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。     

EPHX1 A415G基因多态性与胃肠道肿瘤易感性的Meta分析

目的 探讨微粒体环氧化物水解酶（EPHX1）A415G基因多态性与胃肠道肿瘤易感性的关系。方法 计算机检索PubMed、EMBASE、CBM、维普、万方及中国知网数据库,检索时间截至2013年5月,收集关于EPHX1 A415G基因多态性与胃肠道肿瘤易感性的研究。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STATA 110软件进行Meta分析,计算合并OR值及其95％CI并行敏感性分析和发表偏倚的评估。结果 最终纳入18篇文献,包括5852例胃肠道肿瘤患者和8710例对照人群。纳入的结果在GG vs. AA、GA vs. AA、GG/GA vs. AA和GG vs. GA/AA基因型的比较模型中均无异质性。各遗传模型Meta分析结果显示,EPHX1 A415G基因多态性与胃肠道肿瘤遗传易感性的关联性无统计学意义［GG vs. AA： OR=1.063,95％CI： 0.888～1.273;GA vs. AA： OR=0.935,95％CI： 0.867～1.009;GG/GA vs. AA： OR=0.948,95％CI： 0.882～1.020;GG vs. GA/AA： OR=1.091,95％CI： 0.913～1.304］。结论 EPHX1 A415G基因多态性与胃肠道肿瘤易感性之间无明显相关性。     

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。     

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。     

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.     

IL-10基因-592C>A多态性与宫颈癌易感性的Meta分析

目的:系统评估IL-10基因-592C>A多态性与宫颈癌易感性。方法:计算机检索Pubmed、EBSCO、Web of Science、中国知网、万方等数据库,搜集关于IL-10基因-592C>A多态性与宫颈癌易感性的相关研究文献。遵循文献纳入和排除标准,采用RevMan5.2软件进行Meta分析,计算、合并OR值及95%CI,最后进行偏倚分析和敏感性分析。结果:共纳入9篇文献,累计病例2 913例,对照2 037例。Meta分析结果显示,IL-10基因-592C>A多态性与宫颈癌总体发病风险之间未见显著关系(AA+CA vs CC:OR=0.92,95%CI=0.68~1.26,P=0.62;A vs C:OR=1.01,95%CI=0.82~1.23,P=0.95;AA vs CC:OR=1.04,95% CI=0.65~1.64,P=0.88;AA vs CA+CC:OR=1.08,95%CI=0.82~1.43,P=0.58;CA vs CC:OR=0.9,95%CI=0.67~1.19,P=0.45)。根据人群进行亚组分析结果显示,该基因多态性与亚洲人群及西方人群宫颈癌发病风险均无明显相关性（P>0.05）。结论:IL-10基因-592C>A多态性与宫颈癌易感性可能无关。     

肿瘤坏死因子-α基因G308A多态性与结直肠癌发病风险Meta分析

目的:评价肿瘤坏死因子-α基因G308A多态性位点对于结直肠癌患病风险的影响。方法:以"TNF-α-308、pol-ymorphism和colorectal cancer"作为检索词,检索2000-01-01-2011-09-01PubMed和Embase数据库中所有相关文献,提取其中数据进行统计分析,以比值比(OR)和95%可信区间(95%CI)评价该位点与结直肠癌易感性的关系。结果:最终筛选出9项关于该位点的研究,其中共包含了1 708例结直肠癌病例和1 754名对照。结果显示,A等位基因和G等位基因对于结直肠癌的患病风险差异无统计学意义,OR=1.89,95%CI为0.94～3.78;各种基因模式的对比也无阳性结果,GA对比GG,OR=1.16,95%CI为0.84～1.59,AA/GA对比GG,OR=1.26,95%CI为0.90～1.77,AA对比GA/GG,OR=1.75,95%CI为0.94～3.23。人种与对照来源进行的亚组分析中,也未发现有阳性结果。结论:肿瘤坏死因子-α基因G308A多态性可能对结直肠癌易感性无影响。建议今后应纳入更多的研究证据来明确该多态性位点与结直肠癌易感性的关系。     

谷胱甘肽硫转移酶A1(GSTA1)基因多态性与前列腺癌和膀胱癌易感性的Meta分析

目的 探讨谷胱甘肽硫转移酶A1(GSTA1)基因多态性与前列腺癌及膀胱癌易感性的关系.方法 通过检索PubMed等数据库,获取GSTA1基因多态性与前列腺癌或膀胱癌的文献9篇,对1989例病例和2246例对照进行meta分析,以比值比(OR)和95%可信区间(CI)作为效应指标.结果 各遗传模型的Meta分析显示:GSTA1基因多态性与前列腺癌易感性的相关性无统计学意义[(AA vs BB:OR=0.92,95%CI:0.68~1.23,P=0.56);(AB vs BB:OR=1.02,95%CI:0.86~1.21,P=0.83);(AA/AB vs BB OR=1.01,95%CI:0.86~1.17,P=0.93);(AA vs AB/BB:OR=0.91,95%CI:0.69~1.20,P=0.51)].各遗传模型的Meta分析显示:GSTA1基因多态性与膀胱癌易感性的相关性无统计学意义[(AA vs BB:OR=0.97,95%CI:0.71~1.33,P=0.85);(AB vs BB:OR=1.11,95%CI:0.93~1.31,P=0.25);(AA/AB vs BB OR=1.07,95%CI:0.92~1.25,P=0.37);(AA vs AB/BB:OR=0.87,95%CI:0.64~1.18,P=0.37)].结论 单独的GSTA1基因多态性不是前列腺癌和膀胱癌的易感因素.     

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。     

Current Evidence on Associations Between the MMP-7 (-181A>G) Polymorphism and Digestive System Cancer Risk

Matrix metalloproteinases (MMPs) degrade various components of the extracellular matrix and functionalpolymorphisms in encoding genes may contribute to genetic susceptibility to many cancers. Up to now, associationsbetween MMP-7 (-181A>G) and digestive system cancer risk have remained inconclusive. To better understandthe role of the MMP-7 (-181A>G) genotype in digestive cancer development, we conducted this comprehensivemeta-analysis encompassing 3,518 cases and 4,596 controls. Overall, the MMP-7 (-181A>G) polymorphism wasassociated with higher digestive system cancer risk on homozygote comparison (GG vs. AA, OR=1.21, 95% CI =1.12-1.60) and in a dominant model (GG/GA vs. AA, OR=1.16, 95% CI =1.03-1.46). On subgroup analysis, thispolymorphism was significantly linked to higher risks for gastric cancer (GG vs. AA, OR=1.22, 95% CI = 1.02-1.46; GA vs. AA, OR=1.82, 95% CI =1.16-2.87; GG/GA vs. AA, OR=1.13, 95% CI =1.01-1.27; GG vs. GA/AA,OR= 1.25, 95% CI = 1.06-2.39. We also observed increased susceptibility to colorectal cancer and esophagealSCC in both homozygote (OR = 1.13, 95% CI = 1.06-1.26) and heterozygote comparisons (OR = 1.45, 95% CI= 1.11-1.91). In the stratified analysis by controls, significant effects were only observed in population-basedstudies (GA vs. AA, OR=1.16, 95% CI=1.08-1.50; GA/AA vs. GG, OR=1.10, 95% CI=1.01-1.72). According to thesource of ethnicity, a significantly increased risk was found among Asian populations in the homozygote model(GG vs. AA, OR=1.40, 95% CI=1.12–1.69), heterozygote model (GA vs. AA, OR=1.26, 95% CI=1.02–1.51), anddominant model (GG/GA vs. AA, OR=1.18, 95% CI=1.08–1.55). Our findings suggest that the MMP-7 (-181A>G)polymorphism may be a risk factor for digestive system cancer, especially among Asian populations.     

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.     

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。     

Association between the HSPA1B ±1267A/G Polymorphism and Cancer Risk: a Meta-analysis of 14 Case-Control Studies

Background: Previous epidemiological studies have suggested a potential role of the HSPA1B±1267A/G polymorphism in risk of developing cancer. However, the results were inconsistent. Therefore, we performed this meta-analysis to summarize the possible association with cancer risk. Materials and Methods: We retrieved relevant articles from PubMed, EMBASE, ISI Web of Science, Chinese Biomedical Literature and Chinese National Knowledge Infrastructure. Studies were selected using specific criteria. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess those associations. All analyses were performed using STATA software. Results: Fourteen case-control studies, including 1, 834 cancer cases and 2, 028 controls were included in this meta-analysis. Overall, the results indicated that the G allele of HSPA1B gene ±1267A/G was significantly associated with an increased cancer risk in all genetic models (G vs A: OR=1.51, 95%CI 1.17-1.95, p=0.001; GG vs AA: OR=2.93, 95%CI 1.50-5.74, p=0.002; AG vs AA: OR=1.48, 95%CI 1.10-1.98, p=0.009; GG/AG vs AA: OR=1.69, 95%CI 1.22-2.33, p=0.001; GG vs AG/AA: OR=2.31, 95%CI 1.24-4.32, p=0.009). In the subgroup analysis stratified by ethnicity, a significant association was identified in Caucasians (G vs A: OR=1.35, 95%CI 1.08-1.69, p=0.008; GG/AG vs AA: OR=1.36, 95%CI 1.09-1.70, p=0.007), but not in Asians. In the stratified analysis by cancer types, individuals with the G allele showed an increased risk of hepatocellular carcinoma compared with carriers of the A allele (OR=2.40, 95%CI 1.47-3.91, p< 0.001). Inversely, individuals with the GG genotype showed a decreased risk of gastric cancer compared with carriers of the AG/GG genotypes (GG vs AG/AA: OR=0.39, 95%CI 0.20-0.70, p=0.007). Conclusions: This meta-analysis suggests associations between the HSPA1B ±1267A/G polymorphism and risk of cancer. However, this association might be Caucasian-specific and the G allele of this polymorphism probably increases risk of hepatocellular carcinoma while decreasing risk of gastric cancer. Further well-designed studies based on larger sample sizes are needed to validate these findings.     

MIF-173位点基因多态性与胃癌易感性的Meta分析

目的:探讨胃癌与巨噬细胞迁移抑制因子(macrophage migration inhibitory factor,MIF)基因173位点基因多态性之间风险的相关性。方法:计算机检索Embase、Cochrane、PubMed、中国生物医学文献数据库、中国知网、维普及万方数据库,检索时间截止至2018年3月4 日。收集胃癌的发生发展与MIF-173位点基因多态性的病例-对照研究。依据纳入标准和排除标准，由2名收集者独立获取文献，提取数据并予以评价其质量。RevMan 5.3软件进行系统分析。结果:一共有4个病例-对照研究被纳入研究中,其中有1 014 例患者和1 236 例对照者。系统分析最终结果显示,在3 个遗传模型中MIF基因173位点单核苷酸多态性与胃癌易感性的相关性差异具有统计学意义［显性遗传模型 CC+GC vs GG:OR=1.24,95%CI:1.04~1.47;隐性遗传模型CC vs GC+GG:OR=1.84,95%CI:1.15~2.95;共显性遗传模型CC vs GG:OR=1.87,95%CI:1.34~2.59］,在共显性遗传模型GC vs GG中,两者差异无统计学意义(OR=1.12,95%CI:0.94~1.35)。结论:MIF-173位点单核苷酸多态性与胃癌易感性明显相关,基因型CC+GC和CC会加大胃癌发生的风险。     

MTHFR基因C667T位点多态性与亚洲人群乳腺癌易感性的Meta分析

目的:采用Meta分析的方法定量评价亚甲基四氢叶酸还原酶（MTHFR）基因C667T位点的多态性与亚洲人群乳腺癌易感性的关系。方法:计算机检索PubMed、Web of Science、中国生物医学文献数据库、CNKI、重庆维普和万方数据库,搜索有关MTHFR基因C667T位点的多态性与亚洲人群乳腺癌易感性的研究,检索时间截止2017年2月。采用Stata 12.0软件进行统计分析。结果:共纳入24篇病例对照研究,共计7 268例乳腺癌患者,9 223例健康对照。Meta分析结果显示:MTHFR基因C667T位点的多态性均与亚洲人群乳腺癌易感性有相关性［CC vs CT:OR=0.70,95%CI（0.60,0.83）,P=0.001;CT vs TT:OR=0.87,95%CI（0.79,0.96）,P=0.05;CC vs TT:OR=0.79,95%CI（0.72,0.88）,P=0.002;CT+TT vs CC:OR=0.81,95%CI（0.76,0.87）,P=0.001;CC+CT vs TT:OR=0.85,95%CI（0.77,0.93）,P=0.003］。结论:MTHFR基因C667T位点的多态性增加了亚洲人群乳腺癌的易感性。