Combination of radiofrequency ablation with transarterial chemoembolization for hepatocellular carcinoma: an up-to-date meta-analysis

The aim of this meta-analysis was to compare the effectiveness of combination of radiofrequency ablation (RFA) and transarterial chemoembolization (TACE) with that of RFA alone in patients with hepatocellular carcinoma (HCC). Randomized controlled trials comparing RFA plus TACE with RFA alone for HCC were included into this meta-analysis, and the search strategy followed the requirement of the Cochrane Library Handbook. Overall survival rate and recurrence-free survival rate were analyzed and compared by using Review Manager (version 5). We identified 7 randomized controlled trials comprising 571 patients who were treated by RFA plus TACE versus RFA alone for HCC. Meta-analyses showed that the combination of RFA and TACE was associated with a significantly higher overall survival rates (OR_{1 year}?=?2.39, 95 % CI, 1.35–4.21, P?=?0.003; OR_{3 years}?=?1.85, 95 %CI 1.26–2.71, P?=?0.002), and recurrence-free survival rate (OR_{1 year}?=?2.00, 95 % CI 1.26–3.18, P?=?0.003; OR_{3 years}?=?2.13, 95 %CI 1.41–3.20, P?TACE can improve the overall survival rate and the recurrence-free survival rate for patients with HCC.     

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 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.     

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.     

Survival benefit of hepatic resection versus transarterial chemoembolization for hepatocellular carcinoma with portal vein tumor thrombus: a systematic review and meta-analysis

Background

No consensus treatment has been reached for hepatocellular carcinoma (HCC) with portal vein tumor thrombus (PVTT). Hepatic resection (HR) and transarterial chemoembolization (TACE) have been recommended as effective options, but which is better remains unclear. This meta-analysis is to compare the effectiveness of HR and TACE for HCC with PVTT patients.

Methods

The PubMed, EMBASE, Cochrane Library, VIP, Wan Fang, and Sino Med databases were systematically searched for comparing HR and TACE treating PVTT.

Results

Twelve retrospective studies with 3129 patients were included. A meta-analysis of 11 studies suggested that the 1-, 2-, 3-, and 5-year overall survival (OS) rates (OR?=?0.48, 95% CI?=?0.41–0.57, I² =?37%, P?<?0.00001; OR?=?0.21, 95% CI?=?0.12–0.38, I² =?43%, P?<?0.00001; OR?=?0.35, 95% CI?=?0.28–0.44, I² =?53%, P?<?0.00001; OR?=?0.28, 95% CI?=?0.14–0.54, I² =?72%, P?=?0.0001, respectively) favored HR over TACE. In a subgroup analysis, HR had better 1-, 2-,3, 5-year OS for type I PVTT (OR?=?0.33, 95% CI?=?0.17–0.64, I² =?20%, P?=?0.001; OR?=?0.32, 95% CI?=?0.16–0.63, I2?=?0%, P?=?0.001; OR?=?0.18, 95% CI?=?0.09–0.36, I2?=?0%, P?<?0.00001; OR?=?0.07, 95% CI?=?0.01–0.32, I2?=?0%, P?=?0.0006, respectively) and better 1-, 3-, and 5-year OS for type II PVTT (OR?=?0.37, 95% CI?=?0.20–0.70, I² =?59%, P?=?0.002; OR?=?0.22, 95% CI?=?0.13–0.39, I² =?0%, P?<?0.00001; OR?=?0.16; 95% CI?=?0.03–0.91; I² =?51%, P?=?0.04, respectively). There was no difference in 1-, 3-, or 5-year OS between HR and TACE for type III PVTT (OR?=?0.86, 95% CI?=?0.61–1.21, I² =?0%, P?=?0.39; OR?=?0.83, 95% CI?=?0.42–1.64, I² =?0%, P?=?0.59; OR?=?0.59, 95% CI?=?0.06–-6.04, I² =?65%, P?=?0.66, respectively).

Conclusions

HR may lead to longer OS for some selected HCC patients with PVTT than TACE, especially for type I or II PVTT, with less difference being observed for type III or IV PVTT.

     

MTHFR C677T polymorphism contributes to the risk for gastric cancer

Methylenetetrahydrofolate reductase (MTHFR) has been demonstrated to be involved in carcinogenesis. Increasing individual studies have investigated the role of MTHFR C677T polymorphism in gastric cancer pathogenesis, but with inconsistent findings. The aim of this study was to clarify the potential association of the MTHFR C677T polymorphism with gastric cancer risk by pooling all available data from published case–control studies. We searched the PubMed, Embase, Web of Science, and Wanfang databases for all relevant publications to date. The pooled odds ratio (OR) with corresponding 95 % confidence interval (95 % CI) was calculated. Stratified analysis and sensitivity analysis were also carried out to estimate the strength of this association. A total of 25 case–control studies with 6,572 cases and 9,584 controls were retrieved. Overall, the ORs under five contrast models indicated that the MTHFR C677T variant was positively associated with gastric cancer risk (OR_{T vs. C}?=?1.21, 95 % CI 1.10–1.34, P _OR?<?0.001; OR_{TT vs. CC}?=?1.47, 95 % CI 1.22–1.76, P _OR?<?0.001; OR_{TC vs. CC}?=?1.20, 95 % CI 1.03–1.40, P _OR?=?0.022; OR_{TT?+?TC vs.?CC}?=?1.27, 95 % CI 1.10–1.47, P _OR?=?0.001; OR_{TT vs.?CC?+?TC}?=?1.29, 95 % CI 1.15–1.46, P _OR?<?0.001). Stratified analyses according to ethnicity and source of controls further confirmed the significant correlations. The current meta-analysis provides strong evidence that the MTHFR C677T polymorphism may be a risk factor for gastric cancer among Asians and Caucasians.     

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.     

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 glutathione S-transferase T1 null genotype and risk of myelodysplastic syndromes: a comprehensive meta-analysis

Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal hematologic neoplasms, and the pathophysiology of these disorders is still unclear. Previous studies investigating the association between glutathione S-transferase Tl (GSTT1) null genotype and risk of MDS reported controversial results. We performed a comprehensive meta-analysis to clarify the effect of GSTT1 null genotype on risk of MDS. The strength of the association was measured by odds ratio (OR) with 95 % confidence interval (CI). Fifteen studies were finally included, involving a total of 1,796 cases and 2,502 controls. Subgroup analysis was performed by race. Meta-analysis of all 15 studies showed that the GSTT1 null genotype was significantly associated with an increased risk of MDS (OR?=?1.47, 95 % CI 1.16–1.88, P _OR?=?0.002; I ²?=?54.4 %). Besides, an obvious association was also observed after adjusting the heterogeneity (OR?=?1.32, 95 % CI 1.13–1.54, P _OR?=?0.001; I ²?=?9.0 %). Subgroup analysis by race suggested that this association existed in both Caucasians (OR?=?1.40, 95 % CI 1.04–1.89, P _OR?=?0.027) and Asians (OR?=?1.68, 95 % CI 1.00–2.81, P _OR?=?0.049). This meta-analysis suggests the GSTT1 null genotype is significantly associated with an increased risk of MDS in both Caucasians and Asians.     

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.     

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.     

HIF-1α P582S and A588T polymorphisms and digestive system cancer risk—a meta-analysis

Hypoxia-inducible factor-1 (HIF-1) influences cancer progression and metastasis through various mechanisms, and HIF-1α polymorphisms are reportedly associated with many cancers; however, the associations of HIF-1α P582S and A588T polymorphisms with the risk of digestive system cancer remain inconclusive. To understand the role of HIF-1α P582S and A588T genotypes in digestive cancer development, we conducted a comprehensive meta-analysis involving 1,517 cases and 3,740 controls. Overall, the P582S polymorphism was not significantly associated with digestive system cancers in all genotypes. By contrast, the A588T polymorphism was significantly associated with digestive system cancers in the dominant model (TT/AT vs. AA: OR?=?3.17, 95 % CI: 1.21, 8.25; P _{heterogeneity}?<?0.001). In subgroup analysis for cancer types, the two polymorphisms were only associated with increased risk of pancreatic cancer (P582S: SS vs. PP: OR?=?2.51, 95 % CI: 1.31, 4.81; SS vs. PP/PS: OR?=?8.73, 95 % CI: 1.33, 57.1; A588T: TT vs. AA: OR?=?9.30, 95 % CI: 1.12, 77.6; P _{heterogeneity}?=?0.478; TT vs. AA/AT: OR?=?3.14, 95 % CI: 1.99, 4.97; P _{heterogeneity}?=?0.098; TT/AT vs. AA: OR?=?8.65, 95 % CI: 1.05, 71.6; P _{heterogeneity}?=?0.418). According to the source of ethnicity, the P582S and the A588T polymorphisms are both significantly associated with an increased risk of cancer among Caucasians in the homozygote model (SS vs. PP: OR?=?2.41, 95 % CI: 1.24, 4.691; P _{heterogeneity}?=?0.010; TT vs. AA: OR?=?98.6, 95 % CI: 4.37, 2,224; P _{heterogeneity}?=?0.040) and the recessive model (SS vs. PP/PS: OR?=?9.48, 95 % CI: 1.12, 80.3; P _{heterogeneity}?<?0.001; TT vs. AA/AT: OR?=?82.7, 95 % CI: 3.79, 1,802; P _{heterogeneity}?=?0.041). Our findings suggest that the HIF-1α A588T polymorphism is significantly associated with higher cancer risk and the P582S polymorphism is significantly associated with pancreatic cancer risk. Furthermore, the effect of both polymorphisms on digestive system cancer is more pronounced among Caucasians than that among Asians.     

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.     

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.     

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.     

Association between KIF1B rs17401966 polymorphism and hepatocellular carcinoma risk: a meta-analysis involving 17,210 subjects

Some publications have evaluated the correlation between KIF1B rs17401966 polymorphism and hepatocellular carcinoma (HCC) with conflicting results. We performed this meta-analysis to clarify the association of KIF1B rs17401966 polymorphism and HCC risk. We searched PubMed, ISI Web of Knowledge, ScienceDirect, and Google Scholar. The combined odds ratio (OR) with 95 % confidence interval (CI) was calculated to estimate the strength of the association. Heterogeneity and publication bias were also assessed. In total, 15 case-control studies with 7,596 HCC cases and 9,614 controls were included in the meta-analysis. A significant association between KIF1B rs17401966 polymorphism and HCC risk was detected (OR?=?0.81, 95 % CI 0.72–0.91, P?KIF1B rs17401966 polymorphism and HCC risk in Chinese (OR?=?0.77, 95 % CI 0.67–0.89, P?KIF1B rs17401966 polymorphism was significantly associated with HCC risk in man (OR?=?0.57, 95 % CI 0.51–0.64, P?P?P?P?=?0.11). This meta-analysis showed a significant association between KIF1B rs17401966 polymorphism and HCC.     

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.     

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 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.