| [ Summary ] |
Genetic polymorphisms of alcohol dehydrogenase‒1B (ADH1B) and aldehyde dehydrogenase‒2 (ALDH2) modulate exposure levels to ethanol/acetaldehyde. The combination of alcohol consumption, smoking, slow‒metabolizing ADH1B*1/*1, and inactive heterozygous ALDH2*1/*2 markedly increase the risk of developing esophageal cancer, head and neck cancer, or dysplasia, particularly at multiple sites, because of prolonged exposure to higher concentrations of carcinogenic ethanol and acetaldehyde. A questionnaire asking about current and past facial flushing after drinking a glass (approximately 180 ml) of beer is a reliable tool for detecting the presence of inactive ALDH2. Multiple or large esophageal dysplasia, melanosis in the palate, pharynx, and esophagus, and high mean corpuscular volume serve as high‒risk markers for field cancerization in the esophagus and head and neck. Drinking modulation, drinking cessation, smoking cessation, and high intake of fruit and vegetables decrease the risk of esophageal cancer in a dose‒dependent manner. |