Alcohol, DNA methylation, and cancer.

摘要: Cancer is one of the most significant diseases associated with chronic alcohol consumption, and drinking a strong risk factor for cancer, particularly upper aerodigestive tract, liver, colorectum, breast. Several factors contribute to alcohol-induced cancer development (i.e., carcinogenesis), including actions acetaldehyde, first primary metabolite ethanol, oxidative stress. However, increasing evidence suggests that aberrant patterns DNA methylation, an important epigenetic mechanism transcriptional control, also could be part pathogenetic mechanisms lead development. The effects on global local methylation likely are mediated by its ability interfere availability principal biological methyl donor, S-adenosylmethionine (SAMe), as well pathways related it. may mediate reduced folate levels inhibition key enzymes in one-carbon metabolism ultimately lower SAMe levels, activity expression involved methyltransferases). Finally, variations polymorphisms) several genes modulate alcohol-associated carcinogenesis.