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.     

Quantitative assessment of the association between GSTP1 gene Ile105Val polymorphism and susceptibility to hepatocellular carcinoma

Glutathione S-transferase P1 (GSTP1) gene Ile105Val polymorphism has been suggested to be involved in the development of cancer. However, the results from the studies regarding the association between GSTP1 Ile105Val polymorphism and hepatocellular carcinoma risk have been inconsistent. Thus, we performed a meta-analysis to investigate the association. Published literature from PubMed, Chinese Biomedical Literature, and Wanfang databases was searched for eligible publications. Pooled odds ratios (ORs) with 95 % confidence intervals (95 %CIs) were calculated using random- or fixed-effects model. Six studies with a total of 1,843 participants were finally included into this meta-analysis. The results suggested there was no association between GSTP1 Ile105Val polymorphism and hepatocellular carcinoma risk under all genetic models (for ValVal vs. IleIle, OR?=?0.79, 95 %CI 0.48–1.29, P?=?0.341; for IleVal vs. IleIle, OR?=?1.05, 95 %CI 0.84–1.30, P?=?0.678; for the dominant model, OR?=?0.91, 95 %CI 0.68–1.20, P?=?0.498; and for the recessive model, OR?=?0.76, 95 %CI 0.47–1.24, P?=?0.269). Subgroup analyses by ethnicity showed there was also no association between GSTP1 Ile105Val polymorphism and hepatocellular carcinoma risk in Asians under all genetic models (All P values were more than 0.05), but GSTP1 Ile105Val polymorphism was associated with decreased risk of hepatocellular carcinoma in European under the recessive model (ValVal vs. IleVal/IleIle) (OR?=?0.44, 95 %CI 0.20–0.98, P?=?0.044). In conclusion, the meta-analysis suggests that there is little evidence for the association between GSTP1 Ile105Val polymorphism and hepatocellular carcinoma risk. However, more well-designed studies are needed to further assess this association.     

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.     

Single-nucleotide polymorphisms of GPX1 and MnSOD and susceptibility to bladder cancer: a systematic review and meta-analysis

Reactive oxygen species-related damage plays a critical role in carcinogenesis. Glutathione peroxidase 1 (GPX1) and mitochondrial superoxide dismutase (MnSOD) are two key antioxidant enzymes in the defense system against reactive oxygen species. This systematic review and meta-analysis was designed to evaluate the association of single-nucleotide polymorphisms in GPX1 and MnSOD genes with susceptibility to bladder cancer risk. Online databases of PubMed, Embase, China National Knowledge Infrastructure, and SinoMed were searched to identify eligible studies. Odds ratios (ORs) and 95 % confidence intervals (95 % CIs) were calculated to estimated the association strength. The fixed effects model and random effects model were used to pool the data from different studies. By pooling all eligible studies, we found that the GPX1 Pro198Leu polymorphism was associated with a significantly increased risk of bladder cancer (Leu vs. Pro, OR = 2.111, 95 % CI = 1.020–4.368, heterogeneity (p < 0.001); LeuPro/LeuLeu vs. ProPro, OR = 1.876, 95 % CI = 1.011–3.480, heterogeneity (p < 0.001)). No significant association of MnSOD Ala-9Val polymorphism with cancer risk was observed (AlaVal/ValVal vs. AlaAla, OR = 0.966, 95 % CI = 0.754–1.239, heterogeneity (p = 0.390); Vla vs. Ala, OR = 1.038, 95 % CI = 0.782–1.377, heterogeneity (p = 0.015)). This systematic review and meta-analysis demonstrated that the GPX1 Pro198Leu polymorphism significantly increased susceptibility to bladder cancer, while the MnSOD Ala-9Val polymorphism was not associated with bladder cancer risk.     

Glutathione S-transferase P1 Ile105Val polymorphism contributes to increased risk of gastric cancer in East Asians

Glutathione S-transferase P1 (GSTP1) is an important enzyme playing critical roles in the phase II detoxification pathway. There were many studies investigating the association between GSTP1 gene Ile105Val polymorphism and gastric cancer risk, but studies from East Asians reported inconsistent findings. We performed a meta-analysis to investigate the association in East Asians. Published literature from PubMed and Chinese Biomedical Literature databases were searched for eligible publications. Pooled odds ratios (ORs) with 95 % confidence intervals (95 %CIs) were calculated using random or fixed-effect model according the between-study heterogeneity. A total of 12 studies with 2,552 cases and 5,474 controls were finally included into the meta-analysis. Meta-analysis of those 12 studies showed that there was an obvious association between GSTP1 Ile105Val polymorphism and gastric cancer risk in East Asians under three genetic models (for valine vs. isoleucine, OR?=?1.32, 95 %CI 1.05–1.66, P?=?0.015; for ValVal vs. IleIle, OR?=?2.00, 95 %CI 1.34–2.98, P?=?0.001; for the recessive model, OR?=?1.96, 95 %CI 1.35–2.83, P?<?0.001). Sensitivity analysis by removing one study at a time suggested the pooled results were stable under the three genetic models above. There was no risk of publication bias. In conclusion, the meta-analysis suggests that there is a strong evidence for the association between GSTP1 Ile105Val polymorphism and increased risk of gastric cancer in East Asians and contributes to increased risk of gastric cancer in East Asians.     

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.     

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.     

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.     

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.     

Genetic polymorphisms of methylenetetrahydrofolate reductase (MTHFR) gene Ala222Val and susceptibility to ovary cancer: a systematic review and meta-analysis

Many studies have reported the role of methylenetetrahydrofolate reductase (MTHFR) gene Ala222Val polymorphism with ovary cancer risk, but the results remained controversial. To derive a more precise estimation of the relationship, a meta-analysis was performed. Odds ratios (ORs) with 95 % confidence intervals (CIs) were estimated to assess the association between MTHFR Ala222Val polymorphism and ovary cancer risk. A total of 8 studies including 3,723 cases and 4,001 controls were also involved in this meta-analysis. When all the eligible studies were pooled into this meta-analysis, no significant association between ovary cancer risk and MTHFR Ala222Val polymorphism was found in all genetic models [codominant model: OR?=?0.980, 95 % CI?=?0.756–1.270, P _h?=?0.088, P?=?0.877; dominant model: OR?=?1.022, 95 % CI?=?0.864–1.208, P _h?=?0.033, P?=?0.803; recessive model: OR?=?1.050, 95 % CI?=?0.803–1.373, P _h?=?0.032, P?=?0.723; allele comparison model: OR?=?1.028, 95 % CI?=?0.898–1.178, P _h?=?0.012, P?=?0.685]. In the stratified analysis by ethnicity, no evidence of any associations of this polymorphism with ovary cancer was found in the Caucasian populations. Our meta-analysis supports that the MTHFR Ala222Val polymorphism is not contributed to the risk of ovary cancer from currently available evidence.     

Genetic polymorphisms in glutathione S-transferases P1 (GSTP1) Ile105Val and prostate cancer risk: a systematic review and meta-analysis

Numerous epidemiological studies have evaluated the association between the glutathione S-transferases P1 (GSTP1) Ile105Val polymorphisms and prostate cancer (PCa) risk. However, these studies have yielded conflicting results. A comprehensive search was conducted through researching MEDLINE, PubMed, Web of Science, and EMBASE, and a total of 13 studies including 3,227 cases and 3,945 controls were identified. A meta-analysis was performed to obtain a summary of estimated odds ratios (ORs) and 95 % confidence intervals (CIs) of GSTP1 polymorphisms for PCa, with attention to study quality and publication bias. The GSTP1 Ile158Val variant genotypes are less associated with increased risk of PCa for the homozygote model (Val/Val vs Ile/Ile: OR?=?1.42; I ²? =?63.7 %; 95 % CI?=?1.02–1.97) and the recessive model (OR?=?1.41; I ²? =?45.5 %; 95 % CI?=?1.10–1.80). 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 for Val/Val vs Ile/Ile comparison (OR?=?1.22; I ²? =?0.0 %; 95 % CI?=?1.02–1.47) and for the recessive model (OR?=?1.26; I ²? =?0.0 %; 95 % CI?=?1.06–1.49), 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 provides evidence that GSTP1 Ile105Val gene polymorphisms contributed to PCa susceptibility.     

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.     

Quantitative assessment of the association between glutathione S-transferase P1 Ile105Val polymorphism and bladder cancer risk

Previous studies investigating the association between glutathione S-transferase P1 (GSTP1) Ile105Val polymorphism and bladder cancer risk reported controversial results. This study aimed to quantify the strength of the association between GSTP1 Ile105Val polymorphism and bladder cancer risk by performing a meta-analysis. We searched the PubMed, Embase, and Wanfang databases for publications on the association between GSTP1 Ile105Val polymorphism and bladder cancer risk. We estimated the pooled odds ratios (ORs) with their confidence intervals (95 %CIs) to assess the association. Twenty-five individual studies with a total of 12,360 subjects were finally included. Meta-analysis of all 25 studies showed that GSTP1 Ile105Val polymorphism was associated with increased risk of bladder cancer risk under four genetic comparison models (for G versus A, random-effect OR?=?1.19, 95 %CI 1.05–1.35; for GG versus AA, random-effect OR?=?1.49, 95 %CI 1.12–1.97; for GG/GA versus AA, random-effect OR?=?1.20, 95 %CI 1.03–1.39; for GG versus GA/AA, random-effect OR?=?1.41, 95 %CI 1.10–1.80). Sensitivity analysis showed that GSTP1 Ile105Val polymorphism was still associated with bladder cancer risk under three genetic comparison models (for G versus A, random-effects OR?=?1.13, 95 %CI 1.01–1.26; for GG versus AA, random-effects OR?=?1.29, 95 %CI 1.01–1.65; for GG versus GA/AA, random-effects OR?=?1.19, 95 %CI 1.04–1.35). No evidence of publication bias was observed. This meta-analysis shows that there is an obvious association between GSTP1 Ile105ValIle105Val polymorphism and bladder cancer risk, and GSTP1 ILE105VAL polymorphism contributes to bladder cancer risk.     

Genetic polymorphism of DNA methyltransferase 3B 149 C>T and risk of colorectal cancer: a meta-analysis

Numerous studies have investigated the risk of colorectal cancer (CRC) associated with the polymorphism of DNA methyltransferase 3B (DNMT3B) 149 C>T, but results have been inconsistent. We performed this meta-analysis to drive a more precise estimation of the association between this polymorphism and risk of CRC. A comprehensive search was conducted to identify all case–control studies of the ?149C>T polymorphism of DNMT3B and CRC risk. A total of seven eligible studies, including 2,666 cases and 4,022 controls, relating the DNMT3B polymorphism of ?149C>T to the risk of CRC were identified. It suggested no significant associations between ?149C>T polymorphism of DNMT3B gene and the risk of developing CRC in the recessive, dominant, and co-dominant models (for CC versus TT: OR?=?0.90, 95 % CI?=?0.90–1.25, P _{heterogeneity}?=?0.37; for recessive model: OR?=?0.54, 95 % CI?=?0.28–1.04, P _{heterogeneity}?=?0.00001; for dominant model: OR?=?1.07, 95% CI?=?0.93–1.23, P _{heterogeneity}?=?0.83; and for C allele versus T allele: OR?=?0.70, 95 % CI?=?0.43–1.13, P _{heterogeneity}?=?0.00001). In the subgroup analysis, there is no significant associations were also found in European populations (for CC versus TT: OR?=?1.09, 95 % CI?=?0.92–1.30, P _{heterogeneity}?=?0.88; for recessive model: OR?=?1.00, 95 % CI?=?0.88–1.13, P _{heterogeneity}?=?0.14; for dominant model: OR?=?1.50, 95 % CI?=?0.89–2.54, P _{heterogeneity}?=?0.00001; and for C allele versus T allele: OR?=?0.70, 95 % CI?=?0.38–1.28, P _{heterogeneity}?=?0.00001). In conclusion, no significant association was found between the ?149C>T polymorphisms in DNMT3B and CRC susceptibility.     

CYP2E1 polymorphisms and colorectal cancer risk: a HuGE systematic review and meta-analysis

Studies investigating the associations between Cytochrome P4502E1 (CYP2E1) polymorphisms and colorectal cancer (CRC) risk report conflicting results. We conducted a meta-analysis to assess the association between CYP2E1 gene Rsa I/Pst I, Dral T/A and 96-bp insertion polymorphisms and CRC susceptibility. Two investigators independently searched the Medline, Embase, CNKI, Wanfang, and Chinese Biomedicine Databases. Summary odds ratios (ORs) and 95 % confidence intervals (95 % CIs) for CYP2E1 polymorphisms and CRC were calculated in a fixed-effect model (the Mantel–Haenszel method) and a random-effects model (the DerSimonian and Laird method) when appropriate. Ultimately, 12, 5, and 4 studies were found to be eligible for meta-analyses of Rsa I/Pst I, Dral T/A, and 96-bp insertion polymorphisms, respectively. Our analysis suggested that the variant genotype of Rsa I/Pst I were associated with a significantly increased CRC risk (c2/c2 vs. c1/c1, OR?=?1.36, 95 % CI?=?1.04–1.77; recessive model, OR?=?1.35, 95 % CI?=?1.04–1.75). Moreover, similar results were observed between CYP2E1 96-bp insertion polymorphism and CRC risk (dominant model, OR?=?1.25, 95 % CI?=?1.07–1.45), while no association was observed between CYP2E1 Dral T/A polymorphism and CRC susceptibility in any genetic model. No publication bias was found in the present study. This meta-analysis shows that CYP2E1 Rsa I/Pst I and 96-bp insertion polymorphisms may be associated with CRC risk. The CYP2E1 Dral T/A polymorphism was not detected to be related to the risk for CRC.     

A meta-analysis of evidences on XPC polymorphisms and lung cancer susceptibility

Published data regarding the association between the XPC polymorphisms and lung cancer susceptibility remained controversial. This meta-analysis was performed to draw a precise estimation of the relationship. We systematically searched PubMed, Embase, Elsevier, and Web of Science with a time limit of September 10, 2012. Summary odds ratios (ORs) with 95 % CIs were used to assess the strength of association between these polymorphisms and lung cancer susceptibility using random-effects model. This meta-analysis including 13 case–control studies evaluated the associations between three commonly XPC polymorphisms (Lys939Gln, Ala499Val, and PAT^?/+) and lung cancer susceptibility. No significant associations were found between the three XPC polymorphisms and lung cancer susceptibility (for Lys939Gln polymorphism: CC vs AA, OR?=?1.191, p?=?0.033; AC vs AA, OR?=?0.992, p?=?0.762, the dominant model, OR?=?1.028, p?=?0.521; the recessive model, OR?=?1.205, p?=?0.022). For Ala499Val polymorphism: TT vs CC, OR?=?1.195, p?=?0.071; TC vs CC, OR?=?1.146, p?=?0.133; the dominant model, OR?=?1.161, p?=?0.086; the recessive model, OR?=?1.123, p?=?0.156. For PAT^?/+ polymorphism: +/+ vs ?/?, OR?=?1.094, p?=?0.539; +/? vs ?/?, OR?=?0.925, p?=?0.313; the dominant model, OR?=?0.969, p?=?0.725; the recessive model, OR?=?1.135, p?=?0.290. p?=?0.004 for Bonferroni testing). Significant associations were also not found in the subgroup analysis for the three XPC polymorphisms. This meta-analysis suggested that the three XPC polymorphisms might not be risk factors for developing lung cancer.     

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.     

A let-7 KRAS rs712 polymorphism increases colorectal cancer risk

Growing evidence has indicated that polymorphism present in the miRNA binding site of target gene can alter the ability of miRNAs to bind its target gene and modulate the development and progression of cancer. We aimed to investigate the association between let-7 KRAS rs712 polymorphism and the risk of colorectal cancer (CRC). The let-7 KRAS rs712 was analyzed in a case–control study, including 339 CRC patients and 313 age- and sex-matched controls; the relationship between the polymorphism and the clinicopathological features of CRC was also examined. Individuals carrying the let-7 KRAS rs712 TT genotype and T allele had an increased risk of developing CRC (TT vs. GG, adjusted OR?=?2.18; 95 % CI, 1.00–4.77; T vs. G, adjusted OR?=?1.50; 95 % CI, 1.15–1.96). Stratified analyses revealed that CRC patients with the let-7 KRAS rs712 TT genotype were more likely to have clinical stage III or IV disease (OR?=?3.29, 95 % CI, 1.32–8.20) and distant metastasis (OR?=?4.70, 95 % CI, 1.81–12.25). These findings provide evidence that the let-7 KRAS rs712 polymorphism may play crucial roles in the etiology of CRC.     

The effect of RAD51 135 G>C and XRCC2 G>A (rs3218536) polymorphisms on ovarian cancer risk among Caucasians: a meta-analysis

Genetic polymorphisms of RAD51 135 G>C and XRCC2 G>A (rs3218536) have been reported to change the risk of ovarian cancer, but the results are controversial. To get a more precise result, a meta-analysis was performed. A comprehensive literature search in PubMed, Excerpta Medica Database, and China National Knowledge Infrastructure was carried out to get case–control studies published up to November 2013. The pooled odds ratio (OR) and its corresponding 95 % confidence interval (CI) were conducted to estimate the effect of RAD51 135 G>C and XRCC2 G>A (rs3218536) polymorphisms on ovarian cancer risk. A total of 13 independent case–control studies with 5,927 cases and 10,303 controls were included in this meta-analysis. There was no significant association between RAD51 135 G>C polymorphism and risk of ovarian cancer. However, the result of total studies indicated the XRCC2 G>A (rs3218536) polymorphism could reduce the risk of ovarian cancer (heterozygote model AG vs. GG: OR?=?0.877, 95 % CI?=?0.770–0.999, P?=?0.048; dominant model AA/AG vs. GG: OR?=?0.864, 95 % CI?=?0.763–0.979, P?=?0.022). The result was still significant after Hardy–Weinberg equilibrium-violating studies were excluded (allele contrast A vs. G: OR?=?0.836, 95 % CI?=?0.74–0.943, P?=?0.004; homozygote model AA vs. GG: OR?=?0.562, 95 % CI?=?0.317–0.994, P?=?0.048; heterozygote model AG vs. GG: OR?=?0.859, 95 % CI?=?0.753–0.98, P?=?0.023; dominant model AA/AG vs. GG: OR?=?0.842, 95 % CI?=?0.74–0.958, P?=?0.009). In the stratified analysis by ethnicity, significantly reduced risk was observed among Caucasians in dominant model (AA/AG vs. GG: OR?=?0.867, 95 % CI?=?0.764–0.984, P?=?0.027). No significant association was found between the RAD51 135G>C polymorphism and the risk of ovarian cancer. Interestingly, XRCC2 G>A (rs3218536) polymorphism might reduce the risk of ovarian cancer. Larger-scale and well-designed studies are needed to further clarify the association.     

Glutathione S-transferase P1 gene Ile105Val polymorphism might be associated with lung cancer risk in the Chinese Han population

Genetic variations in glutathione S-transferase P1 (GSTP1) gene have been suggested to be involved in the development of cancer. However, the results from the studies regarding the association between GSTP1 Ile105Val polymorphism and lung cancer risk in the Chinese population have been inconsistent. Thus, we conducted a meta-analysis to investigate the association. Published literature from PubMed, Chinese Biomedical Literature Database, Chinese Wanfang Data, and Chinese National Knowledge Infrastructure databases were searched for eligible publications. Pooled odds ratios (ORs) with 95?% confidence intervals (CIs) were calculated using random or fixed effect model. Ten studies (1,506 cases/1,714 controls) were included in the meta-analysis. The results suggested that GSTP1 Ile105Val polymorphism was marginally associated with lung cancer risk in the Chinese Han population under a multiplicative model (G vs. A, odds ratio (OR)?=?1.22, 95?% confidence interval?=?1.02?C1.46), under a homogeneous codominant model (GG vs. AA, OR?=?1.67, 95?% CI?=?1.14?C2.45), under a heterogeneous codominant model (GA vs. AA, OR?=?1.15, 95?% CI?=?0.98?C1.35), under a dominant model (GG + GA vs. AA, OR?=?1.21, 95?% CI?=?1.04?C1.39), and under a recessive model (GG vs. GA + AA, OR?=?1.59, 95?% CI?=?1.09?C2.31), respectively. Moreover, after adjusted for age, gender, and smoking status, the significant association under dominant model remained (OR?=?1.27, 95?% CI?=?1.07?C1.51). This meta-analysis suggested that there might be an association between GSTP1 Ile105Val polymorphism and lung cancer in the Chinese Han population.