Article

Molecular alterations in hepatocarcinogenesis induced by dietary methyl deficiency.

Division of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA.
Molecular Nutrition & Food Research (impact factor: 4.3). 11/2011; 56(1):116-25. DOI:10.1002/mnfr.201100524 pp.116-25
Source: PubMed

ABSTRACT A chronic deficiency of major dietary methyl group donors--methionine, choline, folic acid, and vitamin B12--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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    Molecular and Cellular Biochemistry 11/2012; · 2.06 Impact Factor
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Keywords

chronic deficiency
 
deregulated one-carbon metabolism
 
endogenous hepatocarcinogenesis
 
folic acid
 
humans-only studies
 
molecular alterations
 
primary liver tumors
 
relevant models
 
rodents
 
shortcomings