagnosed: Various, including breast, bone, gynecological, liver, lung, lymph node, skin, thyroid, urological, and gastrointestional cancers Why performed: A biopsy is performed to diagnose and stage cancer when an abnormality is found during diagnostic tests. It also may be performed to determine the cause of unexplained symptoms or to match organ tissue before a transplant. Patient preparation: Tests before the procedure may include blood tests, urine tests, a chest X ray, an electrocardiogram, CT scanning, magnetic resonance imaging (MRI), and other imaging tests. The patient preparation for a biopsy procedure varies depending on the type of procedure and biopsy location. In some cases, no special preparation is required. In other cases, the patient must not eat or drink for eight hours beforehand and is required to stop taking anticoagulant medications for several days before the procedure. The patient will receive specific preparation instructions from the health care team. Steps of the procedure: Local or general anesthesia may be used, depending on the type of biopsy procedure and biopsy location. The biopsy site is cleansed, and a local anesthetic is injected into the area. In some cases, such as with sentinal node biopsy, a radioactive substance or dye is injected into the tumor and a scanner is used to locate the lymph node or tissue containing the radioactive substance or stained with the dye. The tissue sample or fluid is removed via one of the biopsy techniques. The sample is sent to a laboratory for microscopic analysis by a pathologist. There are a variety of methods for processing tissue samples. Histologic sections involve preparing stained, thin slices of tissue mounted on slides, a process that may take up to forty-eight hours. With the histologic method, the tissue sample is placed in a machine that replaces all water in the sample with paraffin wax. The sample is embedded into a larger block of paraffin, sliced into very thin sections, and stained with dye to aid microscopic analysis. Frozen tissue analysis involves freezing the tissue, slicing it into thin sections, and staining the sections to aid analysis. Smears are tissue samples that are spread onto a slide for examination. The results of smears can usually be obtained very quickly. After the procedure: The length of a patient’s recovery and the steps for recovery vary depending on the type of biopsy procedure and biopsy location. The patient may stay in a recovery room for a certain amount of time after the procedure. The biopsy site is usually covered with a bandage or dressing. Medication is prescribed as needed for relief of pain, which may include discomfort at the bi144
Salem Health: Cancer opsy site or muscle pain. An overnight hospital stay may be required for some fine needle aspiration, laparoscopic, and surgical biopsy procedures. Specific instructions for driving, activity, incision care, medications, nutrition, and follow-up care are provided to the patient, as applicable. In some cases, the patient is not permitted to drive home after the procedure. Depending on the physician’s instructions, the patient may be required to stay on bed rest at home for a certain amount of time after the procedure. Risks: The risks of biopsy procedures are dependent on the type of procedure performed and the biopsy location. Possible risks of all biopsy procedures include bleeding and infection. The risk of death associated with biopsy procedures is generally very low. The physician may discuss specific mortality rates and risks with the patient, depending on the type of procedure performed. Results: The tissue sample removed during the procedure is either normal, which means it is benign or noncancerous, or abnormal, which means it has unusual characteristics and may be malignant or cancerous. In some cases, the tissue that was obtained during the biopsy is not adequate to make a diagnosis, and a repeat biopsy procedure or a different type of biopsy procedure may be performed. The type of cancerous cells and extent of disease will help guide the patient’s treatment. Angela M. Costello, B.S. u
For Further Information DeVita, Vincent, Jr., Samuel Hellman, Steven A. Rosenberg, et al., eds. Cancer: Principles and Practice of Oncology. 7th ed. Philadelphia: Lippincott Williams & Wilkins, 2005. McPhee, Stephen J. Maxine A. Papadakis, and Lawrence M. Tierney, eds. Current Medical Diagnosis and Treatment 2008. New York: McGraw-Hill Medical, 2007. Ota, D. M. “What’s New in General Surgery: Surgical Oncology.” Journal of the American College of Surgeons 196, no. 6 (2003): 926-932.
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Other Resources
American Cancer Society http://www.cancer.org National Cancer Institute http://www.cancer.gov RadiologyInfo http://www.radiologyinfo.org
Salem Health: Cancer Society of Interventional Radiology http://www.sirweb.org See also Anoscopy; Axillary dissection; Bone marrow aspiration and biopsy; Breslow’s staging; Bronchoscopy; Colonoscopy and virtual colonoscopy; Colorectal cancer screening; Colposcopy; Computed tomography (CT)guided biopsy; Conization; Core needle biopsy; Culdoscopy; Cystoscopy; Cytology; Dilation and curettage (D&C); Dukes’ classification; Endoscopic retrograde cholangiopancreatography (ERCP); Endoscopy; Flow cytometry; Gastric polyps; Gleason grading system; Grading of tumors; Hormone receptor tests; Hysteroscopy; Immunocytochemistry and immunohistochemistry; Ki67 test; Laparoscopy and laparoscopic surgery; Laryngoscopy; Liver biopsy; Loop electrosurgical excisional procedure (LEEP); Lumpectomy; Lymphadenectomy; Mediastinoscopy; Needle biopsies; Needle localization; Pap test; Paracentesis; Pathology; Pleural biopsy; Polypectomy; Premalignancies; Progesterone receptor assay; Prostate-specific antigen (PSA) test; Receptor analysis; Screening for cancer; Sentinel lymph node (SLN) biopsy and mapping; Sigmoidoscopy; Staging of cancer; Stereotactic needle biopsy; Surgical biopsies; Thoracoscopy; Thoracotomy; TNM staging; Upper gastrointestinal (GI) endoscopy; Wire localization.
u Birt-Hogg-Dubé syndrome
(BHDS) Category: Diseases, symptoms, and conditions Related conditions: Renal cell carcinoma, pulmonary cysts Definition: Birt-Hogg-Dubé syndrome (BHDS) is a rare, genetically linked syndrome named after the three Canadian doctors who first identified it as a skin disorder. It consists of three types of benign skin growths: fibrofolliculomas, white or flesh-colored tumors that occur in hair follicles; trichodiscomas, overgrowths of tissues in hair disks; and acrochordons, commonly called skin tags. These growths are typically found on the face, neck, chest, and scalp. Since the identification of BHDS in 1977, further study of patients with the syndrome has revealed additional abnormal conditions that characteristically develop in affected individuals. The most common of these conditions include benign and cancerous kidney tumors, lung cysts, and spontaneous pneumothorax.
Birt-Hogg-Dubé syndrome (BHDS) Risk factors: BHDS is genetically linked, meaning that it is associated with a defect in one or more genes. Although in most cases the gene responsible for BHDS has been passed through families, evidence of genetic mutation in people with no familial link has also been identified. People with a defective gene and who also smoke have a higher risk of developing kidney cancer. Etiology and the disease process: BHDS is caused by a mutation in the gene that is responsible for the body’s production of folliculin, a protein that acts as a tumor suppressor. When folliculin is absent or not functioning properly, it cannot control cellular growth and division, which leads to tissue overgrowth and the formation of tumors. Folliculin is present in many types of tissues but is primarily found in skin, lung, and kidney cells. The folliculin gene, otherwise know as FCLN, is located on chromosome 17p11.2. Normally, during conception, the body receives two copies of every gene, one from the mother and one from the father. In BHDS, a single defective copy of the gene, from either the mother or the father, results in a person’s being affected by the disease. BHDS usually begins with the formation of skin growths. As the disease progresses, these growths increase in number and size. Slow-growing kidney tumors can develop as single or multiple tumors in one or both kidneys. Several types of tumors have been associated with BHDS, including benign tumors such as renal oncocytomas and cancerous tumors such as chromophobe renal carcinoma and clear cell carcinoma. Benign tumors often become cancerous as the disease progresses. Research into kidney tumors associated with BHDS indicates that a genetic mutation occurs in the second gene of affected kidney cells, producing two defective genes, which allows these tumors to grow. Incidence: BHDS is very rare, having been identified only in about sixty families worldwide. A precise incidence rate is unknown because people are not routinely tested for the presence of the FCLN gene. There is no indication that race or gender influences a person’s risk of having the gene or developing the disease. The typical age that a person begins to display signs of BHDS is between the late twenties and early forties. The incidence of kidney cancer in people with BHDS may be as low as 15 percent; however, the incidence of lung cysts is estimated to be about 90 percent. Symptoms: Although some people with BHDS have no noticeable symptoms of the disease, the development of fibrofolliculomas or acrochordons is usually the first indication that the person is affected. Initially looking like 145
Birth control pills and cancer small, white pimples, fibrofolliculomas typically become larger and more prolific as time passes. The development of polyps in the mouth or colon may also indicate BHDS and should be investigated further. Lung cysts, which usually do not cause respiratory problems, or lung cancer may be detected during routine examinations or testing for other conditions. Multiple or bilateral kidney tumors are often the first indication of BHDS. Screening and diagnosis: Several recurrent tests are recommended for people with BHDS and those with family members who have BHDS. Recommendations include an annual kidney ultrasound and chest X ray, computed tomography scanning or magnetic resonance imaging every two years, and biopsies of suspicious skin growths. DNA (deoxyribonucleic acid) testing to check for genetic alterations should be considered for individuals who have family members with the disease. Genetic counseling should precede any such testing. The disease is typically diagnosed after skin lesion biopsies are positive for fibrofolliculomas or when multiple kidney tumors and lung cysts are identified. Treatment and therapy: There is no specific medical treatment recommended for the skin tumors associated with BHDS. Surgical removal, electrodesiccation, and dermabrasion have been used without long-term success, as the growths recur. A relatively new procedure for BHDS-related skin tumors is laser skin resurfacing, which has been successful in several cases; however, long-term results are unknown. Both benign and cancerous kidney tumors are removed surgically. However, new tumors often form in place of the ones removed. When possible, only part of the kidney is removed to prolong the patient’s kidney function. Experimental treatments to destroy the cancer cells may be used on recurrent tumors. These include cryoablation, freezing the tumor, and radio frequency ablation, killing the tumor with heat. Prognosis, prevention, and outcomes: The prognosis for BHDS depends on whether kidney cancer develops and the success of its treatment. BHDS cannot be prevented. Dorothy P. Terry, R.N. u For Further Information Lindor, Noralane M., et al. “Birt-Hogg-Dubé Syndrome: An Autosomal Dominant Disorder with Predisposition to Cancers of the Kidney, Fibrofolliculomas, and Focal Cutaneous Mucinosis.” International Journal of Dermatology 40, no. 10 (October, 2001): 653-656. Pavlovich, C. P., et al. “Renal Tumors in the Birt-Hogg-
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Salem Health: Cancer Dubé Syndrome.” American Journal of Surgical Pathology 26 (2002): 1542-1552. Pomery, Chris. DNA and Family History. Toronto: Dundurn Press, 2004. u
Other Resources
Birt Hogg Dube Family Alliance What Is BHD? http://www.birthoggdube.org/id1.html Genetics Home Reference Birt-Hogg-Dubé Syndrome http://ghr.nlm.nih.gov/ condition=birthoggdubesyndrome See also Hereditary leiomyomatosis and renal cell cancer (HLRCC); Kidney cancer; Urinary system cancers.
u Birth control pills and cancer Category: Carcinogens and suspected carcinogens RoC status: Most birth control pills contain two active ingredients, a form of estrogen and a form of progesterone. Collectively, estrogens have been classified as a known human carcinogen since 1985. Progesterone has been listed as a reasonably anticipated human carcinogen since 1985. Also known as: Oral contraceptives Related cancers: Breast cancer, cervical cancer Definition: A birth control pill is a tablet containing a synthetic estrogen, such as ethinylestradiol; a synthetic progesterone, such as norethindrone; or both. These compounds mimic the action of naturally occurring sex hormones and are administered to alter the function of tissues that respond to these hormones. For example, a moderate, consistent dose of estrogen will prevent the typical spike in estrogen that occurs naturally during the middle of the menstrual cycle. This in turn prevents the ovary from releasing an egg. Estrogen and progesterone have different effects on reproductive tissues that, in combination, are highly effective in preventing pregnancy. Although the majority of birth control pills contain a dose of each hormone, minipills that contain only a progesterone are also available. Although contraception is the most common reason for using birth control pills, the pill is also commonly prescribed for other purposes, such as bothersome menstrual symptoms and acne.
Salem Health: Cancer
Birth control pills and cancer
Exposure routes: Birth control pills are tablets that are ingested orally. Several alternative delivery systems, such as transdermal patches, contain similar active ingredients that are taken into the body through other routes. Where found: Birth control pills are manufactured by drug makers and prescribed by health providers. The World Health Organization estimates that approximately 10 percent of all women of reproductive age worldwide use birth control pills. At risk: At highest risk are women of reproductive age, particularly in developed countries where the pill is more widely available and pill use is more prevalent. A small minority of pill users are women who take the pills to manage menopausal symptoms. Etiology and symptoms of associated cancers: The majority of breast cancers, though not all, involve the abnormal growth and proliferation of cells that are responsive to estrogen. Studies in mice and rats indicate that exposure to either synthetic estrogen alone or synthetic progesterone alone caused maligEstrogen, an essential ingredient in birth control pills, is a known human carnant tumors to develop in mammary tissue. cinogen. (Object Gear) Likewise, combinations of synthetic estrogen and progesterone appear to cause developthe risk of cervical cancer even when HPV status is taken ment of both benign and malignant mammary tumors in into account. animals. In humans, breast cancer risk increases with proConversely, the use of birth control pills appears to relonged exposure to estrogen from both internal and exterduce the risk of some types of cancer. There is abundant nal sources, although not all studies of birth control pill usevidence suggesting that birth control pill use reduces a ers have demonstrated an increased risk of breast cancer. woman’s risk of developing ovarian cancer, possibly due Research suggests that breast cancer risk related to pill use to fewer cycles of ovulation over her life span. Birth conis greatest among women who use the pill for several years trol pill use also appears to decrease the risk of cancer of or more before their first full-term pregnancy. After longthe endometrium (the uterine lining), with protective efterm cessation of pill use, the risk of breast cancer appears fects lingering long after cessation of pill use. to decrease to a level comparable to that of women who never used the pill. The risk of cervical cancer is also increased with birth History: The first birth control pill became available in the control pill use and appears to be related to the duration of United States in 1960, and birth control pills were widely pill use, although the risk most likely declines over time adopted in the decades that followed. Early concern about after cessation of use. Research to date has yet to fully exthe safety of birth control pills linked the high doses of plain the relationship between cervical cancer and birth estrogen in birth control pills with an increased risk of control pills. Some researchers have argued that pill users serious cardiovascular events, including heart attack and differ from nonusers in risk factors for human papillostroke. Over time, drug manufacturers lowered the dosmavirus (HPV) infection, which is closely linked to the ages of estrogen in birth control pills. development of cervical cancer. However, to date several By the 1980’s researchers had observed associations studies have suggested that birth control pill use increases between birth control pill use and cancer risk. However, 147
Bis(chloromethyl) ether and technical-grade chloromethyl methyl ether
Salem Health: Cancer
studies were inconsistent in confirming this relationship, and a number of large population-based studies were undertaken to clarify the effect of pill use on cancer risk. After review of multiple such studies, the International Agency for Research on Cancer, a division of the World Health Organization, classified combined estrogenprogesterone birth control pills as carcinogenic to humans. Andrea Bradford, M.A.
u Bis(chloromethyl) ether and
u For Further Information Cerhan, James R. “Oral Contraceptive Use and Breast Cancer Risk: Current Status.” Mayo Clinic Proceedings 81, no. 10 (2006): 1287-1289. Parker, James M., and Philip M. Parker, eds. Birth Control Pills: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. San Diego, Calif.: Icon Health, 2003. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Eleventh Report on Carcinogens. Research Triangle Park, N.C.: Author, 2005. Zonderman, Jon, and Laurel Shader. Birth Control Pills. New York: Chelsea House, 2006.
Related cancer: Lung cancer
u
Other Resources
Mayo Clinic Birth Control Pill Frequently Asked Questions: Benefits, Risks, and Choices http://www.mayoclinic.com/health/birth-control-pill/ WO00098 National Cancer Institute Oral Contraceptives and Cancer Risk: Questions and Answers http://www.cancer.gov/cancertopics/factsheet/Risk/ oral-contraceptives See also Antiestrogens; Cervical cancer; Endocrine cancers; Endometrial cancer; Endometrial hyperplasia; Estrogen-receptor-sensitive breast cancer; Fertility drugs and cancer; Fibrocystic breast changes; Gestational trophoblastic tumors (GTTs); Hormonal therapies; Hormone receptor tests; Hormone replacement therapy (HRT); Ovarian cancers; Ovarian cysts; Progesterone receptor assay; Receptor analysis; Screening for cancer; Vasectomy and cancer.
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technical-grade chloromethyl methyl ether Category: Carcinogens and suspected carcinogens RoC status: Known human carcinogen since 1980 Also known as: BCME, chloro(chloromethoxy) methane dichloromethyl ether, CMME, dimethylchloroether, methyl chloromethyl ether
Definition: Bis (chloromethyl) ether (BCME) and technicalgrade chloromethyl methyl ether (CMME) are chemicals known as chloroalkyl ethers. Both are clear, flammable liquids with strong, unpleasant odors. Exposure routes: After BCME and CMME are released into the air, humans can be exposed by inhalation, dermal contact, and oral exposure via contaminated water. Potential exposure by inhalation can occur to workers who are involved in the production of BCME and CMME. Where found: BCME and CMME are found at production sites where they have been released into the air and at landfill sites where they have been transferred for disposal. Both are found in chemical plants where they are manufactured and in research laboratories where they are used to make other chemicals. They can also be found in plants where they have been used to make several types of polymers, resins, plastics, and textiles. Small quantities of BCME can be formed as an impurity during the production of CMME. CMME can be converted to BCME through hydrolysis. At risk: The greatest risk for contamination from BCME and CMME is to chemical plant workers, laboratory workers, ion-exchange resin makers, and polymer producers. The general public experiences some risk from both chemicals around sites where they are produced or where they are discarded, such as landfills and surface impoundments. Etiology and symptoms of associated cancers: Individuals exposed to BCME and CMME show significant increases in the incidence of lung carcinomas, mostly of the oat-cell type, which is generally not associated with smoking tobacco. The number of lung carcinomas is much higher in people exposed to just BCME, as compared with individuals who are exposed to both BCME and CMME. When exposed to BCME or CMME, individuals have shown a slight increase of incidence of chromosomal aberrations in peripheral lymphocytes. Both chemicals can
Salem Health: Cancer
Bisphenol A (BPA)
induce unscheduled synthesis of deoxyribonucleic acid (DNA) in human fibroblasts in vitro. History: Although BCME and CMME were previously manufactured in the United States, use of both chemicals in the United States has dropped significantly since 1976. Since 1982, only CMME is produced in the United States. In the past, BCME was used to treat vulcanized rubber to increase adhesion and in the production of flame-retardant fabrics. CMME is used as an alkylating agent and solvent in manufacturing polymers, ion-exchange resins, and water repellants. Alvin K. Benson, Ph.D. See also Carcinogens, known; Carcinogens, reasonably anticipated; Occupational exposures and cancer.
u Bisphenol A (BPA) Category: Carcinogens and suspected carcinogens Also known as: 4, 4′-(1-Methylethylidene)bisphenol; 2, 2-bis (4-hydroxyphenyl) propane Related cancers: Prostate and breast cancer Definition: Bisphenol A (BPA) is an organic compound belonging to the aromatic class known as phenols. It is the main monomer used for the manufacture of polycarbonate plastics, which are essentially long chains of individual BPAmolecules linked together. All the BPAmonomers do not react to form the polymer, as a result of which small amounts of the unpolymerized free units leach into the contents of the plastic containers. Exposure routes: Exposure to BPA is mainly through direct contact or by ingesting food or drink that has been in contact with plastic material containing bisphenol A. BPA is known to leach into the contents of polycarbonate containers under certain conditions. It is also released from epoxy resins that are used in dental sealants, food container linings, polyvinyl chloride (PVC) pipes, and flooring materials. As plastics are used ubiquitously in modern society, bisphenol A has many plausible exposure routes for humans. Where found: Bisphenol A is a high-production-volume chemical used as the main building block for the manufacture of many polymers such as polycarbonates and epoxy resins. Polycarbonates are widely used for making food and drink containers, baby bottles, milk containers, and water pipes, and epoxy resins are used in the linings of metal food containers and in dental sealants.
BPA, a suspected carcinogen, is known to leach into the contents of plastic bottles. (©Sean Macdiarmid/Dreamstime.com)
At risk: Infants, children, and adults Etiology and symptoms of associated cancers: The safety data on bisphenol A are controversial. A hazard assessment study by the National Toxicology Program is ongoing. The final peer-reviewed assessment results will be used as a basis for federal regulation of the compound. If the assessment indicates concern about carcinogenicity and other health risks associated with BPA exposure, appropriate measures will be formulated to protect public health and safety. BPA is a known hormone disrupter, and many studies have confirmed this effect. Most research data on the adverse effects of BPA exposure have been collected in rodent studies. Low-level chronic exposure to BPA has been reported to cause endocrine disruption even at levels of 2.3 micrograms per kilogram (mcg/kg) per day, leading to aberrant growth of mammary tissue in mice, which is a pre149
Bisphenol A (BPA) cursor to breast cancer. Additionally it has been reported that prenatal exposure to low levels of BPA causes breast cancer in adult rats. Research reports indicate that BPA at low levels causes adverse effects on the development of the prostate in fetal mice. Studies also suggest that exposure to BPA in the womb alters gene behavior in such a way as to lead to development of prostate cancer in adult rats. A small study involving Japanese women found that the serum levels of BPA were three times higher in women with a recurrent history of miscarriages, providing indirect evidence for BPA as an endocrine-disrupting chemical. History: Bisphenol A was first synthesized in 1891. In the 1930’s it was demonstrated that BPA mimicked the action of estrogens in rats. Around that time, diethylstilbestrol, a more potent estrogen, was discovered, relegating BPA to the background in terms of pharmacological use. In the 1950’s polymer chemists discovered that BPA could be polymerized readily to make plastics such as polycarbonate. BPA thus became a large-volume chemical used in the plastics industry. It is also used as an inert ingredient in antioxidants, pesticides, and flame retardants. Additionally it is used in materials for making reinforced pipes, water-main filters, floorings, and enamels. Its ubiquitous use creates various exposure routes for humans. BPA has been measured in river water, reservoirs, streams, and estuaries. There is ongoing debate about the safety limit for this compound. In the 1980’s the Environmental Protection Agency (EPA) set a reference dose of up to 50 mcg/kg per day in the United States and considers intake below this dose to be safe for health. However, based on research in the late 1990’s and early 2000’s, scientists are of the consensus that exposure to BPA well below the EPA guideline induces adverse effects in rodents in the fetal stage, and these effects are precursors to breast cancer and prostate cancer in adulthood. The cause for concern is that the low levels inducing carcinogenicity in the rodent experiments are within the range of daily human exposure to BPA. European and American regulatory agencies have maintained that exposure to BPA from polycarbonates and epoxy resins does not pose a health risk. Bisphenol A is one of two hundred compounds selected by the Canadian regulatory agency for further safety assessment studies. The U.S. Food and Drug Administration is aware of the need for an objective assessment of the experimental data on the health risks of BPA exposure. The assessment, which will form the basis for regulation of bisphenol A by federal toxicology agencies, will affect the health of millions of people. Lalitha Krishnan, Ph.D. 150
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For Further Information Haighton, L. A., et al. “An Evaluation of the Possible Carcinogenicity of Bisphenol A to Humans.” Regulatory Toxicology and Pharmacology 35 (2002): 238-254. Mittelstaedt, Martin. “‘Inherently Toxic’ Chemical Faces Its Future.” Globe and Mail, April 7, 2007. Stowell, Cheri L., et al. “A Role for Sulfation-Desulfation in the Uptake of Bisphenol A into Breast Tumor Cells.” Chemistry and Biology 13, no. 8 (2006): 891-897. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Eleventh Report on Carcinogens. Research Triangle Park, N.C.: Author, 2005. Vom Saal, Frederick S., et al. “Chapel Hill Bisphenol A Expert Panel Consensus Statement: Integration of Mechanisms, Effects in Animals and Potential to Impact Human Health at Current Levels of Exposure.” Reproductive Toxicology 24, no. 2 (2007): 131-138. Wetherill, Y. B., et al. “Bisphenol A Facilitates Bypass of Androgen Ablation Therapy in Prostate Cancer.” Molecular Cancer Therapeutics 5 (2006): 3181-3190.
u
Other Resources
American Cancer Society Federal Report Looks at Risks from Plastics Chemical http://www.cancer.org/docroot/NWS/content/ NWS_1_1x_Federal_Report_Looks_at_Risks_from_ Plastics_Chemical.asp Breast Cancer Fund Bisphenol A http://www.breastcancerfund.org/site/ pp.asp?c=kwKXLdPaE&b=2638145 National Toxicology Program Bisphenol A http://ntp.niehs.nih.gov/ index.cfm?objectid=BC9825E3-123F-79087BF465F9E25681B0 Toxicology and Chemical Substances/European Chemical Bureau http://ecb.jrc.it See also Acrylamides; Bis(chloromethyl) ether and technical-grade chloromethyl methyl ether; Cadmium and cadmium compounds; Carcinogens, known; Carcinogens, reasonably anticipated; Chromium hexavalent compounds; Di(2-ethylhexyl) phthalate (DEHP); Organochlorines (OCs); Pesticides and the food chain; Plasticizers; Vinyl chloride.
Salem Health: Cancer
Bladder cancer
u Bisphosphonates Category: Chemotherapy and other drugs ATC code: M05BA Definition: Bisphosphonates are medications that act primarily on bone to inhibit resorption or bone destruction resulting from cell-induced bone breakdown. They treat various bone-degenerating conditions. Cancers treated: Breast cancer, hypercalcemia of malignancy (HCM), metastatic bone cancer, multiple myeloma, bone pain, osteoporotic bone loss from cancer treatments Subclasses of this group: Aminobisphosphonates, nonaminobisphosphonates Delivery routes: Bisphosphonates are administered as oral tablets and as intravenous (IV) solutions to outpatients and inpatients. Bisphosphonates in any form are best administered without food to avoid decreased bioavailability. How these drugs work: Bone resorption is part of normal bone regeneration mediated by osteoclasts, or bone breakdown cells. Abnormal osteoclast activity results from lytic bone lesions of multiple myeloma, metastatic bone tumors from breast cancer or other solid tumors, or osteoporosis from glucocorticoids in chemotherapy regimens and from breast-cancer-induced menopause. Bisphosphonates inhibit resorption by decreasing osteoclast activity. This mechanism reduces further bone loss and fracture, minimizes pain associated with osteoclast lesions and weakened bone, and reverses hypercalcemia of malignancy (HCM), which can result when
bone breakdown releases calcium to the blood. Monthly bisphosphonate administration has been shown to reduce the incidence of bone metastases in women with breast cancer as well, and these drugs have substantially reduced the risk of bone loss and fracture in spinal vertebrae and the hip. Side effects: A major side effect of this drug class is irritation of the esophageal mucosa, which can be reduced by taking the drug with a full glass of water and by remaining in an upright position directly after drug ingestion. This side effect may occur even with IV administration. Other side effects include constipation, diarrhea, dyspnea, myalgia, fever, decreased calcium and phosphate, and altered magnesium. Impaired kidney function and renal failure are possible. IV administration causes fever, flulike syndrome, and local injection site reactions. Other side effects noted in trials of patients with cancer include anxiety, headache, insomnia, anorexia, and abdominal pain. Nicole M. Van Hoey, Pharm.D. See also Bone scan; Hypercalcemia; Paget disease of bone.
u Bladder cancer Category: Diseases, symptoms, and conditions Also known as: Transitional cell carcinoma Related conditions: Kidney cancer Definition: Bladder cancer is a cancer that forms in the inner lining of the bladder.
Common Bisphosphonate Agents Drug
Brands
Delivery Mode Cancers/Conditions Treated
Aledronate
Fosamax
Oral
Glucocorticoid-induced osteoporosis
Etidronate
Didronel
Oral, IV
Hypercalcemia of malignancy (HCM)
Ibandronate
Boniva
Oral, IV
Breast cancer bone metastases; menopause-induced osteoporosis
Pamidronate
Aredia
IV
HCM malignancy with or without bone metastases; breast cancer and multiple myeloma; off-label for pain associated with prostatic carcinoma; possible prevention of breast cancer-related bone loss
Risedronate
Actonel
Oral
Glucocorticoid-induced osteoporosis; possible prevention of breast cancer-related bone loss
Tiludronate
Skelid
Oral
Bone metastases
IV
Multiple myeloma; solid tumor bone metastases; HCM
Zoledronic acid Reclast, Zometa
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Bladder cancer Risk factors: Researchers do not completely understand the causes of bladder cancer; however, several carcinogens, family history, and prior diagnosis of bladder cancer remain the chief causes. Smokers are at greatest risk for developing bladder cancer as well as people with exposure to certain chemical dyes in the rubber- and leatherprocessing, textile, and printing industries. Etiology and the disease process: The wall of the bladder is lined with cells called transitional cells and squamous cells. More than 90 percent of bladder cancers begin in the transitional cells and are called transitional cell carcinomas. About 8 percent of bladder cancer patients have squamous cell carcinomas. Cancer that is only in cells in the lining of the bladder is called superficial bladder cancer and often recurs after treatment. Cancer that begins as a superficial tumor may grow through the lining and into the muscular wall of the bladder. This invasive cancer may extend through the bladder
An infiltrating tumor (upper right) in the muscular wall of the bladder. (John Bavosi/Photo Researchers, Inc.)
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Salem Health: Cancer wall into a nearby organ such as the uterus, vagina, or prostate gland or into nearby lymph nodes, in which case cancer cells may have spread to other lymph nodes or other organs such as the lungs and liver or to the bones. Incidence: Primarily occurring in men and women over the age of forty, bladder cancer is diagnosed in 38,000 men and 15,000 women each year in the United States. According to the National Cancer Institute, this is the fourth most common type of cancer in men, and the eighth most common in women. Caucasians get bladder cancer twice as often as African Americans and Hispanics. People with family members who have bladder cancer as well as people who have previously had bladder cancer are more likely to get the disease. Symptoms: Bladder cancer often causes no symptoms until it reaches an advanced state that is difficult to cure. The most common symptom of bladder cancer is blood in the urine (hematuria). Some patients experience pain or burning during urination, or a change in urinary habits, such as a frequent urge to urinate. Screening and diagnosis: Screening tests include a medical interview, a physical examination, urinalysis, urine cytology, and cystoscopy. The urinalysis determines if the urine contains abnormalities such as blood, protein, sugar, and solids. Urine cytology is a microscopic examination of urine to detect any abnormal cells that have sloughed off the bladder wall and have been released in the urine. If necessary, cytoscopy is performed with a very narrow tube with a light and camera inserted through the urethra to examine the inside of the bladder. If bladder cancer is suspected, a physician may order a computed tomography (CT) scan, pyelography, or biopsy. The CT scan is helpful for a three-dimensional view of the bladder and urinary tract to determine if any masses or tumors exist in the bladder or if the cancer has spread to other organs. Pyelography involves injecting a special dye into a vein or the urethra and examining a series of timed-interval X rays of the urinary system to determine if abnormalities exist. The biopsy is typically performed during cytoscopy, and abnormal cells can be detected with a microscope. Staging refers to the size of the cancer and the extent to which it has invaded the bladder wall and spread to other parts of the body. High-grade tumors are significantly more aggressive and life-threatening than low-grade tumors. Approximately 10 per-
Salem Health: Cancer cent of bladder cancer is found to be superficial bladder cancer in situ, which is a highly aggressive, early manifestation of bladder cancer.
Bladder cancer
Incidence of Bladder Cancer per 100,000 People, by Gender 45 Men
Women
40.5 Treatment and therapy: The physi40 cian may treat superficial bladder cancer with transurethral resection (TUR) 35 by inserting a cystoscope into the bladder through the urethra and using a tool 30 with a small wire loop on the end to remove the cancer and to burn away any remaining cancer cells with an electric 25 current. For invasive bladder cancer or 20.3 20.2 cancer involving a large portion of the 20 bladder, surgery is performed to remove 16.4 the entire bladder, nearby lymph nodes, 15 part of the urethra, and the nearby organs that may contain cancer cells. In 10.1 10 some cases of low-grade cancer, only 7.6 part of the bladder is removed in a pro5.5 cedure called segmental cystectomy. 5 3.9 Radiation therapy uses high-energy rays to kill localized cancer cells to 0 shrink the tumor before surgery or if White Black Hispanic Asian/Pacific surgery is not an option. Chemotherapy Islander uses one drug or a combination of drugs to kill cancer cells. Superficial bladder Source: Data from National Cancer Institute, Surveillance Epidemiology and End Results, Cancer Stat Fact Sheets, 2008 cancer can be treated with local cheNote: Based on cases diagnosed in 2000-2004 motherapy; once per week for several weeks, a catheter is inserted through the urethra and remains in the bladder for several hours. If the cancer has deeply u For Further Information invaded the bladder or spread to lymph nodes or other orDunetz, Gary N. Bladder Cancer: A Resource Guide for gans, chemotherapy may be used to treat the entire body. Patients and Their Families. Bloomington, Ind.: Biological therapy, or immunotherapy, uses the body’s AuthorHouse, 2006. natural immune system to fight cancer by inserting a cathEllsworth, Pamela. One Hundred Questions and Answers eter with a solution containing live, weakened bacteria to About Bladder Cancer. Sudbury, Mass.: Jones & Bartkill cancer cells in the bladder. lett, 2005. Schoenberg, Mark P., et al. The Guide to Living with Prognosis, prevention, and outcomes: Bladder cancer Bladder Cancer. Baltimore: Johns Hopkins University has one of the highest recurrence rates of all cancers. If Press, 2000. treated once, patients must continue a course of follow-up screenings. The five-year survival rate for patients with early-stage bladder cancer is 85 percent. Most patients u Other Resources with bladder cancer (up to 80 percent) will be diagnosed with a superficial tumor. Patients with tumors invading Mayo Clinic the bladder wall have a five-year survival rate of 60 to 75 Bladder Cancer percent. http://www.mayoclinic.com/health/bladder-cancer/ Robert J. Amato, D.O. DS00177
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Blood cancers National Cancer Institute Bladder Cancer http://www.nci.nih.gov/cancertopics/types/bladder See also 4-Aminobiphenyl; Bacillus Calmette Guérin (BCG); Cystography; Cystoscopy; Gastrointestinal oncology; Kidney cancer; Squamous cell carcinomas; Transitional cell carcinomas; Urethral cancer; Urinary system cancers; Urography; Urostomy.
u Blood cancers Category: Diseases, symptoms, and conditions Also known as: Hematopoietic neoplasms, malignant neoplasms, bone marrow diseases Related conditions: Leukemia (acute myelogenous or myelocitic leukemia, or AML; acute lymphocytic or lymphoid leukemia, or ALL; chronic myelogenous or myelocitic leukemia, or CML; chronic lymphocytic or lymphoid leukemia, or CLL), lymphoma (Hodgkin disease, or HD; non-Hodgkin lymphoma, or NHL), and myeloma (plasma cell dyscrasia, plasma cell myeloma, multiple myeloma, myelomatosis) Definition: Blood cancers are those that arise from an abnormality in the production of any of the mature blood cells or their precursor stem cells. Not all bone marrow disorders, such as anemia, are cancers. The three main types of blood cancer are leukemia, lymphoma, and myeloma. Leukemia is a cancer of any of the five dominant types of white blood cells. It occurs when the bone marrow produces abnormal white blood cells, which replicate, limiting the ability of healthy cells to function. Chronic leukemia develops slowly, while acute leukemia develops quickly. Of the four subtypes of leukemia, the acute forms exhibit immature blood-forming cells or blasts, and the chronic forms exhibit few or no blast cells but changes in the presentation of marrow cells. Acute lymphocytic leukemia (ALL), also known as acute lymphoid leukemia, is the most common type of blood cancer among those under nineteen years of age. ALL is characterized by lymphoblasts replacing normal cells in the marrow and lymph nodes lowering the affected individual’s ability to fight infection. Chronic lymphocytic leukemia (CLL) is the most common type of blood cancer among those fifty years of age and older and the most prevalent type of leukemia. Acute myelogenous leukemia (AML), in which leukemic blast cells proliferate and block the production of normal marrow cells, results in a deficiency of red blood cells, 154
Salem Health: Cancer white cells, and platelets. Chronic myelogenous leukemia (CML) is seen mostly in adults and begins with a change in a single stem cell, a future red cell, white cell, or platelet. Lymphomas originate in malignant changes in the lymphatic or immune system. The primary types are Hodgkin disease and non-Hodgkin lymphoma. Hodgkin disease is characterized by abnormal T or B white blood cells. As the abnormal cells divide, they proliferate and can spread throughout the body. Non-Hodgkin lymphoma is a cancer of the lymphoid tissue, which is mostly made up of lymph nodes that manufacture and store lymphocytes, white blood cells that protect against infection. Myelomas are progressive blood cancers of plasma cells, which produce antibodies to fight against infections and regulate the immune system. Myeloma results from an overproduction of these antibodies, an impaired immune system, and invasive tumors. Risk factors: The risk factors and causes of many types of blood cancers are not well known, and most cases of blood cancer occur in individuals with no identifiable risk factors. However, for AML, which along with CLL is among the most common types of blood cancer seen in adults, these specific risk factors have been found: Down syndrome and other genetic disorders, chronic exposure to ionizing radiation and chemicals such as benzene in the workplace, high doses of radiation therapy and the chemotherapies used to treat lymphoma or other types of cancer, and tobacco smoke. Those who are immunosuppressed with certain human retroviruses and bacteria, such as the Epstein-Barr virus (EBV) in Africa; those with human immunodeficiency virus (HIV); and those with human T-cell leukemia virus (HTLV) are at greater risk of developing lymphomas. Familial clustering also has been associated with the development of lymphomas. Etiology and the disease process: Cancer develops as a result of a variety of factors and over a number of years. Blood cancers differ widely by group and within each subtype in their progression, causes, and molecular presentation. The leukemias begin in two types of white blood cells: neutrophils and monocytes, which are germ-ingesting cells, and lymphocytes, which are immune-defense cells. Abnormal white blood cells in the bone marrow multiply and enter the bloodstream, crowding out normal cells. Lymphomas develop when these immune-defense cells multiply and cause tumors in the lymph nodes or other parts of the immune system. Development of blood cells through the hematopoietic process is arrested, and abnormal blood cells proliferate. Every stage of hematopoietic development can result in a particular type of cancer. Non-Hodgkin lymphoma (NHL) is manifested by
Salem Health: Cancer well-differentiated cells with slow progression, while other forms are more aggressive with lymphocytes of limited differentiation. Tumors of the bone marrow are characteristic of myelomas. In myeloma, cells that are to become immune cells develop in the bone marrow from stem cells, as will all blood cells. A major type of white blood cells, B lymphocytes, which typically develop into plasma cells, undergo multiple genetic changes as they change into plasma cells, causing malignant plasma cells to develop. These myeloma cells travel throughout the bloodstream, reside in the bone marrow, and damage healthy tissue. The myeloma interferes with the plasma cell’s production of protective proteins called immunoglobulins or antibodies by producing M proteins or abnormal immunoglobulin, making those affected susceptible to infection.
Blood cancers for diagnosis of myeloma was seventy, with the majority, 28.1 percent, between the ages of seventy-five and eightyfour. Incidence rates for all types of leukemia are higher among men than women and higher among African Americans than those of European descent. New cases of multiple myeloma are estimated to be diagnosed at a rate of 5 to 6 per 100,000 people each year. The incidence rate of myeloma is higher for men than women across racial and ethnic groups. Symptoms: Signs and symptoms of blood cancers vary widely and may be similar to those of other, less severe illnesses. Symptoms vary based on the category and subtype of blood cancer; for example, symptoms of acute leukemia may include pallor, shortness of breath with exertion, lack of energy, night sweats or a mild fever, slow healing of cuts and bruises, unexplained weight loss, tiny red spots under the skin, bone and joint aches and pains, and low white blood cell count (especially neutrophils and mono-
Incidence: The most common forms of leukemia seen in adults aged fifty and over are chronic lymphocytic leukemia (CLL) and acute myelogenous leukemia (AML). The incidence of acute lymphocytic leukemia (ALL) increases in those over sixty years of age. In 2007, new cases of CLL were estimated at 15,340 and new cases of AML at 13,410. The National Cancer Institute (NCI) reports that between 2000 and 2004, the average median age at diagnosis for leukemia was sixty-seven, with 23.7 percent between the ages of seventy-five and eightyfour. Based on cases diagnosed during this period, the age-adjusted incidence rate for leukemia was 12.3 per 100,000 men and women per year. Chronic leukemias accounted for 7 percent more cases than acute leukemias. It was estimated that 71,380 cases of lymphoma would be diagnosed in the United States in 2007. The majority of these cases, 63,190, were projected to be of the non-Hodgkin type. Incidence rates of Hodgkin lymphoma tend to be higher among men than women. Non-Hodgkin lymphoma also is more commonly diagnosed among men, particularly those aged sixty to sixtyfour (52.3 in every 100,000 men in this age group). According to the NCI’s cancer surveillance data, the median age for diagnosis of lymphoma was sixty-four, with the majority of cases, 21.3 percent, diagnosed between the ages of seventy-five and eighty-four. Non-Hodgkin lymphoma is the fifth most common cancer among men and women. It was estimated that 19,900 new cases of myeloma would be diagnosed in the United States This X ray reveals a secondary tumor in the humerus; the primary is in the in 2007. NCI data indicated that the median age bronchus. (©Mediscan/Corbis)
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Blood cancers
Salem Health: Cancer
Estimated New Blood Cancer Cases and Deaths by Gender, 2007 New Cases Blood Cancer Type
Men Women
Deaths Total
Men Women
Total
Leukemias (all) Acute myeloid leukemia Chronic myeloid leukemia Acute lymphocytic leukemia Chronic lymphocytic leukemia Other leukemias
24,800 19,440 44,240 7,060 6,350 13,410 2,570 2,000 4,570 3,060 2,140 5,200 8,960 6,380 15,340 3,150 2,570 5,720
12,320 5,020 240 820 2,560 3,680
9,470 21,790 3,970 8,990 250 490 600 1,420 1,940 4,500 2,710 6,390
Lymphomas (all) Hodgkin disease Non-Hodgkin lymphoma
38,670 32,710 71,380 4,470 3,720 8,190 34,200 28,990 63,190
10,370 770 9,600
9,360 19,730 300 1,070 9,060 18,660
Multiple myeloma
10,960
5,550
5,240 10,790
8,940 19,900
Source: Data from American Cancer Society, Cancer Facts and Figures 2007 (Atlanta: Author, 2007)
cytes). Although specific bone marrow and blood tests are needed to diagnose any type of blood cancer, some of those affected with certain subtypes of leukemia may have enlarged lymph nodes in the neck, groin, or armpit, and they may suffer from frequent infections. Often individuals who have Hodgkin disease or nonHodgkin lymphoma experience painless, swollen lymph nodes, loss of appetite, vomiting, bloating, abdominal pain, fullness (due to enlargement of the liver, spleen or abdominal lymph nodes), pain in the lower back, bone pain, constant coughing, and unexplained lethargy. Early symptoms of myeloma are bone pain, particularly with movement, and infections involving the skin, the urinary tract, the bronchial tract, or lungs. These symptoms may also be accompanied by pallor resulting from anemia, weakness, and exaggerated fatigue. Screening and diagnosis: Blood tests and specific bone marrow tests are needed to diagnose blood cancer; however, individuals in early stages of the disease may not have symptoms suggesting cancer. Current evidence does not suggest that routine blood screening before the onset of symptoms will detect cases of blood cancer and lead to improved medical outcomes or be cost effective in those at average risk of developing cancer according to their medical, family, and occupational history. The first indication that a person has blood cancer may be the results of a blood test performed as part of an annual physical. The blood sample may reveal anemia or changes in white blood cells, a possible indicator of leukemia. If an individual has symptoms that suggest blood cancer, the physician will 156
take a medical history and check for swelling of the liver, spleen, or lymph nodes in the armpits, groin, or neck. Urinalysis will also be performed to detect substances or cellular material in the urine. Other tests include a blood test to assess blood cell count, a cytogenetic exam to analyze the number and shape of chromosomes to check for genetic abnormalities, a bone marrow aspirate to check for cancerous cells in liquid bone marrow, and a bone marrow biopsy to check for cancerous cells in the bone specimen. If cancerous cells are present, additional tests may be ordered to ascertain if the disease has spread and to organs or systems. These tests include tumor-marker tests (immunophenotyping, based on the type of antigen or marker on the surface of the cell), a spinal tap or lumbar puncture to obtain a sample of cerebrospinal fluid, chest X rays (for signs of infection or lymph node involvement), or ultrasound scans. Staging is used to assess the extent or severity of the disease, to plan treatment, and to predict the outcome or prognosis. Classification of each type of blood cancer into stages is based on the site that is affected, the progression of the disease, and the appearance of the affected cells. For example, CLL is staged according to the risk-based Rai classification system using symptoms such as blood lymphocyte count, presence of enlarged lymph nodes or organs, platelet count, and anemia. Other forms of leukemia, such as acute leukemia, are not staged because of acute onset, which typically means the cancer has spread to other organs at the time of diagnosis. Although leukemic cancerous cells circulate in the blood and bone marrow, in lymphomas cells form tumors
Salem Health: Cancer in lymphatic tissue. The Ann Arbor staging system is used for staging both Hodgkin disease and non-Hodgkin lymphomas on the basis of specificity of site of lymph node involvement. The TNM (tumor/lymph node/metastasis) system may be used to stage the size of a tumor, lymph node involvement, and existence or extent of spread through other parts of the body. The International Staging System (ISS) is used for staging multiple myelomas based on blood tests for two proteins, albumin and betamicroglobulin, which are markers for the disease. Treatment and therapy: Blood cancers are typically treated with one or more of the following: chemotherapy, radiation therapy, stem cell transplantation, and immunotherapy. A treatment plan is created using an anticancer agent such as chemotherapy, sometimes in combination with radiation therapy. The goal of chemotherapy, drugs given in combination and via different methods of delivery, is to destroy cancerous cells or to stop them from growing and multiplying, producing long-term remission or a cure. Radiation may be used to treat localized cancers such as lymphomas and certain types of leukemia, or it may be used to relieve symptoms when cancerous growths cause pain or pressure on bones, nerves, or organs. However, chemotherapy and radiation therapy can cause longterm or late effects, affecting fertility or growth and causing learning disabilities or illnesses secondary to the primary cancer such as leukemia. Chemotherapy doses considered tolerable by most patients may not be sufficient to arrest, cause remission in, or cure acute leukemia, myeloma, or lymphoma. In patients who may be at high risk of relapse, who relapse after a successful course of treatment, or who do not respond as expected to conventional treatment, stem cell transplantation (transplanting cells from which blood cells and immune cells arise) can enable production of normal blood cells such that intensive chemotherapy can bring about recovery. Immune treatments (using antibodies from the patient or a donor) may be used alone or in combination with other therapies to attack cells that remain after chemotherapy and that may attach to antigens on the malignant cells. They also are used as vaccines to suppress malignant cells that remain in the body following therapy. New chemotherapies, immunotherapies, vaccines, gene therapies, and types of bone marrow transplants to suppress the growth of cancerous cells and affect the course of the disease are always being developed and tested. Patients need to be reminded that pain and uncomfortable symptoms arising from the toxic effects of cancer treatments can be managed by consulting with their physicians. Supportive care to improve functioning and quality of life, transfusions,
Blood cancers antibiotics to protect against infection, and a healthy diet and lifestyle are critical for those undergoing cancer treatment. Prognosis, prevention, and outcomes: Many factors affect the outcome of a patient’s blood cancer, including the type, location, and stage of disease as well as individual and demographic factors such as the person’s general health, age, and response to treatment. A cancer survivor will undergo follow-up care, which includes frequent monitoring of blood counts, X rays, urine tests, imaging tests such as computed tomography (CT) or positron emission tomograph (PET) scans. Those whose remission lasts five years are considered cured. Survival rates for those with blood cancer have been rising since 1975 and the advent of more effective cancer treatments, according to the NCI’s Cancer Trend Report 2005 Update. No specific guidelines for preventing blood cancer exist, as its causes are not known and many types are relatively rare. Limiting exposure to environmental toxins and leading healthy lifestyles may help prevent blood cancers in those of average risk. The relative overall five-year survival rate of leukemia between 1996 and 2003 was nearly 50 percent, a survival rate that has more than tripled in patients diagnosed with leukemia since 1947. Relative survival rates vary by age of diagnosis, race, gender, and type of leukemia. Of all types of leukemia, those with CLL had the highest relative survival rate during this period, with 75.8 percent surviving. Hodgkin disease is considered one of the most curable cancers, with many patients cured after their initial treatment. The five-year survival rate has increased dramatically since the 1960’s, reaching 86 percent of patients of all races who were diagnosed with the disease between 1996 and 2003. Similarly, due to advances in treatment of non-Hodgkin lymphoma, the mortality rate has declined considerably since the 1980’s. Susan H. Peterman, M.P.H. u
For Further Information Adler, Elizabeth M. Living with Lymphoma: A Patient’s Guide. Baltimore: Johns Hopkins University Press, 2005. Hoffman, Barbara, ed. A Cancer Survivor’s Almanac: Charting Your Journey. Minneapolis: National Coalition for Cancer Survivorship, 1996. Mauch, Peter M., et al., eds. Hodgkin’s Disease. Philadelphia: Lippincott Williams & Wilkins, 1999. Wiernik, Peter Harris, ed. Neoplastic Diseases of the Blood. 4th ed. New York: Cambridge University Press, 2003. 157
Bone cancers u
Other Resources
American Cancer Society http://www.cancer.org International Myeloma Foundation http://www.myeloma.org The Leukemia and Lymphoma Society http://www.leukemia-lymphoma.org Memorial Sloan-Kettering Cancer Center http://www.mskcc.org National Cancer Institute http://www.cancer.gov See also Acute lymphocytic leukemia (ALL); Acute myelocytic leukemia (AML); Aleukemia; Amyloidosis; Anemia; Aplastic anemia; Bone marrow aspiration and biopsy; Bone marrow transplantation (BMT); Burkitt lymphoma; Chronic lymphocytic leukemia (CLL); Chronic myeloid leukemia (CML); Cutaneous T-cell lymphoma (CTCL); Disseminated intravascular coagulation (DIC); Down syndrome and leukemia; Eosinophilic leukemia; Fanconi anemia; 5Q minus syndrome; Hairy cell leukemia; Hemolytic anemia; Hodgkin disease; Human T-cell leukemia virus (HTLV); Hypercalcemia; Leukemias; Leukopenia; Leukoplakia; Lymphocytosis; Lymphomas; Multiple myeloma; Myelodysplastic syndromes; Myelofibrosis; Myeloma; Myeloproliferative disorders; Myelosuppression; Neutropenia; Pheresis; Polycythemia vera; Richter syndrome; Sézary syndrome; Stem cell transplantation; Superior vena cava syndrome; Thrombocytopenia; Thymomas; Thymus cancer; Transfusion therapy; Umbilical cord blood transplantation; Waldenström macroglobulinemia (WM).
u Bone cancers Category: Diseases, symptoms, and conditions Also known as: Osteosarcoma, osteogenic sarcoma, bone tumor Related conditions: Li-Fraumeni syndrome, Gardner syndrome, retinoblastoma, leukemia, human immunodeficiency virus (HIV) infection Definition: Bone cancers are malignant, unregulated proliferation of neoplasia (new tissue growth) in bone cells. The most common type of bone cancer is osteosarcoma, a highly malignant tumor composed of cells derived from growing connective tissue cells of bone. Osteochondromas are the most common cancerous primary bone tu158
Salem Health: Cancer mors, with giant cell tumors developing in the thighbone near the knee. Ewing sarcoma is the second most common form of childhood bone cancer and is found mostly in the extremities. Chondrosarcomas are cancerous bone tumors that appear in the cartilage of bone in middle age. Other rare sarcomas are parosteal osteosarcomas involving both the bone and membranous covering, fibrosarcomas originating in the ends of bones in the arm or leg and then spreading to soft tissue, and chordomas that develop on the skull or spinal cord. Multiple myeloma is a hematologic cancer that frequently causes bone tumors. Risk factors: The exact cause of osteosarcoma is not known, but inherited or acquired deoxyribonucleic acid (DNA) mutations are the suggested causes. Risk factors include the presence of a benign bone disease; previous treatment with radiation for another cancer, especially at a young age; teenage growth spurts; and disproportionate tallness with age. Certain rare, inherited cancers are also risk factors, such as Gardner syndrome, Li-Fraumeni syndrome (a rare family predisposition to multiple types of cancers caused by a mutation in a cancer-suppressing gene), and retinoblastoma (a malignant tumor of the retina that usually occurs in children younger than five years old). Studies suggest that occupational exposure to wood preservatives and certain herbicides increases the risk of developing soft-tissue sarcomas. Suggested risk factors for myeloma bone disease include age (it rarely occurs under the age of forty), family history, smoking, exposure to petroleum and other chemicals, and exposure to high amounts of radiation. Atomic radiation from nuclear explosions and high-dose exposure to ionizing radiation are known to be risk factors for bone cancer but on a small scale. Virus infections make relatively minor contributions to human bone cancer, except the human immunodeficiency virus (HIV), which causes sarcoma. Etiology and the disease process: Bone cancers are among the class of mesenchymal cancers that originate from the mesenchyme (bone and other tissues derived from embryonic mesoderm). Abnormal or partially differentiated cells develop in the bone marrow and can enter the general circulation and ultimately cause leukemia. (Leukemia can also result from blocked hemopoietic cell differentiation that causes abnormal cells to accumulate in bone marrow.) Initial mutation in a gene linked to DNA repair will cause other mutations to arise and spread more rapidly. Bone cancers usually develop rapidly and metastasize through the lymph channels of the body. Metastatic tumors frequently involve the axial more than the appendicular skeleton.
Salem Health: Cancer
Bone cancers
Malignant primary bone tumors originate in hard bone, in the soft tissue of blood vessels and nerves, or in tissues containing muscles, fat, or fiber. Osteosarcomas can grow quickly along the edge or end of a fast-growing long bone of the arms or legs, sometimes affecting the pelvis, shoulder, and skull. Osteosarcoma may metastasize into nearby tissues of the foot, tendons, and muscles, or spread through the bloodstream to other organs or bones in the body. Ewing sarcoma originates from immature nerve tissue in the bone marrow of the leg, hips, ribs, and arms, but it is mostly found in the extremities, rapidly infiltrating the lungs and metastasizing to other bones, kidneys, heart, adrenal glands, and other soft tissues. Chondrosarcomas usually originate in cartilage in ribs, legs, or hip bones. These grow slowly and take years to spread to other parts of the body. Incidence: In the United States, about 2,400 cases of cancers of bones and joints are reported annually. The American Cancer Society in 2004 reported incidence rates in the United States to be approximately 1 in 113,333 people, or 2,400 people. In 2005, 2,570 new cases An MRI scan of the spine of a seventy-two-year-old patient reveals myeloma of bone and joint cancer were reported, along that has caused one of the vertebrae (sixth from bottom) to collapse. (Zephyr/ Photo Researchers, Inc.) with 1,210 deaths. Osteosarcoma and Ewing sarcoma occur mostly in children, adolescents, and young Genetic association crops up with bone cancer but adults, accounting for 10 to 15 percent of all childhood scarcely accounts for more than 10 percent of cancers. bone cancers but constituting only 1 percent of all cancers. Most other types of bone cancers are usually found only in Symptoms: Pain is the most common symptom of bone adults. cancer, associated with weakened bones and fractures. Osteosarcoma occurs slightly more often in male than Symptoms may include swelling around the affected site, female children and youths, usually between the ages of increased pain with activity or lifting, limping, and deten and twenty, and represents one-fifth of all bone tumors. creased movement of the affected limb. The soft bone tisApproximately 900 new cases of osteosarcoma are resues grow very large and push aside normal tissue. The iniported each year in the United States. tial symptom is usually a painless lump or swelling, which Ewing sarcoma occurs in 0.6 in one million people in later becomes sore and painful as it presses against nearby the United States, more often in male than female children nerves and tissues. and youths between the ages of ten and twenty, and acSymptoms of Ewing sarcoma include pain, swelling counts for 16 percent of bone cancers. and redness around the site of the tumor, typical small Chronic leukemia, resulting from bone marrow cancer, round blue cells, fatigue, fever, paralysis and incontinence is the most common form of leukemia and is twice as com(if the tumor is in the spinal region), numbness, tingling, mon in men as in women. It is ten times more common in weight loss, and decreased appetite. adults than in children but accounts for 75 percent of childThe symptoms for myeloma bone disease are pain, conhood leukemias, with a five-year survival rate of 80 perstipation, nausea, vomiting, fractures in bones, weakness cent. 159
Bone cancers
Salem Health: Cancer
or numbness in legs, weight loss, weakness, fatigue, repeated infections, and problems with urination. Screening and diagnosis: In addition to a complete medical history and physical examination, diagnostic procedures for bone cancers such as osteosarcoma and Ewing sarcoma may include multiple imaging studies, such as X rays, of the tumor and sites of possible metastasis. Osteosarcomas are classified according to subtypes and grades determined by X rays and histological analysis: • Low grade: intraosseous low grade, parosteal • Intermediate grade: periosteal • High grade: conventional, telangiectatic, central, small cell, high-grade surface A radionuclide bone scan is used to determine the cause of pain or inflammation to rule out any infection or fractures. Magnetic resonance imaging (MRI) is done to rule out any associated abnormalities of the spinal cord and nerves. A computed tomography (CT) scan provides more detailed images than general X rays. A complete blood count (CBC) measures the size, number, and maturity of different blood cells in a specific volume of blood, and urine and blood tests (including blood chemistries) are also used for diagnosis. A biopsy is performed on a tissue specimen to determine if cancer or other abnormal cells are present and to determine other courses of action. Myeloma bone disease is additionally diagnosed with aspiration (an examination of a small amount of bone marrow fluid). Cell sorting devices can identify the number of proliferation cells or ploidy status of the nuclear DNA. Chemical proteins
Age at Death for Cancer of the Bones and Joints, 2001-2005 Age Group
Deaths (%)
Under 20 20-34 35-44 45-54 55-64 65-74 75-84 85 and older
14.8 14.3 7.1 9.5 11.5 13.7 18.3 10.7
Source: Data from National Cancer Institute, Surveillance Epidemiology and End Results, Cancer Stat Fact Sheets, 2008 Note: The median age at death from 2001 to 2005 was fiftyeight, with an age-adjusted death rate of 0.4 per 100,000 men and women.
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(serving as antigens) detected by specific antibodies provide information on the state of cancer cells. Polymerase chain reaction (PCR) kits, which amplify and detect altered DNA base sequences in minute samples of cells, provide additional tumor markers. They make it possible to diagnose cancer types that are difficult to categorize by conventional pathology. Screening of serum sample glycoprotein antigens in the general circulation reveals undetected cancer, and monitors established cancer. Treatment and therapy: Treatment of bone tumors depends on the type of tumor. Treatment is more likely to succeed if fewer cancer cells exist at the beginning of treatment. If the cancer has metastasized, chemotherapy or radiotherapy is used. Chemotherapy is used as a primary therapy or as an addition to other types of treatment and is the main method for treating advanced bone cancer. Typical drugs used are ifosfamide, cisplatin, methotrexate, and doxorubicin, plus some natural products. Drugs are more effective when used in combination. Treatment of osteosarcoma and Ewing sarcoma may include surgery (biopsy, bone/skin grafts, reconstructions, resections, limb salvage procedures), amputation, prosthesis fitting and training, rehabilitation including physical and occupational therapy, psychosocial adapting, supportive care (for the side effects of treatment), antibiotics (to prevent and treat infections), and continued follow-up care (to determine response to treatment, detect recurrent disease, and manage the side effects of treatment). Treatment of osteosarcoma depends on the subtype and grade of the tumor. Low-grade tumors are surgically removed and usually not treated with chemotherapy. Intermediate-grade tumors are treated with both surgery and chemotherapy. High-grade tumors consist of immature cells, which require aggressive chemotherapy. Most osteosarcomas do not respond to radiation therapy. Treatment of myeloma bone disease includes radiation therapy and medications (to control pain), chemotherapy, fracture treatment, bone marrow transplantation, and alpha interferon for immunotherapy. The most common treatment for soft-tissue sarcomas is surgical removal of the tumor, followed by radiation, chemotherapy, or both. Photodynamic therapy involves laser activation of sensitive compounds that generate free radicals. Dietary adjustments, massage, reflexology, acupuncture, and relaxation techniques can relieve pain, anxiety, tension, and depression. Regular exercise provides physical strength and also reduces mental and emotional stress. Prognosis, prevention, and outcomes: Prognosis for bone cancers involves predictions of the rate of growth, the
Salem Health: Cancer likelihood of the cancer to metastasize, the most effective drug or treatment procedure, and the patient’s needs. Prognosis for osteogenic, Ewing, and other sarcomas greatly depends on the extent of the disease; the size and location of the tumor; presence or absence of metastasis; the tumor’s response to therapy; the patient’s age, overall health, and tolerance of specific medications, procedures, and therapies; and continuous follow-up care for the side effects of radiation and chemotherapy as well as secondary malignancies that could occur. Prompt medical attention and aggressive therapy are important for the best prognosis. Five-year event-free survival is expected for 85 percent of patients whose lowgrade osteosarcoma tumors are surgically removed without chemotherapy and for 75 percent of patients with highgrade tumors requiring aggressive chemotherapy. About 50 percent of patients without metastatic Ewing sarcoma may have long-term disease-free survival. The five-year survival rate for sarcomas is about 90 percent if the cancer is discovered before spreading and less than 30 percent for sarcomas that have already metastasized at the time of diagnosis. Since sarcomas arise from chemical reactions within cells, chemoprevention (with minimal side effects) would presumably curb cancer. New legal requirements for carcinogen testing minimize the hazards associated with industrial products; carcinogens cause less than 1 percent of cancers in developed countries. Nevertheless, cancer is still the second highest cause of death in the Western world, suggesting the need for more research and effective controls. Lifestyle modifications for bone cancer prevention include diet management, control of food additive use, tobacco avoidance, regulation of reproductive factors such as contraception, reduction of alcohol consumption, screening for early detection of cancer, and appropriate use and disposal of industrial products. Samuel V. A. Kisseadoo, Ph.D. u
For Further Information Beers, Mark H., ed. The Merck Manual of Medical Information. 2d ed. Whitehouse Station, N. J.: Merck Publishing, 2003. King, Roger J. B., and Mike W. Robins. Cancer Biology. 3d ed. New York: Pearson/Prentice Hall, 2006. O’Neill, Catherine E., ed. New Developments in Bone Cancer Research. New York: Nova Biomedical Books, 2006. Pappo, A. S., ed. Pediatric Bone and Soft Tissue Sarcomas. New York: Springer, 2005. Singh, Gurmit, and Shafaat A. Rabbani, eds. Bone Metastasis. Totowa, N.J.: Humana, 2005.
Bone marrow aspiration and biopsy u
Other Resources
American Cancer Society http://www.cancer.org Free Health Encyclopedia Bone Cancers http://www.faqs.org/health/topics/75/Bonecancers.html Spectrum Health http://www.spectrum-health.org See also Amputation; Bone scan; Childhood cancers; Ewing sarcoma; Fibrosarcomas, soft-tissue; Giant cell tumors (GCTs); Laryngeal cancer; Li-Fraumeni syndrome (LFS); Limb salvage; Metastasis; Nasal cavity and paranasal sinus cancers; Nuclear medicine scan; Orthopedic surgery; Paget disease of bone; Rothmund-Thomson syndrome; Sarcomas, soft-tissue; Simian virus 40; Spinal axis tumors; Uterine cancer; Veterinary oncology; Young adult cancers.
u Bone marrow aspiration and
biopsy Category: Procedures Definition: Bone marrow aspiration involves the removal of a bone marrow sample for laboratory examination. The bone marrow is where all blood cells are created. It is the job of the bone marrow to replace dead and dying red blood cells, white blood cells, and platelets. At times, cancer or other disease may cause this bone marrow production to stop or decrease. Sites for bone marrow aspiration and biopsy are typically the pelvic bone (ilium) or the sternum, larger bones that provide the best samples. A bone marrow biopsy can be performed by a hematologist, medical oncologist, internist, pathologist, or specially trained technologist. The patient can have a bone marrow biopsy at the bedside, in interventional radiology, and even in the operating room. Cancers diagnosed: Leukemia, multiple myeloma, or polycythemia vera, cancers referred to as hematological malignancies; metastatic cancer Why performed: A bone marrow biopsy is done to evaluate the functioning of the bone marrow and to determine the presence or absence of cancer. Patient preparation: The patient will have the procedure explained and provide consent. A numbing medication is 161
Bone marrow aspiration and biopsy injected at the site; it may burn or sting a bit when first used. Once the numbing medication is injected, patients usually feel considerable pressure at the site but not necessarily pain during the procedure. When the biopsy is done in the hip, patients occasionally complain of a quick shooting pain down the leg, but it usually stops once the sample has been taken. A patient with a low platelet count may receive a platelet transfusion immediately before the procedure. Steps of the procedure: The patient will be positioned for the procedure and needs to remain still until its completion. A patient who is having the pelvic bone biopsied will be placed on one side with pillows or blankets used to maintain positioning. A patient who is having the sternum biopsied will lie flat in the bed or on the table. The patient may be given medication for pain and relaxation. The site is scrubbed and cleaned, and then the patient is given medication to numb the site. A small cut is made into the skin. The procedure is done with a device that consists of a large
Salem Health: Cancer hollow needle with an inner attachment (cannula) that allows for the bone to be accessed. The needle is used to make a hole into the bone. Once it is inside the bone, the middle of the needle is removed, and the large hollow needle is then resting in the center of the bone. A large syringe is used to extract a sample of the marrow (aspirate). The section of bone taken when the inner cannula was removed from the needle is also kept for pathology testing. The patient may have this procedure done on both hip bones or at multiple sites in order to establish staging of disease. The samples are placed on slides or in a liquid to preserve them until testing can be completed. After the procedure: Pressure may need to be applied to prevent bleeding. The patient may be asked to lie on that hip to provide extra pressure immediately after the biopsy for ten to fifteen minutes. The cut is typically small enough that a bandage and a little pressure is all that is needed. Some patients may not be able to stop bleeding after the biopsy, usually because their platelet counts are too low. These patients may require a stitch or two at the bone marrow site to stop the bleeding. Patients may remain sore at the site for two to three days after the procedure. If this procedure was performed on an outpatient, then the patient will not be able to drive home and will need a family member or friend to help. Risks: The risks from performing a bone marrow aspiration and biopsy are minimal. As with any invasive procedure, there is a risk for infection. There is also a risk for bleeding and bruising with this procedure. If the sample is taken from the sternum (breast bone), then there is a risk of injury to the heart, lungs, and major blood vessels.
A young patient is undergoing bone marrow aspiration. (National Cancer Institute)
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Results: Findings from the bone marrow aspiration and biopsy show what types of cells are in the bone marrow. The hematologist or pathologist will examine the samples with a microscope to determine what types of cells are present. The physicians are able to determine if these cells are normal, misshapen, or cancerous, as well as the stage of the cancer that may be present. Bone marrow biopsies are also done to evaluate therapy. This is typically seen in leukemia patients. They will have a bone marrow biopsy completed prior to therapy and then a biopsy done at or around day fourteen to determine if the chemotherapy has destroyed the cells in the bone marrow. Katrina Green, R.N., B.S.N., O.C.N.
Salem Health: Cancer u For Further Information Carrier, Ewa, and Gracy Ledinham. One Hundred Questions and Answers About Bone Marrow and Stem Cell Transplantation. Sudbury, Mass.: Jones and Bartlett, 2003. Klag, Michael J., et al., eds. Johns Hopkins Family Health Book. New York: HarperCollins, 1999. Weisbrot, Deborah M., and Alan B. Ettinger. The Essential Patient Handbook: Getting the Health Care You Need—from Doctors Who Know. New York: Demos Medical, 2004.
See also Acute lymphocytic leukemia (ALL); Acute myelocytic leukemia (AML); Aplastic anemia; Blood cancers; Childhood cancers; Chronic lymphocytic leukemia (CLL); Chronic myeloid leukemia (CML); Eosinophilic leukemia; Fanconi anemia; 5Q minus syndrome; Flow cytometry; Hairy cell leukemia; Hematologic oncology; Hemolytic anemia; Histiocytosis X; Hodgkin disease; Immunocytochemistry and immunohistochemistry; Medulloblastomas; Multiple myeloma; Myelofibrosis; Myeloma; Myeloproliferative disorders; Neuroblastomas; NonHodgkin lymphoma; Polycythemia vera; Retinoblastomas; Rhabdomyosarcomas; Stem cell transplantation; Thrombocytopenia; Veterinary oncology; Waldenström macroglobulinemia (WM).
u Bone marrow transplantation
(BMT) Category: Procedures Also known as: Peripheral blood stem cell transplantation (PBSCT) Definition: Bone marrow transplantation (BMT) and peripheral blood stem cell transplantation (PBSCT) are procedures used in cancer therapy to provide stem cells to a patient to replace those lost to disease, chemotherapy, and radiation. Stem cells may be obtained from patients themselves, a related or unrelated donor, or umbilical cord blood taken after the birth of a baby. Autologous transplants use the patient’s own stem cells. Allogeneic transplants use stem cells from a related person; the donor is most often a parent or sibling, but an unrelated but matched donor or umbilical cord blood may be used. A syngeneic transplant is done with stem cells from an identical twin. Cancers treated: Leukemia, lymphoma, multiple myeloma, aplastic anemia, and neuroblastoma; additional
Bone marrow transplantation (BMT) cancers eligible for transplant are being evaluated in clinical trials Why performed: Cancer patients are often treated by high doses of chemotherapy and radiation to rid the body of cancer cells. Chemotherapy and radiation therapy target rapidly dividing cells in the body. Because cancer cells and stem cells divide rapidly, they both may be killed by the therapy. BMT and PBSCT are used to rescue patients after high-dose chemotherapy and radiation by replacing destroyed stem cells with healthy stem cells. Transplanted stem cells allow the bone marrow to begin producing blood cells needed by the body. Additionally, white blood cells from the donor will identify any remaining cancer cells in the patient’s body and attack them as foreign, thus providing additional cancer cell kill. This graft-versustumor (GVT) effect—in this case, stem cells versus cancer cells—is important in some kinds of leukemia treated with allogeneic transplants and enhances the effectiveness of the transplant. To understand bone marrow transplantation, it is important to understand the role of stem cells. Stem cells are found in the bone marrow and can develop into different types of cells in the body, such as blood cells. Blood cells originally begin as immature cells, called hematopoietic stem cells, which are constantly and rapidly dividing. Stem cells used in transplantation are not embryonic stem cells, which are used in cloning experimentation. Mature stem cells are available to the body in the bone marrow, but some stem cells circulate in the bloodstream and are called peripheral blood stem cells. The role of stem cells in the body is to fight infection (stem cells that evolve into white blood cells), carry oxygen (stem cells that evolve into red blood cells), and prevent bleeding (stem cells that evolve into platelets). Patient preparation: The first step in the transplant procedure is determining the type of transplant that will be used by determining if the patient has a potential donor. Doctors try to minimize side effects by using stem cells that match as closely as possible the patient’s own stem cells. There are different proteins on the cell surface, called human leukocyte antigens (HLAs), which are identified with a blood test. The success of the transplant depends on how close a match can be made between the donor stem cells and the patient’s stem cells. Close relatives are the most likely sources of matching stem cells, but less than one-third of patients will have a matched sibling. Finding an unrelated, matched donor is possible in about one-half of cases, and the chance of a match increases if the donor and patient are of the same ethnic and racial 163
Bone marrow transplantation (BMT)
Salem Health: Cancer
Inner spongy layer Hard outer layer
Marrow Bone marrow transplantation is used to treat several types of lymphoma.
background. If a potential donor is identified, then blood work will be used to determine the level of the match. A donor registry may also be used to identify donors who have offered to provide stem cells for transplantation if they match a patient in need. If no donor match can be found, then the patient’s own stem cells may be used in an autologous transplant. Stem cells are obtained from the patient and then treated to remove any cancer cells. Extra stem cells are removed from the patient, as some healthy cells may be damaged when the cancer cells are removed. Once the type of transplant is determined, the stem cells are obtained or harvested. The liquid center of the bone is the source for stem cells used in BMT. The donor is given anesthesia to make the harvest procedure pain-free. General anesthesia or regional anesthesia, which numbs the area below the waist, is used. Large needles are inserted into the hip (pelvic) bone or, rarely, the breastbone (sternum), and marrow is drawn out. The harvest procedure takes approximately one hour. The bone marrow is then treated to remove blood and bone fragments, frozen with a preservative if not to be used immediately, and stored until it is time to administer the stem cells to the patient. Stem cells that are frozen (cryopreserved) can be stored for many years. If the doctor determines that a peripheral blood stem cell transplant is the best choice for the patient, then stem cells are harvested from the bloodstream rather than from the bone marrow. Autologous transplants often use peripheral blood stem cells (PBSCs). Apheresis is used to re164
move PBSCs with a machine that removes the stem cells and then returns the remainder of the blood, minus the stem cells, to the donor. Medicine that stimulates the growth of stem cells in the body may be given to the donor for several days before the harvest. Apheresis may take up to six hours. The cells are processed and frozen for future use. Umbilical cord blood may also be a source of stem cells for transplantation. The mother requests that cells be harvested when the birth occurs. Cord blood banks may store the cells for potential use by the family at a later date or may be given to a public cord blood bank for use by any matching patient. Blood is taken from the umbilical cord and placenta and then frozen for storage. Since only a small amount of blood may be available, cord blood transplants are usually most effective in children or small adults. Steps of the procedure: The patient usually receives high-dose chemotherapy (anticancer drugs) and radiation to rid the body of as many cancer cells as possible. Depending on the hospital program, the patient may be admitted to the hospital or may undergo the preoperative regimen as an outpatient. Once the regimen before the transplant is complete, the patient is ready to have the procedure. The stem cells are thawed and given through an intravenous line, as in a blood transfusion. The infusion of the stem cells may take from one to five hours. After the procedure: Once the infusion of the stem cells is complete, the wait begins for the cells to graft (or take)
Salem Health: Cancer and produce new blood cells for the patients. During this time, the patient may be in a room with special air filters and strict infection control guidelines. Because the patient has very few stem cells until the graft occurs, the body is unable to fight infection or control bleeding. The wait for engraftment ranges from two to six weeks. High fevers, chills, shortness of breath, coughing, low blood pressure, and weakness may occur. With allogeneic transplants, the most significant complication that occurs is graft-versushost disease. Once discharge from the hospital occurs, the patient may face a variety of problems. Fatigue, physical problems lingering after the transplant, and psychological problems may occur. Frequent visits to the physician to follow progress after the transplantation and to manage symptoms are expected. The recovery period may be a year in length. Risks: There is minimal risk involved with donating bone marrow or undergoing apheresis. If the match between donor and patient is not complete, then graft rejection may occur in rare instances. The most significant risk with an allogeneic transplant is graft-versus-host disease. Patients may be unable to have children after a transplant, and this topic should be discussed with the physician prior to the transplant. Results: Survival rates after transplantation vary by disease, type of transplant, and the age of the patient. In related donor patient transplants, survival rates are 55 to 70 percent and 25 to 50 percent if the donor is unrelated. Patricia Stanfill Edens, R.N., Ph.D., FACHE u
For Further Information Jenks Kettmann, J. D., and E. M. Altmaier. “Social Support and Depression Among Bone Marrow Transplant Patients.” Journal of Health Psychology 13 (2008): 39-46. Nadir, Y., and B. Brenner. “Hemorrhagic and Thrombotic Complications in Bone Marrow Transplant Recipients.” Thrombosis Research 120, suppl. 2 (2007): 92-98. u
Other Resources
American Cancer Society http://www.acs.org National Cancer Institute Bone Marrow Transplantation http://www.cancer.gov National Marrow Donor Program http://www.marrow.org
Bone pain See also Blood cancers; Graft-versus-host disease (GVHD); Immunocytochemistry and immunohistochemistry; Leukemias; Lymphomas; Organ transplantation and cancer; Pheresis; Stem cell transplantation; Umbilical cord blood transplantation.
u Bone pain Category: Diseases, symptoms, and conditions Also known as: Skeletal pain Related conditions: Bone metastasis, fracture Definition: Bone pain is an uncomfortable response to disease, infection, inflammation, or trauma to bone. Risk factors: Those at greatest risk for bone pain not caused by fracture or other trauma are those with bone disease, including bone cancers. Etiology and the disease process: Bone pain in cancer may be caused by tumors in or near bones or conditions that cause damage within the bone, such as multiple myeloma. Cancer that spreads, or metastasizes, to bone from another part of the body can result in bone pain. Medications given to stimulate the production of blood cells in the bone marrow may cause temporary bone pain. Incidence: Bone pain is experienced in more than half the cases of bone metastasis. There is a higher incidence in patients with advanced disease, particularly in those with breast and prostate cancers. Symptoms: Symptoms include limited mobility, swelling in the area of pain, fatigue, and lack of appetite. Loss of height is associated with bone compression in the vertebrae. Burning or tingling sensations may indicate nerve involvement. Fracture, a late sign of advanced disease, is another source of pain. Screening and diagnosis: Bone lesions are detected on X rays, positron emission tomography (PET) and computed tomography (CT) scans, and magnetic resonance imaging (MRI). A biopsy is necessary to determine if cancer has spread to the bone. The level of pain is assessed using a variety of scales. A commonly used scale uses a zero to ten rating, where zero correlates with no pain and ten with the worst possible pain. Other evaluations are employed to describe the type and quality of pain. Treatment and therapy: Chemotherapy and radiation alleviate or diminish pain by reducing tumor size. Bone pain is managed with medications, including nonsteroidal anti165
Bone scan inflammatory drugs (NSAIDs), steroids, muscle relaxants, opioids, antidepressants, and antianxiety drugs. Nonpharmaceutical interventions used alone or in conjunction with medication can be effective. Examples include physical therapy, exercise, acupuncture, aromatherapy, biofeedback, breathing exercises, hypnosis, massage, and nerve stimulation. Surgery may be necessary to stabilize weakened bones with rods or special cements. Prognosis, prevention, and outcomes: Prognosis depends on the ability to treat the underlying cause of the pain. An increase in bone pain may indicate disease progression that can lead to serious injury, including fracture, loss of bladder and bowel control, and paralysis. Chronic bone pain can be effectively managed to maximize functionality and quality of life in cases in which it cannot be completely eradicated. Linda August Vrooman, R.N., B.S.N., O.C.N. See also Acute lymphocytic leukemia (ALL); Amputation; Blood cancers; Bone cancers; Bone scan; Chronic lymphocytic leukemia (CLL); Chronic myeloid leukemia (CML); Limb salvage; Multiple myeloma; Myelofibrosis; Myeloma; Neuroblastomas; Neuroectodermal tumors; Orthopedic surgery; Paget disease of bone; Pain management medications; Radiopharmaceuticals; Waldenström macroglobulinemia (WM); Young adult cancers.
u Bone scan Category: Procedures Also known as: Bone scintigraphy Definition: A bone scan is a procedure that can detect abnormalities in the skeleton. A radioactive substance (known as a tracer) is injected into the body and taken up by the bone. The tracer emits radiation in the form of gamma rays, which can be detected by a special scanning camera. More tracer will accumulate in areas of the bone that are actively rebuilding or breaking down (such as that in the presence of cancer) compared to the inactive areas. Cancers diagnosed: Cancers that have spread to the bone (metastatic cancers), primarily breast, prostate, and lung cancers, and kidney and thyroid cancers to a lesser degree Why performed: Cancer cells can spread from their primary location to the bone in a multistep process known as metastasis. Metastatic bone disease can result in bone pain and an overall decrease in the quality of life. Tumor cells residing in the bone can also cause bone destruction (known as resorption) as a result of both direct effects of 166
Salem Health: Cancer the tumor and the activation of osteoclasts (a type of bone cell responsible for resorption). This process may result in weakened bones and a greater risk of bone fractures. Furthermore, calcium may be released from the bone as it breaks down, and elevated levels of calcium in the blood can cause loss of appetite, nausea, and exhaustion and can affect the heart and kidneys. A bone scan is one method to detect if cancer has spread to the bone and to identify where the cancer is located. Bone scans can also be used to determine the stage of disease, as well as to examine how much bone damage is present. Additionally, bone scans may be performed to monitor the response to treatment, as some cases of bone cancers are treated with drugs such as bisphosphonates in order to reduce bone resorption. Patient preparation: Very little prior preparation is required, and patients do not need to fast. At the time of the scan, patients must remove all metal objects (such as jewelry, zippers, and metal buttons), as they may interfere with the scan. In some cases, the clothes should be removed and the patients will wear a hospital gown. Steps of the procedure: A bone scan will usually be performed in a hospital. The two stages of this procedure are the tracer injection and the scan. A radioactive tracer will be injected into a vein in the patient’s arm. Patients will then wait one to four hours to allow the tracer to be incorporated into the bone tissue. Drinking several glasses of water (at least four) will help to eliminate excess tracer through the urine. Patients will be instructed to empty the bladder before the scan begins. For the scan, patients must lie still on a table while the scanning camera moves overhead and scans the body. The camera will detect the gamma rays emitted by the tracer that has concentrated in the bone. Sometimes the scans will be conducted when patients are in different positions in order to view the bones from various angles. On average, the bone scan lasts about thirty to sixty minutes. After the procedure: Care should be taken when sitting up at the completion of the scan, as dizziness or lightheadedness may result from the extended period of lying down. Patients will be instructed to drink plenty of fluids for at least forty-eight hours after the bone scan to help eliminate the remaining radioactive tracer. Patients who are breastfeeding should also discard their breast milk for the first two days after the procedure. Risks: Common risks include redness, soreness, or swelling at the injection site. In rare cases, patients have allergic reactions to the tracer.
Salem Health: Cancer Results: If the radioactive tracer is distributed equally throughout the bones, then the result will be considered normal. An abnormal result will occur when the tracer concentrates in distinct sites of the bone, resulting in “hot spots.” Hot spots indicate that there is a lot of activity in the bone, both building and resorption, which may be a sign of tumor cells within the bone. Hot spots, however, may also be caused by a fracture or bone infection. Therefore, if hot spots are detected, the doctor will often suggest blood tests, biopsies, or other imaging tests in order to confirm the presence of cancer. Elizabeth A. Manning, Ph.D. u For Further Information Coleman, R. E. “Clinical Features of Metastatic Bone Disease and Risk of Skeletal Morbidity.” Clinical Cancer Research 12, no. 20, pt. 2 (2006): 6243s-6249s. Even-Sapir, E. “Imaging of Malignant Bone Involvement by Morphologic, Scintigraphic, and Hybrid Modalities.” Journal of Nuclear Medicine 46, no. 8 (2005): 1356-1367. Hamaoka, T., et al. “Bone Imaging in Metastatic Breast Cancer.” Journal of Clinical Oncology 22, no. 14 (2004): 2942-2953. Rosenthal, D. I. “Radiologic Diagnosis of Bone Metastases.” Cancer 80, suppl. 8 (1997): 1595-1607. Yoneda, T., and T. Hiraga. “Crosstalk Between Cancer Cells and Bone Microenvironment in Bone Metastasis.” Biochem Biophys Res Commun 328, no. 3 (2005): 679-687. u
Other Resources
American Cancer Society How Is Bone Cancer Diagnosed? http://www.cancer.org/docroot/CRI/content/ CRI_2_4_3X_How_is_bone_cancer_diagnosed_2 .asp?sitearea= What Is Bone Metastasis? http://www.cancer.org/docroot/CRI/content/ CRI_2_4_1X_What_Is_bone_metastasis_66.asp Mayo Clinic Bone Scan: Using Nuclear Medicine to Find Bone Abnormalities http://www.mayoclinic.com/health/bone-scan/ CA00020 See also Alveolar soft-part sarcomas; Beckwith-Wiedemann syndrome (BWS); Bone cancers; Childhood cancers; Ewing sarcoma; Exenteration; Gallium scan; Glomus tumors; Imaging tests; Lacrimal gland tumors; Mantle cell
Boron neutron capture therapy (BNCT) lymphoma (MCL); Medulloblastomas; Myeloma; Nuclear medicine scan; Paget disease of bone; Pineoblastomas; Pneumonectomy; Radionuclide scan; Rhabdomyosarcomas; Richter syndrome; Spinal axis tumors.
u Boron neutron capture
therapy (BNCT) Category: Procedures Definition: Boron neutron capture therapy (BNCT) is a form of radiation therapy that brings together a stable isotope of boron (boron 10) and a beam of low-energy neutrons to target and destroy tumor cells while leaving adjacent tissue undamaged. Cancers treated: Glioblastoma multiforme (GBM); perhaps other brain tumors and skin melanomas Why performed: Treatments for high-grade gliomas are supportive but not curative. Patients with GBM die within three months when left untreated. Standard approaches using surgical resection, radiation therapy, and chemotherapy increase the median survival time to twelve months, with few patients surviving beyond five years. This is the case because tumor cells infiltrate into surrounding brain tissue and are not readily available to the surgeon, and because glioma cells tend to resist radiation and chemotherapy. Moreover, older patients respond poorly to all current therapies, and there has been no significant new approach to GBM treatment since the early 1980’s. Researchers hope that BNCT will offer some improvement. Patient preparation: Patient preparation is standard for radiation therapy. The size and location of the patient’s tumor are determined using imaging studies such as magnetic resonance imaging (MRI) or computed tomography (CT) scans. Prior to neutron targeting, the patient’s skin is marked to position the head correctly. Steps of the procedure: The patient first receives an intravenous injection of boron 10 that has been chemically tagged to bind with the tumor cells. Neutrons created in a nuclear reactor and modified for BNCT treatment are beamed into the targeted tissue. Neutron activity slows during the ensuing collisions, resulting in a transformation into low-energy thermal neutrons. The boron atoms are then able to capture the thermal neutrons, resulting in boron disintegration into energetic lithium 7 and alpha particles. These cancer-destroying particles react in a very small area, thus confining the ensuing tissue destruction to the tumor. 167
Bowen disease After the procedure: There are no special procedures following BNCT. Risks: The risks are minimal because the path length of the boron elements produced during the procedure is small, limiting the destructive properties to the size of a single cell and leaving nontargeted tissue unharmed. Results: Although work on boron neutron capture therapy continues to hold promise, in general it has proved no more successful than standard therapies and so is not now a routine approach to treatment. Richard S. Spira, D.V.M. See also Radiation oncology; Radiation therapies.
u Bowen disease Category: Diseases, symptoms, and conditions Also known as: Bowen’s disease, squamous cell carcinoma in situ Related conditions: Squamous cell carcinoma (SCC), Bowenoid papulosis, erythroplasia of Queyrat Definition: Bowen disease refers to a type of skin cancer considered squamous cell in situ, named after John Bowen, who documented it in 1912. It may arise anywhere on the skin or the mucous membranes. Bowen disease of the glans penis is called erythroplasia of Queyrat. Unlike other premalignant cancers, Bowen disease possesses a low potential for progression to invasive SCC (less than 5 percent) and an even lower potential for metastasis. Another characteristic feature of Bowen disease is its greater propensity to spread over skin than to invade deeper skin layers. Although its malignant potential is low, extensive skin damage can result from delays in treatment. Risk factors: Repeated exposure to the sun and exposure to the human papillomavirus (HPV), particularly HPV 16, and to arsenic have been implicated as risk factors for Bowen disease. However, more often than not, no risk factor can account for disease development. Etiology and the disease process: Bowen disease originates from the overproliferation of squamous cells, the flat superficial cells that make up the upper layer of the skin (epidermis). The entire epidermal layer is involved in Bowen disease. Triggers of this overproliferation include ultraviolet light from chronic sun exposure and exposure to HPV 16. Both can damage or alter cellular deoxyribo168
Salem Health: Cancer nucleic acid (DNA) and the cellular controls regulating cell division. The TP53 gene is particularly susceptible to ultraviolet light damage and has been implicated as one of many possible mechanisms of cancer proliferation apart from Bowen disease. Arsenic has been hypothesized to enhance the carcinogenic properties of ultraviolet irradiation, as it has a propensity to accumulate in the skin as well as the lungs, bladder, kidney and liver. Incidence: The incidence of Bowen disease has been estimated to range from 14 to 142 cases per 100,000. There is also a predilection for whites as well as older adults. Symptoms: Bowen disease manifests in an insidious manner and often mimics other diseases before being diagnosed. It often appears as a reddish, nonpigmented, raised, and scaly lesion that gradually enlarges. The lesion is easily identifiable as it is well demarcated from surrounding normal skin. The most common sites are the head, neck, and extremities, although any part of the skin or mucous membrane may be affected. As the lesion enlarges, it thickens and starts to exhibit crusting, fissures, or ulcers. These lesions are usually solitary unless malignancy is present. Nonetheless, a full skin examination is warranted. Screening and diagnosis: Bowen disease can easily be mistaken for other skin cancers such as invasive SCC and basal cell carcinoma. Therefore, a punch or shave biopsy of the lesion is essential to initiate appropriate treatment irrespective of location. The sample must include the full thickness of the epidermis and, as much as possible, hair structures in deeper layers. Staging of Bowen disease as a squamous cell carcinoma is not applicable unless invasion of the underlying dermis is seen during microscopic examination. Apart from routine skin examinations as part of a regular physical examination, there are no formal screening tests for Bowen disease. Treatment and therapy: Medical and surgical treatments are available, although the latter are preferred. Medical treatment consists of topical treatment with either 5fluorouracil (5-FU) or imiquimod 5 percent cream. 5-FU is used on the lesion after keratolytic therapy (controlled chemical breakdown) or cryotherapy (freezing). Iontophoresis can also be used to deliver the drug by inducing a drug “gradient” within the lesion. In women, 5-FU must not be taken during pregnancy. Radiotherapy using X rays or grenz rays is reserved for patients who cannot undergo surgery or those with multiple lesions. Lesions may also be treated with photodynamic therapy, in which a chemical agent increases photosensitivity only within tumor cells. This microenvironment is then exposed to a specific
Salem Health: Cancer
Bowen disease
Bowen disease may arise anywhere on the skin. Here it is in the groin. (Custom Medical Stock Photo)
wavelength of light, which causes local toxin and oxygen radical release and immune system activation, leading to tumor cell death. There are many surgical options including excision of both the lesion and a small margin (4 millimeters) of normal tissue, Mohs micrographic surgery, curettage and electrodesiccation, cryotherapy, and carbon dioxide laser ablation. Simple excision is preferred for small lesions in nonproblematic areas where deformities can be easily corrected. Mohs micrographic surgery, which is a very precise procedure also used in removing other skin cancers, is more suited to removing larger or recurring lesions and in areas where skin conservation is required for cosmetic reasons or functional preservation (for example, the face or joints). Curettage and electrodesiccation, cryotherapy, and carbon dioxide laser ablation are also effective treatments but do not provide pathologic specimens to confirm tumor eradication, particularly with deeper-lying lesions. Prognosis, prevention, and outcomes: The overall prognosis of patients after treatment is excellent. Recurrence
is often associated with inadequate removal of the lesion or malignant transformation and spread. Some of the sequelae of treatment include skin deformity, scarring, infection, and underlying damage to blood vessels and nerves. Prevention is aimed at decreasing unnecessary ultraviolet light exposure. This includes patient education regarding sun exposure and measures such as wearing protective clothing and sunscreen with an SPF of at least 15 and avoiding exposure to the sun between 10 a.m. and 4 p.m. Aldo C. Dumlao, M.D. u
For Further Information Fossel, Michael B. Cells, Aging, and Human Disease. Oxford, England: Oxford University Press, 2004. Gupta, Renu. Skin-Care. Delhi, India: Diamond Pocket Books, 2000. McCally, Michael. Life Support: The Environment and Human Health. Cambridge, Mass.: MIT Press, 2003. 169
Brachytherapy u
Other Resources
American Cancer Society Treating Bowen Disease http://www.cancer.org/docroot/CRI/content/ CRI_2_4_4X_Treatment_of_bowens_disease_51.asp American Osteopathic College of Dermatology Bowen’s Disease http://www.aocd.org/skin/dermatologic_diseases/ bowens_disease.html See also Complementary and alternative therapies; Penile cancer; Premalignancies; Skin cancers; Vulvar cancer.
u Brachytherapy Category: Procedures Also known as: Sealed source radiotherapy, endocurietherapy Definition: Brachytherapy is a form of radiation treatment in which the radioactive source consists of small pellets or seeds, ribbons, or wire, each about the size of a grain of rice, that are placed into or next to the area being treated. Brachytherapy is from a Greek word meaning “short,” so literally brachytherapy means “short distance treatment.” It is unlike radiation from an external source, such as a machine, in which the radioactive beam is directed at the tumor from outside the body. There are three types of brachytherapy delivery. Intracavity treatment involves radioactive implants that are placed inside a body cavity, such as the uterus. In interstitial treatment, radiation implants are placed directly in the tumor. They are often permanent and used in prostate cancer treatment. In unsealed internal radiation therapy, radioactive materials are injected into a vein or body cavity. Brachytherapy can be either permanent or temporary. Permanent brachytherapy, or low dose rate (LDR) brachytherapy, is often called seed implantation and involves placing small radioactive seeds at or near the tumor and leaving them there permanently. This is typically used in the treatment of prostate cancer. The radioactivity of the seeds decreases over time, and the seeds left inside the patient cause no discomfort or harm. Temporary brachytherapy, or high dose rate (HDR) brachytherapy, involves radioactive seeds that are left in the body only for a specific amount of time and then are removed. Treatments may consist of several visits to the physician to have the seeds placed and removed. This method is used in the treatment of most of the other cancers. 170
Salem Health: Cancer Radiation works by killing cancer cells when they are trying to multiply. The deoxyribonucleic acid (DNA) of cancer cells is more sensitive to radiation than that of normal cells, so the normal cells are able to repair themselves and the cancer cells die. Cancers treated: Brachytherapy is used for many types of cancer in the body, including prostate, cervical, head and neck, ovarian, breast, lung, gallbladder, uterine, and vaginal cancers, as well as anal/rectal tumors and sarcomas. It can also be used to treat noncancerous conditions such as benign tumors and coronary artery disease. Additionally, brachytherapy can be used in conjunction with other cancer treatments, including chemotherapy and external beam radiation. It can be used as both a curative and a palliative form of treatment. Why performed: Brachytherapy has been in use since the early twentieth century, and it has been proven to be safe and effective. It allows a higher dose of radioactivity to be used with decreased risk of damage to healthy tissue, quicker healing times, and decreased risk of infection. In breast brachytherapy, for example, the therapy is quicker than external beam radiation, and it only treats a portion of the breast. Brachytherapy often can be performed in five days as opposed to five to seven weeks. The patient has a better cosmetic result and healthy tissue is preserved. Patient preparation: Before the treatment begins, patients meet with the physician and receive instructions on how to care for themselves after the treatment. The physician will determine what tests should be done prior to brachytherapy, which may include blood tests, electrocardiograms (ECG or EKG), and X rays. The actual prepping of the patient depends on where the seeds are being placed. Typically, a radiation oncologist, a radiation physicist, a dosimetrist, and a radiation therapist are involved in planning the treatment. The radiation oncologist determines the type of treatment needed and is responsible for the overall treatment plan, including the area to be treated and the dose to be delivered. The physicist calculates the dose to be prescribed. The dosimetrist assists in dose calculation and helps in delivering the prescribed dose. The radiation therapist operates the equipment and delivers the dose. Through special computer programs, the dose, duration, and delivery method of the treatment are determined. Without this specific calculation, the cancer cells might receive too little radiation and the normal tissue could receive too much. Steps of the procedure: The steps of the procedure also vary depending on where the seeds are being placed in the body. The seeds are generally inserted into the site of the
Salem Health: Cancer tumor through a needle or catheter. Sometimes a device to hold the seeds is placed near the tumor. Often, X rays, ultrasound, computed tomography (CT) scans, or even surgery is used to help position and verify placement of the radioactive material or device. Some doses are delivered to the patient on an outpatient basis, in which radiation is delivered to the tumor in a short amount of time and then the delivery device is removed and the patient goes home. The patient may return at intervals for more treatment. Alternatively, a patient may spend a couple of nights in the hospital so that the delivery device can remain in place and the radioactivity can be delivered at a continuous rate. These patients are placed in private rooms, usually with limited or no visitors allowed. The hospital staff will continue to take care of the patient, but they limit the amount of time that they spend with the patient in order to keep their radiation exposure low. A patient may have an intravenous line inserted in order to receive medications. Sedatives or anesthesia may also be used to place the delivery device, again depending on the location of the treatment. After the procedure: Patients typically can go home after the LDR procedure. The physician will give the patient detailed instructions for self-care at home, which may include limiting contact with pregnant women or children for a limited amount of time so as not to expose them to the radioactivity. The patient may have some pain, swelling, or bleeding at the site of the procedure. Educational materials may be very helpful to the patient and family after the procedure. Side effects and precautions can be outlined. Generally, the patient is to avoid heavy lifting or strenuous physical activity for a few days after the procedure. Sometimes the radiation precautions include instructing the patient to sleep alone for a period of time, to avoid sexual relations for a period of time, and to use tweezers, not bare hands, to pick up any seed that may become dislodged. Instructions on what to do with a dislodged seed are also given. HDR patients are usually in the hospital for forty-eight to seventy-two hours and then are discharged once the radiation device is removed. They also receive detailed instructions on how to protect family members from exposure and to watch for side effects such as pain and bleeding. Risks: Like the preparation of the patient and the steps of the procedure, the risks from brachytherapy also vary depending on the area treated. Although relatively safe, brachytherapy is not totally without risks. Patients with permanent brachytherapy seeds continue to give off small amounts of radiation for several weeks. With this type of
Brachytherapy treatment, there is a risk that the seeds will move out of place. Patients are often told to strain their urine at home in case in seeds do migrate. Patients are given special instructions from their doctor about protecting family members from exposure. Brachytherapy for prostate cancer can cause sexual dysfunction such as impotence and bowel problems such as diarrhea, although these are not very common. Urinary irritation is a more common side effect because the urine stream becomes obstructed by swelling in the prostate after therapy. A urinary catheter or Foley catheter is placed to allow urine to flow. The prostate usually returns to normal size and the blockage disappears after several weeks, and the catheter can then be removed. Patients may continue to have some urinary burning for a few weeks, but this also resolves. Results: The physician may order scans or X rays after brachytherapy in order to determine if the treatment was successful. The effectiveness of brachytherapy varies depending on the location of the treatment and the type of cancer that was treated. It has proven to be effective in many types of cancer, especially cervical and prostate cancer. In early prostate cancer, brachytherapy offers ten-year survival rates comparable to surgical removal of the prostate, according to several studies. In general, patients have fewer side effects and a quicker recovery time with this therapy as compared to external beam radiation or surgery. There is also less risk of infection than with surgery. As a result, patients typically have a better quality of life with this procedure, which is easier to tolerate. Michelle Kasprzak, R.N., B.S.N., O.C.N. u
For Further Information Merrick, G. S., et al. “Long Term Rectal Function After Permanent Prostate Brachytherapy.” Cancer Journal 13, no. 2 (March/April, 2007): 95-104. Mitchell, I. “Patient Education at a Distance.” Radiology 13, no. 1 (February, 2007): 30-34. Nag, Subir, ed. Principles and Practices of Brachytherapy. Malden, Mass.: Blackwell, 1997.
u
Other Resources
American Brachytherapy Society (ABS) http://www.americanbrachytherapy.org American Cancer Society http://www.cancer.org National Cancer Institute http://www.cancer.gov 171
BRAF gene See also Afterloading radiation therapy; Anal cancer; Carcinomas; Cervical cancer; Endometrial cancer; Iridium seeds; Mayo Clinic Cancer Center; Neurologic oncology; Radiation oncology; Radiation therapies; Rhabdomyosarcomas; Veterinary oncology.
u BRAF gene Category: Cancer biology Also known as: BRAF1, RAFB1, v-raf murine sarcoma viral oncogene homolog B1 Definition: BRAF is an internal part of a cellular signaling pathway. This signaling pathway results in cell growth when the correct chemical message is sent. The mutated form of the BRAF gene has a single base (letter) of deoxyribonucleic acid (DNA) changed; this changes the activity of the BRAF protein. This mutant BRAF protein is broken and is continuously on, sending growth signals even when there are no chemical messages and causing runaway growth of cells. The result is like a broken light switch that will not turn off. Etiology and symptoms of associated cancers: The BRAF protein is central to causing many types of cancer, including melanoma, colon cancer, ovarian cancer, thyroid cancer, and gliomas. Knowledge of the BRAF gene, which was first described as a proto-oncogene in 2002, is useful in diagnosing cancer and deciding what type of treatment to use. The advanced state of knowledge in modern biology and medicine makes it likely that drugs that attack cancers with BRAF mutations will be quickly developed. Tumors are called benign (not harmful) or malignant (harmful). Benign tumors can acquire mutations that change them into malignant cancers. Experts believe that cancer requires multiple steps to form. Many normal functions of cells need to be damaged to create a malignant cancer. Cellular functions typically damaged are cell growth (unregulated cell growth), telomere maintenance (cell aging), apoptosis (cell death), angiogenesis (the ability to grow blood vessels), and metastasis (the ability of cells to detach from one part of the body and migrate to another). BRAF mutations primarily affect the first of these functions, cell growth. When BRAF is mutated in a cell, the cell receives a continuous signal to grow and divide. This signal from BRAF also has a smaller effect of reducing the probability of cells dying by apoptosis, an effect promoting metastasis, and effects promoting angiogenesis. BRAF mutations are often found in benign growths. 172
Salem Health: Cancer Mutations of other genes are needed to destroy the remaining cell functions and make a growth malignant. For example, the destruction of the TP53 gene (also known as p53) will help the cancer overcome cell aging (which normally slows down the overgrowing cells) and apoptosis (which normally kills off some of the overgrowing cells). For comparison, TP53 mutations are rarely found in benign growths and are almost always found as secondary changes in cancers. Because BRAF mutations are found in benign and malignant growths, many people believe BRAF is an early change that eventually leads to malignant cancers. Cancers that seem to begin with BRAF mutations also seem to end up being among the most malignant. Even though BRAF is associated with the worst types of malignancies, the silver lining is that since BRAF mutations happen early, while the tumors are still benign, the BRAF mutation can serve as an early warning. BRAF mutation is not found in all cancer but only in cancers of certain tissues. Most of these tissues are what doctors call adenoid tissues. Specifically, BRAF mutation has been found in melanoma (skin), glioma (nerve), thyroid, ovarian, and colon cancer. Researchers have shown that 80 percent of the benign nevi (moles) studied carried the BRAF mutation and that 66 percent of malignant melanomas studied carried the BRAF mutation. In benign gliomas, BRAF mutation is rarely observed, but in malignant gliomas, the BRAF mutation was almost always observed. Testing and treatment: Standard tests of DNA can be done on blood or tumor tissue samples to detect the BRAF mutation. While these tests are very reliable, the knowledge of the BRAF gene mutation and the tests for it are new and are not yet widely available. BRAF mutation tests will help doctors determine the exact type of cancer, how dangerous it is, and what types of treatment to use. One drug in testing is BAY 43-9006. This drug seems to reverse the effect of BRAF mutation and stop the growth of cells. It also seems to kill the cancer cells by restoring normal cell death (apoptosis). Although only laboratory experiments have been done, some researchers expect that actual tests in people with cancers will show that the drug will not only stop the growth of the cancers but may kill the cancers entirely. History: The discovery of the BRAF mutation is a direct result of the Human Genome Project. In the 1990’s the Human Genome Project sequenced the human genome and described the complete set of about 30,000 human genes, the instructions for the body. In the 2000’s the Cancer Ge-
Salem Health: Cancer
Brain and central nervous system cancers
nome Project started examining all 30,000 genes in cancers to find broken genes. One result was the discovery of the BRAF gene mutation in 2002. Christopher Pung, B.S., C.L.Sp. (CG)
tumors of the cerebellum, and central neuroblastomas, which affect the brain cortex. The naming system for pediatric brain tumors is still evolving and remains controversial.
u
Risk factors: Chemicals such as vinyl chlorides, aromatic hydrocarbons, and N-nitroso compounds in cigarettes; ionizing radiation; electromagnetic fields; and viral infections have been suggested as possible environmental risk factors. Some brain cancers appear to be more common in people working with radiation and chemicals, such as employees of nuclear plants and oil refineries. However, none of these environmental factors have been conclusively shown to cause brain cancer. Genetic risk factors include inherited diseases such as tuberous sclerosis and von Hippel-Lindau disease.
For Further Information Begley, Sharon. “Science Journal: Nature’s Quirks Limit DNA-Based Drug Possibilities.” Pittsburg PostGazette, November 11, 2005. Davies, H., et al. “Mutations of the BRAF Gene in Human Cancer.” Nature 417 (2002): 949-954. Shaw, Gina. “BRAF Mutations Predict Tumor Response.” Drug Discovery and Development 8 (2005): 8. u
Other Resources
Atlas of Genetics and Cytogenetics in Oncology and Haematology BRAF http://atlasgeneticsoncology.org/Genes/ BRAFID828.html The Human Genome Melanoma and the BRAF Gene http://genome.wellcome.ac.uk/doc_WTD020812.html See also Genetics of cancer.
u Brain and central nervous
system cancers Category: Diseases, symptoms, and conditions Also known as: Brain tumors, central nervous system (CNS) tumors, gliomas, glioblastomas, astrocytomas, meningiomas, neuromas Related conditions: Seizures, psychiatric symptoms (including abnormal personality and behavioral characteristics), loss of memory and cognition Definition: Brain and central nervous system cancers are masses of abnormal cells (malignant tumors) in the brain and central nervous system that grow rapidly and can invade surrounding normal tissue. Brain tumors are named for both the type of cell from which they arose and their location in the brain. For example, schwannomas are named after the Schwann cells, astrocytomas after astrocytes, oligodendrogliomas after oligodendrocytes, meningiomas after the meninges or brain membranes, and pinealoblastomas after the pineal gland. Exceptions are medulloblastomas, which are undifferentiated neuroectodermal
Etiology and the disease process: The causes of brain and central nervous system cancers are still unproven. Environmental, genetic, medical, and lifestyle factors may all play a role in causing these cancers. Brain tumors can be primary or secondary. Primary tumors originate in the brain and are rarer than secondary brain tumors, accounting for around one-fourth of all brain tumors. Once they occur, primary brain tumors rarely metastasize to other tissues beyond the spinal cord. Examples of primary brain tumors are schwannomas, astrocytomas, medulloblastomas, meningiomas, and oligodendrogliomas. Secondary or metastatic tumors originate elsewhere in the body and migrate or metastasize to the brain. The types of cancer most likely to metastasize to the brain are breast cancer, lung cancer, melanoma, and colon cancer. Nasopharyngeal cancer can also metastasize to the brain via the cranial nerve or through openings in the bone at the base of the skull called foramina. Incidence: The annual incidence of primary invasive central nervous system tumors in the United States is 6.6 per 100,000 people, with an estimated 4.7 deaths per 100,000 people annually. Approximately 20,500 new cases of brain and central nervous system cancers occurred in the United States in 2007, as well as an estimated 12,740 deaths from these cancers. Brain tumors account for 85 to 90 percent of all primary central nervous system tumors. Primary brain tumors have a higher incidence in whites than in blacks and are more common in men than in women, with three out of five sufferers being men. Brain tumors usually arise in early or middle adult life and are most common in people older than sixty-five. However, brain cancer can occur at any age. Primary brain tumors are rarer than secondary brain tumors, with a ratio of 1 primary brain tumor to every 3 sec173
Brain and central nervous system cancers
Salem Health: Cancer
ondary brain tumors. Some experts put this ratio at closer to 1:10, attributing the increased detection of secondary tumors to more sensitive imaging methods. The most common primary brain tumors are astrocytomas, glioblastomas, meningiomas, and other mesenchymal tumors, which make up around 65 percent of all primary brain tumors. The most common primary spinal tumors are schwannomas, meningiomas, and ependymomas, accounting for 79 percent of primary spinal tumors. Secondary or metastatic brain tumors occur in 20 to 40 percent of brain cancer patients. About 80 percent of secondary tumors occur in the cerebral hemispheres, 15 percent in the cerebellum, and 5 percent in the brain stem. Multiple metastases to the brain are more common than solitary metastases, occurring in more than 70 percent of cases.
(including blurred vision, double vision, or loss of peripheral vision), loss of memory and cognition, personality or behavioral changes, abnormal breathing rates, dizziness, nausea or vomiting, loss of hearing, and hormonal disorders. In one study of brain tumors and seizures, seizures were observed in more than 38 percent of patients with primary brain tumors and in 20 percent of patients with cerebral metastases. Oligodendrogliomas are more likely than other types of central nervous system tumors to be associated with seizures. Screening and diagnosis: The first step of brain tumor screening involves a neurological exam to test vision, hearing, balance, coordination, and reflexes. If the neurological exam results warrant further testing, the doctor may order brain imaging scans, such as computed tomography (CT) and magnetic resonance imaging (MRI) scans, which produce pictures of the brain in which tumors can be distinguished by means of dyes or magnetic fields. Com-
Symptoms: Symptoms of brain tumors include persistent headaches that become more intense and frequent, seizures, problems walking and speaking, vision problems
Incidence of Brain and Central Nervous System Cancer per 100,000 People, by Gender 10 Men
9
Women
8.3 8 7 6
5.9
5
6.0
4.7
4.9 3.9
4
3.5
3.5 3.0
3
2.2 2 1 0 White
Hispanic
Black
Asian/Pacific Islander
American Indian/ Alaska Native
Source: Data from National Cancer Institute, Surveillance Epidemiology and End Results, Cancer Stat Fact Sheets, 2008 Note: Based on cases diagnosed in 2000-2004
174
Salem Health: Cancer puted tomography is better at detecting bone calcification and skull lesions. Magnetic resonance imaging is better for detecting soft-tissue and spinal cord tumors. Other tests include an angiogram, in which a dye is injected into the blood to highlight the blood vessels in and around the brain, X-ray scans of the head and skull to reveal changes to skull bones and calcium deposits associated with brain tumors, and positron emission tomography (PET), which identifies areas of abnormal brain metabolism. The discovery of genetic mutations (changes in specific genes) that are linked to different types of cancers has opened the door to future genetic screening for at-risk individuals. A genetic screen involves taking a blood sample and analyzing the deoxyribonucleic acid (DNA) in the sample for genetic mutations that are known to cause a specific type of cancer. When a tumor is detected on a brain scan, a biopsy is usually performed to make a diagnosis. A biopsy involves taking a sample of the tumor; this can be done in a separate procedure or during surgery to remove the tumor. The tumor can be biopsied by open craniotomy, in which the cranium or skull is opened to expose the brain, allowing a sample of the tumor to be surgically removed. Hard-toreach tumors can be sampled by means of a needle biopsy. A small hole, known as the “burr” hole, is drilled in the cranium, and tumor cells are extracted with a narrow-bore needle. The tumor sample is frozen and cut into very thin slices, which are then examined under a microscope. This allows the medical team to confirm the presence of a tumor and determine the specific type of tumor. Additional tests may also be performed to help pinpoint the tumor type. There is no standard method for staging brain tumors. Along with the tumor grade, the type of cell from which the tumor originated and the location in the central nervous system are used for classifying the tumor. Grade I tumors grow slowly and rarely spread to other tissues. The following types of brain tumors are classified as Grade I: pilocytic astrocytomas, Grade I meningiomas, and Grade I ependymomas. Grade II tumors typically grow slowly but may spread to other tissues. Grade II tumors include diffuse astrocytomas, Grade II meningiomas, oligodendrogliomas, Grade II ependymomas, oligoastrocytomas (made up of a mixture of oligodendrogliomal and astrocytomal cells), pinealcytomas, and craniopharyngiomas. Grade III tumors contain fast-growing cells that often spread to other tissues. Grade III tumors include anaplastic astrocytomas, anaplastic oligodendrogliomas, anaplastic ependymomas, anaplastic oligoastrocytomas, and pinealoblastomas. Grade IV tumors grow rapidly, spread aggressively, and contain cells that appear very different from normal cells.
Brain and central nervous system cancers Grade IV tumors include gliobastomas and medulloblastomas, which usually occur in children and adults aged twenty-one to forty. Treatment and therapy: The most common treatment for brain and central nervous system cancers involves surgery to remove as much of the tumor as possible without disrupting neurological function. Surgery usually does not result in the removal of all tumor tissue. In addition, some tumors are located deep in the brain and cannot be reached without considerable damage to the surrounding tissue. These tumors are sometimes diagnosed without conducting a biopsy and treated by nonsurgical means. Radiation treatment and chemotherapy can be used to remove cancer cells remaining after surgery and to treat deep-seated tumors that are not amenable to surgical removal. Radiation therapy is effective for a wider range of brain and spinal cord tumors than chemotherapy. Radiation can enhance the cure rate and prolong disease-free survival. A common type of radiation treatment is external beam radiation therapy (EBRT). Chemotherapy has been shown to prolong disease-free survival in patients with gliomas, medulloblastomas, and some germ-cell tumors. Chemotherapy includes the use of dexamethasone, mannitol, furosemide, and nitrosourea. Anticonvulsants are also used to treat cancer patients with seizures. The majority of brain tumors are accompanied by multiple metastases. These can be treated with a combination of surgery or radiosurgery and whole-brain radiation therapy (WBRT). Radiosurgery is useful for lesions that have a diameter smaller than 3 centimeters. Corticosteroids and anticonvulsants can also be used as needed. Chemotherapy is not as widely used for metastatic brain tumors but may be effective for brain metastases from chemosensitive primary tumors. New therapies that are currently being tested include the use of tyrosine kinase receptor inhibitors, farnesyl transferase inhibitors, viral-based gene therapy, and oncolytic viruses. Patients with tumors that do not respond well to the commonly used treatments can look into clinical trials using combinations of novel therapies with EBRT. Surgery to remove brain tumors can sometimes result in the damage of normal brain tissue. This can cause partial paralysis, changes in sensation, muscle weakness, and defects in thinking and language function. These patients may be referred for physical and speech therapy to regain muscle and language functions, respectively. Follow-up visits are an important part of patient care and usually occur every three to four months for the first two to three years after treatment, then once or twice a year after that. The doctor will discuss treatment side effects, review 175
Brain scan medical history, and conduct various tests to determine if the cancer has recurred or metastasized to other parts of the body. Prognosis, prevention, and outcomes: A cancer patient’s prognosis depends on age (whether younger or older than sixty), the number and location of tumors in the brain and spinal cord, the rate of tumor growth and metastasis, and the tumor’s response to treatment. The prognosis is better for brain metastases from breast cancer and worse for brain metastases from colon cancer. When doctors discuss survival rates, they are referring to the percentage of people with a specific type and stage of cancer who survive for a predetermined period of time after their diagnosis. A common statistic is the five-year survival rate. Doctors may talk about the percentage of people who are alive, the percentage who are symptom-free, or the percentage who are disease-free five years after diagnosis. These numbers are averages for large groups of people and do not predict the specific outcome for an individual patient. Because the causes of brain and central nervous system cancers are not well established, prevention strategies are still evolving. As with other cancers, quitting smoking, maintaining a healthy diet, and exercising probably have beneficial and preventive effects. A novel therapy that has been approved in Switzerland under the brand name DCVax-Brain involves vaccination with dendritic cells that recognize molecules on an individual patient’s tumor cells. When examining outcomes for brain cancer survivors, it is important to also consider their quality of life. A survivor’s quality of life has been directly linked to cognitive impairment, especially defects in speech and language. Ing-Wei Khor, Ph.D. u
For Further Information Connelly, J. M., and M. G. Malkin. “Environmental Risk Factors for Brain Tumors.” Current Neurology and Neuroscience Reports 7 (2007): 208-214. Hutter, A., et al. “Brain Neoplasms: Epidemiology, Diagnosis, and Prospects for Cost-Effective Imaging.” Neuroimaging Clinics of North America 13 (2003): 237-250. Ricci, P. E. “Imaging of Adult Brain Tumors.” Neuroimaging Clinics of North America 9 (1999): 651-669. Wen, P. Y., P. M. Black, and J. S. Loeffler. “Treatment of Metastatic Cancer.” In Cancer: Principles and Practice of Oncology, edited by V. T. DeVita, Jr., S. Hellman, and S. A. Rosenberg. 6th ed. Philadelphia: Lippincott Williams & Wilkins, 2001. 176
Salem Health: Cancer u
Other Resources
Cedars-Sinai Brain Tumors http://www.csmc.edu/5192.html MayoClinic.com Brain Tumor http://mayoclinic.com/health/brain-tumor/DS00281 National Cancer Institute Brain Tumor http://www.cancer.gov/cancertopics/types/brain Revolution Health Brain Cancer http://www.revolutionhealth.com/conditions/cancer/ brain-cancer/ WebMD http://www.webmd.com See also Acoustic neuromas; Astrocytomas; Ataxia telangiectasia (AT); Carcinomatous meningitis; Cell phones; Cognitive effects of cancer and chemotherapy; Craniotomy; Gliomas; Leptomeningeal carcinomas; Meningeal carcinomatosis; Meningiomas; Neuroblastomas; Neuroectodermal tumors; Neuroendocrine tumors; Neurofibromatosis type 1 (NF1); Neurologic oncology; Oligodendrogliomas; Orbit tumors; Pheochromocytomas; Primary central nervous system lymphomas; Schwannoma tumors; Spinal axis tumors; Spinal cord compression; Turcot syndrome; Von Hippel-Lindau (VHL) disease; Wilms’ tumor aniridia-genitourinary anomalies-mental retardation (WAGR) syndrome and cancer.
u Brain scan Category: Procedures Definition: Computed tomography (CT) scan and magnetic resonance imaging (MRI) are two widely used methods of scanning the brain to distinguish normal tissue from abnormal tissue (tumors or masses). The CT scanner uses X rays and a type of ionizing radiation (dye), to acquire images of bone and tissue. MRI uses nonionizing radio frequency signals to acquire its images and is best suited for noncalcified (soft) tissue. Both CT and MRI scanners generate multiple two-dimensional cross-sections, or “slices,” of tissue and produce three-dimensional reconstructions. For purposes of tumor detection and identification, MRI is generally superior. However, CT usually is more widely available, faster, and much less expensive,
Salem Health: Cancer
Brain scan
This series of MRI images, from left to right, show a brain tumor shrinking after radiation therapy, but with development of metastatic brain disease (far right). The scans were taken at the beginning of treatment and at six and fifteen months. (Custom Medical Stock Photo)
and it may be less likely to require the person to be sedated or anesthetized. If cancer is suspected, then the CT scan will provide X-ray images of the brain or other internal organs to detect masses or tumors. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. Acomputer combines the images by “stacking” them on top of each other to offer an exact three-dimensional rendering. MRI is a procedure using a magnet and radio waves to send a series of detailed images of the brain to a computer. A computer then produces cross-sectional or threedimensional images for evaluation. A substance called gadolinium may be injected into the patient through a vein. The gadolinium collects around the cancer cells so that they show up brighter in the picture. This procedure is also called nuclear magnetic resonance imaging (NMRI).
sensation throughout the body and a metal taste in the mouth. Only the head will be covered by the scanner, and those who experience claustrophobia generally do not have problems with a brain scan. After the procedure: Patients are not restricted after this procedure and may eat and drive as normal.
Why performed: Brain scans are ordered by physicians to offer the clearest information available about the brain. The method of scanning depends on the patient’s history and examination and the choice by the physician for diagnostic testing.
Risks: The MRI examination poses almost no risk to the average patient; however, if sedation is necessary, a nurse or technologist will monitor vital signs to avoid excessive sedation. The magnetic field is not harmful to the patient, but metal devices nearby can create malfunction in the MRI. If dye is injected, then there is a rare risk of mild allergic reaction. The CT scan poses a slight risk of cancer as a result of the exposure to radiation. Studies have shown this risk is equivalent to the amount of radiation to which an average person is exposed in three years from other, unavoidable sources. There is a risk to an unborn fetus; therefore CT scanning is not recommended for pregnant women. Nursing mothers must wait twenty-four hours after the dye is injected to return to nursing. There is always a slight chance of cancer from radiation exposure, but the benefit of an accurate diagnosis far outweighs the risk.
Patient preparation: If the brain scan involves injecting or ingesting a dye, then the patient may be asked to avoid eating or drinking four hours before the exam. All jewelry must be removed prior to the brain scan.
Results: The brain scan will be read by a neuroradiologist, and the results will be shared with the physician to discuss with the patient. Robert J. Amato, D.O.
Cancers diagnosed: Brain tumor, metastasized cancer
Steps of the procedure: The patient will be asked to lay down, placing the head in a stabilizer, and remain very still. If contrast (dye) is required, then it will be injected through the intravenous (IV) line that was placed by a radiology nurse or technologist prior to the exam. During the injection, it is normal for patients to experience a warm
u
For Further Information Buthiau, Didier, and David Khayat. CT and MRI in Oncology. New York: Springer-Verlag, 1998. Lee, Howard S., et al. Cranial and Spinal MRI and CT. 4th ed. New York: McGraw-Hill Professional, 1999. 177
BRCA1 and BRCA2 genes Wolbarst, Anthony Brinton. Looking Within: How X-Ray, CT, MRI, Ultrasound, and Other Medical Images Are Created, and How They Help Physicians Save Lives. Berkeley: University of California Press, 1999. See also Astrocytomas; Brain and central nervous system cancers; Computed tomography (CT) scan.
u BRCA1 and BRCA2 genes Category: Cancer biology Also known as: Breast cancer susceptibility genes; breast cancer 1, early onset; breast cancer 2, early onset Definition: BRCA stands for breast cancer susceptibility. BRCA1, the first breast cancer susceptibility gene, was identified and cloned in 1994. A second breast cancer susceptibility gene, BRCA2, was discovered soon after. Identification of BRCA1 and BRCA2 as breast cancer susceptibility genes has had a profound impact on understanding the disease. The immediate clinical use of their discovery for both diagnosis and accurate assessment of increased risk through screening has been one of the foremost success stories in the fight against cancer. Familial disease: Less than 5 percent of breast cancers are hereditary, but more than 90 percent of hereditary breast cancers are caused by mutations in either BRCA1 or BRCA2. Each year approximately 200,000 women in the United States are diagnosed with breast cancer, and about 5 to 10 percent of these women have an inherited mutant BRCA1 or BRCA2 gene. The mutations can be inherited from either the maternal or the paternal side of the family. Mutations in BRCA1 and BRCA2 increase a woman’s lifetime risk of not only breast cancer but also ovarian, colon, and Fallopian tube cancers. Women with an inherited alteration in one of these genes have an increased risk of developing these cancers before the menopause. Altered BRCA2 poses a greater risk in men than altered BRCA1. Men with altered BRCA2 are at a higher risk of breast cancer and prostate cancer. Alterations in the BRCA2 gene have also been associated with increased risks of lymphoma, melanoma, and cancers of the pancreas, gallbladder, bile duct, and stomach in both men and women. Risks and incidence: Estimates of lifetime risks suggest that approximately 12.9 percent of women in the general population will develop breast cancer, as compared with estimates of 78 percent of women with an altered BRCA1 or BRCA2 gene. The ovarian cancer risk is 49.4 percent in carriers versus 1.7 percent in the general population. 178
Salem Health: Cancer Among men, the breast cancer risk is 5.8 percent for carriers versus 0.01 percent in the general population. In carriers, risks for colon, pancreatic, and stomach cancers are also elevated twofold, threefold, and fourfold, respectively, with no increase in prostate cancer risk. Additionally, in BRCA1 mutation carriers, the lifetime risk of developing cancer of the breast can be as high as 85 percent and that of developing ovarian cancer as much as 42 to 63 percent. In BRCA2 carriers, the lifetime risk of developing breast cancer is as high as 86 percent and that of developing ovarian cancer about 27 percent. The likelihood that breast or ovarian cancer is linked with BRCA1 or BRCA2 mutations is highest in families with a history of multiple cases of breast and ovarian cancer, particularly involving a mother, sister, or daughter; diagnosis of breast cancer before the age of thirty-five; presence of male breast cancer in the family; two or more primary cancers such as breast and ovarian cancers or bilateral breast cancer (separate cancers in each breast) in an individual; other multiple cancers in the family, especially prostate cancer; and an Ashkenazi (central and eastern European Jewish) background. It is important to note that not every woman with this sort of background will carry a defective BRCA1 or BRCA2, and not every cancer that occurs in such families will be due to a BRCA1 or BRCA2 defect. Additionally not all women who carry a BRCA1 or BRCA2 mutation will develop breast or ovarian cancer. Mutations in BRCA1 account for breast or ovarian cancers in 45 percent of families with a history of breast cancer and up to 90 percent in families with a history of both breast and ovarian cancers. BRCA2 mutations account for breast cancer in about 35 percent of families with a history of breast cancer. Studies suggest that women who develop breast cancer before the age of fifty have a one in four chance of carrying a BRCA1 or BRCA2 mutation if they have any relative who also develops the disease before the age of fifty. There is a 50 percent chance that mutant carriers will transmit the mutated gene to their offspring. BRCA1-related breast cancer appears to be more aggressive than other types of breast cancer and has a poorer prognosis, and most BRCA1-related ovarian cancers are of the invasive type. Some characteristics of hereditary breast cancer, such as how it occurs at an earlier age, more often affects both breasts, and is associated with other cancers, make it clinically distinct from sporadic cancer. BRCA1 and BRCA2 were identified by linkage analysis of families with multiple cases of early-onset breast and ovarian cancer. BRCA1 is 5,592 kilobases long with 24 exons, and BRCA2 is twice as long with 10,254 kilobases and 27 exons. More than one hundred different alterations scattered throughout BRCA1 and BRCA2 have been iden-
Salem Health: Cancer tified. These alterations tend to be distinct, and in general, most families have a unique alteration. Mutations anywhere along either gene are associated with an increased risk of breast cancer. Some evidence suggests that mutations in the 5′ end of BRCA1 and mutations in exon 11 of BRCA2 might be associated with ovarian cancer. Alterations in certain regions of the BRCA2 gene are known to predispose individuals to a greater risk of ovarian cancer in women and prostrate cancer in men, as compared with alterations in other parts of the gene. This suggests differences in patterns of cancer between individuals with a BRCA1 mutation versus a BRCA2 mutation. Of the more than one hundred alterations identified in each gene (BRCA1 and BRCA2), three alterations have been identified in Ashkenazi Jewish families with a history of breast cancer. These alterations are 185deIAG and 5382insC (BRCA1) and 6174deIT (BRCA2). The estimated frequencies of the three alterations in the general Ashkenazi population are 1.0 percent, 0.1 percent, and 1.4 percent, respectively. Cellular function: BRCA1 and BRCA2 are tumorsuppressor genes, and the BRCA proteins are involved in a multitude of key cellular processes. Research has demonstrated the involvement of BRCA1 and BRCA2 proteins in complexes that activate repair of double-strand breaks and initiate homologous recombination, suggesting a key role of BRCA proteins in maintaining genome stability and integrity. In response to deoxyribonucleic acid (DNA) damage, BRCA1 is engaged in the transcriptional regulation of several genes such as P21 (CDKN1A) and GADD45, which activate cell-cycle check-point induced replication arrest to allow for repair. It is unclear why a defect in BRCA predisposes predominantly to cancer of the breast and ovary, even though the known functions of BRCA proteins are essential to all cell types. Whether estrogen, a known promoter of sporadic breast cancer, affects the risk of BRCA1- and BRCA2-related breast cancers is not clear. Given that factors that contribute to enhanced exposure to estrogen, such as early onset of menarche and late menopause, correlate with a higher incidence of breast cancer and that premenopausal oophorectomy (the surgical removal of the ovaries) exerts a preventive effect, an association is suggested between BRCA1 and BRCA2 and estrogen receptor alpha (ERα). Prevention: The best opportunity to reduce mortality is through early detection. Preventive mastectomy and preventive oophorectomy to reduce the risk of breast cancer and ovarian cancer respectively are possible options. Although oophorectomies are usually performed to reduce ovarian cancer risk, having an oophorectomy before meno-
BRCA1 and BRCA2 genes pause also reduces the risk of breast cancer. Removal of ovaries is associated with a decrease in the production of the hormones estrogen and progesterone, which play a major role in breast cancer progression. For a premenopausal woman with a BRCA mutation, oophorectomy reduces the risk of breast cancer by about 50 percent, and it reduces the risk of ovarian cancer by 80 percent, irrespective of the menopausal status. However, it is important to note that prophylactic surgery reduces but does not eliminate the risk of cancer and carries additional risks related to surgery. Behaviors that can reduce breast cancer risk include regular exercising, decreased alcohol consumption, early childbirth, and breast-feeding for more than twelve months—although effects of these on BRCA mutation carriers are yet unknown. Even though tamoxifen is known to reduce the risk of invasive breast cancer by 49 percent in patients with an increased risk of developing the disease, limited data are available regarding the use of tamoxifen for chemoprevention in women with BRCA1 and BRCA2 alterations. Existing data suggest that use of tamoxifen reduces the risk of breast cancer in BRCA carriers and is recommended for chemoprevention. Banalata Sen, Ph.D. u
For Further Information Bishop, D. T. “BRCA1 and BRCA2 and Breast Cancer Incidence: A Review.” Annals of Oncology 10, suppl. 6 (1999): S113-S119. Venkitaraman, A. R. “Cancer Susceptibility and the Functions of BRCA1 and BRCA2: AReview.” Cell 108, no. 2 (2002): 171-182.
u
Other Resources
Genetics Home Reference http://ghr.nlm.nih.gov HUGO Gene Nomenclature Committee Symbol Report: BRCA1 http://www.genenames.org/data/ hgnc_data.php?hgnc_id=1100 National Cancer Institute Genetics of Breast and Ovarian Cancer http://www.cancer.gov/cancertopics/pdq/genetics/breastand-ovarian National Human Genome Research Institute http://www.genome.gov See also Ashkenazi Jews and cancer; Breast cancer in men; Breast cancer in pregnant women; Breast cancers; 179
Breakthrough pain Carcinomatosis; Clinical breast exam (CBE); Ductal carcinoma in situ (DCIS); Estrogen-receptor-sensitive breast cancer; Family history and risk assessment; Genetic testing; Genetics of cancer; Hereditary cancer syndromes; Hormonal therapies; Invasive ductal carcinomas; Invasive lobular carcinomas; Lobular carcinoma in situ (LCIS); Medullary carcinoma of the breast; Molecular oncology; Mutagenesis and cancer; Oophorectomy; Ovarian cancers; Ovarian epithelial cancer; Pancreatic cancers; Risks for cancer; Salpingectomy and salpingo-oophorectomy; Tumor markers.
u Breakthrough pain Category: Diseases, symptoms, and conditions Also known as: Episodic or incident pain Related conditions: Breakthrough pain may be related to tumor progression or nerve compression as a result of cancer. It may also be a result of a treatment, including surgery, or a variety of painful disorders, such as arthritis. Definition: Breakthrough pain is a transient and intermittent flare of severe pain that “breaks through” analgesic medications. Risk factors: Anyone undergoing treatment for trauma, illness, and other painful conditions is at risk for breakthrough pain. Cancer patients—particularly those with advanced disease—are at high risk for breakthrough pain. Etiology and the disease process: Breakthrough pain generally is the result of whatever is causing a patient’s baseline persistent pain. Incidence: Approximately one-half to two-thirds of cancer patients and up to 86 percent of people taking painreducing medication for chronic pain experience breakthrough pain. The frequency of breakthrough pain varies among individuals; most patients with cancer-related pain have several episodes daily. Often, breakthrough pain flares up just before the patient is to take the next dose of pain medication; this is termed end-of-dose failure. Symptoms: The severity, duration, and cause of breakthrough cancer pain vary among patients. Typically, breakthrough pain happens fast. The average duration is approximately thirty minutes, but it may last from seconds to hours. Breakthrough pain is often unpredictable; it may occur spontaneously or it may be triggered by an activity, such as coughing or moving. It may manifest as an intensified or all-over dull sensation, or it may be a localized sharp pain. 180
Salem Health: Cancer Screening and diagnosis: There is no independently validated measurement available for the evaluation of breakthrough pain. Treatment and therapy: Breakthrough pain medications are generally short-acting and work rapidly to control sudden flares of pain. Breakthrough pain medications may be administered in several ways: orally, by injection, intravenously, under the tongue (sublingually), rectally, or transmucosally. Traditionally, opioid derivatives, such as morphine, administered intravenously, have been one of the fastest ways to alleviate breakthrough pain. A patientcontrolled analgesia device (PCA) allows for convenient intravenous administration of pain medication. One drug that specifically treats breakthrough pain is oral transmucosal fentanyl citrate. Fentanyl citrate dissolves rapidly (within five to ten minutes) via the mucous membranes. Cognitive techniques (including relaxation training, hypnosis, imagery, and distraction) and touch and music therapy may also help relieve breakthrough pain. Prognosis, prevention, and outcomes: Breakthrough pain medications are often called rescue medicines and are taken only at the time of an episode. It is important to take rescue medications at the earliest signs of breakthrough pain, as it is harder to control pain when it is allowed to build up. Anita Nagypál, Ph.D. See also Antinausea medications; Brief Pain Inventory (BPI); Pain management medications.
u Breast cancer in children and
adolescents Category: Diseases, symptoms, and conditions Also known as: Phyllodes tumors Related conditions: Adenocarcinoma Definition: Breast cancer is a malignant tumor that originates from breast cells. Most breast masses in children and adolescents are benign rather than cancerous in nature. One study noted fewer than fifty documented cases of breast cancer in girls between the ages of three and nineteen. Of these cases, juvenile secretory carcinoma was the most common and responsible for more than 80 percent of cases. The second most common form of breast cancer was intraductal carcinoma. Breast tumors called phyllodes tumors, although usually seen in women around forty-five years old, may occur
Salem Health: Cancer
Breast cancer in children and adolescents
Average Incidence of Breast Cancer, 1975-2000 Age Group 15-19 20-24 25-29
Incidence (per million people) 1.3 12.1 81.1
Source: Data from A. Bleyer, M. O’Leary, R. Barr, and L. A. G. Ries, eds., Cancer Epidemiology in Older Adolescents and Young Adults Fifteen to Twenty-Nine Years of Age, Including SEER Incidence and Survival: 1975-2000, NIH Pub. No. 06-5767 (Bethesda, Md.: National Cancer Institute, 2006)
in adolescents and have been reported in girls as young as ten years. These tumors may be benign, intermediate, or malignant. Another form of breast cancer in adolescents is primary breast carcinoma, which has been reported in girls between the ages of three and nineteen. However, in adolescents, most malignant breast masses are metastases from other cancers, such as Hodgkin disease, nonHodgkin lymphoma, primary hepatocellular carcinoma, neuroblastoma, and rhabdomyosarcoma. Risk factors: Risk factors for breast cancer in adolescents include having received chest-wall radiation and having a family history of breast cancer. If a child or adolescent receives radiation therapy to treat cancer of the chest area, the person’s risk for developing breast cancer later in life is significantly higher. The younger radiation was initiated, the higher the risk. This is especially the case when radiation is given to girls whose breasts are developing. Etiology and the disease process: Breast masses in children before and during puberty usually are breast buds. The development of breast buds in children is usually the first sign of puberty. The development of breast buds in children who are too young for puberty may indicate premature thelarche, or precocious puberty. Biopsy is warranted for cystic lesions that do not resolve with aspiration and for suspicious solid lesions. Some cancers start in glandular tissue that basically produces and secretes a substance. The ducts and lobules of the breast are glandular tissue, and the cancers starting in these areas are sometimes called adenocarcinomas. Incidence: Breast cancer in children and adolescents is rare. Generally, the lifetime probability of developing breast cancer is 1 in 6 overall, and 1 in 8 for invasive breast cancer. Globally, and in terms of all ages, breast cancer in-
cidence rates are highest in North America and northern Europe, and lowest in Asia and Africa. Symptoms: The most common finding with breast cancer in adolescents is a hard irregular mass and usually one that does not cause symptoms. As the cancer grows, symptoms may include a change of shape, size, and feel of the breast. Another symptom is bloody, yellow, or green, puslike drainage from the nipple. Advanced symptoms include bone or breast pain, swelling of the arm on the same side of the body as the breast with cancer, and weight loss. If metastasis occurs, other symptoms can include difficulty breathing, skin rash that is generalized, limb swelling, and back pain. Screening and diagnosis: Because a mass may not produce symptoms in the initial stages, all adolescents, especially girls with a family history of breast cancer or other malignancies, should have their breasts clinically examined regularly and should conduct monthly self-examination. Ultrasonography is the preferred imaging modality for breast masses in adolescents because of the increased density of the adolescent breast. Also the large amount of fibroglandular tissue makes mammography difficult to interpret. The accuracy of ultrasonography in differentiating solid from cystic lesions is 96 to 100 percent. Research suggests that an evaluation is warranted if no breast development occurs by the age of thirteen. The stage of breast cancer is based on tumor size; involvement of the skin, chest wall, or local lymph nodes; and whether the cancer has spread to other organs (metastasis). Stage I and Stage II are referred to as early stage or localized breast cancer. In Stage I the tumor size is less than 2 centimeters (cm) with no lymph node involvement. Stage II can exhibit lymph node involvement, but the nodes are small. The primary tumor size is larger than 2 cm but not larger than 5 cm. A tumor that is larger than 5 cm must be node-negative to be considered early stage. Stage III breast cancers are referred to as locally advanced breast cancer. In this stage, the tumors are large and greater than 5 cm across. There can be extensive axillary nodal involvement or nodal involvement of the soft tissues above or below the collarbone. A tumor is also designated Stage III if it extends to underlying muscles of the chest wall or the overlying skin. In Stage III, the breast may be undergoing the inflammatory process and appear red and swollen. Stage IV breast cancer, also known as metastatic breast cancer, consists of tumors that have spread to areas such as the brain, bones, skin, and even other organs. There may be any number of affected lymph nodes, and the primary tumor may be any size. 181
Breast cancer in men Treatment and therapy: The subsequent management of the adolescent with a breast mass depends on the type of mass. Surgical resection (excisional biopsy) may be necessary for cystic lesions that do not resolve with aspiration, when aspiration is not productive or not feasible, and for suspicious solid lesions. Although uncommon, more advanced forms of breast cancer have the potential to be treated similarly to the condition found in adults. Prognosis, prevention, and outcomes: The five-year survival rate refers to the number of patients who live at least five years after their cancer is found. According to the American Cancer Society (ACS), the five-year survival rates for persons with breast cancer that is appropriately treated are 100 percent for Stage I, 81 to 92 percent for Stage II, 54 to 67 percent for Stage III, and 20 percent for Stage IV. Jeffrey P. Larson, P.T., B.S., A.T.C. u For Further Information American Joint Committee on Cancer. AJCC Cancer Staging Manual. 5th ed. Philadelphia: Lippincott-Raven, 1997. Barry, Joanne. “Reaching Out to Educate.” Canadian Nurse 103, no. 8 (October, 2007): 34-35. Mandrell, B. N. “Secondary Breast Cancer in a Woman Treated for Hodgkin Lymphoma as a Child.” Oncology 21 (October, 2007): 27-29. Twombly, R. “Childhood Cancer Survivor Study Doubles to Examine Late Effects of New Treatments.” Journal of the National Cancer Institute 99, no. 21 (November 7, 2007): 1574-1576. u
Other Resources
National Cancer Institute Breast Cancer http://www.cancer.gov/cancertopics/types/breast UpToDate Overview of Breast Masses in Children and Adolescents http://patients.uptodate.com/topic.asp?file=adol_med/ 11491 See also Adenocarcinomas; Breast cancers; Breast selfexamination (BSE); Calcifications of the breast; Childhood cancers; Clinical breast exam (CBE); Cutaneous breast cancer; Phyllodes tumors; Young adult cancers.
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u Breast cancer in men Category: Diseases, symptoms, and conditions Also known as: Infiltrating or invasive ductal carcinoma, ductal carcinoma in situ, inflammatory breast cancer, Paget disease of the nipple Related conditions: Gynecomastia, fibroadenomas, papillomas Definition: Breast cancer occurs in men when malignant (cancerous) cells develop in the breast tissue of the male breast. The cancer can then spread into other tissues. Risk factors: Advanced age is a risk factor for men, just as it is for women. The median age of diagnosis for male breast cancer is sixty-eight. Men who have a close female relative with breast cancer are at risk and may be evaluated for the presence of a mutation in the BRCA2 gene. This mutation is responsible for 15 percent of breast cancers in men, and men with the mutation have a 6 percent lifetime risk for breast cancer. Other risks include radiation exposure (which may be occupational but is more often a result of treatment of other cancers) and liver disease, such as cirrhosis, which causes an increase in estrogen and a decrease in androgen hormones. Obesity and cigarette smoking may also play a role as risk factors. Many male breast cancers are estrogen-receptor-positive, which means that estrogen will increase the risk of development or accelerated growth of the cancer. Estrogen is given to some men to slow the growth of prostate cancer and is used by some men who are undergoing gender transformation. One risk specific to men for the development of breast cancer is Klinefelter syndrome, a genetic mutation involving at least one extra X chromosome, a condition that affects 1 in 850 men. These men have higher levels of estrogen and lower levels of androgens and therefore are at particular increased risk. Etiology and the disease process: There are a number of risk factors for male breast cancer, but none of the known causes can be eliminated. Most male breast cancers are invasive, infiltrating ductal carcinomas and are far more treatable in early localized stages. Therefore, efforts should be concentrated on early identification and treatment by increasing awareness of risk factors, heightening surveillance of those with nonmodifiable risks, and attempting to change those risks that can be modified. Incidence: Both men and women have breast tissue, and breast cancer occurs in men but is much rarer in men than in women, comprising only 1 percent of all cancers in men.
Salem Health: Cancer
Breast cancer in men
Stage at Diagnosis and Five-Year Relative Survival Rates for Invasive Male Breast Cancer, 1988-2001 Stage
Survival Rate (%) a
Localized Regionalb Distantc Unstaged
96.9 78.1 23.0 64.2
Source: Data from L. A. G. Ries et al., eds., Cancer Survival Among Adults: U.S. SEER Program, 1988-2001—Patient and Tumor Characteristics, NIH Pub. No. 07-6215 (Bethesda, Md.: National Cancer Institute, 2007) a Cancer still confined to primary site b Cancer has spread to regional lymph nodes or directly beyond the primary site c Cancer has metastasized
The American Cancer Society states that in the United States in 2005 more than 1,500 cases of male breast cancer were diagnosed and almost 500 deaths occurred. Symptoms: Symptoms of breast cancer in men include breast lumps as well as nipple and skin changes. The cancer is most often diagnosed when a man goes to his doctor after finding a mass below the nipple in one breast. Nipple changes can include redness or patchy scaling of the skin, nipple retraction (pulling inward), and nipple discharge. Skin changes may include puckering and dimpling as well as redness and scaling; however, chest hair may obscure subtle skin changes, and men are not accustomed to examining their breasts in a way that would help them find early lumps. Even when men find early symptoms, they may be misinformed about male breast cancer or embarrassed and delay seeking medical care. Screening and diagnosis: Providing information that male breast cancer does occur and describing early symptoms may be the best screening tools to offer. Screening for male breast cancer is not common among primary care providers, but if a lump is detected or brought to the provider’s attention by the patient, the first step is a mammography done with spot compression or magnification and possibly ultrasound, followed by a biopsy. A biopsy is the only definitive way to diagnose breast cancer. Staging assesses the size, location, lymph node involvement, and degree of metastasis of the cancer, ranging from Stage 0, which is the earliest stage, to Stage IV, which is the most advanced.
Treatment and therapy: Treatment usually involves surgery to remove the breast tissue and often lymph nodes and some of the chest muscles as well. Sentinel lymph node biopsy can be used to attempt to avoid more radical removal of lymph nodes. Radiation therapy and chemotherapy may be employed. If the cancer is determined to be estrogen-receptorpositive, the antiestrogen drug tamoxifen can be used to slow the growth and reproduction of cells that require estrogen. Another drug used in treatment is megace, an antiandrogen drug that blocks the effects of androgen in the breast. Prognosis, prevention, and outcomes: Prognosis is similar for male and female breast cancer when cancers of the same stage are compared; however, male breast cancer often is not discovered as early as is female breast cancer. Early detection is especially important because men have less breast tissue than women, and therefore their cancers can more easily reach and invade the chest muscles. Age at diagnosis and general health influence outcomes. With advanced medical care, five-year survival rates now vary from close to 100 percent for cancers caught in Stage 0 to 25 percent for cancers that have progressed to Stage IV. Prevention efforts center on screening for risk factors that may heighten surveillance for disease and on patient education about early self-detection of changes in the male breast. Outcome also depends on prevention of recurrence, and increased screening as well as adjuvant chemotherapy may improve long term outcomes. Clair Kaplan, R.N., M.S.N., A.P.R.N. (WHNP), M.H.S., M.T. (ASCP) u
For Further Information Berek, J. S., and N. F. Hacker. Practical Gynecologic Oncology. Philadelphia: Lippincott Williams & Wilkins, 2005. DeVita, V. T., S. Hellman, and S. A. Rosenberg. Cancer: Principles and Practice of Oncology. 7th ed. Philadelphia: Lippincott Williams & Wilkins, 2005. Estala, E. M. “Proposed Screening Recommendations for Male Breast Cancer.” The Nurse Practitioner 31, no. 2 (2006): 62-63.
u
Other Resources
American Cancer Society http://www.cancer.org National Cancer Institute Male Breast Cancer Treatment http://www.cancer.gov/cancertopics/pdq/treatment/ malebreast/ 183
Breast cancer in pregnant women See also Breast cancers; Breast self-examination (BSE); Clinical breast exam (CBE); Cutaneous breast cancer; Ductal carcinoma in situ (DCIS); Invasive ductal carcinomas.
u Breast cancer in pregnant
women Category: Diseases, symptoms, and conditions Also known as: Gestational breast cancer, lactational breast cancer, postpartum breast cancer
Salem Health: Cancer forty-four; of these women, only 10 percent will be pregnant at the time of diagnosis. Based on several analyses, the actual incidence of breast cancer during pregnancy has been estimated to fall between 1/3000 and 1/10,000 of all pregnant women. Breast cancer during pregnancy is second only to cervical cancer as the most common malignancy occurring during pregnancy. Of concern is that the incidence will most likely increase as women delay childbearing. In fact, women who have their first term pregnancy after the age of thirty have a twofold to threefold increased risk of breast cancer compared with women who have their first term pregnancy before the age of twenty.
Related conditions: Lactating adenoma, fibroadenoma, cystic disease, lobular hyperplasia, milk retention cyst (galactocele), abscess, lipoma, hamartoma, leukemia, lymphoma, sarcoma, neuroma, tuberculosis
Symptoms: Most often, women with breast cancer during pregnancy complain of a painless mass in the breast or a nipple discharge; a bloody nipple discharge is particularly concerning.
Definition: Gestational breast cancer is defined as breast cancer that occurs during pregnancy or up to one year thereafter.
Screening and diagnosis: All pregnant women should undergo a complete physical examination at the time they register for prenatal care, including a thorough breast examination. All new breast masses or nipple discharges should be evaluated promptly and not delayed until the pregnancy has been completed. The mean age at diagnosis of breast cancer during pregnancy is thirty-two to thirtyfour years. In most cases, the disease is advanced at the time of diagnosis. In general, the number of positive lymph nodes is greater, the tumors are larger, the steroid hormone status is more often negative, the number of cells synthesizing deoxyribonucleic acid (DNA) is greater, the number of mutations involving BRCA1 and BRCA2 is greater, and the tumor suppressor p53 is more often downregulated. Although the usefulness of mammography has been questioned in women less than thirty-five years of age because of higher breast density, mammography during pregnancy (in which breast density is increased) has been shown to be 90 percent sensitive in detecting malignancies. The irradiation exposure to the fetus is negligible and should not be a deterrent. Ultrasound, which carries no fetal irradiation risk, has been shown to be 100 percent sensitive in detecting a malignancy when the breast mass is palpable. The diagnosis rests, however, with pathologic confirmation, which can be obtained with a fine needle biopsy, a core needle biopsy, or an excisional biopsy. Staging is performed to determine if metastasis has occurred.
Risk factors: It is generally believed that breast cancer is years in the making; thus, pregnancy itself can be an aggravating risk factor for breast cancer because the physiologic changes that occur in the breast during pregnancy may mask an occult or nonpalpable mass. Further, there is often denial on the part of the physician or patient that breast cancer can occur during pregnancy, further aggravating the underlying risk. Moreover, the elevated levels of estrogen (hundredfold increase) and progesterone (thousandfold increase) during pregnancy may also stimulate cancer growth. Other traditional risk factors for breast cancer include a history of benign breast disease, menarche (onset of menstrual activity) before the age of twelve, drinking three or more alcohol-containing drinks daily, increased bone density, a sedentary lifestyle, nulliparity (no previous live births), first birth after the age of thirty, a firstdegree relative (mother or sister) with breast cancer, upper socioeconomic status, a history of endometrial or ovarian cancer, chest irradiation, increased breast density, a history of breast cancer, dietary fat intake (especially saturated fat), and obesity. Etiology and the disease process: Like all cancers, breast cancer arises when an oncogene (cancer-causing gene) is activated or the tumor-suppressor gene controlling the oncogene is silenced. Regardless of the precipitating risk factor, breast cancer appears to reflect the cumulative exposure to estrogen and progesterone. Incidence: Of all women diagnosed with breast cancer, only 12.7 percent will be between the ages of twenty and 184
Treatment and therapy: The management of breast cancer during pregnancy has the same goal as in patients who are not pregnant. Termination of pregnancy is not indicated. Surgery is generally delayed until the second trimester, and for nonmetastatic diseases, a modified radical
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Breast cancers
mastectomy is considered the standard conservative procedure. Similarly, even though all chemotherapeutic agents are category D (teratogenic), they have accumulated a favorable safety profile when used in the second and third trimesters. Fetal malformations range from 19 percent in the first trimester to 1.3 percent in the second and third trimesters based on nearly 100 pregnant women treated with 5-fluorouracil, doxorubicin, and cyclophosphamide (a standard chemotherapeutic regimen).
u Breast cancers
Prognosis, prevention, and outcomes: Women who are diagnosed with breast cancer during pregnancy are often diagnosed at a later stage, because breast changes during pregnancy, including increased breast size and changes in breast texture, make small, early-stage tumors harder to detect and diagnose. Roughly half of new cases are found in a late stage (III or IV), as compared with just over a quarter of cases that are diagnosed at Stage I and another quarter or so at Stage II. The five-year survival rate for women with negative lymph nodes is 82 percent; however, lymph node metastasis occurs in 65 percent of women with breast cancer during pregnancy. The overall survival for breast cancer during pregnancy is 70 percent. D. Scott Cunningham, M.D., Ph.D.
Definition: Breast cancer is the occurrence of a malignant tumor in the breast tissue. The most commonly diagnosed breast tumors are ductal carcinoma in situ (DCIS) and lobular carcinoma in situ (LCIS). When discovered early, these tumors are easily treated. However, if gone undetected, the tumors can eventually metastasize, meaning that some of the cancer cells detach from the tumor and spread throughout the body, acting as “seeds” to trigger the further development of malignancy in distant body parts. Once metastatic breast cancer (MBC) forms, the cancer becomes much more difficult to treat.
u For Further Information Barnes, D. M., and L. A. Newman. “Pregnancy-Associated Breast Cancer: A Literature Review.” Surgical Clinics of North America 87 (2007): 417-430. Leslie, K. K., and C. A. Lange. “Breast Cancer and Pregnancy.” Obstetrics & Gynecology Clinics of North America 32 (2005): 547-558. u
Other Resources
National Breast Cancer Foundation http://www.nationalbreastcancer.org/about-breastcancer/ National Cancer Institute http://www.cancer.gov Susan G. Komen for the Cure http://cms.komen.org/komen/AboutBreastCancer/ index.htm See also Adenocarcinomas; Breast cancers; Breast selfexamination (BSE); Calcifications of the breast; Childbirth and cancer; Clinical breast exam (CBE); Cutaneous breast cancer; Duct ectasia; Ductal carcinoma in situ (DCIS); Ductal lavage; Ductogram; Estrogen-receptorsensitive breast cancer; Pregnancy and cancer.
Category: Diseases, symptoms, and conditions Also known as: Metastatic breast cancer (MBC), ductal carcinoma in situ (DCIS), lobular carcinoma in situ (LCIS) Related conditions: Intraductal papillomas, noncancerous adenomas (growths) of the breast tissue, cysts
Risk factors: Some risk factors have been established as very important for determining patients who would benefit from more careful preventative care and observation. However, the presence of one or more risk factors does not necessarily mean that the patient will actually develop a breast tumor. Conversely, up to 70 percent of women who develop breast cancer did not have any known risk factors before diagnosis. Women who previously had a breast tumor in one breast have a significantly increased risk of developing cancer in the other breast. The cancer in the second breast is considered unrelated and not a recurrence of the cancer in the first breast. Several factors are considered to moderately increase the risk of breast cancer in some women. As women age, they develop an increasing risk of developing breast cancer. For example, women between the ages of forty and forty-nine have a 1 in 68 risk of developing breast cancer; this risk nearly doubles to 1 in 37 for women between the ages of fifty and fifty-nine. Nearly half of women diagnosed with breast cancer are over sixty-five and postmenopausal. Mutations in two key genes, BRCA1 and BRCA2, have also been associated with an increased risk of developing breast cancer. These genes are considered tumor suppressors, and mutations can lead to their dysfunction. These mutations seem to be inherited, and having a direct family relative with breast cancer also increases the risk of developing breast cancer. This is most true for first-degree relatives, such as a mother, sister, or daughter. One first-degree relative with breast cancer can nearly double the risk for an individual to develop breast 185
Breast cancers cancer; two first-degree relatives with breast cancer causes the individual to be up to five times as likely to develop breast cancer. Other factors have been shown to only slightly increase the risk of developing breast cancer. These include obesity and increased alcohol intake. Further, women who began to menstruate early (prior to age twelve), who enter into menopause late (after age fifty-five), or who never have children have a small increase in the chance of developing breast cancer. This is thought to be due to the increased exposure these women have to estrogen, a hormone that can increase breast cancer development. Etiology and the disease process: One of the most commonly accepted models of breast cancer formation stems from the development of genetic aberrations in breast cells. Activated mutations in oncogenes, genes responsible for the growth and proliferation of cells, and inhibitory mutations in tumor-suppressor genes that negatively regulate cell growth play an instrumental role in cellular trans-
Salem Health: Cancer formation. Cell transformation is the process by which a normal cell changes into a tumorigenic cell, capable of growing into a malignant mass. A breast tumor begins when one or more tumorigenic cells form within the epithelial layer, the internal tissue lining of the breast. As the tumor grows, it spreads past the epithelium, invading into the deeper tissues of the breast. If left untreated, the breast tumor will eventually metastasize, as the tumor cells break away from the primary tumor and are dispersed throughout the body via the circulatory system. Breast cancers are primarily differentiated as hormonereceptor-positive or -negative. These receptors are the estrogen receptor (ER), progesterone receptor (PR), or both. The distinctions among these tumors are critical, as they are a major determinant in choosing the proper therapy. Both hormone receptors have a similar action: After either hormone binds to its respective receptor inside the cell, it subsequently transports into the nucleus, where it plays a major role in regulating gene expression. Incidence: Breast cancer is one of the most frequently diagnosed cancers in women in the United States, with an estimated more than 175,000 new cases per year. Breast cancer development seems to be affected by race, with a higher incidence occurring in white and African American women compared with Hispanic, American Indian, and Asian American women. Breast cancer is second only to lung cancer in inducing cancer-related deaths in women, but it is the primary cause of cancer-related mortality in younger women, ages twenty to fifty-nine. Since the early 1990’s, the incidence of breast cancer-related deaths has steadily decreased, a reduction most dramatically seen in younger white and African American women. The cause of this reduction is attributed to both improved anticancer therapy and earlier diagnostic abilities. The risk of a woman developing breast cancer at some point in her lifetime is nearly 1 in 8, or 13 percent. Although breast cancer most often occurs in women, it can rarely occur in men. Symptoms: Early breast cancer is usually free of symptoms. The first sign of breast cancer is most often a persistent lump in the breast. As the tumor develops, the individual may begin to experience other symptoms, including swelling of the armpit or breast and thickening of the breast tissue. Patients may also notice slight pain or tenderness in the breast. Changes in how the nipple looks is also frequently observed with breast cancer.
A mammogram showing a breast tumor. (©Visuals Unlimited/ Corbis)
186
Screening and diagnosis: Aclinical breast exam is a common method to detect lumps or abnormal changes in the breast tissue. If a lump is detected, the clinician will assess the characteristics of the lump. Lumps that are soft,
Salem Health: Cancer smooth, and round and move about easily are more likely to be benign, compared to hard, nonsymmetrical lumps that are tightly attached to the breast tissue, which are more likely to be cancerous. It is also recommended that women perform monthly breast self-examinations at home to detect changes between checkups. Subtle changes that may not register as a lump by touch can often be detected by mammograms, X-ray images taken of the breast. Further, many clinicians use mammograms to provide a more detailed look at lumps identified during an examination. Ultrasound and magnetic resonance imaging (MRI) can be used to directly image breast abnormalities. If a clinician feels that a certain breast abnormality warrants further investigation, a biopsy is performed to remove tissue that a pathologist can use to determine if any cancer is present. At the time of first diagnosis, most patients are diagnosed either with early, localized breast cancer or regional breast cancer. Only a small minority of patients receive a primary diagnosis of metastatic breast cancer (MBC). Recurrent breast cancer is a malignancy that has returned after previously being treated to the point of not being detected. Recurrence may occur locally in or near the breast or in distant parts of the body, such as the bone, liver, or lungs. Once a diagnosis is made, the stage of the breast cancer is determined. This is necessary for the physician to determine the extent of the disease and to prescribe the appropriate treatment. Stage 0 is described as in situ carcinoma. In situ carcinoma is noninvasive, meaning the cancer cells have not begun to spread beyond the epithelium, or tissue surface. The most common breast cancer of this stage is ductal carcinoma in situ (DCIS), in which cancerous cells develop within the milk ducts. Stage I is the earliest form of invasive breast cancer. At this point, the tumor is smaller than 2 centimeters (cm) in diameter and is confined to the breast. In Stage II, the tumor is either between 2 and 5 cm and has spread to the lymph nodes under the arm or is larger than 5 cm but has not spread outside the breast. Stage III is characterized by larger tumors that may have spread to lymph nodes and areas beyond the underarm, such as behind the breastbone or near the collarbone. Stage IV is the most advanced stage. At this point, the cancer is classified as distant metastatic cancer. Treatment and therapy: The main goals of breast cancer therapy are to eradicate the tumor and prevent its recurrence. Treatments can be categorized as either local or systemic, and the use of either or both is determined by the extent and stage of disease. Local therapies include surgery and radiation therapy. Surgery can be either minimal, such as a lumpectomy in which only the lump is removed, or
Breast cancers
Stage at Diagnosis and Five-Year Relative Survival Rates for Women with Breast Cancer, 1996-2004 Women Diagnosed (%)
Stage a
Localized Regionalb Distantc Unstaged
61 31 6 2
Survival Rate (%) 98.0 83.5 26.7 56.9
Source: Data from National Cancer Institute, Surveillance Epidemiology and End Results, Cancer Stat Fact Sheets, 2008 a Cancer still confined to primary site b Cancer has spread to regional lymph nodes or directly beyond the primary site c Cancer has metastasized
more drastic, such as a mastectomy in which the majority of the breast is removed. If the breast cancer has spread to local lymph nodes, these also may be removed at the time of surgery. Surgery is often used in conjunction with other therapies, including radiation therapy and systemic drug therapy. Once the breast cancer has metastasized and become MBC, surgery is not a viable therapeutic option. For MBC, systemic therapy is generally the standard treatment and consists of three main categories: chemotherapy, endocrine therapy, and biological therapy. The most effective chemotherapeutic agents for breast cancer are taxanes and anthracyclines, although other drug classes can be used. Despite the benefit these drugs can offer in lengthening patient survival, the accompanying toxic side effects can dramatically decrease the patient’s quality of life. Endocrine therapy is the standard of care for hormone-receptor-positive breast cancer. The most common type of endocrine therapy is the selective estrogen receptor modulator (SERM) tamoxifen, which can reduce the proliferative effect that estrogens have in the breast tumor cells. Although tamoxifen is generally tolerated better than chemotherapies, there is a high risk for developing resistance, after which the drug loses its benefit. The newest addition to the breast cancer therapy arsenal is targeted biological therapy. The prototypical example of this in breast cancer is trastuzumab, an antibody that recognizes and inhibits the human epidermal growth factor receptor (HER2) present on the surface of the breast cancer cell. HER2 is an effective breast cancer target because it is often overactivated in breast cancer, increasing the proliferative signaling downstream of its activation. 187
Breast implants Prognosis, prevention, and outcomes: The improvement of screening and diagnostic techniques has been instrumental in increasing the discovery of breast cancer early in development, when it is most easily treated. Additionally, the development of novel drugs and therapies has caused a significant increase in extending survival of breast cancer patients. Clinicians measure disease outcome by measuring survival rates; a disease-free survival of at least five years is generally considered to be a cure. Currently, the five-year survival rate for patients diagnosed with local breast cancer that has not spread beyond the breast is 98 percent. This survival rate is lowered to 83.5 percent in patients with regional metastasis. Patients with Stage IV metastatic breast cancer have a five-year survival rate of only 26.7 percent. Much effort has gone into determining methods of preventing breast cancer. Because many breast tumors depend on estrogen for growth and survival, decreasing unnecessary estrogen exposure may help prevent breast cancer. Some women with an especially high risk of breast cancer may elect to have an oophorectomy, surgery to remove both ovaries, the primary source of estrogen in premenopausal women. Additionally, regular exercise may reduce the amount of estrogen naturally produced by the body, decreasing the amount of estrogen to which the breast is exposed. An extreme preventative measure in women with a high risk for developing breast cancer is prophylactic mastectomy, a surgical procedure to remove the breast before any signs of cancer. Lisa M. Cockrell, B.S. u For Further Information Bowcock, Anne M, ed. Breast Cancer: Molecular Genetics, Pathogenesis, and Therapeutics. Totowa, N.J.: Humana Press, 1999. Craig, Jordan V., and Barrington J. A. Furr, eds. Hormone Therapy in Breast and Prostate Cancer. Totowa, N.J.: Humana Press, 1999. Grobstein, Ruth H. The Breast Cancer Book: What You Need to Know to Make Informed Decisions. New Haven, Conn.: Yale University Press, 2005. Kufe, Donald W., et al., eds. Holland Frei Cancer Medicine 7. 7th ed. Hamilton, Ont.: B. C. Decker, 2006. Manni, Andrea, ed. Endocrinology of Breast Cancer. Totowa, N.J.: Humana Press, 1999. u
Other Resources
American Cancer Society http://www.cancer.org National Breast Cancer Foundation http://www.nationalbreastcancer.org 188
Salem Health: Cancer National Cancer Institute Breast Cancer http://www.cancer.gov/cancertopics/types/breast Susan G. Komen for the Cure http://www.komen.org See also Accelerated partial breast irradiation (APBI); Adenocarcinomas; Aging and cancer; Antiestrogens; Antiperspirants and breast cancer; Birth control pills and cancer; Breast cancer in children and adolescents; Breast cancer in men; Breast cancer in pregnant women; Breast implants; Breast reconstruction; Breast ultrasound; Calcifications of the breast; Childbirth and cancer; Clinical breast exam (CBE); Cutaneous breast cancer; Diethylstilbestrol (DES); Duct ectasia; Ductal carcinoma in situ (DCIS); Ductal lavage; Ductogram; Estrogen-receptorsensitive breast cancer; Fertility drugs and cancer; Fibroadenomas; Fibrocystic breast changes; Genetic counseling; Genetic testing; Hormone receptor tests; Hormone replacement therapy (HRT); Invasive ductal carcinomas; Invasive lobular carcinomas; Lobular carcinoma in situ (LCIS); Lumpectomy; Lumps; Lymphadenectomy; Lymphangiography; Lymphangiosarcomas; Lymphedema; Mammography; Mastectomy; Medullary carcinoma of the breast; Metastasis; Microcalcifications; Needle localization; Obesity-associated cancers; Phyllodes tumors; Pregnancy and cancer; Premalignancies; Progesterone receptor assay; Tubular carcinomas; Wire localization.
u Breast implants Category: Procedures Also known as: Autologous breast implants, saline breast implants, saline-filled breast implants, silicone breast implants, silicone-filled breast implants Definition: Breast implants are used to reconstruct the natural appearance of one or both breasts following mastectomy for breast cancer. Breast implants may be composed of the patient’s own tissue taken from elsewhere on the body (autologous breast implants) or made of artificial substances (saline or silicone breast implants). Cancers treated: Breast cancer Why performed: Breast reconstruction is a choice for women following mastectomy. Mastectomy involves surgically removing one or both breasts for the treatment of breast cancer. Breast implants are used to replace breasts that have been removed, to create a symmetrical appear-
Salem Health: Cancer
Breast implants
Reconstructed breast Chest wall after mastectomy
Implant
Reconstruction of a breast following a total mastectomy. (©Visuals Unlimited/Corbis)
ance if only one breast was removed, or to replace the one breast that was removed and enhance the appearance of the remaining breast to improve symmetry. Breast implants are an option to wearing breast prosthetics (removable breast forms). Patient preparation: Breast implants come in a variety of shapes, sizes, and compositions. The plastic surgeon guides the patient in the selection process. Tissue expanders may or may not be used to stretch the skin in preparation for breast implant placement. In some cases, the tissue expander may be filled with saline and remain in the body, serving as the breast implant. There are two basic types of artificial implants, saline breast implants and silicone breast implants. Saline breast implants have a silicone outer shell and are filled with saline, a saltwater solution. Saline implants may be prefilled by the manufacturer or filled at the time of surgery and adjusted after surgery. Silicone breast implants have a silicone outer shell and are filled with silicone, a natural substance. Silicone breast implants may be prefilled with silicone by the manufacturer and nonadjustable, prefilled with silicone and allow
for saline insertion at the time of surgery, or prefilled with silicone and allow for saline insertion at the time of surgery and postsurgical adjustments. Saline implants were approved for use in the United States by the Food and Drug Administration (FDA) in 2000. Silicone implants were approved by the FDA in 2006. Both types of implants are not meant to last a lifetime, may need to be replaced, and have a risk of rupture. Saline implants are advantageous in that ruptures are readily identified because the breast size decreases and the saline solution is absorbed by the body. The size of saline implants can be adjusted easily. Some people believe, however, that saline implants do not look or feel as natural as silicone implants. Silicone implants have a texture similar to natural breast tissue. While silicone breast implants may look and feel more natural than saline implants, ruptures may not be as easily noticed with silicone breast implants. Following a rupture, the silicone remains near the implant and is not absorbed by the body. Autologous implants are made of tissue or a tissue flap that is taken from the patient, commonly the abdomen and buttocks. The tissue may contain fat, muscles, blood ves189
Breast reconstruction sels, and nerves. Autologous implants are a more specialized procedure involving microsurgery and take longer to heal, but they do not have the risk of rupture and do not need to be replaced over time. Some people believe that autologous implants produce the most natural results. Steps of the procedure: Breast implants may be inserted at the time of the mastectomy or at a later time in another surgery. Patients receiving radiation therapy following mastectomy may need to delay breast reconstruction. Breast implant procedures do not delay chemotherapy. Breast reconstruction surgery is performed with general anesthesia. Nipple reconstruction may take place following a breast implant procedure. After the procedure: Patients may spend one to six days in the hospital, depending on the procedure. Patients wear bandages and support garments while healing. Activities may be temporarily restricted, but most activities can be resumed in six to eight weeks. Artificial implants typically need to be replaced in time. Breast implants should not affect breastfeeding. Special mammography procedures may be needed, however. Breast implants only rarely obscure the detection of new cancer formation. Risks: The risks of artificial breast implants include rupture, leakage, rippling, infection, and capsular contraction (in which scar tissue surrounding the implants shrinks or hardens). Other risks include the general risks associated with surgery and anesthesia. Results: The optimal result is symmetrical, naturalappearing breasts. Mary Car-Blanchard, O.T.D., B.S.O.T. u
For Further Information Poeppl, N., et al. “Does the Surface Structure of Implants Have an Impact on the Formation of a Capsular Contracture?” Aesthetic Plastic Surgery 31, no. 2 (March/April, 2007): 133-139. “Silicone Gel-Filled Breast Implants Approved.” FDA Consumer 41, no. 1 (January/February, 2007). Stevens, W. G., et al. “A Comparison of Five Hundred Prefilled Textured Saline Breast Implants Versus Five Hundred Standard Textured Saline Breast Implants: Is There a Difference in Deflation Rates?” Plastic and Reconstruction Surgery 117, no. 7 (June, 2006): 21752181. Vázquez, G., and A. Pellón. “Polyurethane-Coated Silicone Gel Breast Implants Used for Eighteen Years.” Aesthetic Plastic Surgery 31, no. 4 (July/August, 2007): 330-336. 190
Salem Health: Cancer u
Other Resources
American Cancer Society http://www.cancer.org American Society of Plastic Surgeons http://www.plasticsurgery.org Breast Implant Safety.org http://www.breastimplantsafety.org See also Breast cancers; Breast reconstruction; Mastectomy; Self-image and body image; Sexuality and cancer.
u Breast reconstruction Category: Procedures Also known as: Breast implants; deep inferior epigastric perforator (DIEP) flap; free flap; gluteal flap; latissimus dorsi flap; pedicle flap; saline breast implants; silicone breast implants; transverse rectus abdominis muscle (TRAM) flap Definition: Breast reconstruction is a complex procedure performed by a plastic surgeon that restores the appearance of a breast after mastectomy to treat breast cancer. Cancers treated: Breast cancer Why performed: Breast reconstruction is performed to reconstruct the size and shape of the breast in a patient who has had a mastectomy. Most women who have had a mastectomy can have breast reconstruction, which may be done either at the time of mastectomy or at a later date. Breast reconstruction may improve the self-esteem and body image of a woman who has had a mastectomy. Patient preparation: A patient facing a mastectomy who is interested in breast reconstruction probably will be advised to consult with a plastic surgeon experienced in breast reconstruction prior to the mastectomy. Ideally, the breast surgeon and the plastic surgeon work together to develop the best surgical and breast reconstruction strategy for each patient, even if the reconstructive surgery will be done later. Two or more operations probably will be needed to achieve a satisfactory result. A patient will be given specific instructions prior to surgery. Since smoking can decrease a patient’s blood circulation, which is critical to the survival of transplanted tissue, a patient who is a smoker will be given instructions and tips to quit smoking prior to reconstruction procedures that involve the use of transplanted tissue. Steps of the procedure: There are two basic types of breast reconstruction, implant procedures and tissue flap
Salem Health: Cancer procedures. A combination of these procedures may also be used. Either type of procedure may be begun either at the same time as the mastectomy (immediate reconstruction) or at a later time (delayed reconstruction). Saline-filled implants are the most common type of implant used and consist of external silicone shells filled with sterile saline. The use of silicone gel-filled implants has decreased because of concerns of possible health risks if silicone leaks from the implant, although recent research has not found any health dangers associated with their use. Sometimes a one-stage procedure is possible, where the implant is placed behind the pectoral muscle in the chest in the first surgery. For most patients, a two-stage procedure is used in which a tissue expander, like a balloon, is implanted beneath the skin and chest muscle. Over a period of several months, the surgeon injects a saline solution at regular intervals to fill the expander and stretch the chest pocket. At the appropriate time, the expander is removed in a second operation and the permanent implant is put into place. Tissue flap procedures involve autologous tissue reconstruction and are the more surgically complex option
Breast reconstruction for breast reconstruction. Tissue from the abdomen or back (more commonly), or buttocks or thighs (less commonly), is used. Two types of methods, pedicle flap and free flap, are in use. In a pedicle flap procedure, some of the blood vessels feeding the tissue to be transferred are cut and some are kept intact. The tissue is tunneled beneath the skin to the chest area, where a new breast mound or pocket for an implant is created. In a free flap procedure, the flap of skin, fat, blood vessels, and muscle tissue is disconnected from its blood supply completely and removed from its original location, and intricate microsurgical techniques are used to reattach the tissue flap to new blood vessels near the chest. This procedure typically takes longer to complete than a pedicle flap procedure. Four main tissue flap procedures are performed: the TRAM (transverse rectus abdominis muscle) flap, the DIEP (deep inferior epigastric perforator) flap, the latissimus dorsi flap, and the gluteal flap. The TRAM flap procedure uses tissue and muscle from the lower abdominal wall, which may be transferred as a free flap or a pedicle flap. This procedure also results in a tightening of the lower abdomen, or a “tummy tuck.” Vari-
A transverse rectus abdominis muscle (TRAM) flap breast reconstruction. (Custom Medical Stock Photo)
191
Breast reconstruction ations on this procedure use different amounts of abdominal muscle. The use of less muscle for reconstruction may help the patient retain abdominal strength after surgery. The newer DIEP flap procedure uses skin, fat, and minimal abdominal muscle tissue, and it uses a free flap approach. Patients generally retain more abdominal strength with this type of breast reconstruction. The latissimus dorsi flap procedure transfers skin, fat, muscle, and blood vessels from the upper back as a pedicle flap, tunneling the tissue under the skin to the front of the chest. The amount of skin and other tissue used in this procedure is generally less than in a TRAM flap surgery, making it useful for reconstructing small and medium-sized breasts or for creating a pocket for a breast implant. The gluteal flap is a free flap procedure that uses skin, fat, blood vessels, and gluteal muscle tissue from the buttocks to create the breast shape. This procedure is an option for women who cannot use the abdominal site due to thinness or incisions, or for patient preference. Nipple and areola reconstruction is optional and, if done, is performed as a last step after the patient has healed from the first surgeries. The nipple is reconstructed using tissue from the breast itself or from another part of the patient’s body such as the inner thigh. The areola may be created by tattooing the skin to make it match the natural nipple and areola. Saving the nipple from the breast with cancer that is removed (called nipple saving or nipple banking) is sometimes done but is risky because the nipple tissue might contain cancer cells. After the procedure: A patient will likely feel tired and sore for a week or two after implant reconstruction, and longer, perhaps months, after tissue flap reconstruction. The patient will probably be discharged from the hospital with a surgical drain in place to allow excess fluids to drain from the surgical site. Stitches will be in place after the surgery, but they will most likely be absorbable sutures that will not have to be removed. Scars will fade over time but never go away entirely. It takes about six to eight weeks for the patient to return to normal, depending on the type of procedure performed. A patient will be advised to take it easy during this period and avoid overhead lifting and strenuous physical activity. Risks: Some risks of breast reconstructive surgery are bleeding, fluid collection, swelling and pain, excessive scar tissue, infection, the death of all or part of the flap, problems at the donor site, fatigue, changes in the affected arm, and the need for additional surgeries to correct problems. If an infection develops after the implant surgery, then the implant may need to be removed until the infection 192
Salem Health: Cancer clears. If an infection develops after flap surgery, then surgical cleaning of the wound may be necessary. Sometimes local complications occur with breast implants. The most common of these is capsular contracture, which can occur if the scar or capsule around the implant begins to tighten and squeeze down on the soft implant, making the breast feel hard. More surgery may be needed to remove the scar tissue, or the implant may need to be removed or replaced. Rarely, rupture of the implant may occur. Implants may not last a lifetime, so additional surgeries may be needed to replace them. Breast reconstruction has no known effect on the recurrence of breast cancer, and neither implant nor flap procedures decrease the likelihood of detection of a recurrence of breast cancer. Results: Breast reconstruction after a mastectomy can improve a woman’s appearance and self-confidence. Although the surgeon will try to create a breast shape that matches the other breast closely, a perfect match is not possible, and a reconstructed breast does not have natural sensations. In some cases, surgery on the other breast is performed to improve the match. Jill Ferguson, Ph.D. u
For Further Information Ahmed, S., et al. “Breast Reconstruction.” British Medical Journal 330 (2005): 943-948. Edlick, R. F., et al. “Advances in Breast Reconstruction After Mastectomy.” Journal of Long-Term Effects of Medical Implants 15 (2005): 197-207. Farhadi, J., et al. “Reconstruction of the Nipple-Areola Complex: An Update.” Journal of Plastic, Reconstructive & Aesthetic Surgery 59 (2006): 40-53. Fentiman, I. S., and H. Hamed. “Breast Reconstruction.” International Journal of Clinical Practice 60 (2006): 471-474. Piasecki, J. H., and K. A. Gutowski. “Breast Reconstruction.” Clinical Obstetics and Gynecology 49 (2006): 401-413. Serletti, J. M. “Breast Reconstruction with the TRAM Flap: Pedicled and Free.” Journal of Surgical Oncology 94 (2006): 532-537. Spear, S. L., and A. N. Mesbahi. “Implant-Based Reconstruction.” Clinics in Plastic Surgery 34 (2007): 63-73. u
Other Resources
American Cancer Society Breast Reconstruction After Mastectomy http://www.cancer.org/docroot/CRI/content/ CRI_2_6X_Breast_Reconstruction_After_ Mastectomy_5.asp
Salem Health: Cancer
Breast self-examination (BSE)
American Society of Plastic Surgeons Breast Reconstruction http://www.plasticsurgery.org/patients_consumers/ procedures/BreastReconstruction.cfm Breastcancer.org Reconstruction http://www.breastcancer.org/bey_tre_recon_idx.html Mayo Clinic Breast Reconstruction After Mastectomy http://www.mayoclinic.com/health/breastreconstruction/WO00083 See also Breast cancers; Breast implants; Mastectomy; Self-image and body image; Sexuality and cancer.
u Breast self-examination (BSE) Category: Procedures Definition: The National Breast Cancer Foundation recommends that all women age twenty and older conduct a breast self-examination (BSE) on a monthly basis, in addition to undergoing a clinical breast examination periodically, depending on age and state of health. Cancers diagnosed: Breast cancer Why performed: Breast self-examinations are performed by women on their own breasts to detect unusual swellings, lumps, thickenings, or other conditions that may suggest the possibility of a breast disorder, including breast cancer. It is believed that, if performed every month at the same time (in relation to the menstrual cycle), this examination will educate a woman about how her breasts feel normally and will alert her to any sudden changes, thereby facilitating early detection of a precancerous or cancerous mass. Patient preparation: It is recommended that the examination take place in the shower (where water smooths the skin and makes it easier to detect changes) or lying prone. Steps of the procedure: Using the left hand to examine the right breast (and vice versa), the woman should, with fingers flat, move gently over every part of the breast in a systematic fashion (vertically up to down or circularly from well beyond the exterial margins inward), starting well above the top margin of the breast and beyond each right and left margin as well. The examination should be conducted three times using light, medium, and heavy
A woman performs a breast self-examination. (PhotoDisc)
pressure. Women must also visually inspect their breasts in a mirror, raising arms overhead and looking at the breasts from all sides. Muscles should be both flexed and relaxed. Women should be particularly alert to any swellings, dimpling of the skin, “orange-peel” (peau d’orange) appearance, discoloration, changes in or discharges from the nipple, lumps no matter how small, or other unfamiliar signs. After the procedure: If a woman detects a change in how her breasts or nipples feel, then she should promptly schedule an appointment with her physician for follow-up tests. Risks: There are no risks in performing the examination, and generally such examinations cause no pain. Results: Women who perform a self-exam become familiar with their own breasts and are able to report abnormalities much earlier than is possible if they wait for an annual clinical examination or mammogram. Early detection of 193
Breast ultrasound precancerous or cancerous tissue greatly increases not only early treatment but also survival rates. Christina J. Moose, M.A. See also Breast cancer in pregnant women; Breast cancers; Calcifications of the breast; Clinical breast exam (CBE); Mammography; Nipple discharge; Palpation; Screening for cancer.
u Breast ultrasound Category: Procedures Also known as: Sonography, ultrasonography Definition: Breast ultrasound is the use of high-frequency sound waves to produce an image of the breast tissue. The sound waves used are in the range of 20,000 to 10,000,000 cycles per second and are inaudible to the human ear. They are bounced off of the breast tissue and are able to distinguish between solid tumors and fluid-filled cysts. The density and elasticity of tissues affect the velocity of the sound waves traveling through them. Tissues that are denser and less elastic slow the sound waves and appear as shaded areas on the screen image. Tissues that are less dense and more elastic do not interfere with the sound waves and appear as clear areas. The interpretation of the sound wave data is performed by a computer. An advantage of breast ultrasound is that it does not use radiation. Cancers diagnosed: Breast cancer Why performed: There are several reasons that breast ultrasounds are performed. After a questionable mammogram, a breast ultrasound may be used to further examine the breast tissue. Some breast conditions may look like a possible cancer on a mammogram but can be identified as benign on ultrasound. For example, breast cysts and some fibroadenomas appear as clear areas on a breast ultrasound, whereas a breast cancer would not. In women under the age of thirty-five, breast ultrasound may be the procedure of choice for screening for breast cancer because younger women have denser breast tissue, which makes it difficult to assess for abnormalities on mammography. Breast ultrasound may also be used to guide a needle biopsy, or needle localization. Ultrasound has proved effective at examining the breasts of women with breast implants. It is often able to illustrate whether the implant has ruptured or not. Mammography does not show fluid leaking from the implant. Patient preparation: No preparation of the patient is required. 194
Salem Health: Cancer Steps of the procedure: For a breast ultrasound, the patient puts on a hospital gown, which is open in the front, and then lies supine on a table. A pillow is placed under the shoulder of the breast to be scanned. The area to be scanned is uncovered. The patient’s arm is placed up over the head, resting on the examination table. The radiology technician or physician uses a transducer (an instrument to transmit and receive sound waves) to scan the breast tissue. A transducer looks like a small cell phone. A gel is used between the transducer and the patient to enhance the transmission of the sound waves for the scan. The transducer is moved slowly and lightly over the breast tissue. Usually, the breast lesion is viewed in several planes, so that its features can be defined. This is accomplished by changing the angle of the transducer in relation to the breast tissue. The images of the breast are printed for further examination. After the procedure: No additional patient care is required, so the patient can go home. Risks: There are no known risks of breast ultrasound for the patient. It appears that sound waves are safe for use on human beings. For the physician, however, there is the risk of making an incorrect diagnosis about the presence of breast cancer. Breast ultrasounds do not differentiate microcalcifications (mineral deposits) in the breast tissue. Microcalcifications that are clustered can be a first sign of a developing breast cancer. The accuracy of breast ultrasounds can vary with the skill of the technician. Once the ultrasound images have been printed, there is no way to determine the angle of the transducer, or to manipulate the images, as can be done with mammograms. Also, breast ultrasound is not as accurate at assessing the whole breast. It is most effective at assessing a small area of breast tissue. Results: The images of the breast ultrasound demonstrate the different breast tissues, with the ducts appearing darker than the adipose (fatty) tissue between the ducts. The breast ultrasound is most accurate at identifying breast cysts, which are fluid-filled. If on ultrasound an area of the breast appears particularly dense and opaque, then a breast cancer could be present. Breast ultrasound does not differentiate between benign tumors and malignant (cancerous) tumors or growths. As a result, a breast biopsy is required to identify the type of lesion. Christine M. Carroll, R.N., B.S.N., M.B.A. u
For Further Information Love, Susan M., and Karen Lindsay. Dr. Susan Love’s Breast Book. Rev. 4th ed. Cambridge, Mass.: Da Capo Press, 2005.
Salem Health: Cancer
Breslow’s staging
Pagana, Kathleen Deska, and Timothy J. Pagana. Mosby’s Manual of Diagnostic and Laboratory Tests. 3d ed. St. Louis: Mosby Elsevier, 2006.
progress, or stage, of the cancer and whether the cancer has spread. The stage helps oncologists choose the best treatment and determine the best prospects for recovery.
u
Patient preparation: No special preparation is needed for a skin biopsy.
Other Resources
American Cancer Society Mammograms and Other Breast Imaging Procedures http://www.cancer.org/docroot/CRI/content/ CRI_2_6X_Mammography_and_Other_Breast_ imaging_Procedures_5.asp Health A to Z Breast Ultrasound http://www.healthatoz/atoz/ency/ breast_ultrasound.jsp Imaginis Breast Cancer Diagnosis http://www.imaginis.com/breasthealth/ ultrasound_images.asp Yale Medical Group Breast Imaging at Yale http://www.yalemedicalgroup.org/news/dxrad/ ymg_breastimaging.html See also Breast cancer in children and adolescents; Breast cancer in men; Breast cancer in pregnant women; Breast cancers; Calcifications of the breast; Clinical breast exam (CBE); Imaging tests; Mammography; Microcalcifications; Needle biopsies; Premalignancies; Screening for cancer; Ultrasound tests.
u Breslow’s staging Category: Procedures Also known as: Breslow thickness, Breslow measurement, Breslow’s depth of invasiveness Definition: Breslow’s staging is a test to measure, in millimeters (mm), the vertical thickness (how far a tumor reaches into the skin) of a malignant melanoma tumor. The test was developed by Alexander Breslow (1928-1980), an American pathologist, in the 1970’s. Cancers diagnosed: Melanoma, the most deadly form of skin cancer Why performed: Once melanoma is confirmed by a skin biopsy, Breslow’s staging helps oncologists establish the
Steps of the procedure: A skin biopsy is usually done in the doctor’s office. A local anesthetic is injected into the area with a small needle. A sample of skin tissue is then removed for examination. After the procedure: The patient feels no pain and may go home. The skin sample is examined in a laboratory. If melanoma is confirmed, then the sample is subjected to Breslow’s staging to help determine prognosis and treatment. Risks: Small skin biopsies are generally safe and carry only a small risk of bleeding or infection. Sometimes a biopsy may leave a scar. Results: Early diagnosis is the most effective way of improving the cure rate for patients with melanoma. When laboratory tests confirm melanoma, Breslow’s staging classifies the progress of the cancer according to one of five stages. In the first stage, malignant melanoma cells are found only in the outer layer of skin and have not yet invaded the deeper layers or spread. Most patients with melanoma only in the outer layer of skin can be cured with surgery. The Breslow thickness of a melanoma tumor predicts the approximate five-year survival rate after the tumor is surgically removed.
• • • •
Smaller than 1 mm: 95-100 percent 1.0-2.0 mm: 80-96 percent 2.1-4.0 mm: 60-75 percent More than 4.0 mm: 50 percent
In the last stage, the melanoma could be any thickness but has spread to other parts of the body, most likely to the nearest lymph nodes. The majority of patients with melanoma that has spread to nearby lymph nodes cannot be cured with current treatments. The average survival of patients with melanoma that has spread to the lymph nodes is only 7.5 months. Only 5 to 10 percent of patients survive beyond five years. Wendell Anderson, B.A. See also Melanomas. 195
Brief Pain Inventory (BPI)
u Brief Pain Inventory (BPI)
Salem Health: Cancer See also Breakthrough pain; Pain management medications.
Category: Procedures Definition: The Brief Pain Inventory (BPI) is a questionnaire used to measure pain in cancer patients and other patients suffering from chronic pain. The BPI provides information on the intensity of pain (known as the sensory dimension) and the impact of pain on a patient’s daily routine (known as the reactive dimension). The BPI was developed in 1989 by Charles Cleeland, M.D., while with the Pain Research group at the University of Wisconsin. Cancers diagnosed or treated: All cancers that cause chronic or severe sporadic pain Why performed: The BPI is administered to determine cancer patients’ level of pain. Once the level of pain is determined, oncologists work to manage the painful symptoms of cancer and to make patients more comfortable. Pain management is especially important for terminal patients. Cancer pain appears when a tumor presses against organs, nerves, or bone. Treatments for cancer—such as chemotherapy, radiation therapy, and especially surgery— also can cause pain. The Veterans Administration and the Joint Commission on Accreditation of Health Care Organizations consider pain the fifth vital sign and require physicians to ask patients about their pain. Patient preparation: Taking the BPI requires no patient preparation. Steps of the procedure: The questionnaire for the BPI is usually filled out by the patient. In some cases, a doctor, nurse, or social worker helps by interviewing the patient and recording the answers. Filling out the short version of the BPI takes about five minutes, while the long version takes about ten minutes. After the procedure: After the patient completes the BPI, it is scored on a scale of 0-10 for both the severity and the impact dimensions of the pain. Risks: There are no inherent risks involved with the BPI. Its validity has been tested many times, and it has been translated into twenty-five languages. The only possible problem involved with the BPI is a patient’s inability or reluctance to report pain accurately. Results: The results of an individual patient’s BPI can be tabulated in a few minutes. The results help oncologists, nurses, and other caregivers develop a pain management plan for the cancer patient. Wendell Anderson, B.A. 196
u Brompton cocktail Category: Chemotherapy and other drugs Also known as: Brompton’s mixture, hospice mix Definition: Brompton cocktail is a palliative elixir containing morphine, cocaine, ethanol, and other ingredients to lessen or prevent the pain and distress associated with terminal illness, especially advanced cancer. It is no longer part of standard care. Cancers treated: Previously used for advanced, painful tumors in patients near death Delivery routes: Oral as a liquid How this substance works: Elixirs of morphine and cocaine were first described in 1896 as treatments for the pain associated with advanced cancer by the English surgeon Herbert Snow. A specific mixture was published under the auspices of the Royal Brompton Hospital in London in 1952; the ingredients included morphine hydrochloride, cocaine hydrochloride, alcohol, and chloroform water. Several different formulations calling for heroin (diacetylmorphine), cannabis, antiemetics, distilled spirits, and sedatives have been promoted over the years. Flavoring syrup is sometimes added. It was widely used in the early 1970’s, mostly in hospice care. Two of its main proponents were Cicely Saunders, founder of the modern hospice movement, and Elisabeth Kübler-Ross, a psychiatrist and authority on end-of-life care. The active ingredients are intended to provide a welcome combination of analgesia, disinhibition, and stimulation. Cough suppression was an important effect in patients with lung or airway malignancies (or end-stage tuberculosis). The mixture was promoted as more cost effective at treating intractable cancer pain than parenteral narcotics. Several significant liabilities have contributed to the disappearance of the Brompton cocktail from modern oncology practice. In 1979, controlled trials showed that oral morphine alone gave pain relief equivalent to the cocktail, that oral morphine and oral heroin were equally effective, and that oral cocaine had no effect on patients’ alertness or sociability. One study concluded that “the Brompton Cocktail is no more than a traditional British way of administering oral morphine to cancer patients in pain.” The potential for diversion and abuse was illustrated by a case report in which an individual obtained the mixture illicitly
Salem Health: Cancer and injected it in lieu of heroin. Each of the cocktail’s active ingredients has addictive and tolerization potential, making discontinuation difficult. Even though terminal cancer patients often require multiple drugs for symptom management, the convenience of an “all-in-one” mixture of drugs such as the Brompton cocktail is outweighed by the benefits obtained by monitoring and adjusting analgesics, antineoplastics, antiemetics, and psychoactive drugs individually. Side effects: The side effects include sedation, confusion, constipation, decreased breathing, tolerization, and addiction. John B. Welsh, M.D., Ph.D. See also Do-not-resuscitate (DNR) order; End-of-life care; Home health services; Hospice care; Pain management medications; Palliative treatment.
u Bronchial adenomas Category: Diseases, symptoms, and conditions Also known as: Bronchial gland tumors, mucous gland adenomas, bronchial carcinoid tumors, cylindromas Related conditions: Carcinoid syndrome Definition: A bronchial adenoma is a slow-growing tumor in the windpipe (trachea) or in the large air passages (bronchi) leading from the windpipe to the lungs. Risk factors: The cause and risk factors for bronchial adenomas are not known. Etiology and the disease process: A bronchial adenoma can be one of several types of tumors that begin in the mucous glands; the main types of tumors are carcinoids and adenoid cystic carcinoma (also called cylindroma). The tumors are usually small and slow growing and therefore may not be diagnosed for years. Symptoms of bronchial adenoma may be confused with those of bronchial asthma or chronic bronchitis. Incidence: Approximately 1 to 3 percent of pulmonary (relating to the lungs) tumors are bronchial adenomas. Bronchial adenomas can be found in individuals of all ages but usually are found in people between the ages of thirty and fifty; the incidence is equal for men and women. Symptoms: Some of the symptoms of bronchial adenomas are difficulty breathing, hoarseness, a persistent cough, coughing up blood (hemoptysis), wheezing sounds, or pneumonia that recurs or is slow to end.
Bronchoalveolar lung cancer Screening and diagnosis: A chest X ray, computed tomography (CT) scan, or magnetic resonance imaging (MRI) can be used to detect a tumor. Often physicians will use a bronchoscopy, a procedure in which a thin, flexible tube with a very small camera is used to look at the trachea and bronchi and to take a sample of cells (biopsy) for testing. This test can distinguish a bronchial adenoma from other types of tissue growths. Sometimes it may be necessary to insert a needle through the chest wall, between the ribs, to take the biopsy for determination of the type of tumor. Treatment and therapy: Treatment of bronchial adenoma is by surgical removal of the tumor. Surgery may be bronchoscopic surgery (during a bronchoscopy) if the tumor is small or open-lung surgery. There is a small chance of recurrence of a bronchial adenoma and a very small chance of metastases. Laser ablation (removal) of a bronchial adenoma may be done through a bronchoscope, especially for tumors that have recurred. Prognosis, prevention, and outcomes: Following removal of the tumor there is an excellent long-term prognosis for individuals with a bronchial adenoma. Vicki Miskovsky, B.S., R.D See also Adenocarcinomas; Adenoid cystic carcinoma (ACC); Bronchoalveolar lung cancer; Bronchography; Bronchoscopy; 1,4-Butanediol dimethanesulfonate; Carcinoid tumors and carcinoid syndrome; Coughing; Laryngeal cancer; Lung cancers; Pneumonia.
u Bronchoalveolar lung cancer Category: Diseases, symptoms, and conditions Also known as: Non-small-cell lung cancer (NSCLC), bronchioloalveolar lung cancer, lung adenocarcinoma Related conditions: Pleural effusion, pneumonia Definition: Bronchoalveolar lung cancer is a type of NSCLC that arises in the alveoli (air sacs of the lung). It can begin as either a single site or multiple sites, or spread rapidly as a pneumonic form. Bronchoalveolar lung cancer is less likely than other types of NSCLC to spread beyond the lungs. Risk factors: The most common cause of lung cancer is smoking cigarettes. Another major cause is exposure to secondhand smoke. Other risk factors include exposure to radon gas or asbestos, environmental pollution, tuberculosis, lung disease, and an inherited predisposition to lung cancer. 197
Bronchoalveolar lung cancer Etiology and the disease process: With bronchoalveolar lung cancer, cells in the alveoli begin to grow wildly. As they grow, they progress along the alveolar walls. Multiple sites may develop and then converge to consolidate some areas of the lungs. An obstructed area of the lung may become pneumonic. Incidence: NSCLCs account for about 75 percent of all lung cancers. Bronchoalveolar lung cancer makes up about 2 to 3 percent of this group. Although 10 percent of patients with lung cancer in the United States are nonsmokers, 25 to 30 percent of patients with bronchoalveolar lung cancer are nonsmokers. It is more common in women. Symptoms: The symptoms of bronchoalveolar cancer are coughing, shortness of breath, wheezing, chest pain, large amounts of watery sputum, and hemoptysis (coughing up blood). On physical examination, the lungs are dull to percussion (tapping on the chest wall), and breath sounds may be weak or absent on auscultation (listening with a stethoscope). If the tumor is pressing on a nerve, it can cause shoulder pain or hoarseness. Screening and diagnosis: Currently, there is no accurate, inexpensive screening test for bronchoalveolar lung cancer. Researchers are working to develop such a test by looking at a marker in the blood and also at breath analysis. To diagnose lung cancer, pulmonary function tests and a chest X ray may be performed. Chest X rays can demonstrate most lung cancers, except the very small. More sensitive tests are computed tomography (CT) scans, magnetic resonance imaging (MRI), and positron emission tomography (PET) scans. To differentiate between the types of lung cancer, a biopsy of the tumor must be performed. Bronchoscopy, thoracoscopy, or mediastinoscopy may be performed to examine pulmonary secretions and the lymph nodes of the lung. If the cancer exists on the periphery of the lung, it may be necessary to perform a needle biopsy through the chest wall. If none of these procedures is effective in determining the type of lung cancer, a surgical procedure called a thoracotomy (opening the chest) can be performed. The actual diagnosis of bronchoalveolar lung cancer is made by the pathologist, who examines the tumor cells under a microscope. The pathologist identifies the type of lung cancer and stages the cancer. All NSCLCs are staged in the same way, using a combination of numeric tumor grading and the TNM (tumor/lymph node/metastasis) stages. The stages are as follows: • Stage IA, T1 N0 M0: The tumor is less than 3 centimeters (cm) and there is no lymph node involvement or metastases. 198
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•
Stage IB, T2 N0 M0: The tumor is greater than 3 cm, but it has not spread beyond the lung. • Stage IIA, T1 N1 M0: The tumor is less than 3 cm, and there is spread to local lymph nodes. • Stage IIB, T2 N1 M0, or T3 N0 M0: Either the tumor is greater than 3 cm, or it has spread into the outside of the lungs, the chest cavity, or the pericardium (sac around the heart). • Stage IIIA, T 1-3 N2 M0, or T3 N1 M0: Either the cancer has spread to distant lymph nodes but has not metastasized, or the cancer has spread into adjacent tissues and muscles and has spread to local lymph nodes. • Stage IIIB, T4 N3 M0: Either the cancer has spread to nearby organs or it has spread to distant lymph nodes but has not metastasized. • Stage IV, M1: The cancer has metastasized to distant organs. Treatment and therapy: Treatment of lung cancer can include surgery, chemotherapy, and radiation. To remove a bronchoalveolar tumor, the surgeon can perform a wedge resection, a lobectomy, or a pneumonectomy. Chemotherapy for lung cancers is effective only 35 percent of the time. The most commonly used drugs are combinations of cisplatin (Platinol), carboplatin (Paraplatin), vinorelbine (Navelbine), vincristine (Oncovin), vinblastine (Velban), paclitaxel (Taxol), docetaxel (Taxotere), and gemcitabine (Gemzar). Newer chemotherapy drugs that interfere with cell growth and reproduction as well as angiogenesis (formation of new blood vessels) are being used. They are gefitinib (Iressa), erlotinib (Tarceva), and bevacizumab (Avastin). Radiation therapy for bronchoalveolar lung cancer is not effective as a cure, so it is reserved for treatment when surgery is not possible. Prognosis, prevention, and outcomes: Patients with lower stage cancers survive longer than those with highstage cancers. Research has shown that patients who have never smoked respond better to treatments for bronchoalveolar cancer. The best way to avoid lung cancer is by not smoking and by avoiding exposure to secondhand smoke. Christine M. Carroll, R.N., B.S.N., M.B.A. u
For Further Information Houlihan, Nancy G. Lung Cancer. Pittsburgh: Oncology Nursing Society, 2004. Hunt, Ian, Martin Muers, and Tom Treasure. ABC of Lung Cancer. Malden, Mass.: Blackwell, 2008. Roth, Jack A., James D. Cox, and Waun Ki Hong, eds. Lung Cancer. 3d ed. Malden, Mass.: Blackwell, 2008.
Salem Health: Cancer u
Other Resources
LungCancer.org http://www.lungcancer.org/ MayoClinic.com Lung Cancer http://www.mayoclinic.com/health/lung-cancer/ DS00038 National Cancer Institute Lung Cancer http://www.cancer.gov/cancertopics/types/lung See also Adenocarcinomas; Adenoid cystic carcinoma (ACC); Bronchial adenomas; Bronchography; Bronchoscopy; 1,4-Butanediol dimethanesulfonate; Carcinoid tumors and carcinoid syndrome; Coughing; Laryngeal cancer; Lung cancers; Pneumonia.
u Bronchography Category: Procedures Also known as: Bronchogram, laryngography Definition: Bronchography is a radiographic evaluation that examines the interior passageways of the larynx, trachea, and bronchi. Bronchography is used somewhat infrequently because of technological advances with computed tomography (CT) scans and bronchoscopy. Cancers diagnosed: Lung cancers Why performed: Bronchography is performed to examine structural or functional abnormalities of the lower respiratory tract. Abnormalities that are commonly investigated with bronchography include bronchiectisis, hemoptysis, chronic bronchitis, chronic pneumonia, and tumors. Patient preparation: The patient is asked to not eat or drink for several hours before the procedure. The patient may also be asked to perform thorough mouth hygiene before the procedure. Steps of the procedure: The patient is asked to remove all clothing, jewelry, and dentures; to dress in a gown; and to empty the bladder. Vital signs (such as blood pressure and respiratory rate) are taken. The patient is positioned on a table that can tilt in various directions. The patient may also be given a sedative. Next, numbing medication is injected into the back of the patient’s throat to prevent gagging. Finally, the physician passes the bronchoscope down the back of the throat into the trachea and bronchi. Contrast dye is released from the bronchoscope as it advances.
Bronchoscopy The dye forms a coating on the lining of the interiors of the bronchi, trachea, and larynx. The physician then takes several X rays from different positions, after which the bronchoscope is removed. After the procedure: The patient is moved to a recovery room and has vital signs monitored for several hours postprocedure. The patient will not be allowed to eat or drink until the gag reflex has returned. The patient may be asked to gently cough up any remaining contrast dye. Normal diet may be resumed after the procedure. The throat may feel sore after bronchography. A follow-up chest X ray is often performed twenty-four to forty-eight hours after the bronchography to verify the removal of the contrast dye from the airways. Risks: Risks of the procedure include infection or pneumonia and airway obstruction from the contrast dye in patients with emphysema or chronic obstructive pulmonary disease (COPD). Results: The contrast dye allows the physician to assess the likely presence or absence of respiratory system abnormalities, such as tumors, in the larynx, trachea, or bronchi. If abnormalities are detected, then the physician will either perform a confirmatory diagnostic procedure or devise a treatment plan based on the specific test results. Jeremy W. Dugosh, Ph.D. See also Adenocarcinomas; Adenoid cystic carcinoma (ACC); Bronchial adenomas; Bronchoalveolar lung cancer; Bronchoscopy; 1,4-Butanediol dimethanesulfonate; Carcinoid tumors and carcinoid syndrome; Coughing; Laryngeal cancer; Lung cancers; Pneumonia.
u Bronchoscopy Category: Procedures Also known as: Fiber-optic bronchoscopy Definition: Bronchoscopy uses a bronchoscope to allow a doctor to see, examine, and biopsy tissues in the respiratory tract and lungs. The procedure is used to check for cancer cells. A bronchoscope is a thin tube equipped with fiber optics or a miniature camera that produces images of the internal airways and lungs. Cancers diagnosed: Respiratory tract cancer, lung cancer Why performed: Bronchoscopy is a diagnostic procedure used to view the inside of the airways and lungs. Suspicious tissues are biopsied and examined in a laboratory in order to detect the presence of cancer cells. 199
Burkitt lymphoma
Salem Health: Cancer gen levels, and heart activity. Oxygen is delivered through a nasal cannula. The bronchoscope is inserted through the nose or mouth. The airways and lungs are inspected. A bronchoalveolar lavage may be performed, which involves inserting sterile fluid to remove mucus or cells for examination. A tissue biopsy is taken by clipping a sample of abnormal tissue. At the end of the procedure, the fluid and bronchoscope are removed. After the procedure: Patients may receive a chest X ray following the procedure to ensure that the lungs were not punctured. Patients should not eat or drink until the anesthesia wears off in order to prevent choking. Patients may be hoarse, experience fever, or cough up small amounts of blood. Risks: Bronchoscopy is considered a safe procedure. The primary risks are infection and bleeding. There is a slight risk of lung perforation, heart attack, irregular heartbeat, and low blood oxygen. Results: A healthy respiratory tract and lungs are free of swelling and abnormal growths. Suspicious growths are biopsied to determine whether cancer is present. Mary Car-Blanchard, O.T.D., B.S.O.T.
A physician uses a bronchoscope. (National Cancer Institute)
Patient preparation: Patients should stop taking aspirin or blood-thinning medication a week before the procedure. Brochoscopy uses local or general anesthesia. Patients receiving general anesthesia should not eat or drink after midnight prior to the day of the procedure. Bronchoscopy is usually an outpatient procedure, and patients should arrange to have someone else drive them home. Patients wear an examination gown, which is removed from the waist up during the procedure, and receive a sedative before the bronchoscopy begins. Steps of the procedure: Patients receive general or local anesthesia, depending on whether a rigid or a flexible bronchoscope is used. Local anesthesia is injected or sprayed into the throat. Patients receive medication to eliminate secretions and to prevent coughing or gagging. Monitors are placed to measure blood pressure, blood oxy200
See also Bronchial adenomas; Bronchoalveolar lung cancer; Bronchography; Carcinoid tumors and carcinoid syndrome; Computed tomography (CT) scan; Coughing; Endoscopy; Gastrointestinal cancers; Hemoptysis; Lambert-Eaton myasthenic syndrome (LEMS); Lung cancers; Mesothelioma; Otolaryngology; Pneumonia; Sputum cytology.
u Burkitt lymphoma Category: Diseases, symptoms, and conditions Also known as: B-cell lymphoma, small noncleaved cell lymphoma Related conditions: Non-Hodgkin lymphoma Definition: Burkitt lymphoma, first described by Denis Parsons Burkitt in 1956, is a type of non-Hodgkin lymphoma that develops from B lymphocytes, the cells that produce antibodies and fight infections. Risk factors: Most people who develop Burkitt lymphoma have no identifiable risk factors, but age, sex, ex-
Salem Health: Cancer
Burkitt lymphoma
posure to chemicals that damage deoxyribonucleic acid (DNA), infections such as the Epstein-Barr virus (EBV), and a weakened immune system may be factors leading to its development. Etiology and the disease process: In North America most cases of Burkitt lymphoma are sporadic and caused by a chromosomal rearrangement. Of these rearrangements, 90 percent involve a chromosomal exchange called a translocation between chromosomes 8 and 14. This translocation moves the MYC gene from its normal position on chromosome 8 to the vicinity of the gene producing immunoglobulin G (IgG) on chromosome 14. In 10 percent of Burkitt lymphoma cases, MYC has been translocated to the vicinity of antibody-producing genes on either chromosome 2 or chromosome 22. In its new chromosomal location, MYC is overactive and results in uncontrolled cell growth. The MYC gene encodes for a transcription factor that activates other genes. One gene that is activated is HMG-I/Y, whose product transforms normal B lymphocytes into rapidly growing tumor cells. Burkitt lymphoma is endemic in equatorial Africa and is associated with not only chromosomal translocations but also the Epstein-Barr virus (EBV), which also causes infectious mononucleosis and other cancers. About 30 percent of Burkitt lymphoma patients in the United States harbor EBV. In children the disease usually begins in the abdomen, develops rapidly, and metastasizes quickly. Abdominal swelling, fluid retention, and vomiting often occur. In adults the disease often begins with a painless enlargement of a lymph gland or abdominal swelling. Depending on the location of the affected lymph node, a variety of conditions may develop. Occasionally, Burkitt lymphoma affects the blood and may result in anemia, increased bleeding, and susceptibility to infections. The B cells may invade other tissues, causing a variety of symptoms. Because the cancer is one of the most rapidly growing human tumors, most cases are in either Stage III or Stage IV at the time of diagnosis. Incidence: Burkitt lymphoma is common in central Africa, where it accounts for as much as 50 percent of cancer deaths in children. The disease is relatively rare in the United States, but when it does occur, the average age at diagnosis is seven years, and the disease accounts for about 3 percent of the total cancer deaths in people under twenty years old. The disease is also three times as likely to occur in boys as in
girls and is more common in white children than children of other races. It is 1,000 times more likely to occur in acquired immunodeficiency syndrome (AIDS) patients. Symptoms: Although most cases in the United States develop in the abdomen, the first symptom is usually a painless swelling of an axillary, neck, or groin lymph node. The affected lymph node or nodes will grow rapidly and may form lumps. Depending on where the disease develops, other symptoms may occur. In Africa, where Burkitt lymphoma is endemic, the disease often affects the face and jaw, causing extensive swelling. Screening and diagnosis: Diagnosis is by biopsy of the affected tissue followed by histological examination. Spinal fluid analysis, blood cell and platelet counts, X rays, computed tomography (CT) scans, gallium scans, and positron emission tomography (PET) scans also can be
A child with a large facial tumor caused by Burkitt lymphoma. (Centers for Disease Control and Prevention)
201
1,3-Butadiene
Salem Health: Cancer
Relative Survival Rates for Burkitt Lymphoma, 1988-2001 Years
Survival Rate (%)
1 2 3 5 8 10
53.5 47.8 47.4 45.4 45.1 45.1
Source: Data from L. A. G. Ries et al., eds., Cancer Survival Among Adults: U.S. SEER Program, 1988-2001—Patient and Tumor Characteristics, NIH Pub. No. 07-6215 (Bethesda, Md.: National Cancer Institute, 2007)
therapy, bone marrow transplants, and monoclonal antibodies also have been used to treat the disease. Prognosis, prevention, and outcomes: If the disease is relatively localized and has not spread, aggressive chemotherapy can cure up to 80 percent of the cases. If the central nervous system or the bone marrow has become involved, the effectiveness of treatment is significantly less. Charles L. Vigue, Ph.D. u
For Further Information Magrath, Ian, ed. The Non-Hodgkin’s Lymphomas. New York: Oxford University Press, 1997. Mauch, Peter, et al., eds. Non-Hodgkin’s Lymphomas. Philadelphia: Lippincott Williams & Wilkins, 2004.
u
used to diagnose the disease. The St. Jude’s Children’s Research Hospital system is commonly used to stage the disease in children. • Stage I: Lymphoma is localized to a single site. • Stage II: Lymphomas involve more than one site but are localized to one side of the body. • Stage III: Lymphomas involve multiple sites on both sides of the body but do not involve bone marrow or the nervous system. • Stage IV: Lymphomas involve the bone marrow or the nervous system. The Ann Arbor system is used for adults with the disease. • Stage I: Lymphoma is limited to one lymph node either above or below the diaphragm or is limited to one organ. • Stage II: Lymphomas are either in two or more lymph nodes on the same side of the diaphragm or are limited to one organ and the lymph nodes near that organ. • Stage III: Lymphomas have spread to lymph nodes on both sides of the diaphragm and may involve an organ. • Stage IV: Lymphomas have metastasized throughout one or more organs and may involve lymph nodes. Treatment and therapy: In children, Burkitt lymphoma is usually treated by aggressive and intense chemotherapy that may last for several months. The most common chemotherapeutic agent used is cyclophosphamide (Cytoxan), usually in combination with another chemotherapeutic agent. If large tumors are involved, radiation therapy may be indicated. In some cases surgery may be required to remove affected tissues. In adults Burkitt lymphoma is treated with chemotherapy involving a combination of chemotherapeutic agents. Radiation therapy is often used in combination with chemotherapy. Stem cell 202
Other Resources
Leukemia and Lymphoma Society http://www.leukemia-lymphoma.org/hm_lls Lymphoma Information Network Burkitt’s Lymphoma/Leukemia http://www.lymphomainfo.net/nhl/types/burkitts.html National Cancer Institute Non-Hodgkin Lymphoma http://www.cancer.gov/cancertopics/types/nonhodgkins-lymphoma See also Childhood cancers; Epstein-Barr virus; Genetics of cancer; Hepatitis C virus (HCV); Hodgkin disease; Infectious cancers; Lymphomas; Molecular oncology; MYC oncogene; Non-Hodgkin lymphoma; Oncogenic viruses; Proto-oncogenes and carcinogenesis; Viral oncology; Virus-related cancers; Young adult cancers.
u 1,3-Butadiene Category: Carcinogens and suspected carcinogens RoC status: Known human carcinogen since 2000 Also known as: Vinylethylene, bivinyl, buta-1,3-diene, α,γ-butadiene Related cancers: Leukemia, lymphosarcoma, reticulosarcoma, hematopoietic cancers Definition: 1,3-Butadiene is a hydrocarbon molecule made up of four atoms of carbon and six atoms of hydrogen. The first and last pairs of carbon atoms are held together by two chemical bonds or four electrons. The two and three carbons share a single pair of electrons. This atomic arrangement makes 1,3-butadiene highly flammable and extremely reactive.
Salem Health: Cancer Exposure routes: Inhalation, ingestion, dermal contact, exhaust from motor vehicles and cigarette smoke Where found: Industries involved in the synthesis of rubber-like materials, resins, and polymers At risk: Workers who deal with synthetic rubber, organic chemicals, and resins Etiology and symptoms of associated cancers: In all species studied, including humans, 1,3-butadiene has been shown to be oxidized to rings that involve two of the carbon atoms and one atom of oxygen. Such epoxides are chemically similar to the known carcinogen ethylene oxide. Tumor production in both rodents and humans involves reaction with deoxyribonucleic acid (DNA), producing genetic alterations in tumor-suppressor genes. History: The shortage of natural rubber in World War II caused an intense search for synthetic latex. It was determined that 1,3-butadiene reacts readily with other similar hydrocarbons to produce a wide variety of polymeric substances. An example is copolymerization with styrene, a molecule involving the carcinogen benzene. Uncertainty in early studies of 1,3-butadiene carcinogenicity resulted when conditions also involved benzene. More than 75 percent of 2 million metric tons of 1,3-butadiene produced in a typical year are consumed by the rubber industry; the compound is also involved in nylon synthesis. Studies of workers in synthetic rubber plants beginning in 1943 gave conflicting evidence concerning the carcinogenicity of 1,3-butadiene. Later animal studies with rats and mice exhibited a strong pattern of incremental risk for a variety of cancers. More carefully controlled studies of production workers in the early 1990’s documented 1,3butadiene’s carcinogenic nature. Extensive federal regulation of 1,3-butadiene exists. The U.S. Department of Transportation (DOT) lists the chemical as hazardous and requires special marking, labeling, and transporting precautions. The U.S. Environmental Protection Agency (EPA), acting under the Clean Air Act (1970), lists 1,3-butadiene as one of thirty-three hazardous air pollutants that present the greatest threat to public health and requires that as little as ten pounds of the substance must be reported. The Occupational Safety and Health Administration (OSHA) has set the permissible exposure limit at one part per million. K. Thomas Finley, Ph.D. See also Air pollution; Carcinogens, known; Carcinogens, reasonably anticipated.
1,4-Butanediol dimethanesulfonate
u 1,4-Butanediol
dimethanesulfonate Category: Carcinogens and suspected carcinogens; chemotherapy and other drugs RoC status: Known human carcinogen since 1985 Also known as: Myleran, busulfan Related cancers: In patients receiving busulfan for chronic myeloid leukemia (CML), cytological anomalies and cancers were observed at a variety of sites, including breast cancer, female genital cancers, and leukemia. Cancer patients given busulfan for bronchial cancer developed leukemia that was not dose related. Definition: Busulfan is a sulfonurea alkylating agent that contains reactive alkyl groups that readily combine with other molecules via cross-linking of deoxyribonucleic acid (DNA) strands in the nuclei of rapidly dividing cells, thereby destroying them. A prescription drug employed in chemotherapy of leukemias, especially CML, busulfan does not selectively harm cancer cells but kills normal cells as well, and it is considered to be mitogenic, carcinogenic, and leukemogenic. Locally it may cause blistering of the skin and damage to the eyes and respiratory tract. Systemic toxic effects include nausea and vomiting, reduction in both leukocytes and erythrocytes, and hemorrhage. Exposure routes: Intravenous (IV), oral/ingestion of tablets Where found: People may be exposed via chemotherapy (oral or IV) for treatment of various types of leukemia, especially CML, and before bone marrow transplants (used to treat CML), in combination with cyclophosphamide used as a conditioning regimen. At risk: There is a potential for occupational exposure in employees who formulate and package busulfan tablets, and for health care professionals who administer IV busulfan to patients. Etiology and symptoms of associated cancers: Busulfan may cause cellular dysplasias and cytologic abnormalities. Busulfan, which is both leukemogenic and carcinogenic, has been shown to cause cancer of the breast and female reproductive organs as well as leukemias in humans, though evidence is limited in animal studies. Related symptoms and signs vary by cancer. For leukemia, they in203
1,4-Butanediol dimethanesulfonate clude weakness, fever, bleeding gums, petechiae, swollen glands, and enlarged spleen or liver; for breast cancer, a new lump or mass in the breast; and, for endometrial cancer, postmenopausal, or irregular vaginal bleeding. History: Introduced in 1950, busulfan raised the median survival time for CML to approximately 3.5 to 4.5 years. However, because busulfan proved more efficient at destroying normal stem cells than CML cells, it has been largely supplanted by more specific and less toxic agents. Malignant tumors and acute leukemias have been reported in patients who were treated with busulfan; the World
204
Salem Health: Cancer Health Organization (WHO) found a cause-and-effect relationship between busulfan and secondary malignancies. The International Agency for Research on Cancer found four cases of acute leukemia among 243 patients treated with busulfan as adjuvant chemotherapy following surgical removal of bronchogenic carcinoma, suggesting that busulfan is leukemogenic. Cynthia Racer, M.A., M.P.H. See also Carcinogens, known; Carcinogens, reasonably anticipated; Chronic myeloid leukemia (CML).
Salem Health: Cancer
u CA 15-3 test Category: Procedures Also known as: Carbohydrate antigen 15-3, cancer antigen 15-3 Definition: CA 15-3 is a transmembrane glycoprotein (carbohydrate-containing protein) found in several tissue types. It is classified as a MUC1 member of the mucin family of proteins. This class of glycoproteins is thought to play a role in reducing cell-to-cell interaction and inhibition of tumor cell cytolysis. The core protein component is identical; the carbohydrate concentration (degree of glycosylation) is the component differentiating between tissue types. Serum/plasma levels are determined by immunoassay. Cancers diagnosed: CA 15-3 is not an organ-specific marker and has been found at elevated levels in ovarian, prostatic, and lung cancer. Additionally, increased CA 15-3 levels can be found concomitant with benign conditions such as breast or ovarian disease, endometriosis, pelvic inflammatory disease, hepatitis, pregnancy, and lactation. Why performed: Because CA 15-3 is not sensitive or specific enough to be used as a screening test, its primarily utility is as a tumor marker for monitoring response to therapy and recurrence in breast cancer patients. At least 70 percent of advanced breast cancer cases have tumors that shed CA 15-3. Blood levels typically are proportional to the tumor burden (mass), with higher levels of CA 15-3 indicative of the presence of a larger tumor. Patient preparation: No special patient preparation is required for accurate CA 15-3 analysis. Steps of the procedure: A blood sample is collected, typically by venipuncture. The collected serum (or plasma) is tested by immunoassay, which involves capturing the CA 15-3 present in the sample by means of monoclonal antiCA 15-3 antibodies. A second, detection (labeled) antibody is then introduced, which subsequently binds to the CA 15-3/anti-CA 15-3 complex. The addition of a substrate results in a detectable signal, the level of which is directly proportional to the amount of the CA 15-3 present in the sample. After the procedure: Pressure should be applied to the venipucture site in order to avoid the development of hematoma (a mass of clotted blood resulting from bleeding under the skin).
CA 19-9 test Risks: The risks of venipuncture are slight but include excessive bleeding, fainting, hematoma, and infection (always a slight risk any time the skin is broken). Results: Although each laboratory establishes reference intervals based on the local, normal population, a basic interpretive guideline would place normal at 0-31 units per milliliter (U/mL) and elevated at more than 31 U/mL. Pam Conboy, B.S. See also CA 19-9 test; CA 27-29 test; CA 125 test; Tumor markers.
u CA 19-9 test Category: Procedures Also known as: Carbohydrate antigen 19-9, cancer antigen 19-9 Definition: CA 19-9 is a glycolipid (carbohydratecontaining fat) characterized glycoprotein (carbohydratecontaining protein, or mucin). It is similar to the type A blood group protein, with additional sialic acid residues. CA 19-9 is found in normal fetal cells as well as in the pancreas, salivary ducts, gastric and colonic epithelium, pancreatic and gastric fluid, saliva, and meconium (first stool of a newborn). It is normally removed from circulation by the biliary system. Serum/plasma levels are determined by immunoassay. Cancers diagnosed or treated: CA 19-9 is elevated in patients with gastrointestinal tract carcinoma, including cancer of the pancreas, stomach, colon, and ovaries. Abnormally high values may also be detected in benign conditions such as acute pancreatitis, cirrhosis, cholecystitis, biliary obstruction, gastric ulcer, pulmonary disease, and chronic hepatitis C and in patients who smoke. Why performed: Because CA 19-9 is not sensitive or specific enough to be used as a screening test, its primarily utility is as a tumor marker for monitoring response to therapy and recurrence in pancreatic cancer patients. Levels are typically proportional to the tumor burden (mass), with higher levels of CA 19-9 indicative of the presence of a larger tumor. Very elevated levels, defined as more than 1,000 kilounits per liter (kU/L), are highly specific for pancreatic cancer and indicate very advanced disease. Patient preparation: No special patient preparation is required for accurate CA 19-9 analysis. 205
CA 27-29 test Steps of the procedure: A blood sample is collected, typically by venipuncture. The collected serum (or plasma) is tested by immunoassay, which involves capturing CA 19-9 present in the sample by means of monoclonal anti-CA19-9 antibodies. A second, detection (radiolabeled) antibody is then introduced, which subsequently binds to the CA 19-9/ anti-CA 19-9 complex. The addition of a substrate results in a detectable signal, the level of which is directly proportional to the amount of the CA19-9 present in the sample. After the procedure: Pressure should be applied to the venipucture site in order to avoid the development of a hematoma. Risks: The risks of venipuncture are slight but include excessive bleeding, fainting, hematoma, and infection (always a slight risk any time the skin is broken). Results: Although each laboratory establishes reference intervals based on the local, normal population, a basic interpretive guideline places normal at 0-40 kilounits per milliliter (kU/mL) and elevated at more than 40 kU/mL. Pam Conboy, B.S. See also Bile duct cancer; CA 15-3 test; CA 27-29 test; CA 125 test; Pancreatic cancers; Tumor markers.
u CA 27-29 test Category: Procedures Also known as: Carbohydrate antigen 27-29, cancer antigen 27-29 Definition: Similar to CA 15-3, CA 27-29 is a transmembrane glycoprotein (carbohydrate-containing protein, or mucin) found in several tissue types. This class of glycoproteins is thought to play a role in reducing cell-to-cell interaction and the inhibition of tumor cell cytolysis. The core protein component is identical; the carbohydrate concentration (degree of glycosylation) is the component differentiating between tissue types. Serum/plasma levels are determined by immunoassay. Cancers diagnosed: CA 27-29 is not an organ-specific marker and has been found at elevated levels in breast, ovarian, colon, stomach, kidney, lung, pancreas, uterus, and liver cancers. Additionally, increased CA 27-29 levels can be found concomitant with benign conditions such as first trimester pregnancy, endometriosis, ovarian cysts, and breast, kidney, and liver disease. Why performed: Because CA 27-29 is not sensitive or specific enough to be used as a screening test, its primary 206
Salem Health: Cancer utility is as a tumor marker for monitoring response to therapy and recurrence in previously treated Stage II and Stage III breast cancer patients. Blood levels are typically proportional to the tumor burden (mass), with higher levels of CA 15-3 indicative of the presence of a larger tumor. Physicians will typically order either CA 27-29 levels or CA 15-3 levels but not both, as they are considered essentially equivalent in diagnostic value. Patient preparation: No special patient preparation is required for accurate CA 27-29 analysis. Steps of the procedure: A blood sample is collected, typically by venipuncture. The collected serum (or plasma) is tested by immunoassay, which involves capturing CA 2729 present in the sample by means of monoclonal anti-CA 27-29 antibodies. A second, detection (labeled) antibody is then introduced, which subsequently binds to the CA 2729/anti-CA 27-29 complex. The addition of a substrate results in a detectable signal, the level of which is directly proportional to the amount of the CA 27-29 present in the sample. After the procedure: Pressure should be applied to the venipuncture site in order to avoid the development of a hematoma. Risks: The risks of venipuncture are slight but include excessive bleeding, fainting, hematoma, and infection (always a slight risk any time the skin is broken). Results: Although each laboratory establishes reference intervals based on the local, normal population, a basic interpretive guideline for CA 27-29 places normal at 0-32 units per milliliter (U/mL) and elevated at more than 32 U/mL. Pam Conboy, B.S. See also CA 15-3 test; CA 19-9 test; CA 125 test; Tumor markers.
u CA 125 test Category: Procedures Also known as: Cancer antigen 125, CA125, CA-125, CA125-II Definition: CA 125 is a mucinous glycoprotein that may be elevated in some cancer cells, particularly those associated with ovarian cancer. Cancers diagnosed: Ovarian cancer, uterine cancer, breast cancer, lung cancer
Salem Health: Cancer
Cachexia
Why performed: CA 125 serves as a biomarker or tumor marker to determine the presence of cancer. It is generated on the surface of cells and released into the bloodstream. Concentrations of CA 125 often are elevated in ovarian cancer patients.
u Cachexia
Patient preparation: No special preparation is necessary.
Related conditions: Anorexia
Steps of the procedure: To determine the level of CA 125 in a patient, blood is drawn from a vein, typically from the inside of an elbow or sometimes from the back of a hand. The site of extraction is first cleaned with an antiseptic. An elastic band is often applied around the upper arm to apply pressure and cause the vein to engorge with blood. After a needle is inserted into the selected vein, blood is collected in a syringe or an airtight vial. Once the blood is collected, the needle is removed and the puncture site is bandaged to stop any subsequent bleeding.
Definition: Cachexia is a complex syndrome in which changes in the way the body uses food—particularly fat and carbohydrates—lead to loss of muscle and fat. Anorexia (loss of appetite) is sometimes, but not always, associated with cachexia.
After the procedure: There may be throbbing or bruising around the extraction site. Risks: The risks involved in collecting blood to ascertain CA 125 levels include the possibility of excessive bleeding, fainting or light-headedness, blood accumulating under the skin (hematoma), and infection around the puncture site. There is always the possibility of multiple punctures being necessary to find a vein that will yield blood. Results: A CA 125 level greater than 35 units per milliliter (U/mL) of blood is considered to be elevated. In many cases, elevated levels are not an indication of cancer but instead can be attributed to other conditions, such as endometriosis and benign ovarian cysts. The lack of specificity is a key problem when using CA 125 as a cancer marker. In 79 percent of women tested with known ovarian cancers, CA 125 levels were elevated, while the other 21 percent showed no elevated CA 125 concentrations. The CA 125 test for ovarian cancer is most reliable in women who have gone through menopause. Tracking CA 125 levels periodically over time to determine the rate at which levels fluctuate is much more definitive than a single CA 125 test. Elevated CA 125 levels, particularly in postmenopausal women, indicate the need for further screening that may include ultrasonic imaging, computed tomography (CT) scans, and surgery. Alvin K. Benson, Ph.D. See also CA 15-3 test; CA 19-9 test; CA 27-29 test; Endometrial cancer; Fallopian tube cancer; Fertility drugs and cancer; Ovarian cancers; Ovarian cysts; Ovarian epithelial cancer; Proteomics and cancer research; Tumor markers; Uterine cancer.
Category: Diseases, symptoms, and conditions Also known as: Wasting syndrome, anorexia-cachexia syndrome
Risk factors: Certain cancers such as lung cancer or any cancer of the digestive tract—particularly of the esophagus, stomach, and pancreas—are more likely to be accompanied by cachexia. It is also common in advanced cancer, although infrequently it occurs in early cancers, sometimes even before diagnosis. Cachexia can also occur with acquired immunodeficiency syndrome (AIDS). Etiology and the disease process: In cancer-related cachexia, it is thought that the tumor releases chemicals that change food metabolism. Patients with cachexia tend to have poor appetites. Even with nutritional supplementation, the wasting cannot be reversed while the cancer remains. Incidence: When diagnosed, about 80 percent of patients with cancers in the upper gastrointestinal tract and 60 percent of patients with cancers of the lung have already lost considerable weight. More than 80 percent of patients who die from any cancer or from AIDS have cachexia. Patients with any solid tumor except breast cancer are generally more prone to cachexia, and it is also more common and more pronounced as the disease progresses in children and in the elderly. Symptoms: Cachexia is one of the most overwhelming symptoms of cancer, demolishing quality of life with numbing fatigue, loss of appetite or changes to taste, and severe weight loss of 10 percent or more of body weight. Screening and diagnosis: When a person experiences unexplained weight or appetite loss or fatigue, medical practitioners without more specific clues might perform such general screens as a complete blood count and a chest X ray. When the source of the problem is suspected, tests are more specific. With a known cancer, cachexia diagnosis is based on clinical history, substantial weight loss, and physical examination. The concentration of plasma albumin in blood will usually be low. Extensive diagnostics are not normally required. 207
Cadmium and cadmium compounds Treatment and therapy: The best course of action for cachexia is treatment of the underlying disease. After successful treatment, patients regain lost muscle and fat mass. Prognosis, prevention, and outcomes: Prognosis is very poor with cachexia in advanced disease. When cachexia occurs in the early stages of cancer, the cancer that causes it is often responsive to treatment, and successful treatment removes the source of changes to metabolism. Jackie Dial, Ph.D. See also Antinausea medications; Appetite loss; Nutrition and cancer treatment.
u Cadmium and cadmium
compounds Category: Carcinogens and suspected carcinogens RoC status: Known human carcinogen since 2000 Also known as: Cadmium chloride, cadmium sulfate, cadmium nitrate, cadmium oxide, cadmium sulfide, cadmium carbonate, greenockite, capsebon, cadmopur yellow Definition: Cadmium is a natural metal, usually occurring in combination with other elements rather than in its pure state. It is most frequently found in zinc deposits as cadmium sulfide. Commercial use of cadmium began at the end of the nineteenth century and became widespread by the middle of the twentieth century. The noncorrosive properties of cadmium led to its use in batteries, electroplating, and coating of other metals, such as steel. Workers are at risk for occupational exposure to cadmium through inhalation, but cadmium also may be released into the environment through these industrial processes. Additionally, cadmium is released into the environment from other sources, including forest fires, volcanos, weathering of rocks, and combustion of fossil fuels such as coal. Both industrial and natural releases of cadmium into the atmosphere put the general public at risk for exposure through contaminated water, air, and soil. Plants can absorb cadmium from contaminated soil, so the major exposure to cadmium in the general public is through the food supply. Tobacco plants are among those that absorb cadmium, so tobacco smoking is another source of exposure in the general public. Related cancers: Lung cancer, possibly prostate and kidney cancer Exposure routes: Inhalation and ingestion 208
Salem Health: Cancer Where found: Food (particularly grain cereal products, potatoes, and other vegetables), cigarette smoke, zinc and lead ores, electroplating and -coating, alloys, pigments (paint, glass, ceramics, porcelain, textiles, plastics, paper, and fireworks), stabilizers in plastics, nickel-cadmium batteries, smoke detectors, radiation detectors, and various electronics and laboratory equipment At risk: Workers who refine and smelt zinc and lead ores, workers in industries using thermal processes (iron production or welding cadmium-coated steel), and tobacco smokers Etiology and symptoms of associated cancers: Cadmium exposure can be acute or chronic. Acute toxicity through ingestion of cadmium may cause only short-term illness, but acute toxicity through inhalation can lead to severe damage to the lungs and even death. Chronic exposure to cadmium can cause damage to the lungs, kidneys, and sometimes bones. Studies have shown that inhalation of cadmium in the workplace is associated with lung cancer. Laboratory studies using cultured cells have shown that cadmium damages the dexoyribonucleic acid (DNA) of the cells and affects the cells’ ability to repair DNAdamage. These factors are likely to be the mechanism through which cadmium contributes to the formation of cancer in humans. Lung cancer can affect one lung or both. Lung cancer detection often occurs when the disease has progressed to late stages because symptoms may take years to appear. When symptoms do appear, they often are mistaken for other less serious conditions. Common signs and symptoms of lung cancer are persistent cough (not related to smoking); persistent pain in the chest, shoulder, or back; coughing up mucus or blood; recurrent respiratory infections; shortness of breath; fatigue; unexplained weight loss; and loss of appetite. Many of these symptoms may be attributed initially to other causes before lung cancer is eventually diagnosed. Lung cancer is the only cancer that has been confirmed to be associated with cadmium exposure. Studies from the 1960’s and later have had conflicting results regarding a connection between cadmium and prostate cancer. A number of studies have shown increases in the occurrence of prostate cancer in workers exposed to cadmium in nickel-cadmium battery plants and other industrial sites, but conflicting studies have indicated no increases or increases that were too small to be statistically significant. Cadmium has also been implicated in kidney cancer, with early studies showing a correlation between exposure and increases in kidney cancer. However, further studies have not confirmed this association.
Salem Health: Cancer History: Industrial use of cadmium became widespread in the middle of the twentieth century, and the toxic effects due to occupational exposure began to be recognized by the early 1950’s. Studies that examined workers who had been exposed to high levels of cadmium were used to examine the toxic effects, and by the 1960’s researchers were investigating cadmium’s potential carcinogenicity. Experimental animal studies also were conducted to research the toxicity and carcinogenicity of cadmium. Regarding the role cadmium played in the development of lung cancer, initial studies were inconclusive or conflicting. Confounding factors, such as workers who were also tobacco smokers or were exposed to additional heavy metals, contributed to the confusing results. Because of its toxic effects, many federal, state, and local agencies, including the Environmental Protection Agency (EPA), began to regulate cadmium in a variety of ways, including stipulation of allowable amounts in air and water. In 1992 the Occupational Safety and Health Administration (OSHA) ruled on permissible exposure limits (PELs) for workers exposed to airborne cadmium in the workplace. By 2000 sufficient studies reported that cadmium contributed to the development of lung cancer for it to be designated as a known human carcinogen by the U.S Department of Health and Human Services. Michelle L. Herdman, Ph.D. u For Further Information Klaassen, Curtis D., ed. Casarett and Doull’s Toxicology: The Basic Science of Poisons. New York: McGrawHill, 2001. Silvera, S. A. N., and T. E. Rohan. “Trace Elements and Cancer Risk: A Review of the Epidemiologic Evidence.” Cancer Causes Control 18 (2007): 7-27. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Eleventh Report on Carcinogens. Research Triangle Park, N.C.: Author, 2005. Waisberg, M., P. Joseph, B. Hale, and D. Beyersmann. “Molecular and Cellular Mechanisms of Cadmium Carcinogenesis.” Toxicology 192 (2003): 95-117. u
Other Resources
Agency for Toxic Substances and Disease Registry http://www.atsdr.cdc.gov U.S. Department of Labor Occupational Safety and Health Administration http://www.osha.gov
Caffeine U.S Environmental Protection Agency http://www.epa.gov See also Chewing tobacco; Coke oven emissions; Free radicals; Kidney cancer; Nickel compounds and metallic nickel; Soots; Urinary system cancers.
u Caffeine Category: Lifestyle and prevention; carcinogens and suspected carcinogens ATC code: N06BC01 Also known as: Trimethylxanthine, coffeine, theine, mateine, guaranine, methyltheobromine Definition: Sometimes considered the most widely used drug in the world, caffeine is an alkaloid stimulant found naturally in coffee, tea, cocoa, and many carbonated drinks. Caffeine is a secondary metabolite substance that plants manufacture as a pesticide against insects and other invertebrates. Humans use the naturally bitter caffeine as a stimulant. Coffee, tea, and cocoa have become extraordinarily popular in most cultures of the world. In the United States, for example, it is estimated that 80 percent of adults drink either coffee or tea and over 70 percent of adults and children consume soft drinks that contain caffeine. Different studies support different arguments that caffeine has a positive or negative correlation with cancer. Related cancers: Skin cancer, breast cancer, colon cancer, rectal cancer, bladder cancer, kidney cancer, ovarian cancer, pancreatic cancer Delivery routes: Caffeine is most often ingested as a stimulant in coffee, tea, cocoa, chocolate, soft drinks, and “energy drinks.” Caffeine tablets are also taken orally as a stimulant. Caffeine is also an ingredient in certain nonprescription drugs designed to address colds, flu, headache, and pain, as well as preparations that function as stimulants to allow users to stay awake. How this drug works: Caffeine acts as a stimulant because it inhibits neurotransmitters that normally act as depressants. Specifically, caffeine occupies the neuron’s receptor sites for adenosine, which is a neuron inhibitor. Instead of being blocked and inhibited, the neuron remains active, thereby increasing neuron activity. Despite numerous studies, the relationships between caffeine intake and cancer risk remain inconclusive at best and contradictory at worst. Some studies show an inverse relationship between caffeine intake and cancer risk, while 209
Caffeine other studies suggest that caffeine increases the risk of certain cancers. Links between caffeine and cancer risk are based on the suggestion that caffeine and some of its metabolites can cause changes in cell reproduction that might enhance growth and proliferation, thereby increasing the growth and spread of cancerous cells that develop. Alternatively, other studies have suggested that caffeine and a related molecule called theophylline can block production of an enzyme that is crucial for cell growth, thereby inhibiting tumor proliferation. Studies at Rutgers University demonstrated that hairless mice treated with caffeine showed much greater resistance to skin tumors than untreated mice, but the experiment has yet to be conducted on human volunteers. Possibly the greatest concern is about a possible relationship between caffeine consumption and breast cancer incidence, with some studies suggesting that a combination of caffeine and methylxanthines showed positive correlation to breast cancer and other diseases of the mammary glands. For example, caffeine and methylxanthines (also found in coffee and tea) are associated with increased severity of fibrocystic breast disease, which may lead to the development of breast cancer, but this finding is contradicted by other studies, leading the American Cancer Institute to announce that there is no evidence between breast cancer and caffeine intake at any level. Although numerous studies have suggested a causal re-
Salem Health: Cancer lationship between coffee intake and pancreatic cancer, none so far has provided conclusive support. The relationship between caffeine and cancer is complex and remains unproven; both the International Agency for Research on Cancer and the American Cancer Society have concluded that there is no evidence that caffeine is carcinogenic. This verdict is echoed by the World Health Organization (WHO) and the Food and Drug Administration (FDA).
Side effects: In the short term caffeine increases attention span and simultaneously decreases the feeling of tiredness and weariness. Caffeine intake in children may cause hyperactive behavior. Caffeine can offset some of the effects of alcohol, but performance and coordination remain unaffected. Caffeine also increases plasma levels of fatty acids, cortisol, and epinephrine. Negative effects of excessive caffeine consumption vary with age, diet, and exercise levels. Generally, higher caffeine intake may elevate blood levels of sugars and fats, increase blood pressure, irritate the lining of the stomach, and cause heartburn, irregular heartbeat, irritability, nervousness, anxiety, depression, insomnia, and the disruption of sleeping habits. Excessive caffeine intake has also been linked to stroke and heart attack. The relationship between caffeine intake and heart problems is of great concern. Recent studies by the Adventist Health Study group reported finding a 50 percent increase in risk of serious heart disease, including heart palpitations and cardiac arrhythmias, both of which can lead to heart attacks. Other studies, however, have failed to demonstrate any relationship between coronary heart disease, stroke, and caffeine intake. Some researchers have also suggested a relationship between caffeine doses and the severity and duration of premenopausal syndrome (PMS) in females among heavy consumers of coffee, tea, and other fluids containing caffeine. Other studies have linked higher-thannormal caffeine consumption with lowered rates of conception, birth defects, retarded fetal growth, reduced birth weight, spontaneous abortion, premature delivery, and stillbirth. There is some evidence that caffeine intake by males prior to mating may result in significant fetal growth retardation, but this too remains problematic A cup of cappuccino contains the alkaloid stimulant known as caffeine. (©Draganr/ and awaits further study. While none of Dreamstime.com)
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Salem Health: Cancer these claims is absolute, women are advised not to consume caffeine while pregnant or planning on becoming pregnant, since blood levels of caffeine can be transferred through the placenta and can be metabolized by a developing fetus. Finally, high caffeine intake reduces the absorption of dietary iron by 40 to 60 percent and reduces calcium intake while simultaneously increasing the rate of calcium loss, all of which may lead to serious calcium imbalance in blood and body fluid levels. Dwight G. Smith, Ph.D. u For Further Information Gilbert, S. G. A Small Dose of Toxicology: The Health Effects of Common Chemicals. Boca Raton, Fla.: CRC Press, 2004. Porta, M., et al. “Coffee Drinking: The Rationale for Treating It as a Potential Effect Modifier of Carcinogenic Exposures.” European Journal of Epidemiology 18, no. 4 (2003): 289-298. Rowley, R., M. Zorch, and D. B. Leeper. “Effect of Caffeine on Radiation-Induced Mitotic Delay: Delayed Expression of G2 Arrest.” Radiation Research 97, no. 1 (January, 1984): 178-185. Waldren, C. A., and I. Rasko. “Caffeine Enhancement of X-Ray Killing in Cultured Human and Rodent Cells.” Radiation Research 73, no. 1 (January, 1978): 95-110.
See also Benign prostatic hyperplasia (BPH); Clinical breast exam (CBE); Diarrhea; Esophagitis; Fatigue; Fibrocystic breast changes; Gastric polyps; Gastrointestinal complications of cancer treatment; Green tea; Hot flashes; Nutrition and cancer prevention; Side effects.
u Calcifications of the breast Category: Diseases, symptoms, and conditions Also known as: Microcalcifications, macrocalcifications Related conditions: Hyperplasia, precancer of the duct, fibroadenoma Definition: Calcifications are calcium deposits in breast tissue, not detectable by touch but visible on mammograms as white spots. Macrocalcifications are large deposits, not indicative of cancer. Microcalcifications appear as tiny white specks on mammograms. Scattered throughout a mammogram, they are usually not cause for concern. They may indicate possible precancer when they appear in irregular patterns or are concentrated in one area of the breast.
Calcifications of the breast Risk factors: Macrocalcifications and 80 percent of microcalcifications are harmless. Women in their childbearing years are prone to microcalcifications. Etiology and the disease process: Macrocalcifications are related to changes in the breast due to inflammation, injury, or aging. Microcalcifications may appear in areas of rapidly dividing cells and therefore can indicate precancer. Incidence: Macrocalcifications occur in about half of women over age fifty and in about 1 in 10 women under the age of fifty. Microcalcifications are usually evident in women only during their childbearing years. Symptoms: No symptoms are associated with calcifications of either kind. Screening and diagnosis: Calcifications are visible only on radiologic images. Macrocalcifications are harmless and require no further attention. Doctors may order special magnified mammographic views of microcalcifications in clusters or in odd patterns. Generally a biopsy is not needed at the first appearance of suspect patterns. Doctors typically have the patient repeat the mammogram three to six months later. If the repeat mammogram does not exhibit any obvious changes in the pattern or number of microcalcifications, a regular schedule of mammograms is adequate to monitor further changes. If microcalcifications appear particularly suspect on first appearance or if changes are noted in the repeat mammogram, a core needle biopsy or a surgical biopsy can be done to rule out precancer. Treatment and therapy: If a patient has microcalcifications removed for biopsy that prove to be precancerous, she should be followed closely with regular mammograms to identify any future occurrences. Prognosis, prevention, and outcomes: Macrocalcifications and the majority of microcalcifications (80 percent) have no relation to cancer. If a precancerous area is identified in microcalcifications, it can be removed completely many years before it has a chance to develop into actual cancer, and the patient’s prognosis is excellent. Any other suspect microcalcifications should be removed fully and analyzed. Patients should be closely followed for the occurrence of new microcalcifications. After menopause, microcalcifications generally no longer occur. Charlotte Crowder, M.P.H., ELS See also Breast ultrasound; Ductogram; Fibroadenomas; Hormone replacement therapy (HRT); Lobular carcinoma in situ (LCIS); Microcalcifications; Tubular carcinomas; Wire localization. 211
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u Calcium Category: Lifestyle and prevention Also known as: Calcium carbonate, calcium citrate, calcium phosphate Definition: Calcium is the most abundant mineral in the body. About 1 percent of calcium is found circulating in the blood, while the remaining 99 percent is stored in bones and teeth. Calcium must be obtained from the diet. It is found primarily in dairy products and is sold as a dietary supplement. Cancers treated or prevented: Colorectal cancer, breast cancer Delivery routes: Oral tablet How this substance works: Circulating levels of calcium help control metabolic events such as muscle contraction and nerve impulse transmission. In healthy people, the amount of calcium in the blood is kept within narrow limits by hormonal regulation. Calcium also helps to build strong bones and delay bone loss caused by aging (osteoporosis). The United States Office of Internal Medicine has established a maximum safe intake level for calcium of 2,500 milligrams per day for persons over one year of age. Animal studies and several human observational and research studies have found that increased intake of calcium is protective against the development of colorectal cancer. The reason for this protective effect is not understood, and not all studies have found calcium to be protective against colorectal cancer. In 2007, the Women’s Health Initiative study of more than 36,000 women aged fifty to seventy-nine found no effect of calcium on the development of colorectal cancer. More research must be done on the relationship between cancer and calcium in different age and gender groups before drawing any firm conclusions. Animal studies have also suggested that calcium may protect against breast cancer. In 2007, a peer-reviewed study of 10,500 premenopausal women found that when the intakes of calcium and vitamin D were simultaneously increased for an extended period, the risk of developing breast cancer was reduced by almost one-third. This effect was not seen in postmenopausal women. Clinical trials examining the relationship between cancer and calcium are under way; information is available at http://www .clinicaltrials.gov. Side effects: Complicating the situation with calcium is evidence that increasing calcium intake in men in amounts ranging from 600 to 2,000 milligrams or more per day may 212
Salem Health: Cancer increase the risk of developing prostate cancer. This is not, however, a consistent finding, and more rigorous studies need to be done. Many tumors that invade bone release stored calcium and cause the blood level of calcium to increase independent of dietary intake. This condition, called hypercalcemia, is the most common life-threatening metabolic disorder associated with cancer. Martiscia Davidson, A.M. See also Bone scan; Breast cancers; Caffeine; Calcifications of the breast; Cartilage supplements; Chemoprevention; Colon polyps; Colorectal cancer; Ductogram; Fiber; Gastrointestinal cancers; Hypercalcemia; Kidney cancer; Microcalcifications; Nutrition and cancer prevention; Polyps.
u Cancell Category: Complementary and alternative therapies; chemotherapy and other drugs Also known as: Entelev, Sheridan’s Formula, Jim’s Juice, Canctron, JS-114, JS-101, 126-F Definition: Cancell (previously known as Entelev) is a controversial and unapproved therapy developed in the late 1930’s. Cancell is a combination of chemicals that is thought to kill cancer cells by affecting their cellular respiration and/or electrical voltage. No clinical trials using Cancell have been published in peer-reviewed journals, and in 1989, the U.S. Food and Drug Administration (FDA) declared it illegal for manufacturers to sell and/or transport Cancell across state lines. Cancers treated or prevented: The manufacturers claim that Cancell can treat all types of cancer; however, it is not approved by the FDA. Delivery routes: Cancell is in liquid form and has been taken by mouth, inserted into the rectum, or applied to the skin (on the wrist or ball of the foot). How this substance works: Cancell (then known as Entelev) was first envisioned in the late 1930’s by the biochemist James V. Sheridan. In 1984, Edward J. Sopcak began making Cancell. Sheridan believed that Cancell affects cellular respiration, a chemical process that uses oxygen and provides energy to a cell. He further speculated that cells which do not require oxygen for respiration are “primitive” and that these primitive cells may be recognized, attacked, and killed by the body’s immune system or through other processes. Accordingly, Sheridan be-
Salem Health: Cancer lieved that Cancell could change cancer cells to a primitive state. Similarly, Sopcak thought that Cancell affected the vibrational frequency and energy of cancer cells, which may disrupt cancer proteins and change cancer cells to primitive cells. In either theory, the hypothesis is that Cancell makes cancer cells become primitive, which would allow the body to get rid of them. Cancell contains various ingredients, including the chemicals inositol, nitric acid, sodium sulfite, potassium hydroxide, sulfuric acid, and catechol. Laboratory studies conducted by the National Cancer Institute (NCI) found that Cancell could not be taken safely by humans at doses high enough to kill cancer cells. Therefore, the NCI concluded that Cancell did not show sufficient anticancer activity to merit continuing the studies. Furthermore, no studies of Cancell (in either animals or humans) have been published in peer-reviewed scientific journals. Side effects: The main side effects of Cancell include tiredness during the first few weeks of treatment, as well as nausea and diarrhea. Elizabeth A. Manning, Ph.D. See also Essiac; Laetrile; Mistletoe; PC-SPES; Sun’s soup.
u Cancer biology Category: Cancer biology Definition: The transformation of a normal cell into a cancerous one is a complicated process consisting of multiple steps and many changes to the cell and its normal control mechanisms. The fact that most human cancers develop later in life reflects the time required for these changes to occur. These changes include the activation of oncogenes, the inactivation of tumor-suppressor genes, and acquisition of a cell’s ability to become immortal, to invade new tissues at distant locations, and to induce the formation of new blood vessels. Characteristics of human cancers: Mutations that are present in the germ cells (egg and sperm) can be passed to the next generation. Mutations that occur in any other cells of the body, called somatic mutations, may affect the cell or tissue in which they occur, but they will not be passed to the next generation. Both germ-line and somatic mutations can cause cancer; it is estimated that approximately 10 percent of cancers are caused by germ-line, or inherited, mutations. Tumors can be either benign (those that remain localized and noninvasive), malignant (those that invade the
Cancer biology basement membrane and underlying tissue), or metastatic (those that shed cells that seed tumors in other locations of the body). Progressive degrees of abnormality are observed in benign, malignant, and metastatic tumors, suggesting that cancer develops in a stepwise process. Cancers can arise in almost all tissue types in the body, although approximately 80 percent of human cancers arise from epithelial cells—those cells that cover internal and external surfaces of the body, including the linings of internal organs and glands. The incidence of many types of cancer varies worldwide, and epidemiologic studies show that environment is the largest factor in variations in cancer incidence from country to country. Indeed, a number of environment and lifestyle elements, tobacco smoking being the most obvious, are known to be strongly correlated with the incidence of certain types of cancer. In 1975, it was shown that many chemicals that are capable of causing mutations in deoxyribonucleic acid (DNA) are also capable of causing cancer in laboratory animals. Later research showed, however, that not all chemicals that cause cancer also cause mutations. Therefore, other mechanisms besides DNA mutation must be involved in at least some cancers. Gene expression and signaling pathways: For the cells of an organism’s various tissues (lung and bone, for example) to display complex, tissue-specific characteristics, large groups of genes must be coordinately expressed while other genes must be repressed. Specialized proteins known as transcription factors are responsible for achieving this coordinated expression. Transcription factors bind to specific DNA sequences in the control region of each gene. The transcription of most genes is controlled by the binding of several distinct transcription factors in the gene’s control region. A single transcription factor can affect the expression of multiple genes that contain its binding sequence in their control regions. In cancer cells, a defective transcription factor may affect the expression of multiple genes, the end result of which is to create a cancer cell from a normal cell. Normal cells within tissues and within an organism communicate with each other in a regulated fashion through a multitude of chemical signals and pathways. Disruption of these normal signaling pathways is an important component of the formation of cancer. In normal cells, signals are transmitted through the various pathways in a number of ways: by a change in the level of activity of signaling molecules by noncovalent modifications, changes in the concentration of a signaling molecule inside a cell, or the direction of signaling molecules to particular locations within the cell. 213
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Salem Health: Cancer surface to which growth factors bind; signal transducers, proteins that make up the signaling pathways between the growth factor receptor and the cell nucleus; and transcription factors.
Tumor-suppressor genes: The class of tumorsuppressor genes includes a large number of genes whose protein products are involved in a multitude of normal cellular functions that in some way regulate a cell’s division and reduce the chance that the cell will become cancerous. Tumor-suppressor genes in cancer cells are often inactivated through mutation or other mechanisms. An inherited increased risk of developing a specific type of cancer in some families is often the result of the presence of a defective tumor-suppressor gene. It is the loss of function of tumor-suppressor genes that can lead to cancer, in contrast to oncogenes, which have gained functions or lost the ability to be controlled in their mutant form. The protein product of a particularly important tumor-suppressor gene, called TP53, causes cessation of cell division and even programmed cell death (apoptosis) in normal cells if the process of cell division malfunctions. In this way the cell’s well-being is monitored, protecting the organism from the effects of runaway division of wayward cells by activating the apoptotic pathway in such Colon cancer under the microscope. (©Micro Discovery/Corbis) cells. Apoptosis is an orderly process in which the DNA of a cell is degraded and the cell itself fragmented into smaller pieces that are taken up by Oncogenes: Normal cells contain a class of genes innearby white blood cells whose job is to clean up such devolved in the regulation of growth and division called bris. Loss of the ability to undergo apoptosis allows cancer proto-oncogenes. A proto-oncogene can mutate into a vercells to survive a variety of environmental stresses and sigsion that is permanently activated and causes uncontrolled naling imbalances. The TP53 gene in the DNA of cancer cell division, one of the hallmarks of a cancer cell. The cells often carries mutations that cause it to malfunction; transformation of a proto-oncogene into an oncogene may more than 90 percent of small-cell lung cancers and more involve a change to the structure of the protein itself or an than 50 percent of breast and colon cancers have been increase in its expression. Achange involving the structure shown to be associated with mutant forms of TP53. of the protein itself may require only very small changes; Normal cells throughout the body grow and divide to in some cases a single base pair mutation is sufficient. A generate two daughter cells in a highly organized and conchange involving an increase in expression often occurs trolled series of events called the cell cycle. A subclass of through increasing the number of copies of the gene in the tumor-suppressor genes controls cell-cycle events in norDNA. There are several ways that amplification of a gene mal cells. Control mechanisms at various steps of the cell can occur: by enhanced replication of a chromosome segcycle function to ensure that a preceding step is completed ment that carries its DNAor by the breaking away of such a before the next step can begin. These control mechanisms are inactivated in many types of cancer cells, allowing chromosome segment to form a small chromosome-like them to divide in an unregulated fashion. A particularly particle that is capable of replicating independently. important tumor-suppressor gene in this class is the retinoScientists have identified more than one hundred oncoblastoma (RB1) gene. The protein product for which the genes. They include growth factors, proteins that signal a RB1 gene codes, pRb, is affected in most if not all types of cell to divide; growth factor receptors, proteins on the cell 214
Salem Health: Cancer human cancer cells. Loss of normal regulation of the signaling pathway of which pRb is a component leads to unrestrained cell proliferation. Cell immortalization: The ability of a cell to divide indefinitely, called cell immortalization, appears to be a characteristic of all cancer cells. This ability has been shown to be related to the structures of the ends of chromosomes, called telomeres, which are composed of several thousand repeats of a six-base-pair sequence element. Every time a cell duplicates its DNA, the telomeres are shortened by fifty to one hundred base pairs, with the result that normal cellular DNA has the capacity for a finite number of replications. The ability to indefinitely maintain telomere length has been observed in virtually all types of cancer cells, the majority of which accomplish this by increasing the expression of the enzyme, telomerase, which is responsible for synthesizing telomeres. Angiogenesis: All cells depend on the availability of oxygen and nutrients for their growth and survival. Virtually all cells in a tissue must be located close to a capillary blood vessel that can deliver nutrients and take away metabolic waste products. For a cancer cell to progress to a macroscopic tumor, it must acquire the ability to induce the formation of new blood vessels, a process called angiogenesis. In normal cells, various negative and positive signaling pathways control the angiogenic process. Cancer cells appear to induce angiogenesis in a number of steps that change the balance of angiogenesis inducers and inhibitors during tumor development. Metastasis: Most types of human cancer will at some point undergo metastasis, the process whereby new tumors are seeded at distant sites from the primary tumor. Metastases are responsible for approximately 90 percent of all cancer deaths. Metastasis involves tumor cells leaving the primary tumor, invading adjacent tissues, and from there traveling to sites where they are able to settle and start the growth of new tumors. The primary route of metastasis is through the circulatory system, although metastatic cancer cells may also spread through lymph ducts to lymph nodes. Sometimes cancer cells traveling through the circulation form small obstructions that lodge in the arterioles and capillaries of various tissues. Complex interactions between the metastasizing cell and the microenvironment of the host tissue in which it lands govern the process of invasion into the tissue and colonization to form a metastasis in a process that is not well understood. Cancer cells that metastasize do not appear to have undergone major changes in their DNA compared with other cells in the original tumor. However, cancer cells that pos-
Cancer biology sess metastatic potential have alterations in several classes of proteins involved in the attachment of cells to their surroundings in a tissue, which render them less able to form such attachments. Cancer cells with metastatic potential may also have an increased ability to degrade proteins in their immediate environment. Metastasizing cells from various types of cancers tend to spread preferentially to some organs; for instance, prostate and breast cancers have a strong tendency to metastasize to the bone marrow, and colon cancer has a strong tendency to metastasize to the liver. The reason for this phenomenon is not well understood. Genomic instability: It has been estimated that multiple genetic changes, perhaps five to seven, are needed for the development of a full-fledged human cancer. A normal cell has numerous control and repair mechanisms that ensure the fidelity of DNA replication and, therefore, that the occurrence of mutations is rare. Malfunctioning of components of these control and repair mechanisms, such as TP53, leads to the observed chromosomal instability and variability of cancer cells. Genetic instability is pervasive in human cancer cells, which commonly exhibit various types of aberrantly structured chromosomes: the loss of entire chromosomes, the presence of extra copies of chromosomes, or the fusion of part of one chromosome with part of another. These chromosomal abnormalities disrupt normal DNA sequence and arrangement and probably help explain how precancerous cells acquire the necessary mutations to render them cancerous. Jill Ferguson, Ph.D. u
For Further Information Hanahan, D., and R. A. Weinberg. “The Hallmarks of Cancer.” Cell 100 (2000): 57-70. Karp, Gerald. Cell and Molecular Biology. 4th ed. New York: John Wiley, 2004. Weinberg, Robert A. The Biology of Cancer. New York: Garland Science, 2007.
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Other Resources
Emory University CancerQuest: Important Tumor Suppressors http://www.cancerquest.org/index.cfm?page=52 Inside Cancer http://www.insidecancer.org National Cancer Institute Cancer Topics http://www.cancer.gov/cancertopics 215
Cancer care team See also Angiogenesis; BRAF gene; BRCA1 and BRCA2 genes; Carcinogens, known; Carcinogens, reasonably anticipated; Cyclin-dependent kinase inhibitor-2A (CDKN2A); Cytokines; Epidemiology of cancer; Estrogen receptor downregulator (ERD); Genetics of cancer; Human chorionic gonadotropin (HCG); Immune response to cancer; Mitochondrial DNA mutations; MLH1 gene; MSH genes; Mutagenesis and cancer; MYC oncogene; Oncogenes; Placental alkaline phosphatase (PALP); PMS genes; Proteomics and cancer research; RB1 gene; RhoGD12 gene; SCLC1 gene; TP53 protein; Tumor necrosis factor (TNF); Tumor-suppressor genes.
u Cancer care team Category: Medical specialties Definition: The cancer care team consists of all the allied health professionals who are involved in a patient’s cancer diagnosis, treatment, and recovery or end-of-life planning. The team can include others who are not health professionals but are nonetheless an important part of the team. These can include spiritual leaders, social workers, and volunteers who provide assistance with transportation or housekeeping, as well as any other people who provide support or care for the individual with cancer. Subspecialties: There is a nearly infinite number of subspecialists who make up the cancer care team. The most important member of the cancer care team is the patient, because this person has the ultimate say in what services and treatment are received. A family member or friend who provides day-to-day care throughout the duration of the cancer treatment and afterward may have no medical training but is nonetheless an integral part of the cancer care team. In addition, the team contains those medical professionals attempting to treat the cancer, such as medical or surgical oncologists, and those whose main function is to help the patient live more fully or more comfortably, such as physical and occupational therapists, psychological counselors, and nutritionists. Also in the team are those whose primary function is to provide emotional support or generalized help for the patient and family, such as social workers, clergy members, and volunteers who provide transportation, help with meals, or simply companionship. Cancers treated: All types of cancer are treated by a cancer care team. The type of cancer the individual has and the planned treatment affect which professionals will be members of the team. The outcome of the cancer treatment 216
Salem Health: Cancer can also determine which professionals are part of the cancer care team. An individual diagnosed with a cancer that is in an early stage and is likely to go into remission probably will be involved with team members to help with the recovery process, such as occupational and physical therapists. An individual diagnosed with a cancer with a high mortality rate that has already spread significantly is likely to have a cancer care team that includes individuals trained in palliative care and end-of-life planning, such as hospice workers and financial planners. Training and certification: The training and certification required to be a member of the cancer care team depends on the role of the team member. A surgical oncologist requires an undergraduate degree, a medical degree, a long surgical residency, and additional surgical oncological training. Depending on the level of care nurses are allowed to provide, they may require various levels of training, including a master’s or doctoral degree. Psychological counselors or therapists usually are required to complete a master’s or doctoral level program. Assistants who are specialists in running certain types of machinery or equipment or assisting other health care professionals may have an associate degree or have completed a special certificate program. Some members of the cancer care team who assist with functions such as changing linens or retrieving necessary items may have received all of their trainin
