环氧化酶COX-2-765G>C多态与结直肠癌易感性关系的meta分析

目的:综合评价COX-2单核苷酸多态-765G>C与结直肠癌易感性的关系。方法:检索中国医学文献数据库和PUBMED,获得有关COX-2-765G>C多态与结直肠癌易感性的关系病例对照研究,并用me-ta分析的方法分析COX-2-765G>C多态与结直肠癌易感性的相关性,然后进行亚组分析、敏感性分析和文献的发表偏倚检验。结果:本次meta分析共纳入10篇文献,显性模型下GC+CC基因型相对于GG基因型的OR值为1.06(95%CI:0.94-1.19),没有统计学显著性意义;但亚洲人中GC+CC基因型相对于GG基因型的OR值为1.40(95%CI:1.11-1.76,P=0.004),具有统计学意义。结论:COX-2-765G>C多态与结直肠癌易感性没有统计学显著性关系,但在亚洲人群中GC+CC基因型与结直肠癌易感性的关系具有统计学显著性意义。     

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。     

DNA损伤修复基因XRCC3 Thr241Met多态与肺癌易感性关系的Meta分析

目的:探讨DNA损伤修复基因X射线交叉互补修复基因3(XRCC3)Thr241Met多态性与肺癌易感性的关系。方法:查找中国医学文献数据库和PubMed,以得到XRCC3基因Thr241Met多态与肺癌易感性关系的病例-对照研究,根据纳入和排除标准筛选符合条件的研究进行Meta分析,合并XRCC3基因Thr241Met多态与肺癌易感性关系的OR值,然后进行亚组分析、敏感性分析和文献的发表偏倚检验。结果:本次Meta分析共纳入13篇文献,累计病例2 986例,对照4 495例,显性模型下TM+MM基因型相对于TT(TM=Thr/Met)基因型OR值为0.96(95%CI为0.86~1.06),差异无统计学意义。结论:尚无足够证据证明XRCC3基因Thr241Met多态同肺癌易感性有关。     

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。     

MDM2启动子309位点多态性与肺癌易感性关系的Meta分析

目的:综合评价MDM2 (murine double minute 2)基因启动子309位点多态性与肺癌易感性的关系.方法:检索中国医学文献数据库和PubMed,以得到MDM2基因SNP309与肺癌易感性关系的病例对照研究,并用Meta分析的方法合并SNP309与肺癌易感性关系的OR值.然后进行亚组分析、敏感性分析和文献的发表偏倚检验.结果:本次Meta分析共纳入6篇文献,累计病例4276例,对照5318例,G等住基因相对于T等位基因OR值为1.11(95%CI为0.97～1.26,P=0.14),差异无统计学意义,但在未吸烟亚组中OR值为1.32(95%CI为1.15～1.52,P=0.000),差异有统计学意义.结论:MDM2基因309T>G多态与肺癌易感性的关系差异无统计学意义,但在未吸烟亚组中SNP309G等位基因是一个肺癌危险因子.     

乙醇和乙醛脱氢酶基因多态与男性结直肠癌的易感性

目的研究乙醇脱氢酶2(ADH2)和乙醛脱氢酶2(ALDH2)基因多态及饮酒习惯与男性结直肠癌易感性的关系。方法在江苏省进行了一项病例-对照研究(结直肠癌患者190例,人群对照222名),调查研究对象的生活习惯,抽取静脉血,提取白细胞DNA,采用聚合酶链反应(PCR)和变性高效液相色谱法(DHPLC)检测研究对象的ADH2Arg47His(G-A)和ALDH2Glu487Lys(G-A)的基因型。结果①ADH2A/A和ALDH2G/G基因型显著增加结直肠癌的易感性。在调整了年龄和吸烟状况后,ADH2A/A基因型者与携带G等位基因者相比,发生结直肠癌的危险性上升到1.61(95%CI:1.09~2.38);ALDH2G/G基因型者与携带A等位基因者相比,发生结直肠癌的危险性上升到1.79(95%CI:1.19~2.69)。②与ADH2G和ALDH2A等位基因携带者相比,同时携带ADH2A/A和ALDH2G/G基因型者发生结直肠癌的OR值上升到3.05(95%CI:1.67~5.57);与不饮酒的ADH2G等位基因携带者相比,拥有ADH2A/A基因型的饮酒者的OR值上升到3.44(95%CI:1.84~6.42);与不饮酒的ALDH2A等位基因携带者相比,拥有AL-DH2G/G基因型的饮酒者的OR值上升到2.70(95%CI:1.57~4.66)。结论ADH2和ALDH2基因多态性与男性结直肠癌的易感性相关。ADH2,ALDH2基因多态之间以及基因多态与饮酒习惯之间,在结直肠癌发生中存在显著的协同作用。     

MDM2启动子309位点多态性与乳腺癌易感性关系的Meta分析

[目的]综合评价MDM2（routine double minute2）基因启动子309位点多态性与乳腺癌易感性的关系。[方法]检索中国医学文献数据库和PubMed中MDM2基因SNP309与乳腺癌易感性关系的病例对照研究,并用Meta分析的方法合并SNP309与乳腺癌易感性OR值。然后进行其中有家族史的乳腺癌亚组分析,敏感性分析和文献的发表偏倚检验。[结果]Meta分析共纳入10篇文献,乳腺癌家族史组有3篇;累计病例7535例,对照8272例,G等位基因相对于T等位基因0R值为1．01（95％CI：0．96～1．06）。乳腺癌家族史组G等位基因相对于T等位基因OR值为1．06（95％CI：0．94～1．19）。[结论]MDM2基因309T〉G多态与乳腺癌易感性无统计学意义。     

细胞周期蛋白D1基因G870A 多态性与结直肠癌易感性的系统评价

 目的 综合评价细胞周期蛋白D1(Cyclin D1) 基因G870A多态性与结直肠癌易感性的关系.方法通过CNKI、PubMed、EMCC等数据库检索文献,获得有关Cyclin D1基因G870A多态性与结直肠癌危险性关系的研究结果,并通过Meta分析进行系统评价。所有文献均采用病例对照研究或者巢式病例对照研究,以OR值为效应指标, 基因型在对照群体中的分布均符合Hardy Weinberg 遗传平衡定律,对文献进行评价筛选、异质性检验。本次Meta分析共纳入23项研究,累计病例6 344例,对照9 018例,利用RevMan5.0对各研究原始结果进行统计处理, 对突变纯合子AA 和杂合子GA 基因型与纯合基因型GG 进行比较,并计算合并OR值及其95%可信区间(CI）。结果 AA和GA与GG基因型在病例组与健康对照组之间差异有统计学意义,OR= 1.10（95%CI：1.01～1.19, P=0.02）;按不同人群进行分层分析,亚洲人群OR= 1.11（95%CI：0.98～1.26, P=0.11）,美洲人群OR= 1.13（95%CI：0.97~1.32,P=0.12),欧洲人群OR= 1.06（95%CI：0.89～1.25, P=0.52）,大洋洲人群OR= 1.05（95%CI：0.80～1.38, P=0.73）;按不同对照进行分组分析,医院基础OR= 1.07（95%CI：0.95～1.20, P=0.28）,人群基础OR= 1.13（95%CI：1.01~1.26, P=0.04）。结论 Cyclin D1基因G870A 多态性与结直肠癌易感性总体分析在统计学上具有相关性,按不同人群进行分组分析,都不支持具有相关性;按不同对照进行分组分析,以医院基础不具有相关性,以人群为基础具有相关性。     

亚甲基四氢叶酸还原酶基因多态性与结直肠癌易感性的关系

目的:研究亚甲基四氢叶酸还原酶(methylenetetrahydrofolate reductase,MTHFR)基因C677T、A1298C多态性与结直肠癌易感性的关系。方法:在江苏省进行了一个病例-对照研究(结直肠癌患者315例,人群对照371例),调查研究对象的生活习惯,抽取静脉血,提取白细胞DNA,采用PCR-RFLP检测研究对象的MTHFR C677T、A1298C基因型。结果:1)男女合计的结直肠癌组、结肠癌组和直肠癌组与对照组之间的MTHFR C677T、A1298C基因型分布频度和等位基因频度差异无统计学意义,MTHFR C677T、A1298C基因多态与结直肠癌、结肠癌和直肠癌的易感性无显著相关。2)在男性中,结肠癌组MTHFR C677T T/T基因型的频度为24.6%,明显高于对照组的14.8%,但差异无统计学意义,χ2=3.42,P=0.064。与C677T C等位基因携带者相比,T/T基因型者发生结肠癌的危险性显著升高,其性别、年龄、居住地区及吸烟、饮酒和饮茶习惯调整后的OR为2.15(95%CI:1.07~4.33)。与同时携带MTHFR C677T C等位基因和A1298C A/A基因型者相比,男性的MTHFR C677T T/T和A1298C A/A基因型携带者发生结肠癌的危险性显著升高,其调整OR为2.64(95%CI:1.20~5.81),而他们发生直肠癌的危险性则明显降低,(调整OR=0.47,95%CI:0.22~1.03)。结论:MTHFR C677T基因多态可以影响男性结、直肠癌的易感性,MTHFR A1298C多态与C677T多态在对男性结、直肠癌易感性的影响中有协同作用。     

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.     

Genetic polymorphisms of cyclooxygenase-2 and colorectal adenoma risk: the Self Defense Forces Health Study

Cyclooxygenase (COX) is a key enzyme in the formation of prostaglandins, and an inducible isoform of COX, COX-2, has been implicated in colorectal carcinogenesis. This study investigated the relation of COX-2 polymorphisms (–1195G>A, –765G>C and 8160A>G) to colorectal adenomas in a case–control study of male officials in the Self Defense Forces (SDF). The study subjects were 455 cases of colorectal adenoma and 1052 controls with no polyps who underwent total colonoscopy. Genotypes were determined using the polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) method with genomic DNA extracted from the buffy coat. Statistical adjustment was made for age, hospital, rank in the SDF, body mass index (BMI), cigarette smoking, and alcohol intake. A statistically non-significant decrease in the risk of colorectal adenomas was observed for the AA versus GG genotype of –1195G>A polymorphism and for the GC versus GG genotype of –765G>C polymorphism. None had the –765CC genotype in either the case or control groups. No effect modification of overweight, smoking or alcohol use was observed for either –1195G>A or –765G>C polymorphism. The variant allele of the 8160A>G polymorphism was extremely rare. A haplotype of –1195G, –765G and 8160A alleles was associated with a modest increase in the risk (adjusted odds ratio [OR] 1.38, 95% confidence interval [CI] 0.99–1.91), and the increase was more evident for distal adenomas (adjusted OR 1.57, 95% CI 1.04–2.38). Another haplotype of –1195A, –765C and 8160A alleles showed an adjusted OR of 0.22 (95% CI 0.06–0.88). These findings add to evidence for the role of COX-2 in colorectal carcinogenesis and warrant further studies focusing on haplotypes. ( Cancer Sci 2008; 99: 576–581)     

Associations of functional polymorphisms in cyclooxygenase-2 and platelet 12-lipoxygenase with risk of occurrence and advanced disease status of colorectal cancer

Aberrant arachidonic acid metabolism by cyclooxygenase (COX)-2 and 12-lipoxygenase (LOX) has implicated in carcinogenesis. Genetic polymorphisms in COX-2 and 12-LOX might therefore affect susceptibility to colorectal cancer (CRC). To examine this hypothesis, genotypes of COX-2 -1290A>G, -1195G>A, -765G>C and 12-LOX 261Arg>Gln polymorphisms were determined in 1000 CRC patients and 1300 controls. Increased risk of developing CRC was associated with the COX-2 -1195GA [adjusted odds ratio (OR) = 1.24, 95% confidence interval (CI) = 1.00-1.54] and -1195AA (adjusted OR = 1.77, 95% CI = 1.38-2.25) genotypes compared with the -1195GG genotype. Similarly, the increased risk for CRC was also associated with the COX-2 -765GC genotype (adjusted OR = 1.73, 95% CI = 1.23-2.43) compared with the -765GG genotype. Consistent with the results of genotype analyses, the ORs for the A_(1195)-C_(765)-containing haplotypes were significantly higher than those for the G_(1195)-G_(765)-containing haplotypes (P < 0.01). Furthermore, the -1195A allele was further associated with advanced CRC, with adjusted ORs of Dukes D CRC against Dukes A CRC being 2.43 (95% CI = 1.15-4.97) and 2.66 (95% CI = 1.23-5.74) for the -1195GA and -1195AA genotypes, respectively. The increased risk of CRC was also associated with the 12-LOX 261Gln/Gln genotype compared with the Arg/Arg genotype (adjusted OR = 1.38, 95% CI = 1.09-1.74). Together, these observations indicate that inherited polymorphisms in arachidonic acid-metabolizing enzymes may confer susceptibility to CRC.     

Interaction of cyclooxygenase-2 promoter polymorphisms with Helicobacter pylori infection and risk of gastric cancer

Overexpression of cyclooxygenase (COX)-2 has been implicated in the development of cancer. This study aimed to evaluate the relationship between genetic variants in COX-2 promoter interacting with Helicobacter pylori and the susceptibility to gastric cancer (GC). Three COX-2 polymorphisms -1290A>G (rs689465), -1195G>A (rs689466), and -765G>C (rs20417) were genotyped in 323 GC patients and 944 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression model. In GC patients, the ORs were 2.33 (95% CI = 1.50-3.63) and 2.70 (95% CI = 1.68-4.33) for -1195AA and -765CG genotype carriers, respectively. Haplotype analysis showed all -1195A allele-containing haplotypes, except G(-1290)-A(-1195)-G(-765), were associated with increased risk for GC, compared with the A(-1290)-G(-1195)-G(-765) haplotype. Moreover, significant multiplicative and additive interactions were observed between H. pylori infection and all these three polymorphisms, and H. pylori-infected subjects carrying the variant allele of -1290A>G, -1195G>A, or -765G>C had increased risk of GC compared with non-H. pylori-infected subjects with wild-type allele (OR = 4.10, 95% CI = 1.90-8.83; OR = 3.46, 95% CI = 1.31-9.11; and OR = 3.32, 95% = 1.27-8.73, respectively). Our results suggested that the COX-2 promoter polymorphisms were associated with increased risk of GC, especially interacting with H. pylori infection.     

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。     

The association between cyclooxygenase-2 1195 G/A polymorphism and hepatocellular carcinoma: evidence from a meta-analysis

Cyclooxygenase-2 (COX-2) is proven to influence the carcinogenesis through immune response suppression, apoptosis inhibition, angiogenesis regulation, and tumor cell invasion. Previous studies assessing the association between COX-2 1195 G/A polymorphism and susceptibility to hepatocellular carcinoma (HCC) reported conflicting results. The objective of the study was to investigate the association between COX-2 1195 G/A polymorphism and HCC by a meta-analysis. PubMed, Embase, Web of Science, and Wangfang databases were searched for studies investigating the association between COX-2 1195 G/A polymorphism and HCC risk. The pooled odds ratio (OR) and its 95 % confidence interval (CI) were used to assess the strength of the association. Five studies with a total of 1,690 HCC cases and 1,961 controls were identified. Meta-analyses of total included studies showed that there was an obvious association between COX-2 1195 G/A polymorphism and HCC risk under two main genetic models (for AA versus GG, fixed-effects OR?=?1.45, 95 % CI 1.15–1.81, P?=?0.001, I ²?=?0.0 %; for AA/GA versus GG, fixed-effects OR?=?1.26, 95 % CI 1.05–1.51, P?=?0.011, I ²?=?0.0 %). Subgroup analysis by ethnicity showed that association was still obvious in Asians under two genetic models (for AA versus GG, fixed-effects OR?=?1.45, 95 % CI 1.16–1.82, P?=?0.001, I ²?=?21.7 %; for AA/GA versus GG, fixed-effects OR?=?1.27, 95 % CI 1.05–1.54, P?=?0.013, I ²?=?0.4 %). The evidence from the meta-analysis supports an association between COX-2 1195 G/A polymorphism and HCC risk in Asians. Further studies with large sample and careful design are needed to identify the possible association in Caucasians.     

DNMT3B -149 C>T and -579 G>T Polymorphisms and Risk of Gastric and Colorectal Cancer: a Meta-analysis

Background: Numerous studies have investigated associations of DNA methyltransferase (DNMT) -149 C>T and -579 G>T polymorphisms with gastric cancer (GC) and colorectal cancer (CRC) susceptibility; however, the findings are inconsistent prompting the present meta-analysis. Materials and Methods: Related studies were identified from PubMed, Google scholar, and SID until 10 October 2015. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of the associations. Results: Eleven studies were included based on the search criteria for CRC and GC related to the DNMT3B 149 C>T (3,353 cases and 4,936 controls) and DNMT3B 579 G>T (1,387 cases and 2,064 controls) polymorphisms. There was no significant association overall between DNMT3B -149 and 579 polymorphisms and the risk of cancer. In the stratified analysis by cancer type, DNMT3B 579G>T polymorphism was associated with the risk of CRC and GC. While the DNMT3B -149C/T polymorphism was related with a significantly increased risk of CRC in two tested models, dominant (GG+GT vs. TT: OR 0.51, 95 % CI 0.38-0.69; P = 0.00, Pheterogeneity=0.69, I2= 0 %) and heterozygote (GT vs. TT: OR 0.50, 95 % CI 0.37-0.69; P=0.00, Pheterogeneity=0.41, I2= 0 %), no evidence of any association with GC risk was observed as in the pooled analyses. Conclusions: More studies are needed to assess associations of DNMT3B -149C/T and DNMT3B 579G>T polymorphisms with cancer in different ethnicities with large population sizes to generate comprehensive conclusions     

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 LEP A19G polymorphism with cancer risk: a systematic review and pooled analysis

The results from the published studies on the association between leptin (LEP) genetic polymorphism and cancer risk are conflicting. The common A19G (rs2167270) genetic polymorphism has been reported to be functional and may contribute to genetic susceptibility to cancers. However, the association between LEP A19G (rs2167270) genetic polymorphism and cancer risk remains inconclusive. To better understand the role of LEP A19G (rs2167270) genetic polymorphism in global cancer, we conducted this comprehensive meta-analysis encompassing 5,679 cases and 7,443 controls. Overall, the LEP A19G (rs2167270) genetic polymorphism was associated with lower cancer risk. In the stratified analysis, significant associations were found between the LEP A19G (rs2167270) genetic polymorphism and colorectal cancer and non-Hodgkin’s lymphoma. For colorectal cancer, there was no significant association of LEP A19G (rs2167270) variant with this disease under heterozygous codominant model [odds ratio (OR)?=?1.11 (0.97–1.27)], dominant genetic model [OR?=?1.03 (0.91–1.17)], and additive genetic model [OR?=?0.94 (0.86–1.03)]; however, there was a marginal association under homozygous codominant model [OR?=?0.80 (0.66–0.97)] and recessive genetic model [OR?=?0.75 (0.63–0.90)]. For non-Hodgkin’s lymphoma, there was a significant association of LEP A19G (rs2167270) variant with the disease under homozygous codominant model [OR?=?0.74 (0.59–0.94)], recessive genetic model [OR?=?0.76 (0.61–0.94)], and additive genetic model [OR?=?0.89 (0.80–0.99)], but not under heterozygous codominant model [OR?=?0.95 (0.82–1.10)] and dominant genetic model [OR?=?0.91 (0.79–1.04)]. Moreover, a significantly decreased cancer risk was found in recessive genetic model among Latin American population. When stratified by study design, significantly elevated susceptibility to cancer was not found among any studies. No significantly differences in genotype method and sample size in cases were found among genotypes. These findings suggest that the LEP A19G (rs2167270) genetic polymorphism may decrease the susceptibility to cancers in colorectal cancer and non-Hodgkin’s lymphoma, when assuming a homozygote codominant model and a recessive genetic model among Latin American population. The phenomenon also indicates that the SNP functions as a recessive mutation, which needs to be verified or linked with functional studies.     

Association of Matrix Metalloproteinase1-1607 1G>2G Polymorphism and Lung Cancer Risk: An Update by Meta-Analysis

Objective: The association between matrix metalloproteinase1 (MMP1)-1607 1G>2G polymorphism and lung cancerrisk is still inconclusive and inconsistent. We conducted a meta-analysis to estimate the potential relationship betweenMMP1-1607 1G>2G polymorphism and lung cancer risk. Methods: The comprehensive searches of the PubMed, Webof Science, Medline, CBM, CNKI, Weipu, and Wanfang databases, published up to Nov 10, 2018. Statistical analyseswere performed with Review Manager 5.3 software. Results: A total of 14 relevant studies containing 6068 cases and5860 controls were included in the study. The results indicated that MMP1-1607 1G>2G polymorphism was significantlyassociated with increased lung cancer risk under four models: 2G vs. 1G model (pooled OR = 1.19, 95% CI = 1.05-1.34,P < 0.0001); 2G/2G vs. 1G/1G (pooled OR = 1.34, 95% CI = 1.09-1.64, P = 0.003); 2G/2G vs. 1G/1G+1G/2G (pooledOR = 1.26, 95% CI = 1.06-1.49, P < 0.0001); 2G/2G+1G/2G vs. 1G/1G (pooled OR = 1.21, 95% CI = 1.05-1.40, P= 0.01). Subgroup analyses showed that there was a higher increase in smoking status under three models: 2G/2Gvs. 1G/1G (pooled OR = 2.07, 95% CI = 1.14-3.77, P = 0.02); 2G/2G vs. 1G/1G+1G/2G (pooled OR = 1.71, 95% CI= 1.17-2.52, P = 0.006); 2G/2G+1G/2G vs. 1G/1G (pooled OR = 2.03, 95% CI = 1.14-3.62, P = 0.02). In addition,subgroup analyses by ethnicity further identified the significant association in Asians. Non-smoking population andethnicity among Caucasian had no relationship with lung cancer susceptibility in four models. Conclusion: Our studysuggested that MMP1-1607 1G>2G polymorphism was a risk factor for developing lung cancer risk.