MMPs基因启动子区多态性与肺癌易感性的Meta分析研究

背景与目的 肺癌是世界范同内最常见的一种癌症,基质金属蛋白酶家族(Malrix metalloproteases,MMPs)在癌细胞的转移和扩散中都起到重要作用.MMPs基因多态性与癌症易感性的关系一直是研究的热点,而它们与肺癌易感性是否相关尚在在争议.为了更好地探讨MMPs基因多态性与肺癌易感性之间的关系,我们收集、整理先前学者研究的数据,并进行Meta分析.方法 使用PubMed和MEDLINE数据库检索2009年3月以前的相关文献,按照纳入标准,全面搜索含有研究MMP1-1607 1G/2G、MMP2-1306C/T、MMP2-735C/T、MMP9-1562C/T多态性与肺癌易感性相关的信息.由至少两位评价员做独立文献筛查和资料提取,并交义审核.使用RevMan(version 5.0)软件进行统计分析.结果 根据我们的榆索条件,8篇文章符合我们的纳入标准.共有4 467例肺癌患者和4 051名正常对照个体被纳入当前的Meta分析.分析结果 表明:MMP2-735C/T多态性与肺癌易感性显著相关,与野牛型等位基因-735C相比,突变型等位基因T显著降低了肺癌的易感件(OR=0.72,95%CI:0.61-0.85,P=0.0001);MMP1-1607 1G/2G、MMP2-1306C/T和MMP9-1562C/T多态性并没有明显影响肺癌的发生.结论 当前研究结果 表明MMP2摹因启动子区-735C/T多态性与肺癌易感性明显相关,MMP9基因-1562C/T多态性与肺癌易感性的关系还需进一步的研究.     

基质金属蛋白酶1、9基因多态性与成人脑星形细胞瘤的易感性

 目的本研究旨在探索MMP-1、MMP-9基因启动子区单核苷酸多态性（Singlenucleotidepoly—morphism，SNPs）与脑星形细胞瘤易感性的关系。方法以聚合酶链反应一限制性片段长度多态性分析方法，检测236例成人星形细胞瘤及366例健康对照的MMP．1-16072G／1G及MMP-9-1562C／T多态性的基因型。结果（1）MMP-1—16072G／1GSNP等位基因型及基因型总体分布在星形细胞瘤患者组和健康对照组之间有显著性差异（P值分别为0．002和〈0．001）。与2G／2G基因型相比，1G／1G基因型可显著降低该肿瘤的发病风险（校正OR=0．58，95％CI=0．42～O．79），而2G／1G基因型对该肿瘤的易感性无显著影响（校正OR=0．74，95％CI=0．51～1．08）。根据性别、发病年龄（≤45岁或〉45岁）进行的分层分析显示了相似的结果。（2）MMP-9-1562C／T的等位基因型及基因型总体分布在肿瘤患者组和健康对照组之间差异无统计学意义（P值分别为0．926和0．818）。与C／C基因型相比，C／T＋T／T基因型不能改变星形细胞瘤的发病风险（校正OR=1．09，95％CI：0．73～1．64）。根据性别、发病年龄、病理分级进行的分层分析，也未发现MMP-9SNP与星形细胞瘤的发病风险相关。结论MMP-1—16072G／1G多态性与星形细胞瘤的易感性有关，而MMP-9—1562C／T多态性可能不是该肿瘤的独立易感因素。     

XPC 基因 rs2228000（C/T）多态性与乳腺癌易感性的Meta分析

目的：定量探讨着色性干皮病 C 组（XPC）基因 rs2228000（C ／T）多态性与乳腺癌易感性之间的关系。方法通过计算机检索 PubMed、Cochrane Library、中国生物医学文献数据库（CBM）、万方医药期刊全文数据库、中国期刊全文数据库（CNKI）及维普数据库（VIP）,检索时间截至2015年12月,搜集有关 XPC rs2228000（C ／T）位点多态性与乳腺癌风险的病例对照研究。采用 STATA 12．0软件进行结果分析,计算比值比（OR）和95％CI。结果总共纳入8篇文献,包括9个病例对照研究（3850例乳腺癌患者和5047例健康对照）。纯合子模型（TT vs．CC：OR ＝1．28,95％CI 为1．08～1．52,Z ＝2．80, P ＝0．005）和隐性模型（TT vs．TC ＋CC：OR ＝1．23,95％CI 为1．05～1．43,Z ＝2．64,P ＝0．008）中 XPC rs2228000（C ／T）多态性与乳腺癌易感性有关,而等位基因模型、杂合子模型、显性基因模型中 XPC rs2228000（C ／T）位点多态性与乳腺癌风险无关（P ＞0．05）。在亚洲人群和 PCR-RFLP 亚组的4种基因模型中,XPC rs2228000（C ／T）多态性与乳腺癌易感性有关（T vs．C：OR ＝1．21,95％CI 为1．05～1．40, Z ＝2．63,P ＝0．009;TT vs．CC：OR ＝1．55,95％CI 为1．13～2．13,Z ＝2．70,P ＝0．007;TT ＋TC vs．CC：OR ＝1．26,95％CI 为1．02～1．55,Z ＝2．19,P ＝0．028;TT vs．TC ＋CC：OR ＝1．39,95％CI 为1．04～1．87, Z ＝2．23,P ＝0．026）。基于对照组来源的亚组分析,社区来源的纯合子模型中 XPC rs2228000（C ／T）多态性与乳腺癌发病风险有关（TT vs．CC：OR ＝1．27,95％CI 为1．02～1．57,Z ＝2．16,P ＝0．031）。结论XPC rs2228000（C ／T）多态性可能与乳腺癌风险有关,尤其在亚洲人群中,基因型 TT 可能增加乳腺癌发病风险。     

基质金属蛋白酶(MMP)-2和-9功能性单核苷酸多态与胃癌

背景与目的：基质金属蛋白酶(matrix metalloproteinase,MMP)-2和-9在胃癌的发生和发展中起重要作用。本研究探讨这2个基因的功能性单核苷酸多态与胃癌发生风险的关系。方法：以聚合酶链反应和变性高压液相色谱以及限制性片段长度多态性分析方法,分别检测228个胃癌患者和774个正常对照者MMP-2-1306T/C和MMP-9-1562C/T多态的基因型;比较不同基因型与胃癌风险的关系,并以效应修饰模型分析基因-基因之间的交互作用。结果：与MMP-2-1306TT或CT基因型携带者比较,MMP-2-1306CC基因型携带者罹患胃癌的风险增加1．67倍(95％CI,1．17～2．38)。MMP-9-1562C/T多态单独与胃癌风险无关,但与MMP-2-1306T/C多态可能有基因-基因交互作用,因为携带MMP-2-1306CC和MMP-9-1562TT或CT基因型的个体,罹患胃癌的风险显著增高(似然比检验,P=0．02)。结论：MMP-2和MMP-9基因单核苷酸多态可能与胃癌的遗传易感性有关。     

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。     

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。     

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。     

XRCC2基因多态性与肺癌易感性关系的研究

目的：探讨中国北方人群中XRCC2基因C41657T、G4234C多态性与肺癌的关系。方法：应用PCR-RFLP方法检测199例肺癌患者和200例正常人的XRCC2 C41657T及G4234C多态位点，比较两组之间等位基因及基因型频率分布及其与肺癌的关系。结果：肺癌患者XRCC2 C41657T多态位点的CC、CT、TT基因型和C、T等位基因频率分布与健康对照组相比差异均无统计学意义（P〉0．05）。G4234C多态位点的GG、GC、CC基因型和G、C等位基因频率分布与健康对照组相比差异也均无统计学意义（P〉0．05）。两多态性位点联合分析显示，肺癌患者与健康对照组的4个单体型分布亦无统计学差异（P〉0．05）。以病理类型、吸烟状况和年龄进行分层分析显示，XRCC2 C41657T多态位点可能与腺鳞癌和不吸烟人群的肺癌发病风险相关；与C／C基因型相比，携带T等位基因的基因型（C／T＋T／T）可显著增加腺鳞癌的发病风险（OR为2．95，95％CI=1．15—7．59）；而C／T基因型可显著增加不吸烟组人群中肺癌的发病风险（OR为2．12，95％CI=1．05-4．27）。对于XRCC2 G4234C多态位点，与G／G基因型相比，G／C基因型和携带C等位基因的基因型（G／C＋C／C）可显著增加小细胞肺癌的发病风险（OR为2．82和2．82；95％CI=1．15～6．91和1．17～6．76）；G／C基因型或与C／C基因型相加可显著增加年龄≥60岁的人群中肺癌的发病风险（OR为2．29和2．37；95％CI=1．11—4．72和1．16—4．88）。结论：对于XRCC2 C41657T多态位点，携带T等位基因的基因型可能增加腺鳞癌的发病风险，C／T基因型可能增加不吸烟者患肺癌风险；XRCC2 G4234C多态位点，G／C基因型或携带C等位基因可能增加小细胞肺癌的发病风险和老年人（年龄≥60岁）患肺癌的风险。     

p21cip1和p27kip1基因遗传多态与食管癌及贲门癌发病风险的关联

背景与目的：有研究表明p21^cip1和p27^kip1的基因多态性与乳腺癌、肺癌、前列腺癌等肿瘤易感性有关。本研究分析中国北方高发区人群食管鳞状细胞癌（ESCC）和贲门腺癌（GCA）与勺p21^cip1和p27^kip1基因多态性之间的关系。方法：应用聚合酶链反应-限制性片段长度多态性（PCR—RFLP）方法检测299例ESCC患者、256例GCA患者及437名健康对照人群p21^cip1 3’非翻译区和p27^kip1第109位密码子基因多态性分布情况。结果：ESCC患者组p21^cip1 T等位基因型频率（42．8％）显著高于健康对照组（36．7％）（P=0．02）,ESCC和GCA患者组p27^kip1等位基因型频率（分别为96．8％和96．1％）均显著高于健康对照组（92．9％）（P值分别为0．00和0．02）。ESCC患者组p21^cip1基因型频率分布与健康对照组相比有显著性差异（P=0．04）,与C／C和C／T基因型相比,T／T基因型可显著增加ESCC的发病风险（校正OR=1．93,95％CI=1．12～3．94）ESCC和GCA患者细p27^kip1基因型频率分布与健康对照组相比均有显著性差异（P分别为0．00和0．01）,与V／G和G／G基因型相比,V／V基因型可显著增加ESCC和GCA的发病风险（校正OR分别为2．44和2．01,95％CI分别为1．2l～4．02和1.12～3．68）。当按吸烟和上消化道肿瘤家族史状况进行分层分析时发现,与V／G和G／G基因型相比,V／V基因型可显著增加吸烟人群患ESCC和GCA（校正OR分别为2．24和2．61,95％C1分别为1.14～4．03和1．25～3．82）以及有家族史人群患ESCC的发病风险（校正OR=2．04,95%CI=1．04～3．43）．两基因联合分析显示,携带p21^cip1T／T和p27^kip1V／V基因型可显著增加患食管癌和贲门癌的发病风险（校正OR分别为3．78和2．56,95?分别为1．46～5．89和1．06～4．78）。结论：在中国北方人群中,p21^cip1基因多态性可能与食管癌的易感性有关,p27^kip1基因多态性可能与食管癌和贲门癌的易感性有关．而且这两个基因的多念性可能存食管癌和贲门癌发病中起联合作用．     

β1-5090／T基因多态性与中国人群NSOLC遗传易感相关性的研究

目的：探讨转化生长因子β1基因（TGF-β1）-509C／T位点多态性与中国人群非小细胞肺癌（non-small cell lung cancer,NSCLC）遗传易感性的关系。方法：采用聚合酶链反应-限制性片段长度多态性PCR—RFLP方法检测210例NSCLC患者和208例健康对照者的TGF-β1—509C／T基因型分布,并分析两组之间的差异。结果：TGF—β1—509CT＋TT基因型相对于CC基N型是NSCLC发生的独立危险因素（P=0．007,OR=2．297,95％CI：1．250-4．219）;携带T等位基因者患NSCLC的风险是携带C等位基因者的1．617倍（P=0．001,95％CI：1．210～2．161）;重度吸烟者相对于不吸烟和轻度吸烟者是NSCLC发生的独立危险因素（P=0．021,OR=1．783,95％CI：1．089～2．918）。结论：TGF-β1—509C／T位点多态性在中国人群中与NSCLC遗传易感性相关,可作为NSCLC发病风险评估的筛选指标。     

The MMP-1, MMP-2, and MMP-9 gene polymorphisms and susceptibility to bladder cancer: a meta-analysis

The relationship between matrix metalloproteinase (MMP) polymorphisms and bladder cancer risk has become a hot topic and was studied extensively in recent years, but the results are still controversial. In order to estimate the relationship of MMP polymorphisms and the risk of bladder cancer, we performed this meta-analysis. We conducted a comprehensive search of databases; PubMed, Web of Science, Embase, Chinese Biomedical Literature Database (CBM, Chinese) and Wanfang Database (Chinese) were searched for all case–control studies which mainly study the relationship between MMP-1-1607 1G/2G, MMP-2-1306 C/T, and MMP-9-1562 C/T polymorphisms and the susceptibility of bladder cancer. The association between the MMP polymorphisms and bladder cancer risk was conducted by odds ratios (ORs) and 95 % confidence intervals (95 % CIs). At last, totally five literatures with 1,141 cases and 1,069 controls were contained in the meta-analysis. Among these articles, four articles with 1,103 cases and 1,053 controls were about MMP-1-1607 1G/2G polymorphism and three studies with 839 cases and 775 controls for MMP-2-1306 C/T polymorphism and MMP-9-1562 C/T polymorphism. With regard to MMP-1-1607 1G/2G polymorphism, significant association was found with bladder cancer susceptibility only under recessive model (2G2G vs. 1G2G/1G1G: OR?=?1.44, 95 % CI?=?1.05–1.97, P?=?0.022), and as to the MMP-2-1306 C/T polymorphism, significant association was found with bladder cancer susceptibility only under homozygote model (TT vs. CC: OR?=?2.10, 95 % CI?=?1.38–3.10, P?=?0), but no associations was found between MMP-9-1562 C/T polymorphism and bladder cancer susceptibility. The results suggest that the MMP-2-1306 C/T and MMP-9-1562 C/T polymorphisms are significantly associated with bladder cancer susceptibility, and no associations were found between MMP-9-1562 C/T polymorphism and bladder cancer susceptibility.     

MMP1-1607 1G/2G polymorphism and lung cancer risk: a meta-analysis

Matrix metalloproteinase-1 (MMP-1) plays an important role in the breakdown of extracellular matrix and mediates pathways of apoptosis, angiogenesis, and immunity. It has been demonstrated that MMP-1 overexpression is associated with tumor initiation, invasion, and metastasis. Many studies have investigated the association between MMP1-1607 1G/2G polymorphism and lung cancer risk, but the impact of MMP1-1607 1G/2G polymorphism on lung cancer is unclear owing to the obvious inconsistence among those studies. This study aimed to quantify the strength of the association between MMP1-1607 1G/2G polymorphism and lung cancer risk. We searched the PubMed, Embase, and Wanfang databases for studies on the association between MMP1-1607 1G/2G polymorphism and risk of lung cancer. We estimated summary odds ratio (OR) with its corresponding 95?% confidence interval (95%CI) to assess the association. Overall, MMP1-1607 1G/2G polymorphism was associated with increased risk of lung cancer under four genetic models (OR_{2G versus 1G}?=?1.21, 95?%CI 1.06?C1.37; OR_{2G2G versus 1G1G}?=?1.36, 95%CI 1.09?C1.70; OR_{2G2G versus 2G1G+1G1G}?=?1.33, 95?%CI 1.10?C1.61; and OR_{2G2G+2G1G versus 1G1G}?=?1.15, 95?%CI 1.04?C1.27). Meta-analyses of studies with high quality showed that MMP1-1607 1G/2G polymorphism was still associated with lung cancer risk under those four genetic models. Subgroup analyses by ethnicity and sensitivity analyses further identified the significant association in East Asians. No evidence of publication bias was observed. Meta-analyses of available data show a significant association between MMP1-1607 1G/2G polymorphism and lung cancer risk.     

Matrix Metalloproteinase-2 -1306 C>T Gene Polymorphism is Associated with Reduced Risk of Cancer: a Meta-analysis

Matrix metalloproteinase-2 (MMP2) is an endopeptidase, mainly responsible for degradation of extracellularmatrix components, which plays an important role in cancer disease. A single nucleotide polymorphism (SNP)at -1306 disrupts a Sp1-type promoter site. The results from the published studies on the association betweenMMP2 -1306 C>T polymorphism and cancer risk are contradictory and inconclusive. In the present study, ameta-analysis was therefore performed to evaluate the strength of any association between the MMP2 -1306C>T polymorphism and risk of cancer. We searched all eligible studies published on association between MMP2-1306 C>T polymorphism and cancer risk in PubMed (Medline), EMBASE and Google Scholar online webdatabases until December 2013. Genotype distribution data were collected to calculate the pooled odds ratios(ORs) and 95% confidence intervals (95%CIs) to examine the strength of the association. A total of 8,590 cancercases and 9,601 controls were included from twenty nine eligible case control studies. Overall pooled analysissuggested significantly reduced risk associated with heterozygous genotype (CT vs CC: OR=0.758, 95%CI=0.637to 0.902, p=0.002) and dominant model (TT+CT vs CC: OR=0.816, 95%CI=0.678 to 0.982, p=0.032) geneticmodels. However, allelic (T vs C: OR=0.882, 95%CI=0.738 to 1.055, p=0.169), homozygous (TT vs CC: OR=1.185,95%CI=0.825 to 1.700, p=0.358) and recessive (TT vs CC+CT: OR=1.268, 95%CI=0.897 to 1.793, p=0.179)models did not show any risk. No evidence of publication bias was detected during the analysis. The results ofpresent meta-analysis suggest that the MMP2 -1306 C>T polymorphism is significantly associated with reducedrisk of cancer. However, further studies with consideration of different populations will be required to evaluatethis relationship in more detail.     

Polymorphisms of matrix metalloproteinases 1, 2, 3 and 9 and susceptibility to lung,breast and colorectal cancer in over 30,000 subjects

A variety of susceptibility genes have been associated with cancer but definitive conclusions have been difficult to draw partly hampered by the small number of subjects in each study. We undertook a comprehensive genetic meta‐analysis of all matrix metalloproteinase (MMP) genes investigated using an allelic‐association case–control model in the 3 major cancers of lung, breast and colorectal cancer. Electronic databases were searched until and including July 2008 for any MMP genetic association study in lung, breast and colorectal cancer. Odds ratio (OR) and 95% confidence intervals (CI) were determined for each gene disease association using fixed and random effect models. Twenty‐five studies addressing 5 polymorphisms in 4 genes were analyzed among 30,651 individuals (15,328 cases and 15,253 controls). The MMP‐1 nt‐1607 polymorphism was significantly associated with colorectal cancer in both the dominant (OR, 1.66; 95% CI, 1.14–2.42; p = 0.008) and recessive (OR, 1.59; 95% CI, 1.15–2.20; p = 0.005) models. MMP‐2^1306C→T (OR, 0.53; 95% CI, 0.40–0.72; p < 0.0001) and 735^C→T (OR, 0.65; 95% CI, 0.53–0.79; p < 0.0001) were significantly associated with protection against lung cancer. No association was found with the MMP 1, 2, 3 or 9 polymorphisms with breast cancer, MMP‐1, 3 or 9 with lung cancer or MMP‐2, 3 or 9 with colorectal cancer. There may be a genetic influence in the development of colorectal and lung cancer. Subjects with the MMP‐1 nt‐1607 polymorphism have an increased association with colorectal cancer. Those homozygous for either the MMP‐2/1306T or 735T allele may be at reduced risk of lung cancer, although the evidence base is small. © 2009 UICC     

MMP1 rs1799750 Single Nucleotide Polymorphism and Lung Cancer Risk: A Meta-analysis

Background: Numerous studies have investigated the association of matrix metalloproteinase 1 (MMP1) rs1799750 single nucleotide polymorphism with lung cancer susceptibility, but the findings are inconsistent.Therefore, we performed a meta-analysis to comprehensively evaluate any possible association. Methods: We searched publications from MEDLINE, EMBASE and CNKI databases which assessed links between theMMP1 rs1799750 polymorphism and lung cancer risk. We calculated the pooled odds ratio (OR) and its 95% confidence interval (95%CI) using either fixed-effects or random-effects models. Results: The meta-analysis was based on 9 publications encompassing 4,823 cases and 4,298 controls. The overall results suggested there was a significant association between the MMP1 rs1799750 polymorphism and lung cancer risk (1G vs. 2G: OR = 0.83,95%CI = 0.73-0.94; 1G1G vs. 2G2G: OR = 0.73, 95%CI = 0.59-0.92; 1G1G vs. 1G2G/2G2G: OR = 0.87, 95%CI = 0.79-0.97; 1G1G/1G2G vs. 2G2G: OR = 0.78, 95%CI = 0.64-0.95). In the subgroup analysis by ethnicity, the association was still obvious in Asians (all P values < 0.05), but there was no association in Caucasians (all P values > 0.05). Conclusions: The MMP1 rs1799750 polymorphism is associated with decreased lung cancer risk,and a race-specific effect may exist in this association.     

Meta-analysis of Associations Between four Polymorphisms in the Matrix Metalloproteinases Gene and Gastric Cancer Risk

Background: Matrix metalloproteinases (MMPs) play important roles in pathogenesis and developmentof cancer. Recently, many studies have show associations between polymorphisms in the promoter regions ofMMPs and risk of gastric cancer. The present meta-analysis was conducted in order to investigate the potentialassociation between four polymorphisms in the MMP gene and gastric cancer risk. Methods: A computerizedliterature search was conducted in databases of Med-line, Embase, Science Citation Index and PubMed till June2013 for any MMP genetic association study of gastric cancer. Odds ratios (ORs) and 95 % confidence intervals(CIs) were estimated for each gene under dominant and recessive models, and heterogeneity between studies wasassessed using the Q test and I2 value. Overall and subgroup analyses according to ethnicity were carried out withStata 12.0. Results: 14 reports covering 8,146 patients (2,980 in the case group and 5,166 in the control group)were included in the present meta-analysis. We found that the MMP-7 (-181A>G) polymorphism increased thegastric cancer risk in therecessive model (GG vs. AA/AG, OR=1.768, 95% CI =1.153-2.712). For MMP2 −1306C>T, MMP1-1607 1G/2G, and MMP9−1 562 C>T, there were no associations between these polymorphisms andthe risk of gastric cancer under dominant or recessive models. Conclusion: This meta-analysis suggested thatthe MMP7-181 A>G polymorphism may contribute to gastric cancer susceptibility. More studies are needed,especially in Europeans, in the future.     

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.