Abstract

ERCC2 is an essential component of the nucleotide excision repair pathway which is involved in the effective maintenance of genome integrity. Association studies on ERCC2 polymorphisms and glioma risk have yielded inconclusive results. This meta-analysis was performed to gain a better insight into the relationship between ERCC2 polymorphisms and glioma risk. A systematic literature search updated to December 2, 2013 was performed in the Pubmed and EMBASE databases. Crude pooled odds ratios (ORs) with their corresponding 95% confidence intervals (95% CIs) were used to estimate the association between ERCC2 polymorphisms and glioma risk under a suitable effect model according to heterogeneity. All analyses were performed using Review Manager 5 (version 5.2) and STATA (version 12.0). The combined results demonstrated rs13181 to be significantly associated with glioma risk (G allele versus T allele: OR=1.15, 95% CI=1.05-1.26, P=0.002; dominant model: OR=1.22, 95% CI=1.07-1.39, P=0.002; recessive model: OR=1.18, 95% CI=0.98-1.41, P=0.070). We also found that rs13181 acts in an allele dose-dependent manner (GG versus TT: OR=1.30, 95% CI=1.07-1.57, P=0.009; TG versus TT: OR=1.20, 95%=CI 1.05-1.37, P=0.009; trend test, P=0.004). However, no evidence was found in analyses for the association between other 3 ERCC2 polymorphisms (rs238406, rs1799793, and rs1052555) and susceptibility to glioma development. Our meta-analysis suggests that rs13181 is significantly associated with glioma risk in an allele dose-dependent manner, whereas, 3 other ERCC2 polymorphisms (rs238406, rs1799793, and rs1052555) may have no influence.

Highlights

  • Glioma is the most common type of primary brain tumors

  • No evidence was found in analyses for the association between other 3 ERCC2 polymorphisms and susceptibility to glioma development

  • Our meta-analysis suggests that rs13181 is significantly associated with glioma risk in an allele dose–dependent manner, whereas, 3 other ERCC2 polymorphisms may have no influence

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Summary

Introduction

Glioma is the most common type of primary brain tumors. Some advances have been made in the detection and management of glioma in the past decades, most of the patients with glioma still have a poor prognosis (Schwartzbaum et al, 2006). Numerous studies have been conducted to uncover the etiology of glioma, but only ionizing radiation has so far been established firmly to be an environmental risk factor for glioma (Ohgaki et al, 2005). An important carcinogenic mechanism of ionizing radiation for glioma is inducing various types of DNA damage including single- and double-strand breaks. The accumulation of DNA damages will result in tumor occurrence if there is the existence of DNA repair defects. DNA repair genes are supposed to be the potential susceptibility genes of glioma

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