Our data demonstrated that reduced MTHFR activities associated with the MTHFR T allele may interact with RBC folate as the risk modifiers of lymphocytic p53 oxidative lesions of HCC patients. The CT/TT genotypes correlated with lower risks of late-stage HCC and a favorable survival of HCC patients, depending on p53 oxidative lesions or RBC folate status.
Previous studies have demonstrated that choline deficiency preceded the formation of adenomas and hepatocellular carcinoma (HCC). Whether dietary intake of one‐carbon nutrients in particular for choline and betaine, risk factors for HCC development, may influence tumour progression was not known. The aims of the study were to investigate the relationships between these two dietary factors, genetic polymorphisms of methylenetetrahydrofolate reductase (MTHFR) and HCC progression. The study included 232 HCC patients with 63 individuals collected for dietary intake data. The database in NAHSIT (Taiwan food data bank) did not contain choline and betaine content values. The hypothetical choline and betaine food composition databases were constructed using the various versions of data sets from US Department of Agriculture (USDA) data sets, by matching identical foods from the NAHSIT database to the USDA database to assign choline and betaine values. The data showed that mean dietary choline intake of HCC patients was lower than the AI value for Taiwanese adults. Dietary betaine intake was inversely correlated with HCC tumor size (r = ‐0.30, p = 0.01) and tumor numbers (r = ‐0.24, p = 0.04). Combining with MTHFR genotype and other dietary one‐carbon factors, HCC patients who carried MTHFR 677 CT/TT genotype had lower lymphocytic mitochondrial DNA large deletion (p= 0.001, p= 0.001) when they got higher choline and betaine from their diet. In summary, dietary choline and betaine intakes were associated with HCC progressive markers, polymorphic or genetic damage markers among HCC patients. The mechanisms require further studies.
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