P53 protein accumulation, iodine-unstained lesions, and alcohol dehydrogenase-1B and aldehyde dehydrogenase-2 genotypes in Japanese alcoholic men with esophageal dysplasia

Abstract

Inactive heterozygous aldehyde dehydrogenase-2 ( ALDH2 *1/ *2 ) and less-active alcohol dehydrogenase-1B ( ADH1B *1/ *1 ) increase the risk of esophageal cancer in East Asian drinkers, and esophageal cancer multiplicity is strongly associated with ALDH2 *1/ *2 . p53 alterations are key molecular events in multifocal carcinogenesis in the esophagus. We studied 260 esophageal-cancer free Japanese alcoholics with esophageal dysplasia diagnosed by biopsy of distinct iodine-unstained lesions (DIULs) ⩾5 mm. The degree of p53 protein accumulation was positively associated with the degree of atypia ( p < 0.0001) and size ( p = 0.040) of DIULs and with the presence of multiple DIULs (p = 0.070), but not with ALDH2 *1/ *2 or ADH1B *1/ *1 .