## Abstract Alterations of the fragile histidine triad (__Fhit__) gene were investigated in rat hepatocarcinogenesis induced by a choline‐deficient L‐amino acid–defined (CDAA) diet. Males of the F344 strain, 6 wk of age, were fed a CDAA diet, and subgroups were killed at 2, 4, 12, 20, and 75 wk aft
Molecular alterations in hepatocarcinogenesis induced by dietary methyl deficiency
✍ Scribed by Igor P. Pogribny; S. Jill James; Frederick A. Beland
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 153 KB
- Volume
- 56
- Category
- Article
- ISSN
- 1613-4125
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✦ Synopsis
Abstract
A chronic deficiency of major dietary methyl group donors – methionine, choline, folic acid, and vitamin B~12~ – can induce the development of liver cancer in rodents. Feeding methyl‐deficient diets causes several molecular alterations, including altered lipid metabolism, oxidative stress, deregulated one‐carbon metabolism, and a number of epigenetic abnormalities that result in progressive liver injury culminating in the development of primary liver tumors. Importantly, this methyl‐deficient model of endogenous hepatocarcinogenesis is one of the most relevant models of human liver carcinogenesis that allows studying liver cancer pathogenesis by substantially complementing many shortcomings of humans‐only studies. In this review, we describe molecular changes and their role in pathogenesis of liver carcinogenesis induced by methyl deficiency.
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