hOGG1, Ser326Cys polymorphism and bladder cancer- Seven case–control studies were identified, including 2474 patients and 2408 controls. Four of them provided the analysis of smoking effects, with 1372 smokers and 947 non-smokers. The odds ratios (ORs) and associated 95- confidence intervals (CIs) were calculated using fixed- or random- effects models. Results Regarding the overall association between the hOGG1 326Cys allele and bladder cancer risk, the meta-analysis did not reveal a significant effect in the additive model (OR: 1.06, 95- CI: 0.96-1.26; p--.49), the recessive genetic model (OR: 1.05, 95- CI: 0.65-1.70; p--.85) or the dominant genetic model (OR: 1.07, 95- CI: 0.87-1.32; p--.53). Similarly, no significant relationship was observed in the stratified analysis by ethnicity, study design and Hardy-Weinberg equilibrium (all p-gt;-.05). In the non-smokers, however, hOGG1 326Cys allele significantly increased the risk for bladder cancer and the ORs in the additive model, homozygote contrast and recessive genetic model were 1.59 (p--.02), 2.53(p--.003) and 2.41(p--.0005), respectively. Nevertheless, in the smoker subgroup, similar findings could not be found in all genetic models (all p-gt;-.05). Conclusions The association between the hOGG1 326Cys allele and bladder cancer was significant in non-smoker population, while was non-detectable in common or smoker populations. This meta-analysis suggests that the hOGG1 Ser326Cys polymorphism may be a risk factor for bladder cancer without exposure to smoking. Further functional studies are needed to elucidate the gene polymorphism-bladder cancer relationship and gene-environment interactions." />