Associations between MTHFR Ala222Val polymorphism and risks of hepatitis and hepatitis-related liver cancer: a meta-analysis

Chronic infection of viral hepatitis is the main cause of liver cancer. There were many studies assessing the associations of methylenetetrahydrofolate reductase (MTHFR) Ala222Val polymorphism with risks of hepatitis and hepatitis-related liver cancer, but no consistent results were reported. To investigate the associations of MTHFR Ala222Val polymorphism with risks of hepatitis and hepatitis-related liver cancer, we performed a meta-analysis of published case–control studies. Eligible studies were searched from PubMed and Chinese National Knowledge Infrastructure (CNKI) databases. The odds ratio (OR) and corresponding 95 % confidence interval (95 %CI) were used to assess the associations. Twenty-one individual studies with a total of 8,187 subjects were included. Overall, MTHFR Ala222Val polymorphism was not significantly associated with risks of liver cancer, hepatitis-related liver cancer, and non-hepatitis-related liver cancer. However, MTHFR Ala222Val polymorphism was significantly associated with risk of hepatitis infection (Val vs. Ala: OR?=?1.15, 95 %CI 1.01–1.32, P?=?0.03; ValVal/AlaVal vs. AlaAla: OR?=?1.37, 95 %CI 1.11–1.68, P?=?0.003). Therefore, MTHFR Ala222Val polymorphism is significantly associated with risk of hepatitis infection but not liver cancer. More studies are needed to further assess the association between MTHFR Ala222Val polymorphism and hepatitis-related liver cancer.     

Association between MTHFR Ala222Val (rs1801133) polymorphism and bladder cancer susceptibility: a systematic review and meta-analysis

Folate metabolism is thought to play an important role in carcinogenesis through its involvement in both DNA methylation and nucleotide synthesis. The association between the MTHFR Ala222Val polymorphism and bladder cancer has been widely reported, however, in general the data from published studies with individually low statistical power were controversial and underpowered. Hence, we performed a meta-analysis to investigate the association between bladder cancer and MTHFR Ala222Val in different inheritance models. Fourteen studies including a total of 3,570 bladder cancer cases and 3,926 controls for MTHFR rs1801133 polymorphism were included in the meta-analysis. Data were extracted from these studies and odds ratios with corresponding 95 % confidence intervals (95 % CI) were computed to estimate the strength of the association. Overall, the MTHFR Ala222Val polymorphism was not associated with the development of bladder cancer in all genetic models (Ala/Ala vs. Val/Val—OR?=?0.961, 95 % CI?=?0.763–1.209; Ala/Ala vs. Ala/Val—OR?=?0.918, 95 % CI?=?0.795–1.060—Ala/Val vs. Val/Val—OR?=?1.022, 95 % CI?=?0.852–1.227; dominant model—OR?=?0.998, 95 % CI?=?0.869–1.145; recessive model—OR?=?0.921, 95 % CI?=?0.794–1.069; Ala allele vs. Val allele—OR?=?0.957, 95 % CI?=?0.857–1.067). In the stratified analyses, no significant associations were found among different descent populations and sources of controls. Our meta-analysis suggests that the MTHFR Ala222Val polymorphism not contributes to the development of bladder cancer.     

Catechol-O-methyltransferase Val158Met polymorphism and breast cancer risk in Asian population

The association between the polymorphism of catechol-O-methyltransferase (COMT) Val158Met and breast cancer risk is still inconclusive. We performed a meta-analysis to derive a more precise estimation of the relationship. A total of 18 studies including 5,175 cases and 6,463 controls were involved in this meta-analysis. When all studies were pooled into the meta-analysis, no significantly elevated breast cancer risk was associated with all genetic models (for additive model: OR?=?1.273, 95 % CI?=?0.947–1.711, P _{heterogeneity}?=?0.000; P?=?0.110; for dominant model: OR?=?1.080, 95 % CI?=?0.945–1.234, P _{heterogeneity}?=?0.001; P?=?0.259; for recessive model: OR?=?1.242, 95 % CI?=?0.941–1.641, P _{heterogeneity}?=?0.000; P?=?0.126; for allele comparison model: OR?=?1.096, 95 % CI?=?0.976–1.230, P _{heterogeneity}?=?0.000; P?=?0.121). In the subgroup analysis by controls source, the same results were found in all genetic models. In summary, this meta-analysis suggests that the COMT Val158Met polymorphism is not a risk factor for breast cancer development. However, large sample and representative population-based studies with homogeneous breast cancer patients and well-matched controls are warranted to confirm this finding.     

Lack of association between MHTFR Glu429Ala polymorphism and breast cancer susceptibility: a systematic review and meta-analysis of 29 research studies

The association between MHTFR Glu429Val polymorphism and breast cancer risk are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed. A total of 29 studies including 8,649 cases and 18,672 controls were involved in this meta-analysis. Overall, no significant associations were found between MTHFR Glu429Ala polymorphism and breast cancer risk when all studies were pooled into the meta-analysis (Glu/Glu vs Ala/Ala: OR?=?0.891, 95 % CI?=?0.782–1.015; Glu/Ala vs Ala/Ala: OR?=?0.874, 95 % CI?=?0.760–1.006; dominant model: OR?=?0.885, 95 % CI?=?0.775–1.012; and recessive model: OR?=?0.989, 95 % CI?=?0.931–1.051). In the subgroup analysis by ethnicity, significantly elevated breast cancer risk was associated with Glu/Glu variant genotype in homozygote comparison and recessive genetic model (Glu/Glu vs Ala/Ala: OR?=?0.78, 95 % CI?=?0.63–0.97; Glu/Glu vs Glu/Ala: OR?=?0.92, 95 % CI?=?0.85–0.99; recessive model: OR?=?0.91, 95 % CI?=?0.85–0.97), while no significant associations were found for all comparison models in other ethnicity populations. In conclusion, this meta-analysis suggests that the MTHFR Glu429Ala polymorphism may be not associated with breast cancer development.     

Association between MTHFR 677C>T polymorphism and risk of gliomas: evidence from a meta-analysis

Folate metabolism plays an important role in carcinogenesis. Methylenetetrahydrofolate reductase (MTHFR) 677C>T polymorphism is a genetic alteration in an enzyme involved in folate metabolism, but its effect on risk of gliomas is still uncertain. To shed some light on these contradictory results from previous studies, we performed a meta-analysis of published data investigating the association between MTHFR 677C>T polymorphism and risk of gliomas. PubMed, Embase, and Web of Science databases were searched for eligible case–control studies. Odds ratios (ORs) and 95 % confidence intervals (CIs) were used to assess the strength of this association. Ten individual case–control studies from six publications with a total of 1,786 cases and 2,076 controls were included into this meta-analysis. There was no obvious heterogeneity under all comparison models of this meta-analysis. Meta-analysis of those ten studies showed that there was no obvious association between MTHFR 677C>T polymorphism and risk of gliomas under all five genetic models (for T versus C, OR?=?1.00, 95 % CI 0.90–1.12, P _OR?=?0.959; for TT versus CC, OR?=?1.02, 95 % CI 0.82–1.27, P _OR?=?0.870; for CT versus CC, OR?=?1.02, 95 % CI 0.89–1.18, P _OR?=?0.733; for TT+CT versus CC, OR?=?1.02, 95 % CI 0.90–1.16, P _OR?=?0.781; for TT versus CT+CC, OR?=?0.99, 95 % CI 0.81–1.21, P _OR?=?0.902). There was also no obvious association between MTHFR 677C>T polymorphism and risk of gliomas in the sensitivity and subgroup analyses of Caucasians. There was no risk of publication bias in this meta-analysis. The evidence from our meta-analysis supports that there is no association between MTHFR 677C>T polymorphism and risk of gliomas.     

Quantitative assessment of the association between MTHFR rs1801131 polymorphism and risk of liver cancer

Methylenetetrahydrofolate reductase (MTHFR) is one of the most important enzymes for folate metabolism which plays a key role in cell metabolism. MTHFR rs1801131 (A1298C) polymorphism can decrease in vitro MTHFR enzyme activity and has been hypothesized to be associated with liver cancer risk. This study aimed to quantify the strength of the association between MTHFR rs1801131 polymorphism and liver cancer risk by performing a meta-analysis. We searched the PubMed and Wanfang databases for studies relating on the association between MTHFR rs1801131 polymorphism and risk of liver cancer. Seven studies with 2,030 cases of liver cancer and 3,096 controls were finally included into the meta-analysis. Meta-analysis of a total of seven studies showed that the homozygote genotype CC of MTHFR rs1801131 polymorphism was significantly associated with decreased risk of liver cancer (for CC versus AA: odds ratio (OR)?=?0.65, 95 % confidence interval (CI) 0.47–0.89, P?=?0.007; for CC versus AA?+?AC: OR?=?0.65, 95 % CI 0.48–0.89, P?=?0.006). Subgroup by race showed that the homozygote genotype CC of MTHFR rs1801131 polymorphism was significantly associated with decreased risk of liver cancer in Asians (CC versus AA: OR?=?0.64, 95 % CI 0.46–0.90, P?=?0.010; for CC versus AA?+ AC: OR?=?0.63, 95 % CI 0.45–0.88, P?=?0.007). However, the association in Caucasians was still unclear owing to the limited data available now. Thus, Asian individuals with the homozygote genotype CC of MTHFR rs1801131 polymorphism are significantly associated with decreased risk of liver cancer. The association in Caucasians needs further studies.     

Association between the Thr241Met polymorphism of X-ray repair cross-complementing group 3 gene and glioma risk: evidence from a meta-analysis based on 4,136 cases and 5,233 controls

Genetic polymorphism of X-ray repair cross-complementing group 3 (XRCC3) Thr241Met has been implicated to alter the risk of glioma, but the results are controversial. Medline, PubMed, Embase, and Cochrane Library databases were independently searched by two investigators up to 13 July 2013. Summary odds ratios (OR) and 95 % confidence interval (CI) for Thr241Met polymorphism and prostate cancer were calculated. Statistical analysis was performed with the software program Stata 12.0. A total of 10 independent studies, including 4,136 cases and 5,233 controls, were identified. Our analysis suggested that Thr241Met was not associated with glioma risk in overall population. In the subgroup analysis, we detected no significant association between Thr241Met polymorphism and glioma risk in different descent populations. Subgroup analysis was held by source of controls, significant association was found between this polymorphism and glioma risk for population-based studies (homozygote model: OR?=?1.747, 95 % CI?=?1.123–2.717, P _h?=?0.059, I ²?=?59.7 %; recessive model, OR?=?1.455, 95 % CI?=?1.179–1.795, P _h?=?0.111, I ²?=?50.1 %; allele model, OR?=?1.258, 95 % CI?=?1.010–1.566, P _h?=?0.011, I ²?=?72.9 %). This meta-analysis showed the evidence that XRCC3 Thr241Met polymorphism was associated with a low risk of glioma development.     

Quantitative synthesis of the association between the cytochrome P450 1A1 Ile462Val polymorphism and prostate cancer risk

The association between the cytochrome P450 1A1 (CYP1A1) Ile462Val polymorphism and prostate cancer risk remains inconclusive owing to the conflicting findings from previous studies. To get a more precise estimate of the possible association, we performed the present meta-analysis. We searched the PUBMED, EMBASE, and Wanfang databases for the studies which met the inclusion criteria. The pooled odds ratio (OR) with corresponding 95 % confidence interval (95 % CI) was used to estimate the association between CYP1A1 Ile462Val polymorphism and prostate cancer risk. A total of 13 studies with 2,350 cases and 2,992 controls were included in the meta-analysis. The results indicated that there was an obvious association between CYP1A1 Ile462Val polymorphism and increased risk of prostate cancer (for Val versus Ile: OR?=?1.27, 95 % CI 1.13–1.43, P?<?0.001; for ValVal versus IleIle: OR?=?1.51, 95 % CI 1.14–2.01, P?=?0.004; for ValVal?+?ValIle versus IleIle: OR?=?1.31, 95 % CI 1.14–1.51, P?<?0.001; for ValVal versus IleIle + ValIle: OR?=?1.38, 95 % CI 1.05–1.81, P?=?0.020). Subgroup analyses by ethnicity suggested that CYP1A1 Ile462Val polymorphism was associated with prostate cancer risk in Asians but not in Caucasians. This meta-analysis suggests that there is an association between CYP1A1 Ile462Val polymorphism and increased risk of prostate cancer. More studies with large sample are needed to further assess the association in Caucasians.     

Quantitative assessment of the influence of CYP1B1 polymorphisms and head and neck squamous cell carcinoma risk

The associations between CYP1B1 polymorphisms and head and neck squamous cell carcinoma (HNSCC) risk have been conflicting. We therefore performed a meta-analysis to derive a more precise relationship. Six published case–control studies were collected; odds ratios (ORs) with 95 % confidence interval (CI) were used to assess the association between CYP1B1 Leu432Val, Asn453Ser polymorphisms, and HNSCC risk. The Sensitivity analysis and publication bias also were performed to guarantee the statistical power. Overall, the pooled OR with 95 % CIs indicated that CYP1B1 Leu432Val polymorphism was significantly related with HNSCC risk (for Val vs. Leu: OR = 1.13, 95 % CI = 1.03–1.25, P?=?0.014, P _{heterogeneity}?=?0.141; for Val/Val vs. Leu/Leu: OR = 1.30, 95 % CI = 1.06–1.60, P?=?0.013, P _{heterogeneity}?=?0.253; for Val/Val vs. Leu/Leu + Leu/Val: OR = 1.23, 95 % CI = 1.05–1.46, P?=?0.013, P _{heterogeneity}?=?0.456). The similar results were also been found in succeeding analysis of HWE and stratified analysis of Caucasian population. Furthermore, no significant association between CYP1B1 Asn453Ser polymorphism and HNSCC risk was found in this meta-analysis. In conclusion, our meta-analysis demonstrates that CYP1B1 Leu432Val polymorphism may be a risk factor for developing HNSCC.     

CCL5-403, CCR5-59029, and Delta32 polymorphisms and cancer risk: a meta-analysis based on 20,625 subjects

Associations between CCL5-403, CCR5-59029, and Delta32 polymorphisms and cancer risk are inconclusive. To derive a more precise estimation of the association, we performed a meta-analysis by searching PubMed, EMBASE, Google scholar, and WanFang databases. A total of 20 eligible articles with 39 studies were included. Of those studies, there were 21 studies for CCR5-Delta32 polymorphism, 9 studies for CCR5-59029 polymorphism, and 9 studies for CCL5-403 polymorphism. Combined analysis revealed no associations between these polymorphisms and cancer risk. However, subgroup analysis by ethnicity suggested that CCR5-59029 polymorphism was associated with the risk of cancer among Asian populations (A vs. G: odds ratio (OR)?=?1.36, 95 % confidence interval (CI) 1.13–1.65, P _H?=?0.27; AA vs. GG: OR?=?2.07, 95 % CI 1.37–3.12, P _H?=?0.17; GA+AA vs. GG: OR?=?1.35, 95 % CI 1.03–1.77, P _H?=?0.92; AA vs. GA+GG: OR?=?1.98, 95 % CI 1.01–3.88, P _H?=?0.08), but not among Caucasian populations. CCL5-403 polymorphism was associated with the risk of cancer among African populations (A vs. G: OR?=?0.68, 95 % CI 0.55–0.83, P _H?=?0.14; AA vs. GG: OR?=?0.51, 95 % CI 0.33–0.77, P _H?=?0.52; AG vs. GG: OR?=?0.58, 95 % CI 0.42–0.80, P _H?=?0.14; AG+AA vs. GG: OR?=?0.56, 95 % CI 0.41–0.75, P _H?=?0.13), but not among Caucasian populations and Asian populations. Overall, this meta-analysis indicated that CCR5-Delta32 was not associated with the risk of cancer. CCR5-59029 polymorphism contributed to cancer risk among Asian populations, and CCL5-403 polymorphism was associated with the decreased risk of cancer among African populations.     

Association between GSTP1 Ile105Val polymorphism and glioma risk: A systematic review and meta-analysis

Glutathione S-transferase P1 (GSTP1) gene Ile105Val polymorphism has been suggested to be involved in the development of glioma. However, the results from the studies regarding the association between GSTP1 Ile105Val polymorphism and glioma risk have been inconsistent. Thus, we performed a meta-analysis to investigate this association. Pooled odds ratios (ORs) with 95 % confidence intervals (95 %CIs) were calculated using random or fixed effects model. Nine studies with 2,078 cases and 3,970 controls were finally included into this meta-analysis. The results suggested there was no association between GSTP1 Ile105Val polymorphism and glioma risk under recessive model (OR?=?1.138, 95 %CI?=?0.966–1.341, P _{heterogeneity}?=?0.088, P?=?0.123). Subgroup analyses by ethnicity showed there was also no association between GSTP1 Ile105Val polymorphism and glioma risk in mixed populations under recessive model (OR?=?1.199, 95 %CI?=?0.928–1.549, P _{heterogeneity}?=?0.060, P?=?0.166) and Caucasian populations(OR?=?1.097, 95 %CI?=?0.885–1.360, P _{heterogeneity}?=?0.186, P?=?0.398). In conclusion, the meta-analysis suggests that there is no association between GSTP1 Ile105Val polymorphism and glioma risk. However, more well-designed and larger studies are needed to further assess this association.     

Association between Cyclin D1 polymorphism and oral cancer susceptibility: a meta-analysis

Data from several case–control studies on the relation between the Cyclin D1 (CCND1) G870A polymorphism and oral cancer susceptibility implicated conflicting conclusions. Thus, a meta-analysis was performed to derive a more precise evaluation of the association. We searched PubMed and Embase for related studies that had been published in English and eight available studies were finally included in the meta-analysis. Odd ratios (ORs) and 95 % confidence intervals (CIs) were calculated for each study. Our meta-analysis suggested that CCND1 G870A polymorphism was not associated with oral cancer risk (OR _{AA vs. GG}?=?1.08, 95 % CI?=?0.90–1.30, P _{heterogeneity}?=?0.175; OR _{AA + GA vs. GG}?=?1.02, 95 % CI?=?0.91–1.14, P _{heterogeneity}?=?0.781; OR _{AA vs. GA + GG}?=?1.16, 95 % CI?=?0.98–1.36, P _{heterogeneity}?=?0.107; OR _{A vs. G}?=?1.05 95 % CI?=?0.96–1.15, P _{heterogeneity}?=?0.211; OR _{GA vs. GG}?=?0.94, 95 % CI?=?0.82–1.08, P _{heterogeneity}?=?0.935). However, in the subgroup analysis by ethnicity, possible significance among Asian groups was indicated in two genetic models (OR _{AA vs. GA + GG}?=?1.27, 95 % CI?=?1.05–1.54, P _{heterogeneity}?=?0.572; OR _{allele A vs. allele G}?=?1.11, 95 % CI?=?1.00–1.24, P _{heterogeneity}?=?0.211). Taken together, the meta-analysis revealed that CCND1 G870A polymorphism might be correlated with the susceptibility of oral cancer in Asians.     

Association between the GSTP1 Ile105Val polymorphism and prostate cancer risk: a systematic review and meta-analysis

Many studies have reported the role of glutathione S-transferase P1 (GSTP1) Ile105Val polymorphism with prostate cancer (PCa) risk. However, these studies have yielded conflicting results. Hence, we performed this meta-analysis to investigate the association between GSTP1 Ile105Val polymorphism and PCa in different inheritance models. A total of 13 eligible studies were pooled into this meta-analysis. There was significant association between the GSTP1 Ile158Val variant genotypes and PCa for Ile/Ile vs Val/Val comparison [odds ratio (OR)?=?0.705; I ²?=?63.7 %; 95 % confidence interval (95 % CI)?=?0.508–0.977], Ile/Val vs Val/Val comparison (OR?=?0.736; I ²?=?8.0 %; 95 % CI?=?0.613–0.883), and dominant model (OR?=?0.712; I ²?=?45.5 %; 95 % CI?=?0.555–0.913). However, no associations were detected for other genetic models. In the stratified analysis by ethnicity, significant associations between GSTP1 Ile105Val polymorphism and PCa risk were also found among Caucasians (Ile/Ile vs Val/Val comparison OR?=?0.818, I ²?=?0.0 %, 95 % CI?=?0.681–0.982; Ile/Val vs Val/Val comparison OR?=?0.779, I ²?=?0.0 %, 95 % CI?=?0.651–0.933; and dominant model OR?=?0.794, I ²?=?0.0 %, 95 % CI?=?0.670–0.941), while there were no associations found for other genetic models. However, no associations were found in Asians and African-Americans for all genetic models when stratified by ethnicity. In conclusion, our meta-analysis indicates that GSTP1 Ile105Val polymorphisms contributed to the PCa susceptibility. However, a study with the larger sample size is needed to further evaluate gene–environment interaction on GSTP1 Ile105Val polymorphisms and PCa risk.     

Associations between polymorphisms of the XPC gene and lung cancer susceptibility: a meta-analysis

Xeroderma pigmentosum complementation group C (XPC) gene plays a critical role in DNA damage recognition, and its functional single nucleotide polymorphisms (SNPs) may alter DNA repair capacity and cancer susceptibility. Numerous epidemiological studies have investigated the associations between XPC Lys939Gln and Ala499Val polymorphisms and lung cancer susceptibility, but the conclusions are inconclusive. We searched three electronic databases (MEDLINE, EMBASE and EBSCO) for eligible publications and performed a meta-analysis assessing the associations between XPC Lys939Gln and Ala499Val polymorphisms and lung cancer risk. We also analysed the genotype-mRNA expression correlation using the data of HapMap phase II release 23 with 270 individuals from 4 ethnicities for exploring biological plausibility of our findings. We included ten published studies of 3,882 cases and 5,219 controls for Lys939Gln, and five studies with 2,605 cases and 3,329 controls for Ala499Val. When all studies were pooled, we found a significantly increased overall lung cancer risk for Lys939Gln polymorphism (recessive model: OR?=?1.14, 95 % CI?=?1.01–1.29, P?=?0.218 for heterogeneity). Stratification analysis also showed a higher lung cancer risk in Asian populations (recessive model: OR?=?1.26, 95 % CI?=?1.04–1.52, P?=?0.263 for heterogeneity). Interestingly, we found significant correlation between Lys939Gln genotypes and XPC mRNA expression for Asian populations as well. However, we did not observe any association between Ala499Val polymorphism and overall lung cancer risk, nor in further stratification analysis. This meta-analysis suggests that XPC Lys939Gln polymorphism may contribute to lung cancer risk, which needs further validation in single larger studies.     

Assessment of the associations between three VEGF polymorphisms and risk of prostate cancer

Vascular endothelial growth factor (VEGF) plays a crucial role in the regulation of angiogenesis and is involved in the development and metastasis of common cancers. There were several case–controls studies published to assess the associations of VEGF polymorphisms with risk of prostate cancer, but the findings were inconsistent. We performed a meta-analysis to provide a comprehensive assessment of the associations of three VEGF polymorphisms with risk of prostate cancer. The pooled odds ratio (OR) with 95 % confidence interval (95 % CI) was calculated to assess the associations. Eleven individual case–control studies with a total of 5,209 cases of prostate cancer and 5,233 controls were finally included into our meta-analysis. Overall, VEGF rs833061 polymorphism was not associated with risk of prostate cancer (T versus C, OR?=?1.14, 95 % CI 0.91–1.44, P?=?0.26; TT versus CC, OR?=?1.09, 95 % CI 0.67–1.76, P?=?0.74; TT versus CC/CT: OR?=?1.46, 95 % CI 0.67–3.18, P?=?0.34; TT/CT versus CC, OR?=?1.08, 95 % CI 0.82–1.43, P?=?0.59). VEGF rs3025039 polymorphism was also not associated with risk of prostate cancer (T versus C, OR?=?1.03, 95 % CI 0.91–1.16, P?=?0.66; TT versus CC, OR?=?1.82 95 % CI 0.16–20.53, P?=?0.63; TT versus CC/CT, OR?=?2.00, 95 % CI 0.18–22.41, P?=?0.57; TT/CT versus CC, OR?=?0.72, 95 % CI 0.38–1.36, P?=?0.31). VEGF rs2010963 polymorphism was not associated with risk of prostate cancer under three models (C versus G, OR?=?1.17, 95 % CI 0.92–1.48, P?=?0.20; CC versus GG, OR?=?2.28, 95 % CI 0.90–5.75, P?=?0.08; CC versus GG/GC, OR?=?1.57, 95 % CI 0.67–3.68, P?=?0.30). In conclusison, current data suggest that those three VEGF polymorphisms are not obviously associated with risk of prostate cancer.     

Meta-analysis of the association between NQO1 Pro187Ser polymorphism and colorectal cancer in Asians

There were a number of studies performed to assess the association between NQO1 Pro187Ser polymorphism and colorectal cancer risk in Asians, but no consensus was available up to now. We conducted a meta-analysis to assess the association between NQO1 Pro187Ser polymorphism and colorectal cancer risk in Asians. Case–control studies investigating the association between NQO1 Pro187Ser polymorphism and colorectal cancer risk in Asians were searched in Pubmed and Wanfang databases. Pooled odds ratio (OR) and 95 % confidence interval (95 % CI) was calculated. Finally, seven studies involving a total of 2,051 cases and 2,798 controls met the inclusion criteria and were included into the meta-analysis. Overall, there was an obvious association between NQO1 Pro187Ser polymorphism and colorectal cancer risk in Asians (Ser versus Pro: OR?=?1.42, 95 % CI 1.08–1.87, P?=?0.013; SerSer versus ProPro: OR?=?1.86, 95 % CI 1.08–3.19, P?=?0.024; SerSer/ProSer versus ProPro: OR?=?1.61, 95 % CI 1.10–2.35, P?=?0.014; SerSer versus ProPro/ProSer: OR?=?1.46, 95 % CI 1.02–2.10, P?=?0.041). There was low risk of publication bias in the meta-analysis. This meta-analysis suggests that there is an obvious association between NQO1 Pro187Ser polymorphism and colorectal cancer risk in Asians.     

TGFβ1 Leu10Pro polymorphism contributes to the development of prostate cancer: evidence from a meta-analysis

Transforming growth factor-β1 (TGFβ1) plays a significant role in regulating cellular proliferation and apoptosis. A large number of studies related to the association between TGFβ1 Leu10Pro polymorphism and prostate cancer (PC) risk, but get conflicting results. We performed a meta-analysis based on six studies, assessing the strength of the association using odds ratios (OR) with 95 % confidence intervals (CI). Overall, our evidence has indicated that TGFβ1 Leu10Pro polymorphism had significantly increased PC risk in the allele comparison model (OR?=?1.081, 95 % CI?=?1.003–1.165, P _{heterogeneity}?=?0.141, P?=?0.041). In the stratified analysis by ethnicity, the same results were found among Caucasians (for heterozygote model, OR?=?1.741, 95 % CI?=?1.004–3.020, P _{heterogeneity}?=?0.000, P?=?0.049; recessive model, OR?=?1.339, 95 % CI?=?1.045–1.717, P _{heterogeneity}?=?0.020, P?=?0.021; allele comparison model, OR?=?1.091, 95 % CI?=?1.005–1.184, P _{heterogeneity}?=?0.048, P?=?0.037). In conclusion, this meta-analysis suggested that TGFβ1 Leu10Pro polymorphism contributed to the development of PC. A well-designed and larger study is still required to evaluate this polymorphism and PC risk.     

Methylenetetrahydrofolate reductase polymorphisms and breast cancer risk in Chinese population: a meta-analysis of 22 case–control studies

The association between methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and breast cancer risk in the Chinese population has been widely reported, but results were inconsistent. In order to derive a more precise estimation of the relationship, a meta-analysis was performed. Eligible articles were identified through search of databases including Medline, PubMed, Web of Science, Embase, Chinese Biomedical Literature Database (CBM, Chinese), China National Knowledge Infrastructure (CNKI, Chinese), and Wangfang Database (Chinese). The association between the MTHFR polymorphism and breast cancer risk was conducted using odds ratios (ORs) and 95 % confidence intervals (95 % CIs). Finally, a total of 22 studies with 6,103 cases and 7,913 controls were included in our meta-analysis: 13 studies with 3,273 cases and 4,419 controls for C677T polymorphism and 9 studies with 2,830 cases and 3,494 controls for A1298C polymorphism. With regard to C677T polymorphism, significant association was found with breast cancer risk under three models (T vs. C: OR?=?1.12, 95 % CI?=?1.02–1.23, P?=?0.015; TT vs. CC: OR?=?1.35, 95 % CI?=?1.10–1.67, P?=?0.005; TT vs. CC/CT: OR?=?1.37, 95 % CI?=?1.11–1.70, P?=?0.004). There was no significant association found between A1298C polymorphism and breast cancer risk under all genetic models (C vs. A: OR?=?0.96, 95 % CI?=?0.89–1.03, P?=?0.268; CC vs. AA: OR?=?0.98, 95 % CI?=?0.77–1.26, P?=?0.899; AC vs. AA: OR?=?0.95, 95 % CI?=?0.88–1.02, P?=?0.174; CC vs. AC/AA: OR?=?1.00, 95 % CI?=?0.78–1.28, P?=?0.996, CC/AC vs. AA: OR?=?0.96, 95 % CI?=?0.89–1.02, P?=?0.196). In summary, during this meta-analysis, we found that MTHFR C677T polymorphism was significantly associated with breast cancer risk in the Chinese population. Meanwhile, MTHFR A1298C polymorphism was not associated with breast cancer risk in the Chinese population.     

XPC gene polymorphisms contribute to bladder cancer susceptibility: a meta-analysis

Numerous studies have investigated the association between three polymorphisms (Lys939Gln, Ala499Val and PAT?/+) of Xeroderma pigmentosum group C (XPC) gene and bladder cancer susceptibility; however, the findings are inconclusive. In order to acquire a more precise estimation of the relationship, we performed a meta-analysis based on 10 studies including 3,934 cases and 4,269 controls for Lys939Gln, five studies including 2,113 cases and 2,249 controls for Ala499Val, and seven studies including 2,834 cases and 3,048 controls for PAT?/+ polymorphism. We searched publications from EMBASE, MEDLINE, and Chinese Biomedical. We calculated pooled odds ratio (OR) and 95 % confidence interval (CI) by using either fixed-effects or random-effects model according to the between-study heterogeneity. We found that all studied polymorphisms were individually associated with increased overall cancer risks, as shown by ORs (95 % CIs) below: the Lys939Gln (Gln/Gln vs. Lys/Lys: OR?=?1.39, 95 % CI?=?1.08–1.79; recessive model: OR?=?1.42, 95 % CI?=?1.11–1.83; and allele comparing: OR?=?1.12, 95 % CI?=?1.003–1.24), the Ala499Val (Val/Val vs. Ala/Ala: OR?=?1.82, 95 % CI?=?1.19–2.79; recessive model: OR?=?1.70, 95 % CI?=?1.18–2.46; and allele comparing: OR?=?1.23, 95 % CI?=?1.01–1.50), and the PAT?/+ (+/+ vs. ?/?: OR?=?1.36, 95 % CI?=?1.03–1.79 and recessive model: OR?=?1.34, 95 % CI?=?1.06–1.70). Furthermore, stratification analyses demonstrated an increased risk for Asian populations as to the Lys939Gln and PAT?/+ whereas for Caucasian populations as to the Ala499Val polymorphism in the homozygous and recessive models. Despite some limitations, this meta-analysis suggests that XPC polymorphisms are associated with bladder cancer risk, but this association warrants further validation in well-designed studies with large sample sizes.     

Vitamin D receptor gene ApaI polymorphism and breast cancer susceptibility: a meta-analysis

Vitamin D receptor (VDR) principally mediates the anticancer activities of vitamin D. Many studies investigated the association between VDR gene ApaI polymorphism and breast cancer, but the results were inconclusive. We performed this meta-analysis to evaluate the association between VDR gene ApaI polymorphism and breast cancer. Twelve studies with a total of 8,254 subjects were identified from PubMed and Wanfang databases. The pooled odds ratio (OR) and confidence intervals (95 % CI) were used to assess the association. The meta-analysis indicated that VDR gene ApaI polymorphism was not associated with risk of breast cancer (a vs. A: OR?=?0.97, 95 % CI 0.91–1.04, P?=?0.378; aa vs. AA: OR?=?0.97, 95 % CI 0.85–1.10, P?=?0.618; aa vs. AA + Aa: OR?=?1.00, 95 % CI 0.89–1.12, P?=?0.972; aa + Aa vs. AA: OR?=?0.95, 95 % CI 0.82–1.11, P?=?0.550). Subgroup analysis by ethnicity further showed that VDR gene ApaI polymorphism was not associated with risk of breast cancer in both Asians and Caucasians. These data from the meta-analysis indicate that VDR gene ApaI polymorphism is not associated with breast cancer susceptibility.