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.     

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。     

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。     

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.     

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。     

CTLA-4启动子及外显子区域基因多态性与胃癌的相关性研究

目的 探讨细胞毒性T淋巴细胞相关抗原4（CTLA-4）基因外显子49位点及启动子1722位点单核苷酸多态性（SNP）与青岛地区人群胃癌发病率的相关性。方法 采用聚合酶链反应-限制性片段长度多态法（PCR-RFLP）检测青岛地区胃癌患者、萎缩性胃炎及健康对照组患者中CTLA-4+49A／G及-1722T／C基因多态性的分布,并分析其多态性与胃癌临床病理特征的关系。结果 萎缩性胃炎组及胃癌组CTLA-4外显子49位点AG及GG基因型的分布频率显著高于健康对照组（P＜0.05）,携带AG及GG基因型者较携带AA基因型者罹患胃癌的风险分别增加至2.63倍（95％CI：1.053～6.542）及5.69倍（95％CI：2.262～14.302）,且男性胃癌患者携带AG及GG基因型明显增加。与健康对照组相比,胃癌组及萎缩性胃炎组的CTLA-4启动子1722位点各基因型分布差异无统计学意义（P＞0.05）,其多态性与胃癌患者的性别、年龄、肿瘤分化程度及TNM分期无相关性。结论 CTAL 4+49A／G基因多态性与胃癌的遗传易感性相关。     

肿瘤坏死因子α-308基因多态性与非霍奇金淋巴瘤易感性的Meta分析

目的 探讨肿瘤坏死因子α(TNF-α)-308G＞A基因多态性与非霍奇金淋巴瘤(NHL)易感性的关系.方法 在PubMed、中国知网、万方数据知识服务平台等数据库,检索淋巴瘤(或lymphoma)和肿瘤坏死因子(tumor necrosis factor或TNF)、基因多态性(polymorphism或SNP或variant或mutation),获取相关文献,采用固定效应模型或随机效应模型进行数据合并统计.发表偏移的评估采用Begg漏斗图和Egger检验.结果 共纳入15篇文献,包含9 738例NHL患者和10 854例对照人群.对入选文献数据进行综合分析,纯合子基因模型(AA比GG:OR=1.55,95％CI 1.30 ～ 1.86,I2=42.4％)和隐性基因模型(AA比AG+GG:OR=1.53,95％CI 1.27～1.83,I2=41.8％)的统计结果显示,TNF-α-308 AA基因可能增加NHL的发病风险.按种族来源不同进行分层分析,结果表明A等位基因可增加高加索人群罹患NHL的风险(A比G、AA比GG、AG比GG、AA比AG+GG、AA+AG比GG),但可降低亚裔人群的发病风险(A比G、AG比GG、AA+AG比GG).结论 TNF-α-308 G＞A基因多态性与NHL的发病风险相关.     

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.     

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。     

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 cytotoxic T lymphocyte antigen-4 +49A/G, −1722T/C,and −1661A/G polymorphisms and cancer risk: a meta-analysis

Cytotoxic T lymphocyte antigen-4 (CTLA-4), a key gene that contributes to the susceptibility and clinical course of cancer, is an important down-regulator of T cell activation and proliferation. The +49A/G polymorphism is commonly studied because of its association with cancer risks. However, other polymorphisms, such as ?1722T/C and ?1661A/G, have not been studied in detail. We performed a meta-analysis using 43 eligible case–control studies with a total of 19,089 patients and 21,388 controls to examine the association between CTLA-4 +49A/G, ?1722T/C, and ?1661A/G polymorphisms and cancer risk. We searched the PubMed and EMBASE databases for all articles published up to July 17, 2013. Individuals with the +49 A allele (AA/AG vs. GG, odds ratio (OR)?=?1.21, 95 % confidence interval (95 % CI)?=?1.16–1.27) and ?1661 G allele (AG/GG vs. AA, OR?=?1.52, 95 % CI?=?1.34–1.73) had increased cancer risk. However, no significant association between cancer risk and the ?1722T/C polymorphism was found (CC/CT vs. TT, OR?=?1.04, 95 % CI?=?0.92–1.16). In subgroup analysis for the +49A/G polymorphism, increased cancer risk remained in the subgroups of Asians (OR?=?1.25, 95 % CI?=?1.18–1.31), patients with breast cancer (OR?=?1.28, 95 % CI?=?1.15–1.42), and patients with lung cancer (OR?=?1.20, 95 % CI?=?1.07–1.35). For the ?1661A/G polymorphism, increased cancer risk remained in the subgroups of Asians (OR?=?1.52, 95 % CI?=?1.34–1.73), patients with breast cancer (OR?=?1.48, 95 % CI?=?1.07–2.03), and patients with oral cancer (OR?=?3.16, 95 % CI?=?1.84–5.45). However, no significant increase in cancer risk was found in the subgroups for the ?1722T/C polymorphism. In conclusion, the results suggest that +49A/G and ?1661A/G polymorphisms in CTLA-4 are risk factors for cancers, whereas the ?1722T/C polymorphism is not associated with an increased risk of cancer.     

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.     

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。     

甘肃汉族妇女XRCC1和CCNH基因多态性与乳腺癌及乳腺良性肿瘤易感性研究

目的： 研究甘肃地区汉族妇女XRCC1 rs25487、CCNH rs2234942基因多态性与乳腺癌及乳腺良性肿瘤发病的相关性。方法：选取经病理组织学确诊的乳腺癌、乳腺良性肿瘤各101例,匹配相同数量健康人作对照。使用聚合酶链式反应-限制性片段长度多态分析技术(PCR-RFLP)对XRCC1、CCNH进行基因型分析,通过Logistic回归分析不同基因型和临床病理特征与乳腺癌发病的风险性关系,通过χ2检验比较两种基因位点不同基因型的初潮年龄、发病年龄与乳腺癌和乳腺良性肿瘤的相关性。结果：Logistic回归分析发现XRCC1 rs25487位点GG基因型携带者的妇女罹患乳腺癌的危险性增加(P=0.001, OR=6.39, 95%CI： 2.18～ 18.65);临床病理免疫组化分析显示,XRCC1基因 rs25487位点携带AA/AG基因型者,在PR+与PR-乳腺癌组织间的分布差异有显著性(P=0.04,OR=0.29);携带AG/GG基因型者,在Her-2+与Her-2-乳腺癌组织间的分布差异有显著性(P=0.008, OR=0.45)。χ2检验显示,乳腺癌和乳腺良性肿瘤患者XRCC1 rs25487位点GG/AG基因型携带者的初潮年龄差异有显著性(P=0.001、0.043);乳腺癌和乳腺良性肿瘤患者CCNH rs2234942位点GG基因型携带者的初潮年龄差异有显著性(P=0.049);乳腺癌和乳腺良性肿瘤患者XRCC1 rs25487和CCNH rs2234942位点GG基因型携带者,发病年龄差异有显著性(P=0.019、0.048)。结论：XRCC1 rs25487 GG基因型将会增加乳腺癌的发病风险,XRCC1 rs25487位点携带AA/AG基因型者,在PR+时乳腺癌的发病风险下降;携带AG/GG基因型者,在Her-2+时可能降低乳腺癌的发病风险。     

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.     

Cyclin D1 G870A polymorphism and breast cancer risk: a meta-analysis involving 23,998 subjects

Cyclin D1 (CCND1) plays an essential role in tumor development and progression through regulating the cell transition from G1 to the proliferative S phase. The CCND1 G870A polymorphism has been associated with an increased susceptibility to squamous cell carcinoma of the head and neck, bladder, prostate, and gastric cardiac cancers. There are a number of studies that explored the relationship between CCND1 G870A polymorphism and breast cancer risk, with inconsistent conclusions. In order to better define the predictive value of CCND1 G870A polymorphism in breast cancer, we searched PubMed and EBSCO for relevant publications. A total of 13 studies were indentified, which included 11,235 cases and 12,763 controls. We calculated the summary odds ratios and the corresponding 95% confidence interval. Our meta-analysis showed that carriers of AA genotype have a significantly higher risk in developing breast cancer compared with that of GG genotype (OR = 1.08, 95% CI = 1.01-1.17, p > = 0.03) in overall population. Furthermore, in subgroup analysis, CCND1 G870A polymorphism was associated with a marginally increased risk of breast cancer for Chinese compared to Caucasian populations with an OR = 1.14, 95% CI = 1.00-1.20, p-trend = 0.06 for AA + GA versus GG, if the controls were hospital-based population with an OR = 1.21, 95% CI = 0.99-1.47, p = 0.06 for AA versus GG and if the distributions of genotypes in control groups were consistent with the Hardy-Weinberg equilibrium (HWE) with an OR = 1.08, 95% CI = 1.00-1.15, p = 0.04 for AA versus GA + GG. Our meta-analysis represents the largest study to date indicating that the G870A polymorphism in CCND1 confers an increased risk for breast cancer. Further studies are warranted to explore the preventive measures to detect and manage the breast cancers attributable to the G870A polymorphism.