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Dietary Protein and Experimental Carcinogenesis

  • Chapter
Essential Nutrients in Carcinogenesis

Abstract

This review summarizes selected information about the influence of proteins, protein-fat interactions, and calorie intake on carcinogenesis. Most of the definitive studies concerning protein and cancer have utilized protein underfeeding and feed restriction. Optimal or less than optimal protein intakes have generally inhibited spontaneous and chemically induced tumor growth as well as the growth of transplantable tumors. Studies have focused on the quantity of protein and its amino acid supply rather than its source. Raising protein intake increases carcinogen metabolizing capacity, and the incidence of tumors depends upon the biologic activity of the metabolites that are formed. The few published studies dealing with the effects of protein on chemically induced colon, mammary, and liver cancers show that the incidence varied with the carcinogen and the level of protein fed at the time of carcinogen administration. With 1,2-dimethyl-hydrazine, a colon cancer-inducing agent, the toxic and tumorigenic responses have varied with the route of administration, the level of protein fed, and the level and duration of exposure to the carcinogen. In some instances, high protein diets may have led to a lower incidence of tumors because of depressed feed intake, a known confounding factor. The existing data about the relation of protein to cancer make generalizations about mechanisms hazardous because experimental models and protocols have varied widely. Some early studies undoubtedly used diets that lacked nutrients now known to be essential. Unfortunately, some recent studies have overlooked established nutritional principles and the known nutritional requirements appropriate for the age and species of animals used as models.

Research conducted in the author’s laboratory was supported by U.S. Public Health Service grants CA22326‚ CA29629‚ and A. M. 28026; Environmental Toxicology Training Grant Number ES0700-17; and NCI Contract No. NCI CP75899.

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Abbreviations

DMH:

1,2-dimethylhydrazine

PAH:

polycyclic aromatic hydrocarbons

AOM:

azoxyraethane

MAM:

methylazoxymethanol

AM:

azomethane

DMBA:

7,12-dimethylbenz(a)anthracene

AHH:

aryl hydrocarbon hydroxylase

AFB1 :

aflatoxin B1

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Authors and Affiliations

  1. University of Illinois College of Medicine, Urbana, Illinois, 61801, USA

    Willard J. Visek

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Editors and Affiliations

  1. Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research Facility, Frederick, Maryland, USA

    Lionel A. Poirier

  2. Department of Pathology, Boston University School of Medicine, Boston, Massachusetts, USA

    Paul M. Newberne

  3. Food Research Institute, University of Wisconsin, Madison, Wisconsin, USA

    Michael W. Pariza

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Visek, W.J. (1986). Dietary Protein and Experimental Carcinogenesis. In: Poirier, L.A., Newberne, P.M., Pariza, M.W. (eds) Essential Nutrients in Carcinogenesis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1835-4_15

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