The molecular and biochemical mechanisms by which chronic alcohol consumption leads to the development of cancers of various organs are not fully understood. It is suggested that these mechanisms differ by target organ and include polymorphisms in genes that encode enzymes responsible for ethanol metabolism (e.g., alcohol dehydrogenase, aldehyde dehydrogenase, and cytochrome P450 2E1), increased oestrogen concentration, and changes in folate metabolism and in DNA repair [60]. For the digestive tract cancers, especially those of the upper digestive tract, acetaldehyde, both from alcohol metabolism in the human body and ingested as a component of alcoholic beverages, has been recently highlighted as an important likely causal pathway [59;61-65].
