Meta-Analysis of the Association between the rs8034191 Polymorphism in AGPHD1 and Lung Cancer Risk

Background: Possible associations between the single nucleotide polymorphism (SNP) rs8034191 in theaminoglycosidephosphotransferase domain containing 1 (AGPHD1) gene and lung cancer risk have been studiedby many researchers but the results have been contradictory. Materials and Methods: A computerized searchfor publications on rs8034191 and lung cancer risk was performed. Odds ratios (ORs) with 95% confidenceintervals (CIs) were calculated to assess the association between rs8034191 and lung cancer risk with 13 selectedcase-control studies. Sensitivity analysis, test of heterogeneity, cumulative meta-analysis, and assessment ofbias were also performed. Results: A significant association between rs8034191 and lung cancer susceptibilitywas found using the dominant genetic model (OR=1.344, 95% CI: 1.285-1.406), the additive genetic model(OR=1.613, 95% CI: 1.503-1.730), and the recessive genetic model (OR=1.408, 95% CI: 1.319-1.503). Moreover,an increased lung cancer risk was found with all genetic models after stratification of ethnicity. Conclusions: Theassociation between rs8034191 and lung cancer risk was significant using multiple genetic models, suggestingthat rs8034191 is a risk factor for lung cancer. Further functional studies of this polymorphism and lung cancerrisk are warranted.     

Matrix Metalloproteinase-2 -1306 C>T Gene Polymorphism is Associated with Reduced Risk of Cancer: a Meta-analysis

Matrix metalloproteinase-2 (MMP2) is an endopeptidase, mainly responsible for degradation of extracellularmatrix components, which plays an important role in cancer disease. A single nucleotide polymorphism (SNP)at -1306 disrupts a Sp1-type promoter site. The results from the published studies on the association betweenMMP2 -1306 C>T polymorphism and cancer risk are contradictory and inconclusive. In the present study, ameta-analysis was therefore performed to evaluate the strength of any association between the MMP2 -1306C>T polymorphism and risk of cancer. We searched all eligible studies published on association between MMP2-1306 C>T polymorphism and cancer risk in PubMed (Medline), EMBASE and Google Scholar online webdatabases until December 2013. Genotype distribution data were collected to calculate the pooled odds ratios(ORs) and 95% confidence intervals (95%CIs) to examine the strength of the association. A total of 8,590 cancercases and 9,601 controls were included from twenty nine eligible case control studies. Overall pooled analysissuggested significantly reduced risk associated with heterozygous genotype (CT vs CC: OR=0.758, 95%CI=0.637to 0.902, p=0.002) and dominant model (TT+CT vs CC: OR=0.816, 95%CI=0.678 to 0.982, p=0.032) geneticmodels. However, allelic (T vs C: OR=0.882, 95%CI=0.738 to 1.055, p=0.169), homozygous (TT vs CC: OR=1.185,95%CI=0.825 to 1.700, p=0.358) and recessive (TT vs CC+CT: OR=1.268, 95%CI=0.897 to 1.793, p=0.179)models did not show any risk. No evidence of publication bias was detected during the analysis. The results ofpresent meta-analysis suggest that the MMP2 -1306 C>T polymorphism is significantly associated with reducedrisk of cancer. However, further studies with consideration of different populations will be required to evaluatethis relationship in more detail.     

MMP1 rs1799750 Single Nucleotide Polymorphism and Lung Cancer Risk: A Meta-analysis

Background: Numerous studies have investigated the association of matrix metalloproteinase 1 (MMP1) rs1799750 single nucleotide polymorphism with lung cancer susceptibility, but the findings are inconsistent.Therefore, we performed a meta-analysis to comprehensively evaluate any possible association. Methods: We searched publications from MEDLINE, EMBASE and CNKI databases which assessed links between theMMP1 rs1799750 polymorphism and lung cancer risk. We calculated the pooled odds ratio (OR) and its 95% confidence interval (95%CI) using either fixed-effects or random-effects models. Results: The meta-analysis was based on 9 publications encompassing 4,823 cases and 4,298 controls. The overall results suggested there was a significant association between the MMP1 rs1799750 polymorphism and lung cancer risk (1G vs. 2G: OR = 0.83,95%CI = 0.73-0.94; 1G1G vs. 2G2G: OR = 0.73, 95%CI = 0.59-0.92; 1G1G vs. 1G2G/2G2G: OR = 0.87, 95%CI = 0.79-0.97; 1G1G/1G2G vs. 2G2G: OR = 0.78, 95%CI = 0.64-0.95). In the subgroup analysis by ethnicity, the association was still obvious in Asians (all P values < 0.05), but there was no association in Caucasians (all P values > 0.05). Conclusions: The MMP1 rs1799750 polymorphism is associated with decreased lung cancer risk,and a race-specific effect may exist in this association.     

CHRNA5 rs16969968 Polymorphism Association with Risk of Lung Cancer - Evidence from 17,962 Lung Cancer Cases and 77,216 Control Subjects

Background: Genetic studies have shown a possible relationship between the rs16969968 polymorphism inCHRNA5 and the risk of lung cancer. However, the results have been conflicting. Thus we rigorously conducteda meta-analysis to clarify any association. Materials and Methods: A total of 10 case-control studies involving17,962 lung cancer cases and 77,216 control subjects were analysed. Odds ratios (ORs) with 95% confidenceintervals (CIs) were used to measure the strength of the association. Results: We found the CHRNA5 rs16969968polymorphism to be associated with the risk of lung cancer (AA vs GG: OR=1.60, 95%CI=1.51-1.71). On stratifiedanalysis by smoking status, a statistically significant increased risk was observed in the smoking group (AA vsGG: OR=1.80, 95%CI=1.61-2.01). However, this polymorphism was not associated with lung cancer risk inAsians (AA vs GG: OR=0.95, 95%CI=0.35-2.59), whereas it was linked to increased risk of lung cancer amongCaucasians (AA vs GG: OR=1.65, 95%CI=1.55-1.76). Conclusions: Our meta-analysis provided statisticalevidence for a strong association between rs16969968 polymorphism and the risk of lung cancer, especially insmokers and Caucasians. Application of this relationship may contribute to identification of individuals at highrisk of lung cancer and indicate a chemoprevention target.     

Significance of Membrane Type 1 Matrix Metalloproteinase Expression in Breast Cancer

Expression of matrix metalloproteinases (MMPs) plays an essential role in tumor metastasis and invasion through the degradation of extracellular matrix (ECM). MT1-MMP (membrane type 1 matrix metalloproteinase), a membrane-type MMP, is responsible for the activation of MMP2. In this study the significance of MT1-MMP expression in human breast tumors was investigated by immunocytochemical assay, and its correlation with clinicobiological features was analyzed. MT1-MMP expression was detected in tumor cells and/or stromal cells, and there was a strong correlation between the expressions of MT1-MMP in the two cell types. Out of 183 primary tumors, 103 (56.2%) showed positive staining of MT1-MMP in tumor cells. MT1-MMP expression showed no significant correlation with any of the clinicobiological parameters examined, including hormone receptor status and angiogenesis. In postoperative survival analysis, MT1-MMP expression itself was not a significant prognostic factor. However, in the particular subgroup with the accumulation of thymidine phosphorylase (TP)-positive stromal cells, which have been activated by various stimuli, such as cytokines and hypoxia, MT1-MMP expression had a significant prognostic value. These data suggested that MT1-MMP might function cooperatively with tumor-associated stromal cells for the progression of breast cancer.     

No Association Between the CYP1B1 C4326G Polymorphism and Endometrial Cancer Risk: a Meta-analysis

Purpose: Any association between the CYP1B1 C4326G polymorphism and endometrial cancer risk remains inconclusive. In order to provide a more precise estimate, we performed the present meta-analysis. Methods: We used fixed effect or random effect models to estimate pooled odds ratios (ORs) with 95% confidence intervals (CIs) for endometrial cancer risk, with the Chi-square-based Q-test used to test for heterogeneity. Begg’s and Egger’s tests were adopted to check publication bias. Results: Six published case-control studies of association between the CYP1B1 C4326G polymorphism and endometrial cancer risk covering 6,577 subjects were included in the meta-analysis, but the results indicated no significant correlation with allele contrast and genotype comparisons (G vs C: OR 1.01, 95% CI 0.93-1.09; GG vs CC: OR 1.04, 95% CI 0.88-1.23; CG + GG vs CC: OR 1.08, 95% CI 0.97-1.21; GG vs CC + CG: OR 1.01, 95% CI 0.87-1.17). Heterogeneity hypothesis test did not reveal any heterogeneity and Begg’s and Egger’s tests did not detect obvious publication bias. Conclusions: There is no association between the CYP1B1 C4326G polymorphism and endometrial cancer risk.     

GSTM1 Polymorphisms and Lung Cancer Risk in the Chinese Population: a Meta-Analysis Based on 47 Studies

Although a number of studies have been conducted on the association between GSTM1 polymorphismsand lung cancer in China, this association remains elusive and controversial. To clarify the effects of GSTM1polymorphisms on the risk of lung cancer, a meta-analysis was performed in the Chinese population. Relatedstudies were identified from PubMed, Springer Link, Ovid, Chinese Wanfang Data Knowledge Service Platform,Chinese National Knowledge Infrastructure (CNKI), and Chinese Biology Medicine (CBM) up to 5th April 2014.A total of 45 articles (47 studies) including 6,623 cases and 7,865 controls were involved in this meta-analysis.Overall, a significant association (OR = 1.45, 95%CI: 1.32-1.60) was found between the null GSTM1 and lungcancer risk when all studies in Chinese population pooled into the meta-analysis. In subgroup analyses stratifiedby quality score, geographic area and source of controls, the same results were observed under all the models.This meta-analysis showed that the null GSTM1 may be a potential biomarker for lung cancer risk in Chinese,but further studies with gene-gene and gene-environment interactions are required for definite conclusions.     

Meta-analysis of the CYP1A2 -163C>A Polymorphism and Lung Cancer Risk

Many published studies have concerned associations between the CYP1A2 -163 C>A polymorphism and riskof lung cancer, but the results have been inconsistent. Therefore, we performed a meta-analysis to obtain a moreprecise estimate. We searched the PubMed database up to March 1, 2013 for relevant cohort and case-controlstudies. Supplementary search was conducted manually by searching the references of the included studies andrelevant meta-analyses. A meta-analysis was performed using RevMan 5.2 software for calculation of pooledodds ratios (ORs) and relevant 95% confidence intervals (CIs) after data extraction. Finally, seven case-controlstudies and one nested case-control study involving 1,675 lung cancer patients and 2,393 controls were included.The meta-analysis showed that there was no association of CYP1A2 -163 C>A polymorphism with risk of lungcancer overall [(OR=0.89, 95%CI= 0.74-1.07) for C vs. A; (OR=0.73, 95%CI= 0.50-1.07) for AA vs. CC ; (OR=0.82,95%CI= 0.62-1.09) for AC vs. CC; (OR=0.79, 95%CI= 0.58-1.07) for (AC+AA) vs. CC; and (OR=0.87, 95%CI=0.67-1.13) for AA vs. (CC+AC)]. Subgroup analysis indicated that there was an associationbetween CYP1A2-163C>A polymorphism and lung cancer risk for population-based controls, a trend risk for SCCL (squamouscell carcinoma of lung) and Caucasians. These results suggested that -163 C>A polymorphism is likely to beassociated with risk of lung cancer compared with population-based controls.     

The 765G>C Polymorphism in the Cyclooxygenase-2 Gene and Gastric Cancer Risk: an Update by Meta-analysis

Background: The 765G>C polymorphism in cyclooxygenase-2 (COX-2) gene has been extensively investigatedfor association with gastric cancer (GC). However, the results of different studies have been inconsistent. The aimof this study is to comprehensively evaluate the genetic risk of -765G>C polymorphism in the COX-2 gene forGC. Materials and Methods: We searched Pubmed, Embase, Medline, CNKI database, Wanfang database, Weipudatabase, and Chinese Biomedical database, covering all publications (last search been performed on Jan 10,2014). Statistical analyses were performed using Revman 5.2 and STATA 10.0 software. Results: A total of 1,874cases and 3,005 controls in 10 case-control studies were included in this meta-analysis. The results indicated thatthe variant C allele carriers (GC+CC) had a 69% increased risk of GC when compared with the homozygote GG(odds ratio (OR)=1.69, 95% confidence interval (CI), 1.10-2.61 for GC+CC vs GG). In the subgroup analysis byethnicity, significant elevated risks were associated with C allele carriers in Asians (OR=1.75, 95%CI=1.40-2.18,and p<0.00001) and in Indians (OR=8.38, 95%CI=4.34-16.16, and p<0.00001) but not in Caucasians (OR=1.07,95%CI=0.81-1.42, and p=0.62) or in Dutch (OR=0.53, 95%CI= 0.33-0.87, and p= 0.01).In the subgroup analysisby Helicobacter pylori (H. pylori) status, a significantly increased risk was identified among H. pylori (+) (OR=3.58,95%CI=2.33-3.50, and p<0.00001) and H. pylori (-) (OR=2.32, 95%CI=1.46-3.69, and p=0.0004). Conclusions:This meta-analysis suggested that the -765G>C polymorphism in the COX-2 gene could be a risk factor for GCin Asians and Indians.     

Updated Assessment of the Association of the XRCC1 Arg399Gln Polymorphism with Lung Cancer Risk in the Chinese Population

Background: Published studies have reported relationships between X-ray repair cross-complementing group1 (XRCC1) Arg399Gln polymorphism and lung cancer risk in Chinese population. However, the epidemiologicalresults remained controversial. The objective of this study was to clarify the association of XRCC1 Arg399Glnpolymorphism with lung cancer risk in the Chinese population. Materials and Methods: Systematic searches wereperformed through the database of Medline/Pubmed, Web of Science, Embase, CNKI and WanFang MedicalOnline. Odds ratios (ORs) with 95% confidence interval (95%CI) were calculated to estimate the strength ofthe association. Results: Overall, we observed an increased lung cancer risk among subjects carrying XRCC1codon 399 Gln/Gln genotype (OR=1.36, 95%CI: 1.09-1.71) in the Chinese population on the basis of 19 studieswith 5,416 cases and 5,782 controls. We did not observe any association between XRCC1 codon 399 Arg/Gln andArg/Gln+Gln/Gln polymorphisms and lung cancer risk (OR=1.00, 95%CI: 0.92-1.08 and OR=1.05, 95%CI: 0.97-1.13, respectively). Limiting the analysis to studies with controls in agreement with Hardy-Weinberg equilibrium(HWE), we observed an increased lung cancer risk among subjects carrying XRCC1 codon 399 Gln/Gln genotype(OR=1.18, 95%CI: 1.01-1.38). When stratified by source of control, we observed an increased lung cancer riskamong subjects carrying XRCC1 codon 399 Arg/Gln+Gln/Gln genotype on the basis of hospitalized patient-basedcontrols (OR=1.21, 95%CI: 1.04-1.42) and among subjects carrying XRCC1 codon 399 Gln/Gln genotype onthe basis of healthy subject-based controls (OR=1.22, 95%CI: 1.04-1.43). Conclusions: Our findings indicatedthat certain XRCC1 Arg399Gln variants might affect the susceptibility of lung cancer in Chinese population.Larger sample size studies are required to confirm our findings.     

CTLA-4 +49 A/G Polymorphism and the Risk of Lung Cancer: a Meta-analysis

Background and objectiveLung cancer is one of the malignant tumors. Gene mutations associated with cellular immune function and regulating the activation and proliferation of immune cells. Several publications have explored the relationship between cytotoxic T lymphocyte antigen-4 (CTLA-4) +49 adenine (A)/guanine (G) polymorphism and susceptibility of lung cancer, but the results remain controversial. Thus, we performed this meta-analysis to derive a more comprehensive estimation of the relationship.MethodsAll articles addressed lung cancer and polymorphisms of CTLA-4 were searched from the PubMed, EMBASE databases published up to June 29, 2019. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association. Publication bias of relevant studies was examined via Begg''s test and funnel plots.ResultsThe meta-analysis included 8 case-control studies covering 4, 430 lung cancer patients and 5, 198 healthy controls from September 2008 to April 2020. The overall eligible data indicated that CTLA-4 +49A/G polymorphisms did not correlate with the elevated lung cancer risk in all genetic comparison models (dominant model: OR=1.037, 95%CI: 0.925-1.161; recessive model: OR=0.968, 95%CI: 0.888-1.055; allele model: OR=0.992, 95%CI: 0.933-1.054; homozygous model: OR=0.980, 95%CI: 0.857-1.121; heterozygous model: OR=1.023, 95%CI: 0.906-1.154). In further stratified analyses, CTLA-4 +49A/G polymorphism was found to be significantly associated with susceptibility to NSCLC in these models (dominant model: OR=1.404, 95%CI: 1.074-1.836; allele model: OR=1.273, 95%CI: 1.034-1.565; homozygous model: OR=1.553, 95%CI: 1.044-2.310; heterozygous model: OR=1.308, 95%CI: 1.062-1.611).ConclusionCTLA-4 +49A/G polymorphism were not associated with the risk of lung cancer but might be a risk factor only in NSCLC.     

The P275A Polymorphism in the Macrophage Scavenger Receptor 1 Gene and Prostate Cancer Risk: a Meta-Analysis

Background: Published data regarding associations between the P275A polymorphism in the macrophagescavenger receptor 1 (MSR1) gene and prostate cancer (PCa) risk are inconclusive. The aim of this study wasto comprehensively evaluate the genetic risk of P275A polymorphism in MSR1 gene for PCa. Materials andMethods: A systematic literature search was carried out in Pubmed, Medline (Ovid), Embase, CBM, CNKI,Weipu, and Wanfang databases, covering all available publications (last search was performed on Apr 27, 2015).Statistical analysis was performed using Revman 5.2 and STATA 10.1 software. Results: A total of 5,017 casesand 4,869 controls in 12 case-control studies were included in this meta-analysis. When all groups were pooled,there was no evidence that the P275A polymorphism had a significant association with PCa under dominant(OR=0.93, 95%CI=0.81-1.06, and p=0.28), co-dominant (homogeneous OR=0.97, 95%CI=0.56-1.68, and p=0.92;heterogeneous OR=0.93, 95%CI=0.74-1.15, and p=0.49), recessive (OR=1.10, 95%CI=0.65-1.87, and p=0.73),over-dominant (OR=0.93, 95%CI=0.75-1.15, and p=0.50), and allelic (OR=0.95, 95%CI=0.77-1.16, and p=0.61)genetic models. For stratified analyses by ethnicity and study design, no significant associations were found in thewhite race, the yellow race, the black race and mixed ethnicity, and the population-based case-control (PCC) andhospital-based case-control (HCC) studies under all genetic models. Conclusions: Based on our meta-analysis,the P275A polymorphism in the MSR1 gene is unlikely to be a risk factor for PCa.     

Association of Promoter Region Polymorphisms of IL-10 Gene with Susceptibility to Lung Cancer: Systematic Review and Meta-Analysis

Objective: Epidemiological studies have suggested that the promoter region polymorphisms of interleukin-10 (IL-10)gene may be associated with an increased risk of lung cancer. However, those studies results are controversial. Thus, acomprehensive meta-analysis was performed to evaluate the association of promoter region polymorphisms of IL-10gene with susceptibility to lung cancer. Methods: a comprehensive search of PubMed, EMBASE, and CNKI databaseswas performed to find all eligible studies up to September 15, 2018. The pooled odds ratios (ORs) with 95% confidenceintervals (CIs) were used to assess the strength of such association. Results: A total number of 19 case-control studies with4084 cases and 6,131 controls were selected. The overall meta-analysis results showed that the -592A>C polymorphismwas significantly associated with lung cancer risk under four genetic models, i.e., allele (CT vs. TT: OR= 1.17, 95% CI1.01-1.35, p=0.02), homozygote (CC vs. AA: OR= 1.64, 95% CI 1.29-2.02, p≤0.001), heterozygote (CA vs. AA: OR=1.26, 95% CI 1.06-1.50, p≤0.001), and dominant (CC+CA vs. AA: OR= 1.31, 95% CI 1.11-1.54, p=0.001). However,there was no significant association between -819T>C and -1082A>G polymorphisms of IL-10 and lung cancer risk.Similarly, subgroup analyses by ethnicity detected significant association between IL-10 -592A>C and lung canceramong Asians and Caucasians. Conclusions: Our meta-analysis suggests that the IL-10 -592A>C polymorphism mightbe risk factor for lung cancer, especially among Asian and Caucasians. In contrast, the IL-10 -819T>C and -1082A>Gpolymorphisms are not significantly associated with increased risk of lung cancer.     

Association between the TP53BP1 rs2602141 A/C Polymorphism and Cancer Risk: A Systematic Review and Meta-Analysis

Background: The p53-binding protein 1 (TP53BP1) gene may be involved in the development of cancer throughdisrupting DNA repair. However, investigation of associations between TP53BP1 rs2602141 A/C polymorphismand cancer have yielded contradictory and inconclusive outcomes. We therefore performed a meta-analysis toevaluate the association between the TP53BP1 rs2602141 A/C polymorphism and cancer susceptibility. Materialsand Methods: Published literature from PubMed, Medline, the Cochrane Library, EMbase, Web of Science,Google (scholar), CBMDisc, Chongqing VIP database, and CNKI database were retrieved. Pooled odds ratios(ORs) with 95% confidence intervals (CIs) were calculated using fixed or random-effects models. Publicationbias was estimated using funnel plots, Begg’s and Egger’s test. Results: A total of seven studies (3,018 casesand 5,548 controls) were included in the meta-analysis. Our results showed that the genotype distribution ofTP53BP1 rs2602141 A/C was not associated with cancer risk overall. However, on subgroup analysis, we foundthat TP53BP1 rs2602141 A/C was associated with cancer risk within an allele model (A vs C, OR=1.14, 95%CI:1.01-1.29) and a codominant model (AA vs CC, OR=1.36, 95%CI: 1.06-1.74) in Asians rather than in Caucasians.Subgroup analysis by cancer type, genotype, and with or without adjustment for controls showed no significantassociation. Conclusions: The findings suggested an association between rs2602141 A/C polymorphism in TP53BP1gene and increased risk of cancer in Asians.     

E2钙黏蛋白基因3′2 U TR + 54C/ T 多态与 肺癌的发病风险

 目的　探讨CDH1 基因3′2 U TR + 54C/ T SNP 与中国北方人群肺癌遗传易感性的关系。方法 采用聚合酶链反应2限制性片段长度多态性( PCR2RFL P) 分析方法检测194 名肺癌患者和223 名健康对 照组3′2 U TR + 54C/ T SNP 的基因型。结果　肺癌患者组吸烟个体比例明显高于对照组,吸烟可增加 肺癌的发病风险(OR = 3. 03 ,95 %CI = 2. 03～4. 54) 。肺癌患者组C 等位基因频率(85. 6 %) 显著高于对 照组(76. 9 %) ,两组相比差异有统计学意义(χ2 = 10. 09 , P = 0. 00) ;肺癌患者组与对照组T/ T、T/ C 和 C/ C 基因型频率分别为1. 0 %、26. 8 %、72. 2 %和4. 0 %、38. 1 %、57. 8 % ,与T/ T 或T/ C 基因型相比,携 带C/ C 基因型可显著增加肺癌的发病风险(OR = 1. 89 ,95 %CI = 1. 25～2. 85) 。结论　CDH1 基因3′2 U TR + 54C/ C 基因型可能是中国北方人群肺癌发病的潜在危险因素。     

The 2518 A/G Polymorphism in the MCP-1 Gene and Cancer Risk: A Meta-analysis

Background: The 2518 A/G polymorphism in the MCP-1 gene has been extensively studied for associationswith cancer; however, results from replication studies have been inconsistent. The aim of this investigationwas to determine links with risk of cancer by meta-analysis. Methods: We searched Pubmed, Embase, CNKI,Weipu and Wanfang databases, covering all case-control studies until March, 2013. Statistical analyses wereperformed using the Revman 5.0 software. Results: A total of 11 case-control studies met our inclusion criteria,including 1,422 cases and 2,237 controls. The results indicated that the MCP-1 2518 gene polymorphism had noassociation with cancer risk overall (GG vs.GA+ AA: OR = 0.89, 95%CI = 0.61–1.28, P = 0.52). However, in thesubgroup analysis by ethnicity, a decrease of cancer risk was found in Asian populations (GG vs.GA+ AA: OR =0.79, 95%CI = 0.63–0.99, P = 0.04). Conclusion: This meta-analysis suggested that the 2518A/G polymorphismof MCP-1 gene is associated with risk of cancer among Asian, but not in Caucasian populations.     

Lack of Association Between the CYP1A1 Ile462Val Polymorphism and Endometrial Cancer Risk: a Meta-analysis

Purpose: Any association between the CYP1A1 Ile462Val polymorphism and endometrial cancer risk remainsinconclusive. For a more precise estimate, we performed the present meta-analysis. Methods: PUBMED, OVIDand EMBASE were searched for the studies which met inclusion criteria. Data in all eligible studies wereevaluated and extracted by two authors independently. The meta-analysis estimated pooled odds ratio (OR) with95% confidence interval (CI) for endometrial cancer risk attributable to the CYP1A1 Ile462Val polymorphism.Results: A total of 7 studies were included in this meta-analysis. The results indicated no association betweenendometrial cancer risk and the CYP1A1 Ile462Val polymorphism (for Val vs Ile allele model [OR 1.09, 95%CI 0.73-1.62]; for Val.Val vs Ile.Ile genotype model [OR 1.54, 95% CI 0.56-4.23]; for (Ile.Val + Val.Val) vs Ile.Ilegenotpye model [OR 1.08, 95% CI 0.71-1.63]; for Val.Val vs (Ile.Ile + Ile.Val) genotype model [OR 1.46, 95% CI0.53-4.04]). Conclusions: This meta-analysis suggests that there is no association between endometrial cancerrisk and the CYP1A1 Ile462Val polymorphism.     

Lack of Association of the Cyclooxygenase-2 Gene 8473T>C Polymorphism with Breast Cancer Risk: a Meta-analysis

Background: Associations between the 8473T>C polymorphism (rs5275) in the cyclooxygenase-2 (COX-2)gene and breast cancer (BC) risk are still inconclusive and ambiguous. The aim of this meta-analysis was tocomprehensively estimate the genetic risk of 8473T>C polymorphism in the COX-2 gene for BC. Materials andMethods: We searched PubMed, Web of Science, Medline, Chinese biomedical (CBM), Weipu, China nationalknowledge infrastructure (CNKI), and Wanfang databases, covering all publications (last search was updated onAug 17, 2014). Statistical analyses were performed using Revman 5.3 and STATA 10.0 software. Results: A totalof 6,720 cases and 9,794 controls in 12 studies were included in this study. The results indicated no significantassociations between the 8473T>C polymorphism of the COX-2 gene and BC risk for the CC+TC vs TT model(pooled odds ratio (OR)=0.97, 95% confidence interval (CI)=0.90-1.03, and p=0.29). On subgroup analysis, wealso found that subdivision on ethnicity among Caucasians, Asians and others also revealed no relationshipwith BC susceptibility. With the study design (CC+TC vs TT), no significant associations were found in eitherpopulation-based case-control studies (PCC), or hospital-based case-control studies (HCC). Conclusions: Thispresent meta-analysis suggests that the 8473T>C polymorphism in the COX-2 gene is not a conspicuous lowpenetrantrisk factor for developing BC.     

Lack of Association Between the Matrix Metalloproteinase-2-1306C>T Polymorphism and Breast Cancer Susceptibility: a Meta-analysis

Background: Since inconsistent results have been reported regarding the relation between the matrix metalloproteinase-2 (MMP-2) -1306C>T polymorphism and susceptibility for breast cancer, we performed a meta-analysis to investigate the issue. Materials and Methods: An internet search of PubMed and EMBASE wasperformed to identify eligible studies. Pooled odds ratios (ORs) with their corresponding confidence intervals (CIs) were calculated to evaluate any association between MMP-2 -1306C>T polymorphism and breast cancer susceptibility. Results: Nine case-control studies were included in the meta-analysis, involving 9,858 cases and 10,871 controls. Overall, there was no evidence of any association between the MMP-2 -1306C>T polymorphism and breast cancer susceptibility in different genetic models (T-allele vs C-allele: OR=0.95, 95%CI, 0.82-1.10, p=0.49; TT vs CC: OR=1.03, 95%CI, 0.90-1.19, p=0.66; TT+TC vs CC: OR=0.93, 95%CI, 0.78-1.10, p=0.38; TT vs TC+CC: OR=1.02, 95%CI, 0.89-1.17, p=0.77). In the subgroup analysis by ethnicity, CC was associated witha significant increase in breast susceptibility among Latin-Americans in the dominant model (OR=0.61, 95%CI,0.40-0.93, p=0.02), but the association disappeared in other models. No significant association was observed among Europeans, East Asians and others in different genetic models. In the subgroup analysis by their source of controls, no significant association between MMP-2 -1306C>T polymorphism and breast cancer susceptibility was noted among population-based studies and hospital-based studies in different genetic models. Conclusions: The results of this meta-analysis suggest that MMP-2 -1306C>T polymorphism is not associated with breast cancer susceptibility, although the association among Latin-Americans in the dominant model was significant.     

Positive Association Between IL-16 rs11556218 T/G Polymorphism and Cancer Risk: a Meta-analysis

Background: Interleukin-16 (IL-16) is a multifunctional cytokine which plays a key role in inflammatory andautoimmune diseases as well as in cancer. Genetic polymorphisms of IL-16 have been implicated in susceptibilityto cancer. However, associations remain inconclusive. The present meta-analysis was therefore carried out toestablish a more conclusive association of IL-16 polymorphisms with cancer risk. Materials and Methods: Relevantstudies were searched through the PubMed, Embase, Web of Science, Google Scholar and Wan fang electronicdatabases updated in October 2013. Odds ratios (OR) and 95% confidence intervals (95% CI) were used toassess the association between IL-16 polymorphisms and cancer risk. Results: Eight eligible studies (rs4778889T/C: 8, rs11556218 T/G: 7, rs4072111 C/T: 6) that met our selection criteria were included. The meta-analysisindicated that rs11556218 T/G was associated with a significant increased risk of cancer (G vs. T, OR=1.321,95% CI=1.142-1.528, P ﹤0.001; TG vs. TT, OR=1.665, 95% CI=1.448-1.915, P﹤0.001; GG+TG vs. TT, OR=1.622,95% CI=1.416-1.858, P﹤0.001),as well as nasopharyngeal carcinoma and colorectal cancer. Furthermore, in thesubgroup of Chinese, significant associations were found between rs11556218 polymorphism and cancer risk.There was no statistically significant association between the other two variants (rs4778889, rs4072111) and riskof cancer. Conclusions: This meta-analysis suggests that the IL-16 rs11556218 polymorphism is associated withincreased cancer risk. Large well-designed studies involving various cancer types and different populations arenow needed.