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Alleles of alcohol and acetaldehyde metabolism genes modulate susceptibility to oesophageal cancer from alcohol consumption.
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In February 2007, the IARC convened a new working group to consider new evidence that had come to light since 1988. The 2007 working group, which included one of us (P.J.B.), drew several conclusions which substantially altered the way we think about the relationship between alcohol consumption and cancer, from both epidemiological and mechanistic standpoints [1]. First, on the basis of the evidence available, both from epidemiological and from animal studies, the 2007 working group concluded that ethanol itself is carcinogenic to humans. Secondly, the group added two additional alcohol-related cancers: colorectal cancer and cancer of the female breast. Regarding mechanism, the group concluded that there is substantial evidence to indicate a role for acetaldehyde, the first metabolite of ethanol, in the pathogenesis of oesophageal cancer resulting from alcohol consumption. This last conclusion was based largely on studies by Yokoyama and colleagues of oesophageal cancer risk in Asian individuals, who are ALDH2 deficient owing to the ALDH2 G487K allele [2]. A summary of the 2007 IARC working group conclusions has been published [3].