Cancer Prevention International

Editor: Daniel W. Nixon

ISSN: 1083-9984

Softbound

Aims & Scope

Cancer Prevention International (CPI) is an international journal devoted to publishing scholarly works in the broad field of cancer prevention, detection, and control. To this end it will cover such areas as basic mechanisms of cancer prevention, chemoprevention, nutrition, alcohol, tobacco, and environmental sciences, epidemiologic and behavioral studies, prevention clinical trials, and other areas related to prevention and control of cancer.

VOLUME 3, NUMBER 3/4, 1998

Cancer Prevention and Control
Joni Shulman and Daniel W. Nixon

State Cancer Pain Initiatives: A Decade of Progress
June L. Dahl

Proactive Approaches to Nutritional Care During Radiation Therapy
Marylou S. Anton

A Mixture of Chemopreventives Modifying the Oxidative State and Inducing Programmed Cell Death in Human and Hamster Oral Carinonoma Cells
Joel L. Schwartz

Application of Behavioral Theory Within Diet-Based Clinical Trials to Improve Outcome
Wendy Demark-Wahnefried

Conjugated Linoleic Acid (CLA) and Carcinogenesis
David Kritchevsky

Nutritional Intervention With n-3 Polyunsaturated Fatty Acids in Advanced Pancreatic Cancer
Matthew D. Barber and Kenneth C. H. Fearon

Rethinking Vitamin C and Cancer: An Update on Nutritional Oncology
Michael J. González, Edna Mora, Neil H. Riordan, Hugh D. Riordan, and Pablo Mójica

Molecular Biology Editorial Board

Nutrition Editorial Board

Studies of a Newly Described Gastrointestinal Factor and Its Role in Protecting Against the Negative Effects of Food
Yulian Rafes

Medical Oncology Board

The Force of Long-Term Mortality in Breast Cancer Patients
Rowan T. Chlebowski, James Sayre and Linda M. Lillington

Occupational and Environmental Health Editorial Board

Xenoestrogen Exposure and Dietary Fat Connection in Breast Cancer Risk: Is There a Scientific Basis for Concern? Part 1: Breast Cancer Risk and Estrogenicity
Narayanan K. Narayanan

Medical Ethics

Alternative Medicine

Hope, Meaning, and Music Therapy in the Treatment of Life-Threatening Illness
David Aldridge

Spirituality, Healing, and Medicine
David Aldridge

Volume 3 Subject and Author Index

Conference Announcement

EDITOR-IN-CHIEF
Daniel W. Nixon, M.D.
Folk Professor of Experimental Oncology
Professor of Medicine
Associate Director of Cancer Prevention and Control
Hollings Cancer Center
Medical University of South Carolina, Charleston, SC, 29425

 

SECTION EDITORS AND SECTION EDITORIAL BOARDS:

Medical Oncology Editor
Rowan T. Chlebowski, M.D., Ph.D., Harbor/UCLA Medical Center, Torrance, CA, USA

Medical Oncology Editorial Board
Ronald H. Blum, M.D., NYU Medical Center, New York, NY, USA
Scott M. Lippman, M.D., M.D. Anderson Cancer Center, Houston, TX, USA
Frank L. Meyskens, Jr., M.D., University of California, Irvine, Orange, CA, USA
James L. Mulshine, M.D., National Cancer Institute, Rockville, MD, USA

SECTION DESCRIPTION: Dedicated to the review and timely publication of the latest updates on cancer chemoprevention trials, as well as information on the clinical ramifications of promising new chemopreventive agents, biomarkers, and intermediate end points. Related issues of trial conduction, such as recruitment, adherence, and study design, also fall into the scope of this section.

 


Occupational and Environmental Health Editor
William R. Hendee, Ph.D., Medical College of Wisconsin, Milwaukee, WI, USA

Occupational and Environmental Health Editorial Board
Henry Anderson, M.D., Bureau of Public Health, Madison, WI, USA
Carl Barrett, Ph.D., Natl. Inst. Environmental Health Sciences, Research Triangle Park, NC, USA
John B. Conway, Ph.D., M.P.H., State University of New York at Albany, NY, USA
Devra Lee Davis, M.D., Health and Human Services, Washington, DC, USA
Alan Ducatman, M.D., West Virginia University School of Medicine, Morgantown, WV, USA
Tee L. Guidotti, M.D., University of Alberta Faculty of Medicine, Edmonton, Alberta, Canada

SECTION DESCRIPTION: Addresses environmental and occupational exposures to carcinogens, their impact on human health, and ways to reduce the impact through remediation, education, and policy-making.

 


Nutrition Editor
Myron Winick, M.D., Columbia University, New York, NY, USA

Nutrition Editorial Board
David Kritchevsky, M.D., Wistar Institute, Philadelphia, PA, USA
Pedro Rosso, Catholic University Medical School, Santiago, Chile
Harold Sandstead, M.D., University of Texas, Medical Branch, Galveston, TX, USA
Richard Weindruch, Ph.D., University of Wisconsin, Madison, WI, USA
John H. Weisburger, M.D., American Health Foundation, Valhalla, NY, USA
James Whittam, Shaklee Corporation, San Francisco, CA, USA

SECTION DESCRIPTION: Epidemiological studies, human case control studies, experimental clinical trials, animal studies, and any other scientifically valid studies relating general diet or individual nutrients to the etiology and any type of cancer are included. In addition, articles related to the nutrition of patients with cancer are included if they involve lowering or increasing the risk of further spread.

 


Molecular Biology Editor
Edward Bresnick, M.D., University of Massachusetts Medical School, Worcester, MA, USA

Molecular Biology Editorial Board
Leonard Augenlicht, Ph.D., Albert Einstein Medical Center, Bronx, NY, USA
James M. Phang, M.D., Lab. of Nutrition & Molecular Regulation, Frederick, MD, USA
Max Wicha, M.D., Comprehensive Cancer Center, Ann Arbor, MI, USA

SECTION DESCRIPTION: Publishes the latest advances in the use of molecular bioloigical techniques in the design of specific biomarkers for predicting populations that are susceptible or resistant to the development of cancer and for assessing the efficacy of chemopreventive agents.

 


Alternative Medicine Editor
Barrie R. Cassileth, Ph.D., University of North Carolina at Chapel Hill, NC, USA

Alternative Medicine Editorial Board
David Aldridge, Ph.D., Universitat Witten Herdecke, Witten, Germany
Joe Jacobs, M.D., Guilford, CT, USA
Wayne B. Jonas, M.D., National Institutes of Health, Bethesda, MD, USA
Charles L. Loprinzi, M.D., The Mayo Clinic, Rochester, MN, USA
John C. Reed, M.D., Pain and Stress Recovery Center, Phoenix, AZ, USA
Sidney L. Saltzstein, M.D., M.P.H., Univ. of California San Diego Med. Ctr., San Diego, CA, USA
Zeng Yi, M.D., Chinese Academy of Preventive Medicine, Beijing, China

SECTION DESCRIPTION: This section broadens oncologists' access to alternative research information and providers a forum for alternative researchers.

 

Medical Ethics Editor
Jan van Eys, Ph.D., M.D., Vanderbilt University School of Medicine, Nashville, TN, USA

Medical Ethics Editorial Board
L. Ray Patterson, University of Georgia School of Law, Athens, GA, USA
Stuart L. Spicker, Ph.D., Baylor College of Medicine, Houston, TX, USA

SECTION DESCRIPTION: Publishes original articles, analyses, and reviews of topics touching upon the ethical and legal implications of initiatives toward cancer prevention.

VOLUME 3, 1998

Author Index

Aldridge, D., 279, 287
Anton, M. S., 165

Barber, M. D., 207
Bhagavathiammai, A., 3

Castañeda-Méndez, K., 55
Chlebowski, R. T., 241

Dahl, J. L., 157
Demark-Wahnefried, W., 191

Fearon, K. C. H., 207

Gittinger, C., 3
González, M. J., 215

Holladay, E. B., 3

Imai, K., 79

Jones, W., 3

Kritchevsky, D., 199
Kucuk, O., 99

Lillington, L. M., 241

McShane, F. P., 19
Mójica, P., 215
Mora, E., 215

Nakachi, K., 79
Narayanan, N. K., 251
Nixon, D., 3, 19

Pentz, R. D., 123

Rafes, Y., 229
Riordan, H. D., 215
Riordan, N. H., 215

Sayre, J., 241
Schwartz, J. L., 37, 175
Sueoka, N., 79
Suga, K., 79

Torosian, M. H., 93

Unander, D. W., 143

van Eys, J., 131

Wilson, D. B., 19

Zoller, J., 19
 

Subject Index

Activity-based costing, 55
Antioxidants, 99
Apoptosis, 175
Appetite, 165
Archival, 3

Baldrige, 55
Behavioral theory, 191
Benefit-burden, 123

Cachexia, 165
Cancer prevention, 79
CaSki cells, 3
Cell cycle kinetics, 93
Cervical intraepithelial neoplasia, 3
Chemoprevention, 37
Chemopreventive mixture, 175
Chemotherapy, 99
Confidentiality, 123
Cost of quality, 55

Diet-based clinical trials, 191
Discrimination, 123
Disease prevention, 19

 

E6-E7 transcription, 3
Endocrine, 251
Environmental exposure, 251
Ethics, 123
Ethnobotany, 143

Genetic, 123
Green tea, 79

Health promotion, 19
Health services, 19
Hepatitis B., 143
Hormone, 251
Hospitals, 19
Human papilloma virus, 3

Index of relative risk, 37

Late effects, 165
Lifestyle change, 191

Micronutrients, 99

Nutrition, 55, 165

p53, 3
Phase I trial, 79
Phyllanthus, 143
Phytoestrogens, 251
Prevention, 123
Protective oxygen systems, 37

Quality, 55

Radiation, 99, 165
Reactive oxygen substances, 37
Redox state, 175
Retinoblastoma, 3
RT-PCR, 3

Solid tumors, 215

Total parenteral nutrition, 93
Toxicity prevention, 99
Tumor growth, 93
Tumor metastasis, 93

Vitamin C, 215

Xenoestrogens, 251


CANCER PREVENTION INTERNATIONAL

ABSTRACTS
VOLUME 3, NUMBER 3/4, 1998

CancerPrevention International, Vol. 3, pp. 165-173, 1998
1083-9984 $10.00 + .00
Copyright © 1998 Cognizant Comm. Corp.
Printed in the USA. All rights reserved.

Proactive Approaches to Nutritional Care During Radiation Therapy

Marylou S. Anton

Department of Radiation Oncology, University of Pennsylvania Medical Center, 3400 Spruce Street-2 Donner, Philadelphia, PA 19104

Nutrition as it relates to cancer and radiation is discussed in terms of anorexia, cachexia, mechanical barriers to nutrition, effects of chemotherapy on nutrition, fatigue, and depression. The stated general measures for nutritional support are education and physiological implications related to nutritional support. The assessment of nutritional status is described through diet history, anthropometric measurements, exemplified by weight, mid-arm circumferences, and triceps, skinfold; biochemical; measurements, further described as albumin, transferin, nitrogen balance, and immune function evaluation. Obstacles to nutritional assessment are also described. The effects of radiation and their relationship to nutrition are described. Early and late effects are reviewed with side effect management descriptions given.

Key words: Nutrition; Radiation; Appetite; Cachexia; Late effects

Address correspondence to Marylou S. Anton. Tel: (215) 349-8892; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

 



Cancer Prevention International, Vol. 3, pp. 175-190, 1998
1083-9984 $10.00 + .00
Copyright © 1998 Cognizant Comm. Corp.
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A Mixture of Chemopreventives Modifying the Oxidative State and Inducing Programmed Cell Death in Human and Hamster Oral Carcinoma Cells

Joel L. Schwartz

Howard University, College of Dentistry, 600 W Street, N.W., Washington, DC 20059

The chemopreventives such as carotenoids, retinoids, tocopherols, ascorbic acid, and reduced glutathione were studied for their effects on the modification of the oxygen state and the induction of programmed cell death. A previous study indicated that the combination of chemopreventives was more effective than any single agent inhibiting oral carcinogenesis. Additional in vitro studies were conducted to verify this relationship. Hamster- and human-derived oral carcinoma cells (HCPC-1 and SCC-25) were used as targets. Tritiated thymidine ([3H]TD) incorporation identified a dose-response (8, 35, 70 mM) effect for the combination treatment, b-carotene (BC), canthaxanthin (CAN), retinyl palmitate (RP), and dl-alpha tocopherol acid succinate (VES), while ascorbic acid (AS) and glutathione (reduced) (GSHred) did not appear to produce this level of depression of cell growth. This became more evident at 70 mM compared to the 8 mM dose. In conjunction a viability test (tetrazolium salt assay, MTT) produced a similar response. The levels of mercaptan (mM, nonprotein sulfhydryls) and glutathione (GSHred) were found to be depressed by the combination and BC, RP, and AS treatments, while VE and GSHred treatments significantly elevated their levels. The result of these oxidative changes was the induction of apoptosis as identified through nucleosome formation, changes in mRNA levels for tumor necrosis factor-a (TNF-a) and enhanced expression of p53. The combination of nutrients induced the highest level of apoptosis while the next highest to lowest levels were BC > RP > CAN > VES > AS > GSHred. A mixture of chemopreventives compared to any single nutrient forming the mixture could produce a greater suppressive effect in oral cancer cells inducing apoptosis.

Key words: Chemopreventive mixture; Apoptosis; Redox state

Address correspondence to Joel L. Schwartz. Tel: (202) 806-0094; Fax: (202) 806-0354; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

 



Cancer Prevention International, Vol. 3, pp. 191-197, 1998
1083-9984 $10.00 + .00
Copyright © 1998 Cognizant Comm. Corp.
Printed in the USA. All rights reserved.

Application of Behavioral Theory Within Diet-Based Clinical Trials to Improve Outcome

Wendy Demark-Wahnefried

Box 2619, Duke University Medical Center/MSRB, Durham, NC 27710

Theories developed in the area health behavior serve as valuable tools in helping to explain human behavior and strategies to achieve change. Thus, the application of behavioral theory to clinical trials aimed at lifestyle change can enhance recruitment; the ability to distinguish compliant from noncompliant subjects; the development of uniform and effective messages and program strategies; and the ability to interpret, generalize, and ultimately disseminate research findings. Behavioral theories developed to explain intra- and interpersonal human behavior may have particular merit for application to clinical trials. The Health Belief Model, the Transtheoretical Stages of Change Model, and Social Cognitive Theory are described. These models are examples of the many behavioral models that exist, which have demonstrated success in trials aimed at behavioral change. Researchers therefore can strengthen clinical trials aimed at lifestyle change through the thoughtful application of behavioral theory.

Key words: Behavioral theory; Diet-based clinical trials; Lifestyle change

Address correspondence to Wendy Demark-Wahnefried. Tel: (919) 681-3261; Fax: (919) 684-9990; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

 



Cancer Prevention International, Vol. 3, pp. 215-224, 1998
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Rethinking Vitamin C and Cancer: An Update on Nutritional Oncology

Michael J. González,1 Edna Mora,2 Neil H. Riordan,3 Hugh D. Riordan,3 and Pablo Mójica2

1University of Puerto Rico, Medical Sciences Campus, School of Public Health, Department of Human Development, Nutrition Program , San Juan, Puerto Rico
2University of Puerto Rico, School of Medicine, Cancer Center and Experimental Surgery Division, San Juan, Puerto Rico
3The Center for the Improvement of Human Functioning, RECNAC Program, Wichita, KS

The effect of vitamin C on cancer, especially on solid tumor malignancies, has been a subject of great controversy. In this article we address general aspects of vitamin C and cancer, while reviewing and analyzing existing literature on the subject. In addition, we present and discuss our own hypothesis on the effect of vitamin C on cancer (solid tumors). This article is an attempt to ease the existing controversy while providing an updated scientific basis for the use of vitamin C in nutritional oncology.

Key words: Vitamin C; Solid tumors

Address correspondence to Dr. Michael J. González, University of Puerto Rico, Medical Sciences Campus, Graduate School of Public Health, Department of Human Development, Nutrition Program, PO Box 365067, San Juan, Puerto Rico 00936-5067. Tel: (787) 758-2525, Ext. 1405; Fax: (787) 759-6719.

 



Cancer Prevention International, Vol. 3, pp. 229-238, 1998
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Copyright © 1998 Cognizant Comm. Corp.
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Studies of a Newly Described Gastrointestinal Factor and Its Role in Protecting Against the Negative Effects of Food

Yulian Rafes

YIVO Institute for Jewish Research, 555 West 57th Street, Suite 1100, New York, NY 10019

There is a great deal of evidence that the postgastrectomy syndrome that accompanies the ingestion of food (``dumping syndrome'') is one of the most severe forms of a disease spectrum that exists in many people with intact gastrointestinal tracts. Symptoms may vary from weakness, drowsiness, dizziness, headache, cold sweats, palpitations, nausea, vomiting, epigastric and abdominal pain to only one or two of these symptoms. The common factor, however, is that these symptoms are always the direct result of food ingestion. The author presents a concept, supported by all of the available evidence, that the gastrointestinal tract secretes a substance that prevents this food-induced syndrome. He has named this substance the Food Asthenia Preventive Factor (F.A.P.F.). In animals this factor appears to have physiologic activity outside of its effects on the gastrointestinal tract. Administration of F.A.P.F. to farm animals increases their growth, raises birth weight, and decreases dyspepsia rates. When this factor is given to experimental animals, it reduces stress-related lesions, and increases physiologic resistance to several types of stress and a variety of malignant tumors. The factor has been shown to be present in extracts of both porcine and human gastrointestinal tracts. Whether this factor has more general effects in humans similar to those seen in animals has not yet been determined. Nevertheless, even today it is obvious that this factor defends an individual from certain negative influences of food.

Address correspondence to Yulian Rafes. Dr. Rafes is former head and professor of Clinic of Ukraine Institute of Gastroenterology and presently a senior research fellow at the YIVO Institute.

 



Cancer Prevention International, Vol. 3, pp. 241-247, 1998
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Copyright © 1998 Cognizant Comm. Corp.
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The Force of Long-Term Mortality in Breast Cancer Patients

Rowan T. Chlebowski,1 James Sayre,2 and Linda M. Lillington1

1Harbor-UCLA Medical Center, Department of Medicine, Division of Medical Oncology and Hematology, Torrance, CA
2UCLA School of Medicine, Department of Biostatistics, Los Angeles, CA

Optimal patient management and public policy decision making with respect to breast cancer is dependent on reliable determination of the clinical course of this disease. However, substantial differences in long-term mortality patterns of breast cancer patients emerge from consideration of recent Surveillance, Epidemiology, and End Results (SEER) Program cancer statistics compared to Early Breast Cancer Trialists' Cooperative Group (EBCTCG) reports. SEER results suggest decreasing risk of death with time over long-term (15 years) follow-up whereas EBCTCG results suggest a more sustained, relatively constant mortality risk over the same period. To explore this issue, results from a hospital-based tumor registry were examined after enhanced follow-up procedures. For 508 consecutive local-regional breast cancer cases from the Harbor-UCLA Tumor Registry, a survival pattern over 15 years most consistent with EBCTCG results was seen, suggesting the force of long-term mortality related to breast cancer diagnosis is both sustained and relatively constant over time. To definitely resolve this important question regarding the clinical course of breast cancer, individual patient results from SEER and EBCTCG databases should be directly compared.

Address correspondence to Rowan T. Chlebowski, Harbor-UCLA Medical Center, Division of Medical Oncology and Hematology, 1000 W. Carson Street, Bldg. J3, Torrance, CA 90509. Tel: (310) 222-2217; Fax: (310) 320-2564.

 



Cancer Prevention International, Vol. 3, pp. 251-273, 1998
1083-9984 $10.00 + .00
Copyright © 1998 Cognizant Comm. Corp.
Printed in the USA. All rights reserved.

Xenoestrogen Exposure and Dietary Fat Connection in Breast Cancer Risk: Is There a Scientific Basis for Concern? Part 1: Breast Cancer Risk and Estrogenicity

Narayanan K. Narayanan

Hollings Cancer Center, Medical University of South Carolina, 171 Ashley Avenue, Charleston, SC 29425

Breast cancer is the leading hormone-dependent malignancy in women, and the incidence is reported to be increasing in industrial nations. In this review we have summarized evidence from environmental, experimental, and epidemiological perspectives, to evaluate various risk factors associated with breast cancer development. This article is intended to document the association and controversies between exogenous and endogenous estrogens, and plausible mechanistic pathways involved in breast cancer development. A review of the English-language literature was conducted in several areas, which included environmental, experimental, epidemiological, medical, and social sciences with emphasis on articles published in the last 10 years. More than 350 articles were reviewed. Many factors--environmental, genetic, reproductive, etc.--have been linked to breast cancer development. Exogenous and endogenous estrogens have been implicated in the etiology of benign and neoplastic tumors of the breast. A number of compounds and their metabolites have estrogenic activity, including steroids, phytoestrogens, and synthetic chemicals. Dietary fat intake is a major concern for increased breast cancer incidence in women because diets high in total fat and certain polyunsaturated fatty acids have been linked to increased incidence of carcinogen-induced breast cancer in animals. The association between persistent lipophilic xenoestrogenic substances carried in dietary fat and potentially adverse environmental factors with breast cancer susceptibility genes may increase the risk of breast cancer. The potential of xenoestrogens to cause harmful effects in animals and humans is highly controversial. Though experiments with animal models and limited human studies suggest that dietary fat intake increases the incidence of breast cancer, epidemiological evidence seems to be inconsistent. Studies focused on the mechanism of action of both xenoestrogens and dietary fat at the cellular and organism level might explain these apparent discrepancies and narrow down the uncertainties.

Key words: Environmental exposure; Phytoestrogens; Xenoestrogens; Endocrine; Hormone

Address correspondence to Narayanan K. Narayanan. Tel: (843) 876-1967; Fax: (843) 876-1963; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

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