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Carcinogenesis Advance Access published online on January 15, 2009
Carcinogenesis, doi:10.1093/carcin/bgp018
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Association between Genetic Polymorphisms of DNA Base Excision Repair Genes and Evolution of Precancerous Gastric Lesions in a Chinese population

Wen-qing Li1, Lian Zhang1, Jun-ling Ma1, Yang Zhang1, Ji-you Li2, Kai-feng Pan1 and Wei-cheng You1,*

1 Key laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Cancer Epidemiology
2 Department of Pathology, Peking University School of Oncology, Beijing Cancer Hospital & Institute, 52 Fu-cheng Road, Hai-dian District, Beijing 100142, P.R. China

* To whom correspondence should be addressed. Key laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Cancer Epidemiology, Peking University School of Oncology, Beijing Cancer Hospital & Institute, 52 Fu-cheng Road, Hai-dian District, Beijing 100142, P.R. China. Tel: +86-10-88141035; Fax: +86-10-88122437; Email: weichengyou{at}yahoo.com

Correspondence may also be addressed to Kai-feng Pan. Tel: +86-10-88196701; Fax: +86-10-88122437; Email: pankaifeng2002{at}yahoo.com

Base excision repair pathway may play an important role in repairing DNA damage related to Helicobacter pylori-induced inflammatory process. To evaluate the association between genetic polymorphisms of X-ray repair cross-complementing group 1 (XRCC1, Arg194Trp and Arg399Gln), adenosine diphosphage ribosyl transferase (ADPRT, Val762Ala), 8-oxoguanine DNA glycosylase (OGG1, Ser326Cys) and apurinic/apyrimidinic endonuclease 1 (APE1, Asp148Glu), and evolution of H. pylori-associated precancerous gastric lesions, a population-based cohort study was conducted in Linqu County, a high-risk area of gastric cancer in China. Genotypes were determined by PCR-based denaturing high-performance liquid chromatography and PCR-restriction fragment length polymorphism analysis in 1281 H. pylori infected subjects. We found that subjects carrying the combined XRCC1-194Arg/Trp+Trp/Trp genotype had an elevated chance of regression of gastric lesions [adjusted odds ratio (OR) 1.44; 95% confidence interval (CI) 1.06-1.96], whereas subjects carrying the XRCC1-399Arg/Gln+Gln/Gln genotype had a decreased chance of regression (OR 0.68; 95% CI 0.49-0.92). Stratified analysis indicated that an increased risk of progression was observed in subjects carrying the XRCC1-399Arg/Gln+Gln/Gln genotype (OR 1.60; 95% CI 1.09-2.36) or OGG1-326Ser/Cys+Cys/Cys genotype (OR 1.95; 95% CI 1.03-3.71) with intestinal metaplasia or dysplasia at baseline, or carrying the XRCC1-399Arg/Gln+Gln/Gln genotype and smoking (OR 1.58; 95% CI 1.02-2.45). Furthermore, a significantly increased risk of progression was observed in subjects carrying one or two hazard genotypes of XRCC1-399 or OGG1-326, the OR was 2.83 (95% CI 1.32-6.08), 2.22 (95% CI 1.24-3.98), or 2.27 (95% CI 1.26-4.10), respectively. These findings suggest that genetic polymorphisms in XRCC1-Arg194Trp, XRCC1-Arg399Gln and OGG1-Ser326Cys may play important roles in the evolution of H. pylori-associated gastric lesions in this high-risk population.

Key Words: polymorphism • DNA base excision repair gene • evolution • H. pylori • precancerous gastric lesion

Received November 12, 2008; revised January 8, 2009; accepted January 10, 2009.


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