CTLA-4+49A／G基因多态性与乳腺癌易感性的Meta分析

目的 探讨细胞毒性T淋巴细胞相关抗原4（CTLA-4）+49A／G基因多态性与乳腺癌易感性的关系。方法 计算机检索PubMed、MEDLINE、Web of Science、EMBASE、中国知网及万方等数据库,检索时间截止于2014年6月。收集关于CTLA-4+49A／G基因多态性与乳腺癌易感性关系的研究,由2名评价者按照纳入和排除标准独立选择文献、提取资料、评价质量。采用RevMan 5.1软件进行Meta分析,计算比值比（OR）及其95％可信区间（CI）并行敏感性分析和发表偏倚评估。结果 最终纳入5篇文献,包括3237例乳腺癌患者和3242例对照人群。纳入数据在AA vs. GG、AG vs. GG、AG／AA vs. GG和A vs. G基因型的比较中均无异质性。各模型Meta分析结果显示,CTLA-4+49A／G基因多态性与乳腺癌易感性有统计学意义（AA vs.GG：OR=1.49,95％CI：1.10～2.00;AG vs.GG：OR=1.23,95％CI：1.10～1.37;AG／AA vs.GG：OR=1.27,95％CI：1.14～1.40;A vs.G：OR=1.19,95％CI：1.11～1.29）。结论 CTLA-4+49A／G基因多态性与乳腺癌易感性有关,值得进一步研究。     

IL-10 基因-1082A ＞G位点多态性与非霍奇金淋巴瘤易感性的Meta分析

目的:用Meta分析法评价IL-10基因-1082A＞G位点的多态性与非霍奇金淋巴瘤(non-Hodgkin lymphoma,NHL)易感性的相关性.方法:利用计算机检索PubMed、EMBASE、Web of Science、中国生物医学文献数据库、中文科技期刊全文数据库、中国期刊全文数据库和万方数据库,检索日期自各数据库建库到2017年1月止,全面检索IL-10基因-1082A＞G位点的多态性与NHL易感性的病例对照研究文献,采用STATA 12.0统计软件进行Meta分析.结果:最终纳入16篇病例对照研究文献进行Meta分析,共计4 718例NHL患者和3 877例健康对照人员.分析结果显示,IL-10基因-1082A＞G位点在等位基因模型(A vs G∶OR=1.12,95％ CI=1.04～1.21)、共显性模型(AA vs AG:OR=1.27,95％ CI=1.06～1.52)、相加模型(AA vs GG:OR=1.22,95％ CI=1.06～1.40)和显性模型(AA vs AG+GG:OR=1.29,95％ CI=1.08～1.53)下与NHL易感性有关;而在隐性模型(GG vs AA+AG:OR=1.11,95％ CI=0.92～ 1.34)与NHL易感性无关.结论:IL-10基因-1082 A＞G位点多态性可能与NHL易感性相关.     

pre-miR-27a基因rs895819多态性与大肠癌易感性的Meta分析

目的 近年来,有关pre-miR-27a基因rs895819位点多态性与大肠癌易感性关系的研究日益增多,但结论并不一致.本研究从循证医学角度,综合评价pre-miR-27a基因rs895819位点多态性与大肠癌易感性的关系.方法 通过检索数据库PubMed、Cochrane Library、EMBASE以及中国知网数据库、万方数据库,收集有关pre-miR-27a基因rs895819位点多态性与大肠癌罹患风险关系的病例-对照研究.检索时间1998-01-01-2015-11-01.依据文献纳入及排除标准筛选相关文献,提取基本数据信息并进行文献质量评估.采用Stata 12.0软件行Meta分析,计算合并OR值和95％CI,并进一步行亚组分析和敏感性分析.结果 最终纳入6个病例-对照研究(包括2 025例大肠癌患者和2 320例非肿瘤对照者).Meta分析结果显示,pre-miR-27a基因rs895819多态性与大肠癌罹患风险具有显著的相关性,GvsA:OR=1.18,95％CI=1.08～1.30;GG vs AA/AG:OR=1.52,95％CI=1.26～1.97;GG vs AA:OR=1.53,95％CI=1.26～1.86,P值均＜0.05.亚组分析结果发现,亚洲人群也有相似的结论,Gvs A:OR=1.21,95％CI=1.09～1.35;AG/GG vs AA:OR=1.15,95％CI=1.00～1.32;GG vs AA/AG:OR=1.57,95％CI=1.27～1.93;GG vs AA:OR=1.59,95％CI=1.27～1.98,P值均＜0.05.结论 pre-miR-27a基因rs895819多态性与大肠癌易感性之间具有相关性,并且GG基因型具有增加罹患大肠癌的风险.     

GSTP1 Ile105Val（A/G）多态性与进展期胃癌铂类药物化疗敏感性的Meta分析

目的 定量评价进展期胃癌患者中谷胱甘肽S转移酶pi（GSTP1）基因105氨基酸位点Ile/Val多态性与铂类药物化疗敏感性的关系.方法 检索中国期刊全文数据库（CNKI）、中文科技期刊全文数据库（VIP）、中国生物医学文献数据库（CBM）、万方数据库、PubMed、EMBASE、Cochrane Library,收集国内外公开发表的关于GSTP1 Ilel05Val基因多态性与胃癌铂类药物化疗敏感性关系的文献.临床有效（完全缓解＋部分缓解）作为评价化疗敏感性的指标.运用RevMan 5.2进行Meta分析,计算合并比值比（OR）及95％可信区间（CI）,运用Stata 12.0识别是否存在发表偏倚.结果 本研究纳入6项研究共计病例724例,Meta分析结果显示,各基因型间（GG＋GAvs AA：OR=2.38,95％ CI为1.29～4.38;GG vs GA＋ AA：OR=3.66,95％ CI为1.18 ～ 11.39;GG vs AA：OR=4.42,95％ CI为1.28～15.26）以及亚洲人群亚组（GG＋ GA vs AA：OR=2.93,95％CI为1.33 ～ 6.48）中GSTP1 Ilel05Val多态性与化疗敏感性的差异有统计学意义.结论 GSTP1 Ile105VaI（A/G）基因多态性可能与进展期胃癌铂类化疗药物敏感性相关.     

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。     

CCND1 G/A位点基因多态性与肝细胞癌发生风险相关性的Meta分析

目的探讨细胞周期蛋白D1(CCND1)G/A位点基因多态性与肝细胞癌(HCC)发生风险的相关性。方法利用Pub Med、CNKI和EMbase数据库系统检索:CCND1 G/A位点基因多态性与肝细胞癌发生风险相关性的病例-对照研究。以病例组与对照组CCND1 G/A位点各种基因模型的比值比(OR)及95%可信区间(CI)为效应指标,并用Egger检验和Begg检验进行发表偏倚评价。结果有7项研究符合纳入标准。共纳入1108例肝癌患者和1477例对照。Meta分析结果表明:CCND1 G/A位点基因多态性与肝细胞癌发生风险无明显相关性,其中(AA vs GG:OR=1.33,95%CI:0.98~1.82,P=0.07;GA vs GG:OR=1.07,95%CI:0.92~1.24,P=0.37;GA+AA vs GG:OR=0.93,95%CI:0.82~1.05,P=0.23;AA vs GG+GA:OR=1.08,95%CI:0.95~1.22,P=0.24)。结论基于目前研究结果,尚不能认为CCND1 G/A位点基因多态性与肝细胞癌发生风险有显著相关性。     

CCND1基因G870A位点多态性与宫颈癌易感性的Meta分析

目的:运用Meta分析方法研究CCND1基因G870A位点多态性与宫颈癌易感性的发生风险。方法:检索PubMed和CNKI数据库中有关CCND1基因G870A位点多态性与宫颈癌易感性的相关性研究,根据纳入标准提取文献数据,应用STATA 11.0软件以OR值和95%可信区间为效应指标,进行Meta统计分析,并对发表偏倚及检测敏感性进行检测。结果:纳入9篇对照研究,共计2638例宫颈癌患者和3651例健康对照人群,Meta分析结果显示,总人群中,CCND1基因G870A位点多态性与宫颈癌风险之间没有显著关联(GA vs GG:OR=1.07,95%CI=0.86-1.34,P=0.53,I2=57.6%;AA vs GG:OR=1.09,95%CI=0.79-1.51,P=0.59,I2=75.0%;(GA+AA) vs GG:OR=1.08,95%CI=0.86-1.36,P=0.49,I2=64.6%;AA vs (GG+GA):OR=1.07,95%CI=0.83-1.36,P=0.61,I2=73.3%)。在针对种族和对照人群来源设计的亚组分析中,仍没有发现CCND1基因G870A位点多态性和宫颈癌的发生风险具有相关性。结论:CCND1基因G870A位点多态性可能与宫颈癌的发生无关。     

细胞周期素D1 G870A基因多态性与胃癌易感性关系的Meta分析

摘 要：［目的］采用Meta 分析方法研究细胞周期素D1（CCND1）基因G870A多态性与胃癌易感性的关系。［方法］ 通过关键词与主题词检索PubMed,Ovid,CNKI,维普和万方数据库中有关CCND1基因G870A多态性与胃癌易感性的相关性研究,数据分析应用Review Manager 5.3和STATA 10.0 软件。［结果］ 纳入6篇文献,包括7个病例-对照试验研究,共计1283例胃癌患者为病例组与1760例非肿瘤患者为对照组。Meta分析结果显示,总人群中,CCND1基因G870A多态性与胃癌发生风险之间无显著相关性（A vs G：OR=0.90,95%CI：0.77～1.06,P=0.21;AA+AG vs GG：OR=0.85,95%CI：0.60～1.21,P=0.37;AG+GG vs AA：OR=1.15,95%CI：0.97～1.37,P=0.10）。在种族与肿瘤类型的亚组分层分析中,结果同样显示CCND1基因G870A多态性与胃癌的发生风险无明显相关性。［结论］ CCND1基因G870A多态性可能与胃癌的发生风险无关。     

微粒体环氧化物水解酶EPHX1基因多态性与肝细胞性肝癌易感性的Meta分析

目的探讨微粒体环氧化物水解酶编码基因EPHX1多态性与肝细胞性肝癌（HCC）遗传易感性的关系。方法按照制定的检索策略,枪索相关数据库中的文献,获取有关EPHX1基因多态性与HCC易感性的病例一对照研究,提取相关数据进行Meta分析。以病例组和对照组基因型分布的比值比（OR）为效应指标,对纳入文献进行异质性检验,应用Statal2．0软件以不同合并模型对各研究原始数据进行Meta合并,计算合并效应量OR值及其95％可信f）（间（CI）。结果共纳入9篇文献,EPHX1337T〉C多态位点的共8个研究,累计病例584例,对照989例。等位基因比较模型（CYST）的OR值为1．47（95％CI=1．26～1．72,P〈0．001）;纯合子比较模型（CC vs TT）的OR值为1．88（95％CI=1．40～2．52,P〈0．001）;隐性模型（CCV vs CT/TT）的OR值为1．73（95％CI=1．36～2．21,P〈0．001）。EPHX1416A〉G多态位点共6项研究,累计病例432例,对照699例。等位基因比较模型（GVSA）的OR值为0．75（95％CI：0．59～0．95,P=0．018）。结论EPHX1337T〉C多态位点CC基因型与HCC易感性升高有关;416A〉G多态位点等位基凶G可能降低HCC易感性,为保护基因型。     

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。     

Association between the Interleukin-17A -197G>A (rs2275913) Polymorphism and Risk of Digestive Cancer

Interleukin-17A (IL-17A) is a multifunctional cytokine which plays a crucial role in the initiation andprogression of cancer. To date, several studies have investigated associations between IL-17A -197G>A (rs2275913)polymorphism and digestive cancer risk, but the results remain conflicting. We here aimed to confirm the roleof this single nucleotide polymorphism (SNP) in susceptibility to digestive cancer through a systemic reviewand meta-analysis. Ten eligible case-control studies were identified by searching electronic databases, involving3,087 cases and 3,815 controls. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were usedto estimate the strength of the association. The results of overall analyses indicated that the variant A allele wasassociated with an increased risk of digestive cancer (AA vs GG: OR=1.51, 95%CI=1.18-1.93; AA vs GG+GA:OR=1.45, 95%CI=1.12-1.87; A vs G: OR=1.21, 95%CI=1.05-1.39). In subgroup analysis stratified by specificcancer type, elevated risk among studies of gastric cancer was found (AA vs GG: OR=1.68, 95%CI=1.24-2.28;AA vs GG+GA: OR=1.62, 95%CI=1.16-2.26; A vs G: OR=1.23, 95%CI=1.04-1.46). According to ethnicity, therewas evidence in the Asian populations for an association between this polymorphism and cancer risk (GA vs GG:OR=1.19, 95%CI=1.05-1.36; AA vs GG: OR=1.56, 95%CI=1.15-2.12; AA+GA vs GG: OR=1.28, 95%CI=1.13-1.44; AA vs GG+GA: OR=1.42, 95%CI=1.01-2.00; A vs G: OR=1.24, 95%CI=1.08-1.44), while in the Caucasianpopulations an association was found in the recessive model (AA vs GG+GA: OR=1.62, 95%CI=1.17-2.24). Inconclusion, the results of this meta-analysis suggest that the IL-17A -197G>A polymorphism contributes to anincreased risk of human digestive cancer, both in the Asian and Caucasian populations and especially for gastriccancer.     

The CCND1 G870A Gene Polymorphism and Brain Tumor Risk: a Meta-analysis

Background: In recent years, numerous studies have been performed to investigate the CCND1 G870Agene polymorphism impact on brain tumors susceptibility. Unfortunately, the results of previous studies wereinconsistent. Therefore, we performed a meta-analysis to derive a more precise estimation of any association.Materials and Methods: We conducted a search in PubMed, Embase and CNKI covering all published papersup to November, 2013. Odds ratios (ORs) and their 95% confidence intervals (95%CIs) were applied to assessassociations. Results: A total of 6 publications including 9 case-control studies met the inclusion criteria. Thepooled ORs for the total included studies showed significant association among comparison A vs G (OR= 1.246,95%CI= 1.092-1.423, p= 0.001), homozygote comparison AA vs GG (OR= 1.566, 95%CI= 1.194-2.054, p= 0.001),heterozygote comparison AG vs GG (OR= 1.290, 95%CI= 0.934-1.782, p= 0.122), dominant model AA/GA vsGG (OR= 1.381, 95%CI= 1.048-1.821, p= 0.022) and recessive model AA vs GA/GG (OR= 1.323, 95%CI= 1.057-1.657, p= 0.015) especially in glioma. Conclusions: CCND1 G870A polymorphism may increase brain tumorrisk, especially for gliomas. However, more primary large scale and well-designed studies are still required toevaluate the interaction of CCND1 G870A polymorphism with brain tumor risk.     

Association Analysis of GSTP1-rs1695 Polymorphism with the Risk of Oral Cancer: A Literature Review,an Updated Meta- Analysis,and a Structural Assessment

Background: This study aimed to investigate the association of rs1695 polymorphism in glutathione S-transferase P1 (GSTP1) with risk of oral cancer in a meta-analysis which was followed by a bioinformatics approach. Materials and methods: Related articles were collected through a systematic search in PubMed, Google Scholar, and EMBASE databases up to June 2022 and then screened. Finally, seven studies, including 1249 cases of oral cancer and 1861 healthy individuals, were included in our meta-analysis. Seven different genetic models including G vs. A, GG+GA vs. AA, GG vs. GA+AA, GA vs. GG+AA, GG vs. GA, GG vs. AA, and GA vs. AA were used for the calculation of odds ratio and 95% confidence interval in order to assess the association between GSTP1-rs1695 polymorphism and oral cancer risk. Also, the ethnicity-based stratified analyses were performed using the seven mentioned models. Some bioinformatics software was used to investigate the effect of rs1695 polymorphism on the primary, secondary, and three-dimensional structure of GSTP1. Results: Our results showed that rs1695 polymorphism was not associated with the risk of oral cancer in any seven genetic models (G vs. A: OR= 0.9331, 95%CI= 0.6339-1.3737, P= 0.726; GG vs. GA+AA: OR= 0.9112 , 95%CI= 0.6865-1.2093, P= 0.520; GG+GA vs. AA: OR= 0.9006, 95%CI= 0.5522-1.4690, P= 0.675; GA vs. GG+AA: OR= 0.8732, 95%CI= 0.5763-1.3230, P= 0.522; GG vs. AA: OR= 0.9516, 95%CI= 0.5503-1.6456, P= 0.859; GG vs. GA: OR= 1.0645, 95%CI= 0.7891-1.4359, P= 0.683; GA vs. AA: OR= 0.8825, 95%CI= 0.5499-1.4162, P= 0.604). Also, we did not observe any significant associations in ethnicity-based stratified analyses. But bioinformatics studies have shown that this polymorphism can alter the physicochemical properties and secondary structure of the protein. Conclusions: Based on results, the rs1695 polymorphism could not be considered a risk factor for oral cancer.     

The CCND1 G870A Gene Polymorphism and Leukemia or Non-Hodgkin Lymphoma Risk: a Meta-analysis

In recent years, mounting evidence has indicated that the CCND1 G870A gene polymorphism, which impacts the mitotic cell cycle, may influence leukemia or non-Hodgkin lymphoma risk. Unfortunately, the previous results were inconsistent. Therefore, a meta-analysis was performed to obtain a more precise estimation of any association. We conducted a search in PubMed, Embase and CNKI covering all published papers up to March, 2014. A total of 9 publications including 10 case-control studies met the inclusion criteria. Odds ratios (ORs) and their 95% confidence intervals (95%CIs) were applied to assess association. The pooled ORs showed significant association in non-Hodgkin lymphoma (comparison A vs G: OR= 1.114, 95%CI=1.053-1.179, p=0.000; homozygote comparison AA vs GG: OR=1.245, 95%CI=1.110-1.396, p=0.000; heterozygote comparison AG vs GG: OR=1.095, 95%CI=1.000-1.199, p=0.05; dominant model AA/GA vs GG: OR=1.137, 95%CI=1.043-1.239, p=0.003; and recessive model AA vs GA/GG: OR=1.177, 95%CI=1.066-1.301, p=0.001). However, there was no association between the CCND1 G870A polymorphism and leukemia risk. In conclusion, the CCND1 G870A polymorphism may increase risk of non-Hodgkin lymphoma, but not leukemia. However, more primary large scale and well-designed studies are still required to evaluate the interaction of CCND1 G870A polymorphism with leukemia and non-Hodgkin lymphoma risk.     

The Cyclin D1 G870A Polymorphism and Colorectal Cancer Susceptibility: A Meta-analysis of 20 Populations

Purpose: Studies of the association between the cyclin D1 (CCND1) G870A genetic polymorphism and riskof colorectal cancer (CRC) have generated conflicting results. In order to derive a more precise estimation, ameta-analysis was here performed. Materials and methods: An extensive search of relevant studies was carriedout as a meta-analysis of twenty studies with 5,975 cases and 8,333 controls. Results: Overall, a significantlyelevated colorectal cancer risk was associated with variant allele 870A when all studies were pooled (AA vs.GG: OR = 1.23, 95%CI = 1.04-1.44; GA vs. GG: OR = 1.13, 95%CI = 1.01-1.26; dominant model: OR = 1.16,95%CI = 1.03-1.31). In the subgroup analysis by ethnicity, significantly increased risks were detected amongCaucasians (AA vs. GG: OR = 1.27, 95%CI = 1.04-1.44; and dominant model: OR = 1.17, 95%CI = 1.02-1.34).With stratification into sporadic CRC and hereditary nonpolyposis colorectal cancer (HNPCC), the formerdemonstrated increased cancer susceptibility (AA vs. GG: OR = 1.24, 95%CI = 1.04-1.48; dominant model:OR = 1.17, 95%CI = 1.04-1.33). However, no significant associations were found in either Asians or HNPCCpatients for any genetic model. Conclusion: The results suggest that the cyclin D1 870A allele is a low-penetrantrisk factor for development of sporadic colorectal cancer, especially among Caucasians.     

Association of Cytotoxic T-lymphocyte Antigen-4 Polymorphisms with Malignant Bone Tumors Risk A Meta-analysis

Background Previous studies have assessed the association between the Cytotoxic T-lymphocyte Antigen- 4(CTLA-4) polymorphism with the risk of malignant bone tumor, but the conclusions were inconsistent. We aimed to clarify association of cytotoxic T-lymphocyte antigen-4 polymorphisms with malignant bone tumors risk by performing a meta-analysis. Materials and Methods The databases including PubMed, EMBase databases and the Cochrane Library were searched to identify the eligible studies prior to January 30 2016. Odds ratio (OR) with 95% con dence interval (95%CI) were used to estimate the strengths of the association between the CTLA-4 polymorphism and the malignant bone tumor risks. The meta-analysis was performed by STATA 12.0. Results Four individual studies with a total of 1003 cases with malignant bone tumor and 1162 controls were included in our meta-analysis. The results of meta-analysis on those data demonstrated that CTLA-4 +49G>A polymorphism was associated with the risk of Ewing's sarcoma and osteosarcoma strongly (A vs. G OR1.36, 95%CI1.20- 1.54, p0.000; AA+AG vs. GG OR1.35, 95%CI1.14-1.61, p0.001; AA vs. GG OR2.24, 95%CI1.67-2.99, p0.000; AA vs. AG+GG OR2.00, 95%CI1.53-2.62, p0.000), but CTLA-4 -318C/T polymorphism was not associated with the risk of malignant bone tumor (C vs. T OR0.76, 95%CI0.76-1.08, p 0.262; CC+CT vs. TT OR0.70, 95%CI0.41-1.20, p0.198; CC vs. TT OR0.69, 95%CI0.40-1.19, p 0.183; CC vs. CT+TT OR0.92, 95%CI0.75-1.13, p 0.419). Subgroup analysis showed that there are signi cantly positive correlations between CTLA-4 +49G>A polymorphism and increased risks of malignant bone tumors in large size of sample (A vs. G OR1.347, 95%CI 1.172,1.548, p0.000; AA vs. GG OR2.228, 95%CI 1.608,3.085, p0.000), Ewing's Sarcoma or Osteosarcoma (A vs. G OR1.361, 95%CI 1.201,1.540, p0.000; AA vs. GG OR2.236, 95%CI 1.674,2.986, p0.000), and PCR-RFLP or Sequencing(A vs. G OR1.361, 95%CI 1.201,1.540, p0.000; AA vs. GG OR2.236, 95%CI 1.674,2.986, p0.000), but CTLA-4 -318C/T polymorphism was not associated with the risk of malignant bone tumors in diagnosis, genotype method, and sample size (all p>0.05). Conclusions CTLA-4 +49A/G variant was associated with an increased risk of developing the malignant bone tumors, such as Ewing's sarcoma and osteosarcoma. However, it failed to show the association between CTLA-4 -318C/T polymorphism and the risk of malignant bone tumors. Future large-scale studies remain to be done to con rm our conclusions.     

EGF61基因多态性与胃癌易感性Meta分析

目的：探讨表皮细胞因子（epidermalgrowthfactor,EGF）基因61A／G多态性与胃癌风险的相关性。方法：计算机检索PubMed、EMABSE、CJFD、CBM、CNKI、VIP及万方数据库,检索时间截至2013-0l-01,收集关于EGF 6lAG;基因多态性与胃癌易感性的病例＝对照研究。由2名评价者按照纳入和排除标准独立选择文献,提取资料,评价质量,采用RevMan5．1和Stata12．0软件进行Meta分析。结果：共纳入5个病例-对照研究,1388例患者和2642例对照。与基因型AA比较,AG＋GG和GG基因型可增加罹患胃癌风险,AG＋GGvsAA的OR=1．28,95％CI：1．03～1．59,Z=2．19,P=0．03;GGvsAA的OR—1．34,95％C1：1．05～1．70,Z=2．36,P=0．02。AG基因型与胃癌风险无关,AGvsAA的OR—1．22,95％CI：0．97～1．53,Z=1．68,P=0．09;与等位基因A比较,等位基因G可增加罹患胃癌风险．OR=1．27,95％CI：1．13～1．43,Z=3．98,P〈0．0001。人种和对照来源的亚组分析结果显示,在中国人、日本人群及医院来源的对照组中,EGF基因多态性与胃癌风险存在相关性。其中,中国人GGWSAG＋AA的OR=1．3／1,95％CI：1．11～1．61,Z=3．04,P=0．002;GGvsAA的OR=1．55,95％CI：1．09～2．20,Z=2．44,P=0．01。日本人GGvsAA的OR=1．68,95％CI：1．O5～2．69,Z＝2．16,P＝0．03。医院来源GGVSAG＋AA的0R_=1．54．95％C1：1．19～2．00,Z＝3．29,P＝0．001;GG圳AA的OR=1．81,95％CI：1．14～2．88,Z＝2．53,P＝0．01．结论：EGF61A／G基因多态性与胃癌易感性相关,等位基因（j与基因型AG＋GG和GG均可增加罹患胃癌的风险。