MKK4基因启动子区-1304T〉G多态与食管癌易感性研究

目的：探讨MKK4基因-1304T〉G位点单核苷酸多态基因型在中国东部人群中的分布及其对食管癌易感性的影响。方法：设计以医院为基础的病例对照研究,进行食管癌患者与对照人群频数匹配,采用聚合酶链反应-限制性片段长度多态性的方法（PCR-RFLP）对571例食管癌患者和785名正常人的MKK4基因-1304T〉G位点（rs3826392）进行基因分型。利用Logistic回归分析基因多态性与食管癌发病风险的关联,并校正年龄和性别。结果：MKK4基因-1304T〉G位点基因多态性在病例和对照组中分布差异无统计学意义,GG基因型（OR=0.98,95%CI：0.67～1.61）,TG基因型（OR=1.12,95%CI：0.90～1.43）,P=0.435。结论：MKK4基因-1304T〉G位点的单核苷酸多态可能与中国东部人群食管癌易感性无关。     

MKK4基因启动子区遗传变异与中国南方人群肺癌易感性的相关性研究

目的:探讨丝裂原活化蛋白激酶激酶4(mitogen-activated protein kinase kinase4,MKK4)基因启动子区单核苷酸多态性与中国南方人群肺癌发病风险的关系。方法:采用病例对照研究方法,收集800例肺癌病例和900例正常对照,采用TaqMan技术检测MKK4基因启动子区多态位点rs3826392(-1304T>G)的基因型。应用SAS9.3软件分析其与肺癌易感性的相关性。结果:MKK4基因启动子区-1304T>G基因型在对照组中的频率分布符合Hardy-Weinberg平衡(P=0.149),其在病例组和对照组的分布差异有统计学意义(P=0.001);与携带TT基因型个体相比,携带TG杂合子的个体患肺癌的风险下降25%[校正比值比(oddratio,OR)=0.75,95%可信区间(confidence interval,CI)=0.58～0.97],而携带GG变异纯合子者患肺癌的风险下降45%(校正OR=0.55,95%CI=0.33～0.94);随着变异型等位基因G的个数增加,肺癌发病风险逐步降低(P趋势<0.001)。结论:MKK4基因启动子区-1304T>G基因遗传变异可能降低肺癌发病风险。     

COX-2基因单核苷酸多态性与肝细胞癌关联的研究

目的:探讨广西地区COX-2基因-1195G>A(rs689466)和8473T>C(rs5275)位点单核苷酸多态性与肝细胞癌(HCC)遗传易感性的关系。方法:采用以医院为基础的病例对照研究方法。研究对象为780例经组织学确诊的HCC患者和780例相同地区、年龄、性别和民族频数匹配的非肿瘤患者。运用Taq Man MGB探针等位基因分型技术进行COX-2基因单核苷酸多态性的检测,以χ2检验和非条件Logistic回归模型分析比较病例和对照两组间各位点基因型频率分布的差异及其与HCC患病风险的关系,并进一步探讨基因-环境的交互作用对HCC患病风险的影响。结果:COX-2基因单位点-1195G>A或8473T>C多态与HCC患病风险无统计学相关性(显性模型下SNP-1195G>A:校正OR=1.32,95%CI:0.94~1.85;SNP8473T>C:校正OR=0.87,95%CI:0.64~1.18)。分层分析显示,显性模型下COX-2基因-1195G>A位点GA+AA基因型增加年龄<55岁者患HCC的风险(校正OR=1.56,95%CI:1.03~2.37),而8473T>C位点TC+CC基因型可降低女性患HCC的风险(校正OR=0.50,95%CI:0.25~0.99)。进一步交互作用分析显示,COX-2基因-1195G>A位点与年龄、8473T>C位点与性别分别存在交互作用(P=0.002;P=0.007)。结论:COX-2基因-1195G>A或8473T>C位点SNP的单独效应可能与HCC易感性无关联,但是-1195G>A与年龄、8473T>C位点与性别存在交互作用,影响HCC的患病风险。     

EGFR基因rs763317多态性与胃癌遗传易感的相关性研究

目的:探讨EGFR基因第一内舍子区rs763317位点单核苷酸多态性(SNP)与江西地区汉族人群胃癌遗传易感性的相关性.方法:应用MassARRAY(R)SNP分型技术检测138例胃癌患者和170名正常对照EGFR基因多态位点rs763317的基因型.用χ2检验统计分析病例组和对照组基因型和等位基因的频率;采用非条件Logistic回归分析,计算比数比(OR)和95%CI,评价多态性位点与胃癌遗传易感性的相关性.结果:EGFRrs763317多态位点AA、AG和GG基因型在胃癌人群中的分布频率为5.8%、52.2%和42.0%,与对照组(2.4%,31.8%和65.9%)相比差异有统计学意义,P≤0.001.与rs763317 GG基因型相比,携带AA或AG基因型的个体能显著增加患胃癌的发病危险(OR=3.909,95%CI:1.108～13.786;OR=2.540,95%CI:1.565～4.123).等位基因A在胃癌患者的分布频率显著高于正常对照组(OR=3.277,95%CI:1.103～9.738).结论:首次发现EGFR基因第一内含子区rs763317位点多态性与江西地区汉族人群胃癌的遗传易感性相关.     

XRCC1基因单核苷酸多态性与食管癌易感性的关系

目的探讨X线修复交叉互补基因(X-ray cross complementing group1,XRCC1)单核苷酸多态性(single nucleotide polymorphism,SNPs)与食管癌易感性及临床病理的关系。方法应用Sequenom MassARRAY时间飞行质谱系统对200例食管癌及200例对照者XRCC1基因10个多态位点进行基因型分型。统计分析基因型频率和食管癌易感性的关系,统计基因多态与食管癌临床病理之间的关系。结果 XRCC1基因10个多态位点,rs25491位点、rs3213242位点没有多态性。条件Logistic回归分析显示,rs25487位点在显性模型中等位基因频率在病例组和对照组间差异有统计学意义(OR=1.558,95%CI=1.020-2.381,P=0.040);rs1799778位点在显性模型中等位基因频率在病例组和对照组间差异有统计学意义(OR=1.558,95%CI=1.019-2.381,P=0.041);rs2682585位点基因频率在病例组和对照组间差异有统计学意义(OR=14.313,95%CI=5.188-39.489,P=0.000);其余位点两组间差异无统计学意义。没有发现有意义的单体型。未发现基因多态与食管癌临床病理特征之间的关系。结论 XRCC1基因SNP位点rs2682585、rs25487和rs1799778与食管癌发病风险有显著相关性,很可能是决定食管癌个体遗传易感性的重要因素,以上3个SNP位点与食管癌临床病理特征之间无相关性。     

江苏淮安人群食管癌发病危险与易感基因多态性

目的探讨江苏淮安食管癌高发地区人群食管癌相关代谢酶基因与DNA修复酶基因的分布特征,为食管癌的病因学研究及该地区人群食管癌一级预防提供依据.方法通过1:1配对病例-对照研究,应用PCR-RFLP技术分析106对原发性食管癌患者及其对照样本代谢酶基因CYP1A1、CPY2E1、GSTM1、GSTT1和DNA修复酶基因XPD、XRCC1的多态性.结果CYP1A1、CYP2E1、GSTM1、GSTT1基因多态性与淮安人群食管癌易感性升高之间没有明显相关性.XPD基因多态性和XRCC1基因194位点多态性未见与食管癌易感性相关;XRCC1基因399位点的多态性与食管癌易感性相关,携带突变纯合子Gln/Gln的个体患食管癌的易感性显著高于对照人群(OR=3.447,95%CI=1.078～11.026,P=0.029).代谢酶基因与DNA修复酶基因在食管癌发生中交互作用的分析发现,CYP2E1基因突变基因型与GSTT1基因缺失型同时存在的个体,其患食管癌的危险性下降(OR=0.305,95%CI=0.116～0.802);同时,XRCC1基因194位点与399位点的突变基因型也可使食管癌发生的危险性有所降低(OR=0.329,95%CI=0.121～0.897).结论XRCC1基因399位点多态性与淮安人群食管癌易感性有关;相关基因之间存在一定的交互作用,这种交互作用对基因功能的影响及其在食管癌发生中的意义值得深入探讨.     

p73基因多态性与食管癌、贲门癌遗传易感性的关系

背景与目的:p73作为一种抑癌基因,其第二外显子非编码区存在两个单核苷酸多态性(G4C14-A4T14),可以形成茎环结构而影响基因表达。本研究旨在探讨河北省食管癌高发区人群中这两个连锁多态性与食管癌、贲门癌易感性的关系。方法:采用病例-对照研究,以聚合酶链反应-限制性片段长度多态性方法,分析348例食管癌患者、259例贲门癌患者和630例健康对照者的p73基因多态性。结果:具有上消化道肿瘤家族史可明显增加食管癌和贲门癌的发病风险,经性别、年龄和吸烟状况校正的OR值分别1.68(95%CI=1.28～2.20)和1.68(95%CI=1.24～2.26)。p73G4C14-A4T14基因型及等位基因型在食管癌患者、贲门癌患者和健康对照中总体分布差异无显著性。在根据吸烟状况和上消化道肿瘤家族史进行分层分析,发现在无上消化道肿瘤家族史亚组中,携带GC/AT基因型明显增加贲门癌的发病风险(OR=1.71,95%CI=1.14～2.57),而其他亚组中未见p73G4C14-A4T14多态性增加食管癌、贲门癌的发病风险。结论:p73G4C14-A4T14多态性中,携带GC/AT基因型明显增加河北省食管癌高发区无上消化道肿瘤家族史人群贲门癌的发病风险。     

DNA修复基因XPD G312A多态性与肺癌易感性关系的meta分析

背景与目的已有的研究结果显示DNA修复基因XPD G312A多态位点与肺癌发生存在相关性,但研究结果尚未有一致性结论。本研究旨在通过meta分析的方法,综合评价DNA修复基因XPD G312A多态位点与肺癌发病风险的相关性。方法检索PUBMED、EMBASE、清华CNKI全文数据库、万方全文数据库中XPD基因G312A多态位点与肺癌易感性关系的病例对照研究。对符合纳入标准的研究用meta分析的方法进行数据合并,采用RevMan5.0和STATA11.0评价研究间异质性,计算合并OR值及95%CI。并进行敏感性分析和发表偏倚检验。结果共纳入18项研究,累计病例6554例,对照8322例。总体人群中A等位基因及AA基因型携带者肺癌风险明显升高(A vs G:OR=1.06,95%CI:1.00-1.12;AA vs AG+GG:OR=1.20,95%CI:1.06-1.36;AA vs GG:OR=1.19,95%CI:1.04-1.36)。亚洲人群中,AA基因型携带者肺癌风险明显升高(AA vs AG+GG:OR=7.15,95%CI:1.90-26.94;AA vs GG:OR=7.20,95%CI:1.91-27.15)。高加索人群中,AA基因型携带者肺癌风险升高(AA vs AG+GG:OR=1.15,95%CI:1.01-1.31)。结论XPD312A等位基因为肺癌发生的风险等位基因,AA基因型携带者肺癌风险升高,尤其在亚洲人群这种影响更为明显。     

MAP3K1及LSP1基因单核苷酸多态与中国北方汉族绝经前妇女乳腺癌风险相关性

目的:探讨MAP3K1及LSP1基因单核苷酸多态与中国北方汉族绝经前妇女乳腺癌风险的关系。方法:采用多重单碱基延伸单核苷酸多态性分型技术(Snapshot)分析方法,检测280例绝经前乳腺癌患者和287例绝经前正常对照者MAP3K1基因rs889312和LSP1基因rs3817198多态性位点基因型,并比较不同基因型与乳腺癌风险的关系。结果:MAP3K1基因rs889312和LSP1基因rs3817198多态性位点基因型频率在乳腺癌和对照样本之间未存在显著差异(P=0.937、P=0.323)。Logistic回归分析结果显示,对于MAP3K1的rs889312位点,与AA携带者相比,AC携带者、CC携带者和AC+CC基因型携带者与乳腺癌的患病危险无关(OR=0.814,95%CI=0.537-1.236,P=0.335;OR=0.999,95%CI=0.627-1.594,P=0.998;OR=0.876,95%CI=0.591-1.298,P=0.509);对于LSP1的rs3817198位点,与TT携带者相比,CT携带者、CC携带者和CT+CC基因型携带者与乳腺癌的患病危险无关(OR=0.832,95%CI=0.565-1.223,P=0.349;OR=0.651,95%CI=0.108-3.936,P=0.640;OR=0.839,95%CI=0.573-1.229,P=0.369)。结论:上述两个基因MAP3K1和LSP1位点多态性与中国北方汉族绝经前妇女乳腺癌易感性之间无明显相关性。     

ATM基因单核苷酸多态性与鼻咽癌易感性及复发的相关性

目的:探讨ATM基因单核苷酸多态性与鼻咽癌易感性与复发的关系.方法:采用病例对照研究,采集来自北方地区不同医院的鼻咽癌病人193例、正常人群231例静脉血,酚-氯仿法提取基因,Taqman real-time PCR方法及SDS软件对ATM基因型进行分型.SPSS 13.0软件包进行数据分析,以χ2检验比较SNPs基因型在病例与对照之间分布的差异,以单因素和多因素logistic回归计算比值比(odds ratio,OR)及95%可信区间(confidence interval,CI).结果:单因素分析显示,ATM126713位点的各基因型与鼻咽癌易感性不相关,P值0.075,OR值1.422,95%CI为0.963~2.199.但ATM126713位点的杂合基因型(G/A)经校正年龄、性别、吸烟状态后显示与鼻咽癌易感性相关,P值0.024,OR=1.636,95%CI为1.067~2.509.ATM126713位点各基因型与鼻咽癌复发不相关.结论:ATM126713位点G/A杂合型基因是鼻咽癌风险基因型,ATM126713位点各基因型与鼻咽癌复发无相关性.     

The protective role of polymorphism MKK4-1304 T>G in nasopharyngeal carcinoma is modulated by Epstein-Barr virus' infection status

MKK4 is a candidate tumor suppressor, which acts as a critical mediator of Epstein-Barr Virus (EBV)-induced c-Jun N-terminal kinase (JNK) activation. Functional polymorphism MKK4 -1304T>G has been showed to be protective in colorectal cancer or lung cancer. We hypothesized that genetic variants in the MKK4 promoter were associated with the risk of nasopharyngeal carcinoma (NPC). Two common polymorphisms in MKK4, -1304T>G and -1044A>T were genotyped in two independent case-control panels of Eastern and Southern Chinese populations, totally containing 1237 NPC and 1328 controls. We found that compared to the most common -1304TT genotype, carriers of variant genotypes (-1304TG+GG) were associated with a significantly reduced risk for NPC in total subjects (adjusted OR = 0.78; 95%CI = 0.67-0.94). Further stratification analysis showed that the protective effect was more pronounced in EBV negative status (adjusted OR = 0.51; 95%CI = 0.41-0.68) but restrained in those with EBV infection (adjusted OR = 1.05; 95%CI = 0.88-1.26), and that the -1304GG variant genotypes interacted with EBV negative status on reducing cancer risk (p = 0.011). However, no significant association was observed between the -1044A>T polymorphism and risk of NPC. Our data suggest that the protective role of genetic variant MKK4 -1304T>G is restrained in NPC with EBV infection. These findings implicate the role of EBV and MKK4 -1304 T>G interaction as a causative factor for the NPC.     

The association between −1304T>G polymorphism in the promoter of MKK4 gene and the risk of sporadic colorectal cancer in southern Chinese population

MKK4 (mitogen‐activated protein kinase kinase 4, NM_003010.2), which belongs to the mitogen‐activated protein kinase pathways, possesses functions in tumorigenesis. We hypothesized the genetic variants in MKK4 gene may alter its functions and thus cancer risk. In current hospital‐based case‐control study of 706 patients with sporadic colorectal cancer (CRC) and 723 sex‐age–frequency‐matched control subjects in a southern Chinese population, we genotyped two polymorphisms of MKK4 promoter (i.e., ?1304T>G, rs3826392 and ?1044A>T, rs3809728) and assessed their associations with the risk of sporadic CRC. Compared with ?1304TT genotypes, ?1304TG had a significantly decreased risk of CRC (adjusted odds ratios [OR] = 0.56; 95% CI = 0.44–0.72; p = 3.53 × 10^?6), the ?1304GG carriers had a further decreased risk of CRC (OR = 0.40; 95% CI = 0.23–0.70; p = 1.32 × 10^?3), and there was a significant trend for an allele dose effect on risk of CRC (p_trend = 2.64 × 10^?7). The decreased risk associated with ?1304G variant genotypes (i.e., TG+GG) was more pronounced in the subjects older than 60 years (adjusted OR = 0.41; 95% CI = 0.29–0.57; p = 2.25 × 10^?7), in ever drinkers (adjusted OR = 0.41; 95% CI = 0.28–0.59; p = 2.42 × 10^?6). The age and alcohol drinking status interacted with ?1304G variant genotypes on reducing cancer risk (p values for interaction were 0.015 and 0.043, respectively). Western blotting analysis showed that the levels of Mkk4 protein in sporadic CRC neoplastic tissues were significantly higher in the carriers of ?1304G variant genotypes than that in those with ?1304TT genotypes. However, no significant association was observed between ?1044A>T polymorphism and risk of CRC. To the best of our knowledge, this is the first study of genetic variants in MKK4 and cancer susceptibility. Larger studies are needed to validate our findings. © 2009 UICC     

基质金属蛋白酶基因多态性与食管癌易感性的 Meta 分析

目的：探讨 MMP 基因多态性与食管癌易感性之间的关系。方法：使用 Pubmed、Web of science、Em-base、中国生物医学文献数据库、中国知网、万方数据库检索2015年5月以前 MMP1－16071G／2G、MMP2－1306 C ＞T、MMP9－1562 C ＞T 与食管癌易感性的相关病例－对照研究,采用 STATA 12．0软件进行 Meta 分析。结果：共纳入10篇文献,3159例食管癌患者和4405名正常对照者。MMP1－16071G／2G 多态性与高加索人食管癌的发生相关,与1G 等位基因相比,2 G 等位基因显著增加食管癌的患病风险（2G vs 1G,OR ＝1．38,95％CI ＝1．18～1．61,P ＜0．05）。但在亚洲人群的亚组分析中,未发现有统计学意义。MMP2－1306 C＞T 基因多态性中,相对于 C 等位基因,T 等位基因是食管癌的保护因素（OR ＝0．75,95％CI ＝0．65～0．85,P＜0．05）。而 MMP9－1562 C ＞T 多态性并没有影响食管癌的发生。结论：MMP1和 MMP2基因多态性可能与食管癌易感性相关,尚不能排除 MMP9在食管癌发病中的作用,仍需进一步研究。     

基质金属蛋白酶-7启动子（-181A/G）基因多态性与消化道肿瘤易感性的Meta分析

目的:评价基质金属蛋白酶-7（MMP-7）启动子（-181A/G）基因多态性与消化道肿瘤易感性的关系。方法:计算机检索各大医学数据库,对2017年7月前公开发表的关于MMP-7（-181A/G）基因多态性的病例对照研究进行Meta分析。结果:共19项研究符合纳入标准,累计病例数3 296例,对照组4 362例。从总体效应量分析,除隐性基因模型外,MMP-7（-181A/G）基因多态性与消化道肿瘤易感性有关,差异有统计学意义（G vs A,OR=1.25,95%CI:1.09~1.43,P=0.00;GG/AG vs AA,OR=1.25,95%CI:1.12~1.39,P=0.00;GG vs AA,OR=1.42,95%CI:1.03~1.94,P=0.03;AG vs AA,OR=1.21,95%CI:1.07~1.35,P=0.00）。进一步分层分析表明MMP-7（-181A/G）基因多态性与胃癌、食管鳞癌的易感性有关,但并不能确定是否增加结直肠癌的发生风险。按照种族进行亚组分析,提示MMP-7（-181A/G）基因多态性能够显著增加亚洲人群的消化道肿瘤的发生率。结论:MMP-7（-181A/G）基因多态性与消化道肿瘤有关,G等位基因增加了食管鳞癌、胃癌的发生风险。     

XRCC1-77T>C polymorphism and cancer risk: a meta- analysis

Variants of X-ray repair cross-complementing group 1 (XRCC1) are involved in the development of cancer, but studies investigating the association of XRCC1-77T>C polymorphism with cancer risk have reported conflicting results. To clarify the effect of the XRCC1 -77T>C polymorphism on cancer risk, we performed a meta-analysis by conducting searches of the published literature in PubMed, Embase and CBM databases. Finally, 13 studies were included into our meta-analysis, involving a total of 11, 678 individuals. Subgroup analyses were performed by ethnicity and cancer type. The results of this meta-analysis showed that there was significant association between the C variant of XRCC1-77T>C polymorphism and cancer risk in all four genetic comparison models (ORC vs. T =1.19, 95%CI 1.07-1.31, P = 0.001; OR homozygote model =1.28, 95%CI 1.07-1.52, P = 0.007; OR recessive genetic model =1.22, 95%CI 1.04-1.44, P = 0.015; OR dominant model =1.21, 95% CI 1.07-1.35, P = 0.001). In the subgroup analyses based on ethnicity, the association was still significant in the Asian population (all p values<0.001), but not in the Caucasian population (all p values > 0.05). Thus, the XRCC1 -77T>C polymorphism is associated with cancer risk, and individuals with XRCC1 -77C variant have a significantly higher cancer risk, particularly in the Asian population.     

XRCC1 Arg399Gln基因多态性与中国人群肝细胞癌易感性的Meta分析

目的 探讨XRCC1 Arg399Gln基因多态性与肝细胞癌（HCC）易感性的关系。方法 计算机检索PubMed、中国生物医学文献（CBM）、中国知网、万方及维普等数据库,收集有关XRCC1 Arg399Gln基因多态性与HCC易感性关系的病例对照研究,提取纳入文献的相关数据进行Meta分析,以病例组与对照组XRCC1 Arg399Gln各种基因模型的比值比（OR）为效应指标,发表偏倚采用Eggers检验和Beggs检验。结果 共17篇文献符合纳入标准,累计病例数3301例,对照组4156例。XRCC1 Arg399Gln基因多态性与中国人群HCC易感性有明显关联性（G/G vs. A/A：OR=1.32,95％CI：1.13～1.54,P=0.000;A/G vs. A/A：OR=1.25,95％CI：1.10～1.41,P=0.000;A/G+G/G vs. A／A：OR=1.22,95％CI：1.09～1.36,P=0000;G／G vs. A／A+A／G：OR=1.20,95％CI：1.04～1.39,P=0.014）。根据健康对照组来源不同的亚组分析中,所有地区或者控制人口来源医院的研究结果均显示,XRCC1 Arg399Gln 基因多态性与HCC易感性有明显关联性,但控制人口非医院来源的研究结果显示XRCC1 Arg399Gln 基因多态性与HCC易感性无明显关联性;根据地区不同分组的亚组分析中,在广西地区,除隐性遗传模型外（G/G vs. A/A+A/G：OR=1.25,95％CI：0.95～1.65,P=0.115）,其余遗传模型结果显示XRCC1 Arg399Gln基因多态性与广西地区HCC易感性有明显相关性（G/G vs. A/A：OR=1.47,95％CI：1.10～1.95,P=0.009;A/G vs. A/A：OR=1.35,95％CI：1.17～1.56,P=0.000;A/G+G/G vs.A／A：OR=133,95％CI：1.16～1.52,P=0.000）。结论 XRCC1 Arg399Gln 基因多态性可能增加中国人群HCC的易感性,尤其在广西地区。     

Associations of ERCC4 rs1800067 Polymorphism with Cancer Risk: an Updated Meta-analysis

Background: Results from previous studies concerning the association of ERCC4 rs1800067 polymorphismwith risk of cancer were inconsistent. To explore the exact relation with susceptibility, we conducted the presentmeta-analysis. Materials and Methods: Literature of electronic databases including PubMed, Web of Science,EMBASE, Wanfang and Chinese National Knowledge Infrastructure (CNKI) were systematically searched. ORsand their 95%CIs were used to assess the strength of associations between ERCC4 polymorphism and cancerrisk. Results: There was no significant association between ERCC4 rs1800067 AA or AG genotypes and overallrisk of cancer (AA vs. GG: OR=0.998, 95%CI=0.670-1.486, P=0.992; AG vs. GG: OR=0.970, 95%CI=0.888-1.061, P=0.508). A dominant genetic model also did not demonstrate significant association of (AA+AG)genotype carriers with altered risk of overall cancer (OR=0.985, 95%CI=0.909-1.068, P=0.719). In addition,no significant association was observed between A allele of ERCC4 rs1800067 A/G polymorphism and alteredcancer risk compared with G allele (OR=0.952, 95%CI=0.851-1.063, P=0.381). Subgroup analysis suggestedthat AA genotype carriers were significantly associated with decreased risk of glioma compared with wild-typeGG genotype individuals (OR=0.523, 95%CI=0.275-0.993, P=0.048). For subgroup of lung cancer, A allele ofERCC4 rs1800067 A/G polymorphism was significantly associated with decreased risk of lung cancer comparedwith G allele (OR=0.806, 95%CI=0.697-0.931, P=0.003). Conclusions: This meta-analysis indicated that ERCC4rs1800067 A/G polymorphism might not be associated with risk of overall cancer. However, individuals with theAA genotype were associated with significantly reduced risk of glioma compared with wild-type GG genotype;The A allele was associated with significantly reduced risk of lung cancer compared with G allele. Future largescalestudies performed in multiple populations are warranted to confirm our results.