Volume 31, Issue 6 pp. 802-809

XRCC1 genetic polymorphism Arg399Gln and hepatocellular carcinoma risk: a meta-analysis

Fei Liu

Fei Liu

Department of Liver and Vascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China

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Bo Li

Bo Li

Department of Liver and Vascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China

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Yonggang Wei

Yonggang Wei

Department of Liver and Vascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China

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Lvnan Yan

Lvnan Yan

Department of Liver and Vascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China

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Tianfu Wen

Tianfu Wen

Department of Liver and Vascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China

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Jichun Zhao

Jichun Zhao

Department of Liver and Vascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China

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Mingqing Xu

Mingqing Xu

Department of Liver and Vascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China

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First published: 07 June 2011
Citations: 38
Correspondence
Yonggang Wei, Department of Liver and Vascular Surgery, West China Hospital, Sichuan University, 37 Guo Xue Road, Chengdu, 610041, Sichuan Province, China.
Tel: +86 28 85422476
Fax: +86 28 85423724
e-mail: [email protected]

Abstract

Background: Studies investigating the association between X-ray repair cross-complementing group 1 (XRCC1) genetic polymorphism Arg399Gln and hepatocellular carcinoma (HCC) risk report conflicting results. The aim of this study was to quantitatively summarize the evidence for such a relationship.

Methods: Two investigators independently searched the Medline, Embase, CNKI and Chinese Biomedicine Database. Summary odds ratios (ORs) and 95% confidence intervals (95% CIs) for XRCC1 polymorphism and HCC were calculated in a fixed-effects model (the Mantel–Haenszel method) and a random-effects model (the DerSimonian and Laird method) when appropriate. The pooled ORs were performed for a codominant model (Gln/Gln vs. Arg/Arg, Arg/Gln vs. Arg/Arg), a dominant model (Gln/Gln+Arg/Gln vs. Arg/Arg) and a recessive model (Gln/Gln vs. Arg/Gln+Arg/Arg).

Results: This meta-analysis included 11 case–control studies, which included 2208 HCC cases and 3265 controls. Overall, the variant genotypes (Gln/Gln and Arg/Gln) of Arg399Gln were not associated with HCC risk when compared with the wild-type Arg/Arg homozygote (Gln/Gln vs. Arg/Arg, OR=1.01, 95% CI=0.79–1.28; Arg/Gln vs. Arg/Arg, OR=1.09, 95% CI=0.81–1.45). Similarly, no associations were found in the dominant and recessive models (dominant model, OR=1.12, 95% CI=0.85–1.47; recessive model, OR=0.99, 95% CI=0.79–1.25). Limiting the analysis to the studies within Hardy–Weinberg equilibrium, the results were persistent and robust. When stratifying for ethnicity, country/region and source of controls, no evidence of a significant association was observed in any subgroup. No publication bias was found in the present study.

Conclusion: No association is found between the XRCC1 polymorphism Arg399Gln and the risk of HCC.

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