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Background: In 2009, a genome-wide association study (GWAS) identified two variants (rs12425791 and rs11833579) nearNINJ2gene that confer susceptibility to stroke in Caucasian populations. Recently, a number of studies have been conducted to replicate this finding in Asian populations. However, the results are conflicting. Thus, we performed a quantitative analysis to summarize the evidence regarding the association between these two polymorphisms and ischemic stroke risk.Methods: Pertinent studies were identified by searching PubMed and Embase through September 2014. Studies that reported odds ratio (OR) with 95% confidence interval (CI) for the association between these two polymorphisms and stroke risk were included.Results: Eight independent publications, with 8626 cases and 8046 controls for rs12425791 and 9142 cases and 8657 controls for rs11833579, were included. Overall, significantly increased ischemic stroke risk was associated with rs12425791 A allele when all studies were pooled into the meta-analysis (AA/GA vs. GG: OR = 1.08, 95% CI: 1.01–1.14). However, rs11833579 was not associated with increased stroke risk in any genetic model.Conclusions: These findings indicate that rs12425791 G>A polymorphism may be a low-penetrance susceptibility marker of stroke in Asian populations and further studies are warranted to verify this association. [ABSTRACT FROM AUTHOR]

Background: P53 is a tumor suppressor gene and plays important role in the etiology of breast cancer. Intron 3 sixteen-bp duplication polymorphism of p53 has been reported to be associated with breast cancer risk. However, the reported results remain conflicting rather than conclusive. Methods: A meta-analysis including 19 case-control studies was performed to address this issue. Odds ratios (ORs) with 95% confidence intervals (CIs) were adopted to evaluate the association. Results: The overall results suggested that the variant genotypes were associated with a significantly increased breast cancer risk (Del/Ins vs Del/Del: OR = 1.18, 95% CI: 1.00–1.40; Ins/Ins vs Del/Del: OR = 1.42, 95% CI = 1.09–1.84; Ins/Ins+Del/Ins vs Del/Del: OR = 1.21, 95% CI = 1.03–1.41). When stratifying by sample size of studies, a significantly elevated risk was also observed among large sample studies (>500 subjects) but not among small sample studies (≤500 subjects). Conclusion: These results suggested that the 16-bp duplication polymorphism of p53 may contribute to susceptibility to breast cancer. Additional well-designed large studies were required to validate this association in different populations. [ABSTRACT FROM AUTHOR]

The Ser326Cys polymorphism in the human 8-oxogunaine DNA glycosylase (hOGG1) gene had been implicated in cancer susceptibility. Studies investigating the associations between the Ser326Cys polymorphism and cancer susceptibility showed conflicting results. To derive a more precise estimation of the relationship, a meta-analysis was performed. This meta-analysis was performed from 83 case–control studies, including 27 918 cases and 33 399 controls. The fixed and random effect models were used to estimate the odds ratios (ORs) and their 95% confidence interval (CI) for various contrasts of this polymorphism. The combined results based on all studies showed that the hOGG1 Ser326Cys polymorphism was associated with an increased cancer susceptibility in different genetic models. In the stratified analyses, the association was significantly in head and neck cancer (homozygote comparison: OR = 2.19, 95% CI: 1.20–4.01, Pheterogeneity = 0.002; heterozygote comparison: OR = 1.48, 95% CI: 1.11–1.99, Pheterogeneity = 0.004; dominant model comparison: OR = 1.58, 95% CI: 1.14–2.19, Pheterogeneity < 0.001; recessive model comparison: OR = 1.73, 95% CI: 1.02–2.94, Pheterogeneity = 0.002; and additive model comparison: OR = 1.43, 95% CI: 1.09–1.88, Pheterogeneity < 0.001) which remained for studies of the Asian populations and hospital-based of control sources. But it was not observed in other cancer types of the European population and population based of control sources. This meta-analysis suggested that the hOGG1 Ser326Cys polymorphism might contribute to an increased risk on cancer susceptibility. More studies based on larger sample size should be performed to confirm the findings. [ABSTRACT FROM PUBLISHER]

Methylenetetrahydrofolate reductase (MTHFR) is involved in DNA methylation and nucleotide synthesis. Accumulated evidence has demonstrated that C677T and A1298C polymorphisms of the MTHFR gene are associated with acute lymphoblastic leukemia (ALL) risk, but the results have been inconclusive. To determine a more precise estimation, we performed a meta-analysis of 28 studies with 4240 cases and 9289 controls. We found that the 677TT genotype showed a reduced risk of ALL compared with the 677CC genotype in the overall population (odds ratio [[OR]] 0.76, 95%% confidence interval [[CI]] 0.61-0.92). The reduced risk was pronounced only among the Caucasian population (OR 0.68, 95%% CI 0.51-0.90), not the Asian (OR 0.89, 95%% CI 0.75-1.05). For the MTHFR A1298C polymorphism, no significant association with ALL susceptibility was observed in the pooled analyses. However, significantly increased ALL risk was found in childhood inthe comparison of 1298CA versus AA genotype. This study provides evidence that MTHFR polymorphisms may play animportant role in the development of ALL. [ABSTRACT FROM AUTHOR]

Myeloperoxidase (MPO) is an endogenous oxidant enzyme that generates reactive oxygen species and plays an important role in the aetiology of cancer. The MPO −463G>A polymorphism influences MPO transcription and has been implicated in cancer risk. However, results from published studies on the association between the MPO −463G>A polymorphism and risk of cancer are conflicting. To derive a more precise estimation of association between the MPO −463G>A polymorphism and risk of cancer, we performed a meta-analysis based on 43 case–control studies, including a total of 14 171 cancer cases and 17 319 controls. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association. Overall, individuals with the −463A allele had a 0.93-fold lower cancer risk in a dominant model (OR = 0.93, 95% CI = 0.87–1.00). In the stratified analyses, we observed a similar association in European populations (heterozygote comparison: OR = 0.90, 95% CI = 0.82–0.99) and hospital-based studies (dominant model: OR = 0.88, 95% CI = 0.79–0.99). When stratified by cancer type, however, no significant association was found. The results suggested that the MPO −463A allele does not contribute to the development of cancer. Additional well-designed large studies are required to validate these findings in different populations. [ABSTRACT FROM PUBLISHER]

Abstract: Objective: p53 is a tumor suppressor gene and is involved in the etiology of ovarian cancer. Studies investigating the associations between the p53 codon 72 polymorphism and ovarian cancer risk showed conflicting results. We performed this meta-analysis from eligible studies to evaluate this purported relationship. Methods: This meta-analysis was performed from 9 case-control studies, including 825 ovarian cases and 1073 controls. T he fixed and random effect models were used to estimate the odds ratios(ORs) for various contrasts of this polymorphism. Results: The combined results based on all studies showed that a significantly decreased risk was associated with the variant Pro/Pro genotype, compared with Arg/Pro+Arg/Arg genotypes(OR, 0.70; 95%CI, 0.51∼0.95). When stratifying the studies by ethnicity, we found that individuals with the variant genotype Pro/Pro had a significantly decreased risk of ovarian cancer compared with Arg/Arg genotype(OR, 0.43; 95%CI, 0.20∼0.89) and Arg/Pro+Arg/Arg genotypes(OR, 0.61; 95%CI, 0.37∼0.99) among Africans. Conclusion: This meta-analysis suggests that the p53 codon 72 polymorphism may contribute to genetic susceptibility to ovarian cancer. More studies based on larger sample size should be performed to confirm the findings. [Copyright &y& Elsevier]