Alcohol consumption and cigarette smoke are risk factors for esophageal cancer, especially for multicentric carcinogenesis.

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Alcohol metabolism: A loss of fragile histidine triad (FHIT) expression is associated not only with alcohol-induced esophageal carcinogenesis, but also with multicentric carcinogenesis, in the metabolic pathway of ethanol. Aldehyde dehydrogenase 2 (ALDH2) is a major enzyme for detoxification of acetaldehyde, and it is important for esophageal and ling carcinogenesis. Both inactive and active forms of ALDH2 are induced in the esophagus by heavy drinking and also support a hypothesis that ALDH2 deficiency might be a high-risk factor of esophageal cancer for the individuals having a heavy-drinking habit. The expression level of Cyp2e1 was increased in the liver from Aldh2-null mice. Therefore, Aldh2-null mice may be useful model animals for the investigation of alcohol metabolism and related diseases.Tobacco smoking: The methylation of p16 was more frequently observed in patients who were heavy smoker and with squamous cell carcinoma and than in never/ light smokers and adenocarinoma, respectively. The mutations in the epidermal growth factor receptor (EGFR) gene were more frequently observed in patients who smoked p20 pack-year, and in patients who quit at least 20 years before the date of diagnosis for lung cancer. The K-ras mutations were more frequently found in smokers than in never smokers, and in high-dose smokers than in low-dose smokers, suggesting that mutations of EGFR and k-ras might be strongly associated with exposure of tobacco smoking.