Abstract
Various mechanisms may contribute to alcohol-mediated carcinogenesis, including the action of acetaldehyde, the first and most toxic ethanol metabolite, and the generation of oxidative stress by various pathways including the induction of cytochrome P450-2E. Other important mechanisms include the effect of alcohol on epigenetics (DNA, histone methylation and acetylation), the interaction with retinoid metabolism, and special effect of ethanol on intracellular signal transduction pathways. In addition, tissue specific effects of alcohol are of considerable importance. This is relevant for hepatocellular carcinoma, where cirrhosis is a major factor, and for breast cancer where estrogens act as a carcinogen and are increased by alcohol consumption. Chronic alcohol consumption even at smaller amounts increases the risk for hepatocellular cancer in patients with hepatitis B and C, in hemochromatosis, and in nonalcoholic steatohepatitis. Alcohol related carcinogenesis may interact with other factors such as smoking, diet, comorbidities, and depends on genetic susceptibility.
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