Editorial

Epidemiological data have shown that chronic alcohol consumption increases the risk for cancer of the organs and tissues of the respiratory tract and the upper digestive tract (ie upper aerodigestive tract), liver, colon, rectum and breast. Although the exact mechanism of ethanol-associated carcinogenesis still remains unknown, a number of factors may contrib-ute to the development of alcohol-associated cancer, including ethanol metabolising enzymes. Ethanol is metabolised to acetaldehyde, the first and most toxic metabolite of alcohol, mainly by alcohol dehydro-genase (ADH) enzymes. Acetaldehyde is then metabolised to acetic acid by aldehyde dehydrogen-ases (ALDHs). A recent study in Nature Genetics1 has indicated that genetic variants of ADH1B an