Alcohol consumption is a risk factor associated to several forms of cancer and the International Agency for Research on Cancer (IARC) has defined acetaldehyde (the first intermediate product of alcohol degradation) associated with consumption of alcoholic beverages as “carcinogenic to humans” (Group 1) [IARC Working Group on the Evaluation of Carcinogenic Risks to Humans 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans 2012]. In particular, alcohol carcinogenesis mostly affects tissues directly exposed to alcohol ingestion (e.g., the oral cavity, pharynx, esophagus, larynx, and colon), tissues involved in alcohol metabolism (e.g., liver), and tissue exposed to alcohol-associated oxidative stress (e.g., breast) [Persson and others 2013; Toh and others 2010; Varela-Rey and others 2013]. The full set of carcinogenic mechanisms of alcohol, including formation of acetaldehyde-DNA adducts, hyperregeneration, and epigenetic changes, is still to be elucidated and confirmed [Brooks and Zakhari 2014]. Genetic studies (candidate gene studies, meta-analyses, and GWAS) of alcohol-associated cancers (AAC; e.g., upper aerodigestive tract cancers, hepatocellular carcinoma, breast cancer, colon cancer, and thyroid cancer) have repeatedly implicated risk alleles in alcohol metabolism genes, including
