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[Dietary fatty acids and experimental carcinogenesis].
Bull Cancer. 2005 Jul; 92(7):685-96.BC

Abstract

Experiments in animal models of mammary carcinogenesis suggest that fatty acids promote mammary tumors development. This effect depends first on the amount then on the type of fatty acids available. n-6 fatty acids such as linoleic acid generally stimulates mammary tumor growth, while n-3 fatty acids oppose this effect. Conjugated diene fatty acids (CLA) inhibit mammary carcinogenesis when brought at elevated amount. There are limitations in using an animal model in the analysis between nutrition and colorectal cancers. This is ascribable to the following: firstly, the digestive tract of rodents if different from that of humans and secondly, the induction of colon cancer in these animals (chemical carcinogenesis, injection of cancerous cells or transgenesis) does not mimic human colon carcinogenesis. However, on the basis of numerous published data, some important correlations have arisen that could generate hypotheses and guide new epidemiological/interventional and experimental studies. In these animal models it appears that an adequate supply of n-3 PUFAs and oleic acid in food may exert a protective effect at all stages of colon carcinogenesis. On the other hand, an excessive consumption of n-6 PUFAs and of saturated fatty acids could promote colon cancers.

Authors+Show Affiliations

Inserm E 0211, Equipe de recherche Nutrition, croissance et cancer, Corad, CHU de Tours 2, boulevard Tonnellé 37044 Tours Cedex.No affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

fre

PubMed ID

16123007

Citation

Bougnoux, Philippe, and Jean Menanteau. "[Dietary Fatty Acids and Experimental Carcinogenesis]." Bulletin Du Cancer, vol. 92, no. 7, 2005, pp. 685-96.
Bougnoux P, Menanteau J. [Dietary fatty acids and experimental carcinogenesis]. Bull Cancer. 2005;92(7):685-96.
Bougnoux, P., & Menanteau, J. (2005). [Dietary fatty acids and experimental carcinogenesis]. Bulletin Du Cancer, 92(7), 685-96.
Bougnoux P, Menanteau J. [Dietary Fatty Acids and Experimental Carcinogenesis]. Bull Cancer. 2005;92(7):685-96. PubMed PMID: 16123007.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Dietary fatty acids and experimental carcinogenesis]. AU - Bougnoux,Philippe, AU - Menanteau,Jean, PY - 2005/8/27/pubmed PY - 2005/9/10/medline PY - 2005/8/27/entrez SP - 685 EP - 96 JF - Bulletin du cancer JO - Bull Cancer VL - 92 IS - 7 N2 - Experiments in animal models of mammary carcinogenesis suggest that fatty acids promote mammary tumors development. This effect depends first on the amount then on the type of fatty acids available. n-6 fatty acids such as linoleic acid generally stimulates mammary tumor growth, while n-3 fatty acids oppose this effect. Conjugated diene fatty acids (CLA) inhibit mammary carcinogenesis when brought at elevated amount. There are limitations in using an animal model in the analysis between nutrition and colorectal cancers. This is ascribable to the following: firstly, the digestive tract of rodents if different from that of humans and secondly, the induction of colon cancer in these animals (chemical carcinogenesis, injection of cancerous cells or transgenesis) does not mimic human colon carcinogenesis. However, on the basis of numerous published data, some important correlations have arisen that could generate hypotheses and guide new epidemiological/interventional and experimental studies. In these animal models it appears that an adequate supply of n-3 PUFAs and oleic acid in food may exert a protective effect at all stages of colon carcinogenesis. On the other hand, an excessive consumption of n-6 PUFAs and of saturated fatty acids could promote colon cancers. SN - 1769-6917 UR - https://www.unboundmedicine.com/medline/citation/16123007/[Dietary_fatty_acids_and_experimental_carcinogenesis]_ L2 - http://www.jle.com/medline.md?issn=0007-4551&vol=92&iss=7&page=685 DB - PRIME DP - Unbound Medicine ER -