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.
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 -