One possibility may be that in populations with fully active ALDH2, where acetaldehyde generated from ethanol oxidation is rapidly converted to acetate, different mechanisms of alcohol-related UADT carcinogenesis are operative. Specifically, the reduced ability to clear ethanol in ADH1B R48 homozygotes could result in the induction of CYP2E1, which generates genotoxic oxygen radicals and lipid peroxidation products. Although ethanol induction of CYP2E1 levels are most well documented for the liver, CYP2E1 is present in oesophageal cells, and is also ethanol inducible in this tissue [9].
