Esophageal Cancer
Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 7, 2005; 11(17): 2531-2538
Published online May 7, 2005. doi: 10.3748/wjg.v11.i17.2531
Phase I/II enzyme gene polymorphisms and esophageal cancer risk: A meta-analysis of the literature
Chun-Xia Yang, Keitaro Matsuo, Zhi-Ming Wang, Kazuo Tajima
Chun-Xia Yang, Department of Epidemiology, Huaxi Public Health School, Sichuan University, Chengdu 610041, Sichuan Province, China
Chun-Xia Yang, Keitaro Matsuo, Kazuo Tajima, Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan
Zhi-Ming Wang, Huaxi Public Health School, Sichuan University, Chengdu 610041, Sichuan Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Keitaro Matsuo, Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan. kmastuo@aichi-cc.jp
Telephone: +81-52-762-6111 Fax: +81-52-763-5233
Received: September 24, 2004
Revised: September 25, 2004
Accepted: November 19, 2004
Published online: May 7, 2005
Abstract

AIM: Phase I/II enzymes metabolize environmental carcin-ogens and several functional polymorphisms have been reported in their encoding genes. Although their significance with regard to esophageal carcinogenicity has been examined epidemiologically, it remains controversial. The present systematic review of the literature was performed to clarify associations.

METHODS: Eligible studies were case-control or cohort studies published until September 2004 that were written in any language. From PubMed and a manual review of refe-rence lists in relevant review articles, we obtained 16 studies related to the CYP1A1 Ile-Val substitution in exon 7, CYP1A1 MspI polymorphisms, CYP2E1 RsaI polymorphisms, GSTM1 null type, GSTT1 null type and GSTP1 Ile104Val. All were of case-control design. Summary statistics were odds ratios (ORs) comparing heterozygous-, homozygous-non-wild type or these two in combination with the homozygous wild type, or the null type with the non-null type for GSTM1 and GSTT1. A random effect model was used to estimate the summary ORs. A meta-regression analysis was applied to explore sources of heterogeneity.

RESULTS: Individuals with the Ile-Val substitution in CYP1A1 exon 7 had increased esophageal cancer risk, with ORs (95%CI) compared with Ile/Ile of 1.37 (1.09-1.71), 2.52 (1.62-3.91) and 1.44 (1.17-1.78) for Ile-Val, Val/Val genotype and the combined group. No significant association was found between esophageal cancer risk and the other genetic parameters.

CONCLUSION: A significant association exists between the CYP1A1 Ile-Val polymorphism and risk of esophageal cancer. Polymorphisms that increase the internal exposure to activated carcinogens may increase the risk of esophageal cancer.

Keywords: CYPs; GSTs; Gene polymorphisms; Esophageal cancer; Meta-analysis