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.     

Association between NAD(P)H:quinone oxidoreductase 1 rs1800566 polymorphism and risk of bladder cancer

NAD(P)H:quinone oxidoreductase 1 (NQO1) rs1800566 (Pro187Ser) is a functional polymorphism which leads to a proline-to-serine amino acid substitution at codon 187 in the NQO1 protein and enzyme activity changes. NQO1 rs1800566 polymorphism was implicated to be associated with a risk of bladder cancer, but published studies showed inconclusive results. We performed a meta-analysis of nine publications with a total of 2,661 cases and 2,738 controls on the association between NQO1 rs1800566 polymorphism and risk of bladder cancer. Data were extracted from those included studies, and the pooled odds ratio (OR) with the corresponding 95 % confidence interval (95 % CI) was calculated to assess the association. We found that there was no association between NQO1 rs1800566 polymorphism and risk of bladder cancer under all four genetic models (Ser vs. Pro, OR?=?1.06, 95 % CI?=?0.97–1.16, P?=?0.21, I ²?=?31 %; SerSer vs. ProPro, OR?=?1.12, 95 % CI?=?0.89–1.42, P?=?0.33, I ²?=?44 %; SerSer/ProSer vs. ProPro, OR?=?1.08, 95 % CI?=?0.96–1.21, P?=?0.20, I ²?=?27 %; SerSer vs. ProPro/ProSer, OR?=?1.06, 95 % CI?=?0.85–1.32, P?=?0.59, I ²?=?36 %). Meta-analysis of those eight studies from Europeans also showed that there was no association between NQO1 rs1800566 polymorphism and risk of bladder cancer under all four genetic models (Ser vs. Pro, OR?=?1.02, 95 % CI?=?0.93–1.13, P?=?0.66, I ²?=?20 %; SerSer vs. ProPro, OR?=?0.99, 95 % CI?=?0.75–1.30, P?=?0.93, I ²?=?38 %; SerSer/ProSer vs. ProPro, OR?=?1.04, 95 % CI?=?0.92–1.17, P?=?0.55, I ²?=?6 %; SerSer vs. ProPro/ProSer, OR?=?0.98, 95 % CI?=?0.75–1.28, P?=?0.87, I ²?=?39 %). This meta-analysis suggests that the NQO1 rs1800566 polymorphism is not associated with a risk of bladder cancer. Further studies with larger samples are needed, especially for studies in Asians and Africans.     

No significant association between p53 codon 72 Arg/Pro polymorphism and risk of oral cancer

The genetic polymorphism of p53 codon 72 Arg/Pro has been implicated in oral cancer risk, but the results of previous studies remain controversial and ambiguous. To estimate the effect of the p53 codon 72 Arg/Pro polymorphism on the risk of oral cancer, a meta-analysis was performed. Based on a comprehensive search in PubMed, Embase, Web of Science, and China National Knowledge Infrastructure (CNKI) databases, we identified all available publications assessing the association between p53 codon 72 Arg/Pro polymorphism and oral cancer risk. The pooled odds ratio (OR) with its corresponding 95 % confidence interval (CI) was calculated to assess the association. Subgroup analyses by ethnicity and study quality were performed to further identify the correlation. Totally, 17 studies with 2,975 cases and 3,413 controls were included into this meta-analysis. There was no statistically significant association between the p53 codon 72 Arg/Pro polymorphism and oral cancer risk in all genetic contrast models (OR_{Pro allele vs. Arg allele}?=?1.05, 95 % CI 0.94–1.18, P_OR?=?0.379; OR_{Pro/Pro vs. Arg/Arg}?=?1.11, 95 % CI 0.89–1.40, P_OR?=?0.356; OR_{Pro/Arg vs. Arg/Arg}?=?1.10, 95 % CI 0.93–1.30, P_OR?=?0.256; OR_{Pro/Arg + Pro/Pro vs. Arg/Arg}?=?1.10, 95 % CI 0.93–1.31, P_OR?=?0.263; and OR_{Pro/Pro vs. Arg/Arg + Pro/Arg}?=?1.03, 95 % CI 0.90–1.18, P_OR?=?0.647). In the subgroup analysis of high-quality studies, we failed to find the susceptibility of p53 codon 72 Arg/Pro polymorphism to oral cancer. Moreover, the results were similar among Asians, Caucasians, and mixed populations when stratifying by ethnicity. Sensitivity analysis further confirmed the stability of the results. The present meta-analysis of currently available data shows no association between the p53 codon 72 Arg/Pro polymorphism and oral cancer risk.     

P53 codon 72 polymorphism and lung cancer risk: evidence from 27,958 subjects

The role of p53 codon 72 polymorphism in the development of lung cancer remains obscure due to inconsistent findings of individual case–control studies published to date. A meta-analysis was conducted to better estimate the association between the p53 codon 72 variant and lung cancer risk. All relevant publications from the PubMed, Embase, Web of Science, and Wanfang databases were retrieved. Based on the inclusion criteria, 39 publications involving 44 independent case–control studies were finally included into this meta-analysis. Data were extracted and the pooled odds ratio (OR) with the corresponding 95 % confidence interval (95 % CI) was calculated. The overall pooled ORs showed no significant relationship of the p53 codon 72 polymorphism with increased or decreased risk of lung cancer in all gene contrast models (OR _{Pro vs. Arg}?=?1.04, 95 % CI?=?0.96–1.13, P _OR?<?0.001; OR _{Pro/Pro vs. Arg/Arg}?=?1.07, 95 % CI?=?0.91–1.25, P _OR?<?0.001; OR _{Arg/Pro vs. Arg/Arg} =1.04, 95 % CI?=?0.94–1.15, P _OR?<?0.001; OR _{Pro/Pro + Arg/Pro vs. Arg/Arg}?=?1.04, 95 % CI?=?0.94–1.16, P _OR?<?0.001; OR _{Pro/Pro vs. Arg/Arg + Arg/Pro}?=?1.07, 95 % CI?=?0.93–1.23, P _OR?<?0.001). According to the ethnicity, no significant association was observed in subgroup analyses of the Asians, Caucasians, Africans and the mixed population. Similar finding was found in subgroup analyses of hospital-based and population-based studies. Concerning the histological types of lung cancer, the p53 codon 72 variant exerts risk effect on the lung carcinogenesis in patients with adenocarcinoma (OR _{Arg/Pro vs. Arg/Arg}?=?1.10, 95 % CI?=?1.00–1.22, P _OR?=?0.048). Additionally, subgroup analysis by the smoking status demonstrated that the p53 codon 72 variant seemed to play a protective role in lung carcinogenesis among the non-smokers but not the smokers in the contrast model of Arg/Pro vs. Arg/Arg (OR _{Arg/Pro vs. Arg/Arg}?=?0.71, 95 % CI?=?0.50–1.00, P _OR?=?0.049). The present meta-analysis suggests the p53 codon 72 polymorphism may weakly modify the risk for lung cancer among the adenocarcinoma patients and non-smokers. Nevertheless, this association needs further confirmation in future studies with high quality.     

Association between cytochrome P450 1A1 MspI polymorphism and endometrial cancer risk: a meta-analysis

Many studies proposed that cytochrome P450 1A1 (CYP1A1) MspI polymorphism may be associated with endometrial cancer risk, but the findings from previous studies reported conflicting results. A meta-analysis of all relevant studies was performed to get a comprehensive assessment of the association between CYP1A1 MspI polymorphism and endometrial cancer risk. Eligible studies were searched in PubMed and China National Knowledge Infrastructure databases. The pooled odds ratios (ORs) with the corresponding 95 % confidence intervals (95 % CIs) were calculated to evaluate the association. Twelve studies with a total of 2,111 cases and 2,894 controls were finally included into the meta-analysis. Overall, meta-analysis of a total of 12 studies showed that there was no obvious association between CYP1A1 MspI polymorphism and endometrial cancer risk (OR_{C vs. T}?=?0.97, 95 % CI 0.77–1.22, P _OR?=?0.808; OR_{CC vs. TT}?=?1.00, 95 % CI 0.57–1.76, P _OR?=?0.994; OR_{CC vs. TT/TC}?=?0.88, 95 % CI 0.65–1.20, P _OR?=?0.425; OR_{CC/TC vs. TT}?=?0.98, 95 % CI 0.74–1.29, P _OR?=?0.861). Subgroup analyses by ethnicity further showed that there was no obvious association between CYP1A1 MspI polymorphism and endometrial cancer risk in both Caucasians and Asians. There was no obvious risk of publication bias. Therefore, the meta-analysis suggests that CYP1A1 MspI polymorphism is not associated with endometrial cancer risk.     

Quantitative assessment of the association between CYP1A1 A4889G polymorphism and endometrial cancer risk

Cytochrome P450 1A1 (CYP1A1) A4889G polymorphism was supposed to be associated with endometrial cancer risk, but previous studies reported conflicting results. We therefore performed a meta-analysis of all relevant studies to get a comprehensive assessment of the association between CYP1A1 A4889G polymorphism and endometrial cancer risk. The pooled odds ratios (OR) with the corresponding 95 % confidence interval (95 % CI) was calculated to assess the association. Finally, ten studies with a total of 1,682 endometrial cancer cases and 2,510 controls were finally included into the meta-analysis. Meta-analysis of the total ten studies showed that CYP1A1 A4889G polymorphism was not associated with endometrial cancer risk (OR_{G versus A}?=?1.14, 95 % CI 0.83–1.57, P _OR?=?0.417; OR_{GG versus AA}?=?1.23, 95 % CI 0.70–2.18, P _OR?=?0.470; OR_{GG versus AA/AG}?=?1.03, 95 % CI 0.59–1.81, P _OR?=?0.919; OR_{GG/AG versus AA}?=?1.22, 95 % CI 0.82–1.81, P _OR?=?0.336). Subgroup analyses by ethnicity further showed that there was also no obvious association between CYP1A1 A4889G polymorphism and endometrial cancer risk in both Caucasians and Asians. Sensitivity analysis by excluding single study in turns showed that the pooled estimations were not stable. Therefore, evidence for currently available data suggests that CYP1A1 A4889G polymorphism is not associated with endometrial cancer risk. However, more studies with large number of participants are needed to further assess the association precisely.     

Association between the p53 codon 72 Arg/Pro polymorphism and hepatocellular carcinoma risk

Previous studies regarding the association of p53 codon 72 Arg/Pro polymorphism with hepatocellular carcinoma (HCC) risk have provided conflicting and inconclusive findings. Thus, a meta-analysis of all currently available publications was performed to address this issue. Eleven individual case–control studies involving a total of 2,718 cases and 3,752 controls were identified after a systematic search of the PubMed, Embase, Web of Science, and Wanfang databases. The strength of the association of p53 codon 72 Arg/Pro polymorphism with HCC risk was estimated by the pooled odds ratio (OR) with its corresponding 95 % confidence interval (95 % CI). Subgroup analyses stratified by ethnicity, source of controls, gender, hepatitis virus infection status, and family history of HCC were also conducted to assess the association. Overall, significantly increased risk of HCC was identified among carriers of the homozygous genotype ProPro (OR_{ProPro vs. ArgArg}?=?1.38 (95 % CI, 1.03–1.85), P _OR?=?0.033; OR_{ProPro vs. ArgArg + ArgPro}?=?1.28 (95 % CI, 1.03–1.59), P _OR?=?0.026). In subgroup analysis by ethnicity, the pooled results suggested that the p53 codon 72 Arg/Pro polymorphism was associated with an increased risk of HCC in Asians and Caucasians (for Asians, OR_{ProPro vs. ArgArg + ArgPro}?=?1.17 (95 % CI, 1.02–1.34), P _OR?=?0.025; for Caucasians, OR_{ProPro vs. ArgArg}?=?1.65 (95 % CI, 1.07–2.56), P _OR?=?0.025; OR_{ProPro vs. ArgArg + ArgPro}?=?1.74 (95 % CI, 1.14–2.66), P _OR?=?0.010). Subgroup analyses by source of controls and hepatitis virus infection status further demonstrated the significant association, whereas stratification factors involving gender and family history of HCC did not modify the association between p53 codon 72 Arg/Pro polymorphism and HCC risk. This meta-analysis suggests that the p53 codon 72 Arg/Pro polymorphism may play a critical role in the development of HCC, and gender and family history of HCC may not modulate the effect of p53 codon 72 Arg/Pro in HCC risk.     

P53 codon 72 Arg/Pro polymorphism and glioma risk: an updated meta-analysis

P53 codon 72 Arg/Pro is a C/G variation upstream of the p53 gene on human chromosome 17p13. Many case–control studies have investigated the association between p53 codon 72 Arg/Pro polymorphism and glioma risk but provided inconsistent findings. To better understand the pathogenesis of glioma, we performed the current meta-analysis by pooling data from all available individual studies. According to the inclusion criteria, ten independent publications with 11 case–control studies were included into this meta-analysis. The pooled odds ratio (OR) with 95 % confidence interval (95 % CI) was calculated to estimate the effect of p53 codon 72 Arg/Pro variant on the development of glioma. Overall, no appreciable correlation was observed among the total studies in all gene models (OR_{Pro allele vs. Arg allele}?=?1.04, 95 % CI?=?0.90–1.20, P _OR?=?0.581; OR_{Pro/Pro vs. Arg/Arg}?=?0.95, 95 % CI?=?0.80–1.14, P _OR?=?0.614; OR_{Pro/Arg vs. Arg/Arg}?=?1.01, 95 % CI?=?0.79–1.29, P _OR?=?0.993; OR_{Pro/Arg + Pro/Pro vs. Arg/Arg}?=?1.03, 95 % CI?=?0.82–1.29, P _OR?=?0.799; OR_{Pro/Pro vs. Arg/Arg + Pro/Arg}?=?1.02, 95 % CI?=?0.86–1.22, P _OR?=?0.785). In stratified analyses by ethnicity, source of controls, and glioma subtypes, the p53 codon 72 Arg/Pro polymorphism did not alter the risk for glioma in population-based, hospital-based, astrocytoma, and oligodendroglioma studies among Caucasian. Interestingly, the Pro/Pro genotype seemed to be negatively associated with the glioma risk among patients with glioblastoma (OR_{Pro/Pro vs. Arg/Arg}?=?0.68, 95 % CI?=?0.48–0.95, P _OR?=?0.026). Our study suggests that the polymorphism of p53 codon 72 Arg/Pro may play a protective role in the development of glioblastoma. The relationship of p53 codon 72 Arg/Pro polymorphism with the susceptibility to glioma needs further estimation by more individual studies with high quality across ethnicities.     

Association between NQO1 C609T polymorphism and colorectal cancer risk

NAD(P)H: quinone oxidoreductase 1 (NQO1) is a cytosolic enzyme, and the NQO1 C609T polymorphism is associated with the enzymatic activity of NQO1. Many studies were performed to assess the association between NQO1 C609T polymorphism and colorectal cancer risk, but no consensus was available up to now. We conducted a meta-analysis to examine the association between NQO1 C609T polymorphism and colorectal cancer risk, and the pooled odds ratios (OR) with their 95 % confidence intervals (95 % CI) were used to assess the association. Finally, 12 studies involving 4,026 cases and 4,855 controls were included into the meta-analysis. Overall, there was an obvious association between NQO1 C609T polymorphism and colorectal cancer risk (T versus C: OR?=?1.28, 95 % CI 1.08–1.51, P?=?0.005; TT versus CC: OR?=?1.60, 95 % CI 1.10–2.33, P?=?0.015; TT/CT versus CC: OR?=?1.36, 95 % CI 1.09–1.69, P?=?0.006; TT versus CT/CC: OR?=?1.37, 95 % CI 1.05–1.80, P?=?0.022). Subgroup analysis by ethnicity showed that the association was obvious in both Caucasians and Asians. Therefore, the meta-analysis provides strong evidence for the association between NQO1 C609T polymorphism and colorectal cancer risk, and the T allele of NQO1 C609T polymorphism is an important risk factor of colorectal cancer.     

The NQO1 C609T polymorphism and hepatocellular carcinoma risk

NAD(P)H quinine oxidoreductase 1 (NQO1) enzyme plays a crucial role in the protection against oxidative stress. The polymorphism of NQO1 C609T has been implicated in the development of hepatocellular carcinoma (HCC). However, the findings were inconsistent due to different ethnicity, sample size, and source of controls in individual studies. To better estimate the association of NQO1 C609T polymorphism with HCC risk, we performed a meta-analysis of all currently available studies on the susceptibility to HCC. The meta-analysis included three independent studies with a total of 1, 595 subjects. The association was assessed under five different gene models. The overall analysis suggested that the variant allele and genotypes were significantly related to increased risk of HCC (OR_{T vs. C}?=?1.47, 95 % CI 1.07–2.00, P _OR?=?0.016; OR_{TT vs. CC}?=?2.06, 95 % CI 1.06–3.98, P _OR?=?0.032; OR_{TC vs. CC}?=?1.33, 95 % CI 1.06–1.67, P _OR?=?0.012; OR_{TT?+?TC vs. CC}?=?1.46, 95 % CI 1.19–1.81, P _OR?TT vs. CC?+?TC?=?1.62, 95 % CI 1.25–2.09, P _OR?NQO1 C609T variant allele and genotypes are more susceptible to HCC, particularly for Asians.     

Association between X-ray repair cross-complementing group 1 Arg194Trp polymorphism and colorectal cancer risk

The polymorphism of X-ray repair cross-complementing group 1 (XRCC1) Arg194Trp, a substitution of Arg to Gln at position 194, has been implicated in the development of colorectal cancer (CRC) in a number of case–control studies with contradictory and inconclusive findings. The current meta-analysis of all currently available publications was conducted to assess the gene susceptibility to CRC and improve our understanding of the CRC pathogenesis. The pooled odds ratio (OR) with corresponding 95 % confidence interval (95 % CI) was calculated by use of fixed-effects model or random-effects model when appropriate. A total of 15 eligible case–control studies with 4,501 cases and 8,038 controls were retrieved after a comprehensive search of the PubMed, Embase, Web of science, and Chinese Biomedicine (CBM) databases up to December 2012. The overall meta-analysis identified a positive but not statistically significant association between the XRCC1 Arg194Trp polymorphism and CRC risk under all genetic contrast models (OR_{Trp vs. Arg}?=?1.07, 95 % CI 0.90–1.26, P _OR?=?0.441; OR_{TrpTrp vs. ArgArg}?=?1.28, 95 % CI 0.91–1.81, P _OR?=?0.163; OR_{ArgTrp vs. ArgArg}?=?1.00, 95 % CI 0.85–1.19, P _OR?=?0.956; OR_{ArgTrp + TrpTrp vs. ArgArg}?=?1.06, 95 % CI 0.90–1.24, P _OR?=?0.502; OR_{TrpTrp vs. ArgArg + ArgTrp}?=?1.11, 95 % CI 0.91–1.34, P _OR?=?0.306). The genotype TrpTrp carriers among Caucasians were more susceptible to CRC, although lack statistical evidence (OR_{TrpTrp vs. ArgArg}?=?2.69, 95 % CI 0.97–7.49, P _OR?=?0.058; OR_{TrpTrp vs. ArgArg + ArgTrp}?=?2.77, 95 % CI 0.99–7.72, P _OR?=?0.051). Interestingly, the XRCC1 Arg194Trp variant was significantly associated with an increased risk of colon cancer. The present meta-analysis suggests that the XRCC1 Arg194Trp polymorphism may modify the risk for CRC, particularly colon cancer. However, the precise genetic association needs to be further estimated in future studies.     

Association between the XRCC3 C241T polymorphism and lung cancer risk in the Asian population

X-ray repair cross-complementing group 3 (XRCC3) plays a vital role in maintaining the stability of genome by homologous recombination repair for DNA double-strand breaks. The genetic polymorphism of XRCC3 C241T has been implicated in lung cancer risk, but the findings across published studies in Asians are inconsistent and inconclusive. To estimate the precise association of XRCC3 C241T polymorphism with lung cancer risk, a meta-analysis of all currently available studies in Asians was performed. A comprehensive search of the PubMed, Embase, Web of Science, and China National Knowledge Infrastructure databases was conducted for eligible studies based on the inclusion criteria. The pooled odds ratios (ORs) with corresponding 95 % confidence intervals (CIs) were calculated to assess the association. Besides, subgroup analysis and sensitivity analysis were also performed for further estimation. Seven available studies with a total of 7,398 subjects were finally included into this meta-analysis. The overall ORs indicated that the XRCC3 C241T polymorphism was not associated with a lung cancer risk among Asians in all genetic contrast modes (OR_{T allele vs. C allele}?=?1.08, 95 % CI 0.95–1.24, P _OR?=?0.252; OR_{TT vs. CC}?=?1.30, 95 % CI 0.69–2.45, P _OR?=?0.426; OR_{CT vs. CC}?=?1.07, 95 % CI 0.93–1.24, P _OR?=?0.363; OR_{TT + CT vs. CC}?=?1.08, 95 % CI 0.94–1.24, P _OR?=?0.300; OR_{TT vs. CC + CT}?=?1.29, 95 % CI 0.68–2.43, P _OR?=?0.439). We failed to identify significant association between the XRCC3 C241T polymorphism and risk of lung cancer in Chinese and population-based studies. Interestingly, the pooled ORs in hospital-based studies indicated that the XRCC3 C241T variant carriers were more susceptible to lung cancer (OR_{T allele vs. C allele}?=?1.27, 95 % CI 1.04–1.56, P _OR?=?0.019; OR_{CT vs. CC}?=?1.26, 95 % CI 1.01–1.57, P _OR?=?0.045; OR_{TT + CT vs. CC}?=?1.28, 95 % CI 1.03–1.59, P _OR?=?0.027). Sensitivity analysis confirmed the stability and liability of all results. This meta-analysis suggests that the XRCC3 C241T polymorphism may not exert a risk effect on the lung cancer risk in Asians, although a statistically significant association was observed among the hospital-based studies. Thus, the precise relationship between the XRCC3 C241T variant and lung cancer risk needs further confirmation in future studies with large available data.     

No significant association between the XRCC3 Thr241Met polymorphism and lung cancer risk: a meta-analysis

The development of lung cancer is significantly associated with genetic susceptibility. Findings from previous individual studies regarding the effect of X-ray repair cross-complementing group 3 Thr241Met (XRCC3 Thr241Met) polymorphism on lung cancer risk remained conflicting and inconclusive. Thus, a meta-analysis of previous relevant studies was performed to estimate this effect more precisely and to shed some light on the contradictory findings. The pooled odds ratios (ORs) with the corresponding 95 % confidence intervals (95 % CIs) were calculated to assess the correlation of XRCC3 Thr241Met polymorphism with lung cancer susceptibility. Stratified analysis according to ethnicity and sensitivity analysis was both conducted for further confirmation. Seventeen independent case–control studies involving 12,610 subjects totally were included into this meta-analysis. Overall, meta-analysis of total included studies showed that the XRCC3 Thr241Met polymorphism was not associated with risk of lung cancer in all genetic contrast models (OR_{Met allele vs. Thr allele}?=?1.01, 95 % CI 0.91–1.13, P _OR?=?0.810; OR_{Met/Met vs. Thr/Thr}?=?1.16, 95 % CI 0.88–1.54, P _OR?=?0.281; OR_{Thr/Met vs. Thr/Thr}?=?0.95, 95 % CI 0.86–1.04, P _OR?=?0.240; OR_{Met/Met?+?Thr/Met vs. Thr/Thr}?=?0.97, 95 % CI 0.89–1.06, P _OR?=?0.538; OR_{Met/Met vs. Thr/Thr?+?Thr/Met}?=?1.18, 95 % CI 0.91–1.52, P _OR?=?0.204). Stratified analyses in Asians and Caucasians showed similar results. Sensitivity analysis confirmed the stability and reliability of the findings. This meta-analysis of all available data did not support any appreciable association between the XRCC3 Thr241Met polymorphism and lung cancer risk in any populations.     

Association between NQO1 C609T polymorphism and bladder cancer susceptibility: a systemic review and meta-analysis

There is growing evidence for the important roles of genetic factors in the host’s susceptibility to bladder cancer. NAD(P)H:quinone oxidoreductase 1 (NQO1) is a cytosolic enzyme that catalyzes the two-electron reduction of quinoid compounds into hydroquinones. Since the NQO1 C609T polymorphism is linked to enzymatic activity of NQO1, it has also been hypothesized that NQO1 C609T polymorphism may affect the host’s susceptibility to bladder cancer by modifying the exposure to carcinogens. There were many studies carried out to assess the association between NQO1 C609T polymorphism and bladder cancer risk, but they reported contradictory results. We conducted a meta-analysis to examine the hypotheses that the NQO1 C609T polymorphism modifies the risk of bladder cancer. Eleven case–control studies with 2,937 bladder cancer cases and 3,008 controls were included in the meta-analysis. Overall, there was no obvious association between NQO1 C609T polymorphism and bladder cancer susceptibility (for T versus C: odds ratio (OR) = 1.12, 95 % confidence interval (95 %CI) 0.99–1.26, P _OR = 0.069; for TT versus CC: OR = 1.31, 95 %CI 0.95–1.81, P _OR = 0.100; for TT/CT versus CC: OR = 1.06, 95 %CI 0.95–1.18, P _OR = 0.304; for TT versus CT/CC: OR = 1.29, 95 %CI 0.94–1.77, P _OR = 0.112). After adjusting for heterogeneity, meta-analysis of those left 10 studies showed that there was an obvious association between NQO1 C609T polymorphism and bladder cancer susceptibility (for T versus C: OR = 1.18, 95 %CI 1.06–1.31, P _OR = 0.003; for TT versus CC: OR = 1.47, 95 %CI 1.14–1.90, P _OR = 0.003; for TT/CT versus CC: OR = 1.16, 95 %CI 1.01–1.34, P _OR = 0.036; for TT versus CT/CC: OR = 1.39, 95 %CI 1.10–1.75, P _OR = 0.006). There was low risk of publication bias. Therefore, our meta-analysis suggests that NQO1 C609T polymorphism is associated with bladder cancer susceptibility.     

Polymorphism of 8q24 rsl3281615 and breast cancer risk

Several genome-wide association studies on breast cancer have reported similar findings of a new cancer susceptibility locus, 8q24 rsl3281615. Subsequent case–control studies have rapidly investigated the association between the single nucleotide polymorphism of rsl3281615 at chromosome 8q24 and breast cancer risk, but the effect of 8q24 rsl3281615 polymorphism on breast cancer is still unclear due to the inconsistence among those studies. Given the contradictory findings, a meta-analysis was performed to determine the association between 8q24 rsl3281615 polymorphism and breast cancer risk. 12 eligible case–control studies with a total of 42,508 cases and 53,928 controls were finally included into this meta-analysis by searching the PubMed, Embase, and China Biology Medicine (CBM) databases. We estimated the summary odds ratio (OR) with its corresponding 95 % confidence interval (95 % CI) to assess this association. Meta-analyses of total 12 studies showed 8q24 rsl3281615 polymorphism was significantly associated with an increased risk of breast cancer in all contrast models (OR_{G vs. A}?=?1.10, 95 % CI 1.05–1.14, P _OR?<?0.001; OR_{GG vs. AA}?=?1.20, 95 % CI 1.11–1.29, P _OR?<?0.001; OR_{AG vs. AA}?=?1.08, 95 % CI 1.05–1.12, P _OR?<?0.001; OR_{GG vs. AA +AG}?=?1.13, 95 % CI 1.07–1.19, P _OR?<?0.001; OR_{GG+AG vs. AA}?=?1.13, 95 % CI 1.07–1.19, P _OR?<?0.001). Meta-analyses of studies with high quality showed that 8q24 rsl3281615 polymorphism was still significantly associated with an increased risk of breast cancer under the five genetic contrast models. Sensitivity analyses by sequential omission of any individual studies and subgroup analyses by ethnicity further identified the significant association between 8q24 rsl3281615 polymorphism and breast cancer risk. Conclusively, this meta-analysis shows a significant association between 8q24 rsl3281615 polymorphism and breast cancer risk.     

The polymorphism of EGFR 142285G > A exerts no risk effect on breast cancer

The association between the epidermal growth factor receptor (EGFR) 142285G?>?A polymorphism and the susceptibility to breast cancer is unclear. We conducted a meta-analysis of all published studies to estimate the association of EGFR 142285G?>?A polymorphism and breast cancer risk. Systematic computerized searching of the PubMed, Web of Science, and Wanfang databases was performed for relevant publications. Overall, there were three eligible case–control studies with 1,360 cases and 1,522 controls included into our study. The pooled ORs showed that the EGFR 142285G?>?A variant genotypes did not increase or decrease the risk of breast cancer under the following gene models: A vs. G, OR?=?1.07, 95 % CI 0.96–1.19, P _OR?=?0.240; AA vs. GG, OR?=?1.14, 95 % CI 0.91–1.42, P _OR?=?0.239; GA vs. GG, OR?=?0.99, 95 % CI 0.83–1.17, P _OR?=?0.892; GA?+?AA vs. GG, OR?=?1.03, 95 % CI 0.87–1.21, P _OR?=?0.727; AA vs. GG?+?GA, OR?=?1.17, 95 % CI 0.97–1.42, P _OR?=?0.096. The between-study heterogeneity was not significant among all studies. The current meta-analysis showed no evidence for significant association between EGFR 142285G?>?A polymorphism and breast cancer risk. Subsequent studies with large sample size are needed for further elucidation.     

EPHX1 A139G polymorphism and lung cancer risk: a meta-analysis

Microsomal epoxide hydrolase 1 (EPHX1) plays an important role in both the activation and the detoxification of polycyclic aromatic hydrocarbons and aromatic amines. Polymorphisms at exon 4 of the EPHX1 gene have been reported to be associated with variations in EPHX1 activity. Many studies have investigated the association between EPHX1 A139G polymorphism and lung cancer risk, but the impact of EPHX1 A139G polymorphism on lung cancer risk is not clear owing to the apparent inconsistence among those studies. This study aimed to identify the association between EPHX1 A139G polymorphism and lung cancer risk by performing a meta-analysis. We used the pooled odds ratio (OR) with its corresponding 95 % confidence interval (95 % CI) to explore the association. Finally, 26 studies with a total of 14,494 subjects were included into this meta-analysis. Meta-analyses of total studies showed the EPHX1 A139G polymorphism was associated with lung cancer risk under three genetic models (OR _{G versus A}?=?1.17, 95 % CI 1.04–1.31, P _OR?=?0.01; OR _{AG versus AA}?=?1.21, 95 % CI 1.06–1.37, P _OR?=?0.004; OR _{AG + GG versus AA}?=?1.22, 95 % CI 1.06–1.39, P _OR?=?0.005). Sensitivity analyses and subgroup analyses further identified the significant association between the EPHX1 A139G polymorphism and lung cancer risk. No evidence of publication bias was observed. Meta-analyses of available data supported the concept of EPHX1 A139G polymorphism as a genetic susceptibility factor for lung cancer.     

Vascular endothelial growth factor gene polymorphism (-634G/C) and breast cancer risk

The aim of this meta-analysis was to assess if the -634G/C polymorphism represents a predisposition factor for the risk of breast cancer. We included eight published case-control studies, in which a total of 6,175 cancer cases and 6,421 cancer-free controls were included. Pooled ORs and 95 % CIs were calculated by the fixed effects model to evaluate the association of the -634G/C polymorphism and breast cancer risk. When all studies were pooled, we did not find statistical evidence of any significant association with overall breast cancer risk (OR_{BB vs. bb}?=?1.00, 95 % CI?=?0.93–1.07, P?=?0.999; OR_{BB + Bb vs. bb}?=?1.00, 95 % CI?=?0.95–1.05, P?=?0.999; OR_{BB vs. Bb + bb}?=?1.03, 95 % CI?=?0.96-1.09, P?=?0.984; OR_{allele B vs. allele b}?=?1.01, 95 % CI?=?0.97–1.05, P?=?0.998; OR_{Bb vs. bb}?=?0.99, 95 % CI?=?0.92–1.06, P?=?0.992). In further stratified analyses by ethnicity and control source, no significant association was revealed. This study suggests that the -634G/C polymorphism does not appear to represent a risk factor for breast cancer.     

Association between the P53 codon 72 polymorphism and nasopharyngeal cancer risk

The P53 codon 72 polymorphism has been identified as a critical biomarker in modifying the risk of nasopharyngeal cancer (NPC). Many studies have investigated the association between the polymorphism of P53 codon 72 and NPC risk; however, the findings across the published studies are inconsistent and inconclusive. To acquire a more precise assessment for this association, we conducted an updated meta-analysis. The PubMed, Embase, Web of Science, and Wanfang databases were searched for relevant case–control studies. Totally, seven independent publications with 1,133 cases and 1,678 controls were retrieved. The pooled odds ratio (OR) with corresponding 95 % confidence interval (95 % CI) was calculated. Increased risk of NPC was observed among individuals carrying the variant allele and genotypes of P53 codon 72 (OR _{Pro vs. Arg}?=?1.32, 95 % CI 1.18–1.47, P _OR?<?0.001; OR _{ProPro vs. ArgArg}?=?1.90, 95 % CI 1.51–2.39, P _OR?<?0.001; OR _{ProArg + ProPro vs. ArgArg}?=?1.33, 95 % CI 1.13–1.57, P _OR?=?0.001; OR _{ProPro vs. ArgArg + ProArg}?=?1.65, 95 % CI 1.35–2.01, P _OR?<?0.001). Stratified analyses by ethnicity and source of controls also identified this significant relationship in Asians, Caucasians, and hospital-based case–control studies. There was no publication bias risk in our study. The updated meta-analysis supports the evidence that the polymorphism of P53 codon 72 is a risk factor for the development of NPC among the populations of both Asian and Caucasian.     

Association between the NBS1 Glu185Gln polymorphism and breast cancer risk: a meta-analysis

Nijmegen breakage syndrome 1 (NBS1), a vital DNA repair protein in the homologous recombination repair pathway and a signal modifier in the intra-S phase checkpoint, plays a critical role in cellular response to DNA damages and the maintenance of genomic stability. The NBS1 Glu185Gln (NBS1 E185Q, NBS1 8360G>C, rs1805794) polymorphism has been indicated to be involved in the development of cancer, but results of previous individual studies on the association between NBS1 Glu185Gln polymorphism and breast cancer risk remain controversial and inconclusive. Our meta-analysis investigated this association for the first time by pooling the odds ratios with corresponding 95 % confidence intervals (95 % CIs) of all individual publications available to date. Overall, 14 separate studies with 6,642 cases and 7,138 controls were finally included into the present meta-analysis after a comprehensive literature search of the PubMed, Embase, Web of Science, and China National Knowledge Infrastructure databases up to October 21, 2012. Overall analysis and subgroup analyses by ethnicity and source of controls were performed. Meta-analysis of total studies showed that the NBS1 Glu185Gln variant carriers were not susceptible to breast cancer (OR_{Gln vs. Glu}?=?1.05, 95 % CI 0.80–1.39, P _OR?=?0.719; OR _{Gln/Gln vs. Glu/Glu}?=?0.82, 95 % CI 0.62–1.08, P _OR?=?0.154; OR _{Glu/Gln vs. Glu/Glu}?=?1.00, 95 % CI 0.90–1.13, P _OR?=?0.939; OR_{Gln/Gln + Glu/Gln vs. Glu/Glu}?=?0.96, 95 % CI 0.83–1.11, P _OR?=?0.551; OR_{Gln/Gln vs. Glu/Glu + Glu/Gln}?=?0.84, 95 % CI 0.67–1.05, P _OR?=?0.134). Similar results were observed in heterogeneity-adjusted meta-analysis of all studies. Furthermore, subgroup analyses by ethnicity and source of controls did not identify any appreciable relationship of the NBS1 Glu185Gln polymorphism with breast cancer susceptibility in any populations. Sensitivity analysis by sequentially omitting individual studies confirmed the stability and reliability of our results. Our meta-analysis of currently available data shows no association between the NBS1 Glu185Gln polymorphism and breast cancer risk.