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SULT1A1 polymorphism and esophageal cancer in males
Author(s) -
Wu MingTsang,
Wang YiTing,
Ho ChiKung,
Wu DengChyang,
Lee YungChie,
Hsu HonKi,
Kao EinLong,
Lee JangMing
Publication year - 2002
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.10805
Subject(s) - esophageal cancer , areca , genotype , medicine , allele , gastroenterology , alcohol consumption , carcinoma , cancer , oncology , alcohol , genetics , biology , gene , biochemistry , structural engineering , nut , engineering
Sulfotransferase (SULT) 1A1 detoxifies and bioactivates a broad spectrum of substrates including xenobiotics. It has been suggested that the SULT1A1 his ( histidine ) allele, which is caused by a his for arg ( arginine ) substitution due to a G→A transition at codon 213, carries a significantly higher risk for women to develop breast cancer. We investigated the association between the SULT1A1 arg / his genotype and esophageal cancer in men, 187 cases of esophageal squamous cell carcinoma and 308 controls from 3 medical centers in Taiwan. Cigarette smoking, areca chewing and alcohol consumption were the major risks for developing esophageal cancer. The frequencies of arg / his in cases and controls were 27.8% (52/187) and 11.0% (34/308), respectively ( p < 0.0001). No subjects carried his / his . After adjusting for substance use and other covariates, individuals with arg / his had a 3.53‐fold higher risk (95% CI = 2.12–5.87) of developing esophageal cancer than those with arg / arg . Unexpectedly, this positive association was found to be even stronger (adjusted OR = 4.04–4.80) among non‐smokers, non‐drinkers or non‐chewers. Our findings suggest that the SULT1A1 his 213 allele is important in the development of esophageal cancer in men. © 2002 Wiley‐Liss, Inc.