In addition to the deficient ALDH2 variant that is common in Asians, there is now also evidence that genetic variation in other alcohol and acetaldehyde metabolism genes increases susceptibility to cancer after alcohol consumption. Much of this evidence comes from large studies carried out by intramural investigators at the IARC on cancer risk in several central European countries. Central Europe has some of the highest rates of squamous cell oesophageal cancer in the world, owing in large part to high rates of smoking and alcohol abuse [4]. A 2006 study [4] provided evidence that in these populations, which do not carry the inactive ALDH2 allele common in Asians, other polymorphisms in the alcohol dehydrogenase (ADH) and aldehyde dehydrogenase 2 (ALDH2) genes are associated with UADT cancers, and these interact substantially with alcohol consumption to elevate cancer risk. Specifically, the high-activity ADH1B R48H allele (also known as ADH1B*1) was protective against UADT cancer, whereas three ALDH2 variants were associated with an increased risk of alcohol-related UADT cancers. It should be noted, however, that, unlike the ADH1B R48H and the Asian ALDH2
