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Essential Nutrients in Carcinogenesis PDF

548 Pages·1986·18.998 MB·English
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ESSENTIAL NUTRIENTS IN CARCINOGENESIS ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY Editorial Board: NATHAN BACK, State University of New York at Buffalo NICHOLAS R. DI LUZIO, Tulane University School of Medicine EPHRAIM KATCHALSKI-KATZIR, The Weizmann Institute of Science DAVID KRITCHEVSKY, Wistar Institute ABEL LAJTHA, Rockland Research Institute RODOLFO PAOLETTI, University of Milan Recent Volumes in this Series Volume 201 LIPOPROTEIN DEFICIENCY SYNDROMES Edited by Aubie Angel and Jiri Frohlich Volume 202 INFECTIONS IN THE IMMUNOCOMPROMISED HOST Laboratory Diagnosis and Treatment Edited by Paul Actor, Alan Evangelista, James Poupard, and Eileen Hinks Volume 203 EXCITATORY AMINO ACIDS AND EPILEPSY Edited by Robert Schwarcz and Yehezkel Ben-Ari Volume 204 NEUROBIOLOGY OF CENTRAL D,-DOPMAINE RECEPTORS Edited by George R. Breese and Ian Creese Volume 205 MOLECULAR AND CELLULAR ASPECTS OF REPRODUCTION Edited by Dharam S. Dhindsa and Om P. Bahl Volume 206 ESSENTIAL NUTRIENTS IN CARCINOGENESIS Edited by Lionel A. Poirier, Paul M. Newberne, and Michael W. Pariza Volume 207 THE MOLECULAR AND CELLULAR BIOLOGY OF FERTILIZATION Edited by Jerry L. Hedrick Volume 208 PHOSPHATE AND MINERAL HOMEOSTASIS Edited by Shaul G. Massry, Michel Olmer, and Eberhard Ritz A Continuation Order Pian is available for this series. A continuation order will bring delivery of each new volume immediately upon publication. Volumes are billed only upon actual shipment. For further information please contact the publisher. ESSENTIAL NUTRIENTS IN CARCINOGENESIS Edited by Lionel A. Poirier National Cancer Institute Frederick, Maryland Paul M. Newherne Boston University Boston, Massachusetts and Michael W. Pariza University of Wisconsin Madison, Wisconsin PLENUM PRESS • NEW YORK AND LONDON Library .of Congress Cataloging in Publication Data Essential nutrients in carcinogenesis. (Advances in experimental medicine and biology; v. 206) Based on a symposium held Feb. 1, 1985, at the National Institutes of Health, Bethesda, Md., under the auspices of the National Cancer Institute. Includes bibliographies and index. 1. Cancer-Nutritional aspects-Congresses. 2. Carcinogenesis-Congresses. 3. Nu tritionally induced diseases-Congresses. I. Poirier, Lionel A. II. Newberne, Paul M., 1920- . III. Pariza, Michael W. IV. National Cancer Institute (U.S.) V. Series. [DNLM: 1. Diet - adverse effects - congresses. 2. Neoplasms - etiology - congresses. WI AD559 v.206/QZ 202 E78 1985) RC268.45.R65 1986 616.99'4071 86-25356 ISBN-13: 978-1-4612-9025-4 e-ISBN-13: 978-1-4613-1835-4 DOl: 10.1007/978-1-4613-1835-4 Proceedings of a symposium on The Role of Essential Nutrients in Carcinogenesis, held February 1, 1985, at the National Institutes of Health, Bethesda, Maryland © 1986 Plenum Press, New York Softcover reprint ofthe hardcover lst edition 1986 A Division of Plenum Publishing Corporation 233 Spring Street, New York, N.Y. 10013 All rights reserved No part of this book may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the Publisher PREFACE For more than 50 years, it has been recognized that diet influences cancer formation both in humans and in experimental animals. In fact, early investigators successfully retarded the onset of tumors in animals by dietary manipulation. Such findings led to an early optimism that cancer would prove to be yet another disease resulting from dietary imbalances and might thus be amenable to prevention or cure by appropriate nutritional changes. Subsequent studies showed that the influence of diet on cancer formation was not only very complex, it also did not appear to playa direct causative role in carcinogenesis. Thus during the mid-1950s scientific interest in diet and cancer greatly waned. By the early 1970s, however, a resurging interest in diet and cancer became evident. This field of activity has continued to grow. Yet for over 20 years, no comprehensive meeting has been held to summarize the major developments concerning dietary modification of carcinogenesis over a broad range of essential nutrients. To fill this void, a workshop was held on the role of essential nutrients in carcinogenesis from January 30 to February 1, 1985, in Bethesda, Maryland, under the auspices of the National Cancer Institute. This volume is a compilation of the presenta tions made at that meeting. The financial support of the Division of Cancer Etiology and of the Division of Cancer Prevention and Control at NCI is gratefully acknowl edged. Special thanks are also due to the staff of Program Resources, Inc., particularly to Rachelle Daigneault, Carole Benson, Margaret Fanning, E1ynor Sass, and Jennifer Sipes, for the technical operation of the work shop and for extensive editorial assistance without which this endeavor would not have been possible. This volume is dedicated to three pioneer investigators in the field of nutrition and cancer: 1) Dr. Albert Tannenbaum, for his early studies on the protective effect of caloric restriction on carcinogenesis; 2) Dr. Carl Baumann, for establishing, at the University of Wisconsin, a long and continuing tradition of investigating the modulating effect of diet on carcinogenesis; and 3) Dr. William D. Salmon, for the early recognition that dietary imbalance alone may cause cancer. The influence of these men and their scientific heirs will be felt throughout this volume. L. A. Poirier M. W. Pariza P. M. Newberne v CONTENTS 1. Introductory Remarks • • • • • • • • • • • • • • • • • • • • • • 1 J.M. Rice 2. Brief History of the Role of Nutrition in Carcinogenesis • • •• 5 L.A. Poirier 3. Epidemiologic Studies of Vitamins and Cancer of the Lung, Esophagus, and Cervix ••••••••••••• • • 11 R.G. Ziegler 4. Selenium, Vitamin E, Fiber, and the Incidence of Human Cancer: An Epidemiologic Perspective ••• 27 W.C. Willett 5. Studies of Nutrients and Their Relationship to Cancer in the Mu1tiethnic Population of Hawaii •••• 35 L.N. Ko1one1, J.H. Hankin, A.M.Y. Nomura, and M.W. Hinds 6. Diet and Carcinogenesis: Historical Perspectives • • • • • • •• 45 K.K. Carroll 7. Influence of Caloric Intake on Experimental Carcinogenesis: A Review • • • • •••• 55 D. Kritchevsky and D.M. K1urfe1d 8. Dietary Fat and Experimental Carcinogenesis: A Summary of Recent In Vivo Studies • • • • • • • • • • • • • 69 D.F. Birt 9. Dietary Fat and Neop1asia--The Role of Net Energy in Enhancement of Carcinogenesis: Effects of Fat and Calories on the Immune System •• • • • • • • • • •• 85 G.A. Boissonneault, C.E. Elson, and M.W. Pariza 10. Oil Gavage Effects on Tumor Incidence in the National Toxicology Program's 2-Year Carcinogenesis Bioassay 99 B.S. Appleton and R.E. Landers 11. Modification of Experimental Colon Carcinogenesis by Dietary Fibers • • • • • • • • • • • • • • • • • • • • • 105 L.R. Jacobs 12. Dietary Fiber and Human Cancer: Critique of the Literature • •• 119 D.M. K1urfe1d and D. Kritchevsky vii 13. Dietary Cholesterol, Serum Cholesterol, and Colon Cancer: A Review • • • • • • • • • • • • • • • • • 137 S.A. Broitman 14. Proteins and Amino Acids: Effects of Deficiencies and . . . . . Specific Amino Acids • • • • • • • • • • • • • • 153 A.E. Harper 15. Dietary Protein and Experimental Carcinogenesis •••••••• 163 W.J. Visek 16. Role of Tryptophan in Carcinogenesis • • • • • • • • • • • • •• 187 H. Sidransky 17. Hereditary Tyrosinemias (Type I): A New Vista on Tyrosine Toxicity and Cancer ••••••••• 209 C. Laberge, A. Lescault, and R.M. Tanguay . . . . . . . . . . 18. Lipotropic Factors and Oncogenesis • 223 P.M. Newberne 19. Choline Deficiency and Chemical Carcinogenesis • • • • • • • •• 253 H. Shinozuka, S.L. Katyal, and M.I.R. Perera 20. The Role of Methionine in Carcinogenesis • • • • • • • • • • •• 269 L.A. Poirier 21. Ethionine in the Analysis of the Possible Separate Roles of Methionine and Choline Deficiencies in Carcinogenesis • • • • • 283 A.K. Ghoshal, D.S.R. Sarma, and E. Farber 22. The Role of Vitamin B12 and Folate in Carcinogenesis • • • • •• 293 V. Herbert 23. Role of Vitamin B12 and Folate Deficiency in Carcinogenesis • • • • • • • • • • • • • • • • •• 313 I. Eto and C.L. Krumdieck 24. The Influence of Niacin and Nicotinamide on In Vivo . . . . . . Carcinogenesis • • • • • • • • • • 331 G.T. Bryan 25. Vitamin B6 Deficiency and Carcinogenesis • • • • • • • • • • •• 339 R.D. Reynolds . . . . . . . . . . . . . . . . . . . . . . . . 26. Riboflavin • • • 349 R.S. Rivlin 27. The Role of Ascorbic Acid in Carcinogenesis •••••••••• 357 B.E. Glatthaar, D.H. Hornig, and U. Moser 28. Some Thoughts on the Relationship Between Vitamin A and C~ncer • • • • • • • • • • • • • • • • • •• 379 J.A. Olson 29. Anticarcinogenic Effects of Retinoids in Animals • • • • • • •• 399 R.C. Moon and R.G. Mehta viii 30. The Relationship Between the Vitamin D System and Cancer • • •• 413 H.F. DeLuca and V. Ostrem 31. The Chemopreventive Role of Selenium in Carcinogenesis • • • •• 431 C. Ip 32. Inhibition of Chemical C.a .rc .in .og .en .e s.is .a n.d .T .um .o r.ig .e n.e s.is . . . . . by Selenium 449 J.A. Milner 33. Mechanisms of Selenium Inhibition of Tumorigenesis • • • • • •• 465 D. Medina . . . . . . . . . . . . . . . . . 34. Alcohol and Cancer • • • • • • 473 A.E. Rogers and M.W. Conner 35. The Role of Calcium, Magnesium, and Zinc in Carcinogenesis • •• 497 K.S. Kasprzak and M.P. Waalkes 36. Role of Zinc Deficiency in Carcinogenesis ••••••••••• 517 D.H. Barch and P.M. Iannaccone 37. The Role of Iodine in Carcinogenesis. • • • • • • • • • • • •• 529 J.M. Ward and M. Ohshima 38. Summery and OVerview • • • • • • • • • • • • • • • • • • • • •• 543 K.N. Prasad Contributors • 549 Index 553 ix 1 INTRODUCTORY REMARKS Jerry M. Rice Laboratory of Comparative Carcinogenesis Division of Cancer Etiology National Cancer Institute-Frederick Cancer Research Facility Frederick, Maryland 21701 In 1980, the National Cancer Institute commissioned the National Research Council to conduct, in the words of the Preface to the resulting report,1 "a comprehensive study of the scientific information pertaining to the relationship of diet and nutrition to cancer ••• [to] review ••• the state of knowledge and information pertinent to diet/nutrition and the incidence of cancer; develop a series of recommendations related to dietary components (nutrients and toxic contaminants) and nutritional factors which can be communicated to the public, and, based on the above state-of-the-art appraisals and the identification of gap areas, develop a series of research recommendations related to dietary components and nutritional factors and the incidence of cancer." The recommendations of the Committee on Diet, Nutrition, and Cancer, published in 1982, were understandably cautious. Their most definite conclusion was that a causal relationship exists between fat intake and the occurrence of cancer. With respect to more specific substances, for example, copper, zinc, molybdenum, and iodine, the committee concluded that the data concerning dietary exposure to these elements were insuffi cient and provided no basis for conclusions about association of these elements with cancer risk. In fact, the committee compared its task to that of evaluating the risk of cigarette smoking 2 decades ago, when the data base associating human cancer with cigarettes was much narrower than it is today. And there is a ylaintive note regarding its task of making recommendations to the public: "The public often demands certain kinds of information before such information can be provided with complete cer tainty. For example, weather forecasting is often not exact; nevertheless, the public asks that the effort be made, but has learned to accept the fact that the results are not always reliable." We clearly have a pressing need for more and better data, from both laboratories and epidemiologists, to achieve one of the goals of the cancer prevention effort: to minimize the risk of human cancer through wise choice of diet. The goals and scope of this symposium are narrower than those of the National Research Council committee and mercifully do not include the biomedical equivalent of weather forecasting. The focus of this symposium is exclusively on components of diet that can be described as "normal." Additives and contaminants, whether naturally occurring or man-made, are specifically excluded from consideration. This is not because additives and contaminants are not important. On the contrary, some of the most potent organic carcinogens known, the aflatoxins, are produced by fungi that readily contaminate beans, corn, and peanuts, and although their roles in the genesis of human cancer are still suspected rather than proved, these substances have clearly been responsible for major episodes of acute poisoning in human populations, especially in third world countries. The carcinogenic by-products of cooking foods, for example, aromatic hydrocarbons, protein and amino acid pyrolysates, and nitrosa mines, include carcinogens that have shown great potency in experimental animals and that cannot be ignored. However, in one sense, to focus attention on contaminants deflects attention from diet itself as a modulating factor in the susceptibility of the organism to carcinogenesis. To the investigator studying a putative carcinogen, the diet given the experimental animals is simply a possible source of confounding variables to be controlled. In contrast, the goal of this symposium is to critically review the roles of normal dietary components in carcinogenesis. Some of these substances, especially by their absence or their presence in deficient quantities, have profound effects in experimental systems, and this has aroused increased interest among experimentalists. Other nutrients, notably ascorbic acid and certain retinoids, protect against carcinogenesis, and this too has captured well-deserved attention. Appreciation of the roles of specific nutrients in carcinogenesis has evolved to its present state in a manner that parallels our under standing of tumor promotion, and indeed these subjects overlap. In the not-too-distant past, tumor promotion was the exclusive province of a few harmless eccentrics whose preoccupation was the painting of an ill-defined irritant cathartic onto the skins of mice to induce the growth of warts. To date, many compounds have been identified that possess high potency for promotion and apparently high specificity in rodents for various non squamous epithelia. These include many of the internal lining epithelia, such as those of the urinary bladder and the renal cortex, from which a significant fraction of human carcinomas evolve. Among the promoting compounds are substances that have been taken internally by humans for decades, such as phenobarbital, and the neoplasms seen in initiation/ promotion studies include carcinomas as well as their histologically benign precursors. The perceived importance of the phenomenon has increased as a result, and the prospect of understanding the mechanisms of promotion at the cellular and molecular levels has attracted the attention of increasing numbers of capable investigators. Similarly, as progress is made toward understanding mechanisms for dietary effects in carcinogenesis, interest will continue to increase. However, nutrition research in relation to carcinogenesis, especially in relation to cancer in humans, appears intrinsically more difficult because of the often intractable problem of separating variables, but in many cases this is being accomplished. Zinc deficiency, long implicated in esophageal cancer, has recently been shown to alter microsomal metabolism of a nitrosamine that in rats is highly selective for esophageal epithe lium, and this effect occurs in the target tissue in that species. Iodine deficiency, with its resulting goitrous hyperplasia of the thyroid, has been shown to have a pronounced promoting effect on thyroid follicular carcinogenesis in rats, initiated by transient exposure to a carcinogen before dietary iodine deficiency was imposed. Dietary methyl deficiency in rats reduces methylation of DNA in the target tissue, liver, and thus possibly contributes directly to a reduction in control of genetic expres sion. As these and many other recent developments are discussed during the next 3 days, I feel sure we will be encouraged by the current rate of progress in defining the roles of essential nutrients in carcinogenesis. 2

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