端粒酶逆转录酶基因多态性与胃癌遗传易感性的研究

目的探讨端粒酶逆转录酶（TERT）基因rs2736098 和 rs2736100位点单核苷酸多态性与胃癌遗传易感性和幽门螺杆菌（Hp）感染的关系。方法 采用限制性片段长度多态性聚合酶链反应（PCR RFLP）检测297例胃癌患者（病例组）和306例非萎缩性胃炎患者（对照组）中TERT基因rs2736098和rs2736100位点的多态性;采用病理学诊断和13C尿素酶呼气试验检测Hp感染。结果 rs2736098位点各基因型频率在病例组和对照组中的分布差异无统计学意义（P＞0.05）,病例组rs2736100位点仅GG基因型频率显著高于对照组（27.0％ vs. 16.4％,P＜0.05）。Logistic回归分析显示,携带GG基因型个体罹患胃癌的风险是携带TT基因型个体的1.371倍（OR=1.371,95％CI：1.063～1.775,P=0.005）;在Hp阴性者中,GG型罹患胃癌的风险较TT型增加（OR=1.421,95％CI：0.988～2.042,P=0.046）;而在Hp阳性者中,未发现rs2736100位点的基因型与罹患胃癌的风险有关。结论 TERT基因rs2736100位点基因多态性可能与胃癌遗传易感性相关,而与Hp感染无关。     

IL-17基因多态性与胃癌易感性的关系

目的 探讨白介素-17（Interleukin-17,IL-17）基因rs2275913、rs763780多态性与胃癌易感性的关系。方法 收集青岛地区355例汉族胃癌患者为胃癌组,同期进行健康体检的300名正常者为对照组,采集两组患者外周血,提取全血基因组DNA,PCR扩增目的基因片段,采用DNA直接测序法检测IL-17基因rs2275913、rs763780位点基因型,分析其位点多态性与胃癌易感性的关系。结果 胃癌组与对照组IL-17基因 rs2275913位点基因型分布差异有统计学意义（χ²=17.192,P＜0.001）。与GG基因型相比,携带AA基因型的个体胃癌发病风险增加,差异有统计学意义（χ²=16.829,P＜0.05;OR=2.891,95%CI=1.721~4.857）;携带GA基因型的个体胃癌发病风险增加,但差异无统计学意义（χ²=0.878,P＞0.05）。胃癌组与对照组相比,IL-17基因 rs763780位点基因型分布差异无统计学意义（χ²=1.381,P=0.501）。结论 IL-17基因 rs2275913 A等位基因的携带会增加青岛地区汉族人群胃癌发病风险,IL-17基因 rs763780位点多态性与胃癌发病风险无明显相关性。     

ZO-1 SNPs与胃癌遗传易感性及预后*

目的:探讨中国福建地区汉族人群中ZO- 1 基因TJP1 4 个已知位点单核苷酸多态性（SNPs）与胃癌遗传易感性及进展和预后的相关性。方法:应用PCR-LDR法检测福建医科大学附属第一医院200 例健康体检个体及220 例原发性胃腺癌患者TJP1基因4 个SNP 位点的基因型。结果:福建地区汉族人群中,TJP-1 SNP rs 7179270 位点稀有等位基因C 的频率为0.2,而其他三个位点（rs 34771010,rs 28578444和rs 41280058）稀有等位基因频率为0.0。TJP1 基因SNP 位点rs 7179270 200 例对照组等位基因C、T 的频率分别为20% 和80% ,胃癌病例组等位基因C、T 的频率为32.6% 和67.4% ;CC、C/T和TT的基因型频率在对照组分别为4% 、32%和64% ,而在病例组为10.9% 、43.2% 和45.9% ,差异具有统计学意义（OR= 1.953,95%CI 1.425～2.677,P<0.001）。 TJP1 rs 7179270位点基因型与胃癌患者的性别、年龄、分化程度、浸润深度、淋巴结转移及手术后生存时间无显著相关（P>0.05）。 结论:TJP1rs 7179270 位点携带等位基因C 的CC和C/T基因型个体的胃癌患病风险提高,提示检测该位点基因型有助于评估胃癌的遗传易感性;TJP1 rs 7179270 位点的基因型频率与临床病理学参数及胃癌患者手术后生存时间无显著相关性,提示TJP1 rs 7179270 位点多态性可能不参与胃癌的进展和预后;TJP1 rs 34771010、rs 28578444和rs 41280058稀有等位基因频率为0.0,推测中国福建地区人群可能无这三个位点的多态性分布。      

TNF-A基因多态性及其单体型与新疆维、汉民族胃癌的关系

目的:探讨新疆维吾尔族(维族)和汉族胃癌患者肿瘤坏死因子-α基因(TNF-A)rs1800629和rs361525位点多态性及其单体型与胃癌易感性的关系。方法:采用Snapshot技术分析322例胃癌患者(其中维族93例,汉族229例)和作为对照的487例非胃癌患者(其中维族231例,汉族256例)TNF-A基因rs1800629和rs361525位点基因型的分布;利用SHEsis软件分析其构成的单体型在病例组和对照组中的分布频率,比较基因型和单体型在病例组和对照组间的分布差异。结果:在维族人群中,TNF-A基因rs1800629和rs361.525位点不论是等位基因位点、基因型还是单体型在病例组和对照组中的分布频率差异均无统计学意义(P>0.05)。在汉族人群中,TNF-A基因rs361525位点AA+GA基因型在病例组和对照组之间的分布差异有统计学意义(χ=4.56,P=0.03),即携带A等位基因者发生胃癌的风险增加(OR=2.41,95%CI:1.06～5.49);rs1800629位点基因型与胃癌之间未发现明显关联;A-A单体型在病例组及对照组分布频率分别为0.92%和0.86%,差异有统计学意义(χ~2=7.03,P=0.01)。结论:TNF-A基因单核苷酸多态性与汉族人群胃癌发病风险相关,这种相关性具有民族差异。     

Relationship between tagSNPs and haplotype of TNF-A gene and gastric cancer in Uygur and Han ethnic groups in Xinjiang

目的:探讨新疆维吾尔族(维族)和汉族胃癌患者肿瘤坏死因子-α基因(TNF-A)rs 1800629和rs361525位点多态性及其单体型与胃癌易感性的关系.方法:采用Snapshot技术分析322例胃癌患者(其中维族93例,汉族229例)和作为对照的487例非胃癌患者(其中维族231例,汉族256例)TNF-A基因rs1800629和rs361525位点基因型的分布;利用SHEsis软件分析其构成的单体型在病例组和对照组中的分布频率,比较基因型和单体型在病例组和对照组间的分布差异.结果:在维族人群中,TNF-A基因rs1800629和rs361525位点不论是等位基因位点、基因型还是单体型在病例组和对照组中的分布频率差异均无统计学意义(P＞0.05).在汉族人群中,TNF-A基因rs361525位点AA+GA基因型在病例组和对照组之间的分布差异有统计学意义(X2=4.56,P=0.03),即携带A等位基因者发生胃癌的风险增加(OR=2.41,95％ CI:1.06～5.49);rs1800629位点基因型与胃癌之间未发现明显关联;A-A单体型在病例组及对照组分布频率分别为0.92％和0.86％,差异有统计学意义(X2=7.03,P=0.01).结论:TNF-A基因单核苷酸多态性与汉族人群胃癌发病风险相关,这种相关性具有民族差异.     

胃癌高发区IL-1基因多态性、H.pylori感染和胃黏膜萎缩关系的研究

目的:分析胃癌高发区普通人群的IL-1B-511基因多态性、H.pylori感染率及胃粘膜萎缩的血清学指标(血清胃蛋白酶原I(pepsinogenI,PGI)、胃蛋白酶原I/胃蛋白酶原II的比值(PGI/PGII)和胃泌素(gastrin)浓度,探讨IL-1B-511基因多态性对幽门螺旋杆菌(Helicobacterpylori,Hp)感染后胃黏膜萎缩的影响。以期进一步明确IL-1B基因多态性与胃黏膜萎缩关系,IL-1B基因多态性增加胃癌发病危险性的可能机理。方法:采用PCR-限制性长度片段多态性(RFLP)分析法检测胃癌高发区陕西省普通人群169例的基因型。采用酶联免疫吸附法(ELISA)检测上述人群的Hp感染率、PGI、PGII和Gastrin的浓度。结果:在胃癌高发区,Hp阳性者PGI/PGII显著低于Hp阴性者(P<0.01),但1L-1B-511T/T基因型人群PGI/PGII与1L-1B-511C/T和C/C基因型者无显著差异(P值均>0.05)。血清胃泌素浓度与IL-1B-511的基因型没有明确的关系(P>0.05)。结论:在胃癌高发区,Hp感染可能在20~23岁年龄段已是胃黏膜萎缩的危险因素,1L-1B-511T/T基因型者可能增加Hp后胃黏膜萎缩形成的危险性;胃黏膜萎缩的发生、发展除与Hp感染和遗传有关外,环境因素可能起相当重要的作用。     

福建地区汉族人群中CLDN23基因SNPs多态性与胃癌遗传易感性及预后的相关性CSCD

目的探讨福建地区汉族人群中已知的三种claudin-23基因CLDN23单核苷酸多态性(SNPs)与胃癌遗传易感性及预后的相关性。方法应用PCR-LDR法检测CLDN23基因3个SNP位点rs12153、rs1060106 和rs11249884的基因型。结果 CLDN23基因SNP位点rs12153、rs1060106及rs11249884三个位点的基因型及等位基因频率在胃癌病例组和健康者之间差异均无统计学意义(P>0.05);胃癌病例组中三个位点的基因型分布频率与肿瘤分化程度、pT分期显著相关(P<0.05);rs12153、rs1060106的基因型分布频率与患者术后生存时间显著相关(P<0.05);CLDN23基因SNP位点rs12153、rs1060106和rs11249884两两之间未见明显的遗传连锁不平衡性;rs12153、rs1060106和rs11249884可能存在的基因单体型中,C-T-G单体型在胃癌病例组与正常对照组之间有显著差异(P<0.01)。结论福建汉族人群中,CLDN23基因SNP位点rs12153、rs1060106及rs11249884的多态性与胃癌的分化、pT分期具有相关性,可能参与胃癌的进展,rs12153、rs1060106的多态性与胃癌患者的预后有关。     

EGFR基因rs763317多态性与胃癌遗传易感的相关性研究

目的:探讨EGFR基因第一内舍子区rs763317位点单核苷酸多态性(SNP)与江西地区汉族人群胃癌遗传易感性的相关性.方法:应用MassARRAY(R)SNP分型技术检测138例胃癌患者和170名正常对照EGFR基因多态位点rs763317的基因型.用χ2检验统计分析病例组和对照组基因型和等位基因的频率;采用非条件Logistic回归分析,计算比数比(OR)和95%CI,评价多态性位点与胃癌遗传易感性的相关性.结果:EGFRrs763317多态位点AA、AG和GG基因型在胃癌人群中的分布频率为5.8%、52.2%和42.0%,与对照组(2.4%,31.8%和65.9%)相比差异有统计学意义,P≤0.001.与rs763317 GG基因型相比,携带AA或AG基因型的个体能显著增加患胃癌的发病危险(OR=3.909,95%CI:1.108～13.786;OR=2.540,95%CI:1.565～4.123).等位基因A在胃癌患者的分布频率显著高于正常对照组(OR=3.277,95%CI:1.103～9.738).结论:首次发现EGFR基因第一内含子区rs763317位点多态性与江西地区汉族人群胃癌的遗传易感性相关.     

ERCC1基因多态性与胃癌发生发展的关系

  目的  本研究拟探讨切除修复互补交叉基因1(ERCC1)3个单核苷多态性(SNPs)与胃癌发生发展的关系。  方法  选取2007年1月至2009年12月福建地区组织学确诊的452例胃癌患者和469例健康体检人群, 利用基质辅助激光解吸电离飞行时间质谱(MALDI-TOF-MS)方法进行rs11615 T > C、rs2298881 C > A和rs3212930 T > C、3个位点多态性检测, 以评估ERCC1不同基因型与胃癌发病风险和病理特征的关系。  结果  rs11615 T > C位点携带C等位基因的个体患胃癌的风险较野生纯合基因型降低一半(OR=0.49;95%CI: 0.52~0.47;P=0.01), 但是罹患弥漫型胃癌的风险上升1.68倍, 预后更差(OR=1.68;95%CI: 0.76~0.61;P=0.048)。单体型分析显示, 基于这3个位点的单体型C-C-C降低了体患胃癌的风险(OR=0.729;95%CI: 0.531~1.001;P=0.0499), 而单体型T-C-T则增加了胃癌患病的风险(OR=1.321;95%CI: 1.063~1.641;P=0.0118)。  结论  ERCC1基因rs11615 T > C位点多态性与胃癌发生发展密切相关, 携带该基因2种不同单体型的个体在胃癌患病风险上存在差异。      

IL-1B基因多态性和H.pylori感染与胃癌关系的研究

目的:通过比较胃癌低发区广东省胃癌患者与匹配人群的幽门螺旋杆菌(Helicobacterpylori,H.pylori)感染率和IL-1B-31基因多态性,探讨IL-1B-31基因多态性是否增加H.pylori感染后胃癌发生的危险性。方法:1)采用PCR-限制性片段长度多态性(restrictionfragmentlengthpolymorphism,RFLP)分析法检测胃癌低发区广东省84例胃癌患者和84例与之性别、年龄匹配的普通人群的lL-1B-31基因多态性。2)采用酶联免疫吸附法(enzyme-linkedimmunosorbentassay,ELISA)检测上述人群的H.pylori感染率。结果:1)IL-1B-31T/T基因型频率在对照人群与胃癌患者两组间差异无统计学意义,(3·6%vs1·2%,χ2=1·0,P=0·3)。2)84例胃癌患者的H.pylori感染率显著高于对照人群,81·0%vs59·5%,χ2=9·2,P=0·002,OR=2·9。结论:在胃癌低发区广东省,H.py-lori感染是胃癌发生的危险因素,OR=2·9;IL-1B-31T/T基因型不是通过影响HP感染后发生胃癌的危险性,是通过遗传或其他途径增加胃癌发病的危险性。     

白细胞介素-1B 基因多态性、幽门螺杆菌感染与胃癌发生的相关性

 目的 探讨湖南衡阳地区白细胞介素-1B（IL-1B）基因多态性与胃癌的关系以及幽门螺杆菌（Helicobacter pylori,HP）感染后胃癌发生的易感基因型。方法 52例胃癌患者癌旁正常胃粘膜组织和55例慢性胃炎患者胃粘膜组织,均经快速尿素酶和PCR检测HP,应用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）分析技术,进行基因型检测,并对C/C、T/T进行测序,比较各基因型在胃癌组和胃炎组中的分布差异。结果 IL-1B-31T、IL-1B-511T等位基因和IL-1B-31T/T、IL-1B-511T/T基因型在胃癌组的分布频率高于胃炎组（P〈0.05）,OR值分别为1.97（95%CI=1.15-3.59）、2.52（95%CI=1.45-4.39）和2.71（95%CI=1.10-6.66）、3.33（95%CI=1.14-9.73）。在伴有HP感染的群体中进行比较,IL-1B-31位点各基因型未见明显差异;但IL-1B-511T等位基因和IL-1B-511T/T基因型在胃癌组的分布频率高于胃炎组（P〈0.05）,OR值分别为2.16（95%CI=1.10-4.23）和3.43（95%CI=1.01-11.62）。结论 在湖南衡阳地区IL-1B-31T/T、IL-1B-511T/T基因型与胃癌发病风险相关,在HP被感染后IL-1B-511T/T基因型可能为湖南衡阳地区胃癌易感基因型。     

胃蛋白酶原C基因插入-缺失多态和幽门螺杆菌感染的交互作用与胃癌发病风险

目的 探讨胃癌发生发展过程中,胃蛋白酶原C(PGC)基因插入-缺失多态与幽门螺杆菌(Hp)及其不同基因亚型菌株感染的交互作用.方法 1:1频数配伍,选择基本正常(NOR)、胃糜烂溃疡(GU)、萎缩性胃炎(AG)和胃癌(Gc)各141例,分析PGE基因多态和Hp感染的交互作用.同时选择177例Hp感染阳性者,分析PGC基因多态与不同基因亚型Hp感染的交互作用.以聚合酶链反应(MR)检测PGC基因多态型及Hp基因亚型.以酶联免疫吸附实验(ELISA)检测血清Hp-IgG抗体.结果 PGG基因多态与Hp感染两因素交互作用,PGC等位基因1纯合型、Hp-IgG阳性者罹患GU、AG和GC的OR值分别为8.69、11.16和10.61(P值分别为0.049、0.02和0.03),交互作用指数分别为5.40、6.48和4.34,归因比分别为0.721、0.770和0.697.P02基因多态与不同基因亚型Hp感染对于AG和GC患病均无交互作用.结论 GC发生发展过程中,PGC基因多态与Hp感染存在正交互作用,而与不同基因亚型Hp菌株感染无交互作用.     

Glulathione-S-transferases Gene Polymorphism in Prediction of Gastric Cancer Risk by Smoking and Helicobacter Pylori Infection Status

Aim: To evaluate the association of glutathione S-transferases gene polymorphisms with the risk of gastriccancer, with reference to smoking and Helicobacter pylori infection. Methods: We conducted a 1:1 matched casecontrolstudy with 410 gastric cancer cases and 410 cancer-free controls. Polymorphisms of GSTM1, GSTT1 andGSTP1 were determined using PCR-CTPP. Results: The GSTM1 and GSTT1 null genotypes were significantlyassociated with the risk of gastric cancer after adjusting for potential confounding factors (OR=1.68, 95%CI=1.32-2.23 for null GSTM1, OR=1.73; 95% CI=1.24-2.13 for null GSTT1). The combination of null GSTM1and null GSTT1 conferred an elevated risk (OR=2.54, 95% CI=1.55-3.39). However, no association was foundfor GSTP1 polymorphism The smoking modified the association of GSTM1 and GSTT1 null genotypes withthe risk of gastric cancer. Conclusion: GSTM1 and GSTT1 null genotypes are associated with increased risk ofgastric cancer, and smoking modifies the association.     

IL-1B (C+3954T) Gene Polymorphism and Susceptibility to Gastric Cancer in the Iranian Population

Background: Gastric cancer as one of the most important diseases affecting health in all worldwide. Currentstudies have confirmed associations of cytokine gene polymorphisms with the risk of gastric cancer development.The current research aimed to assess the association of IL-1B+3954 genotypes with the risk of gastric cancerin the Iranian population. Materials and Methods: This case-control study covered 49 gastric cancer patientscompared to 53 cancer free individuals as a control group. Genomic-DNA extraction was carried out from biopticsamples of patients and peripheral blood of healthy volunteers. Polymorphism of IL-1B +3954 genotypes wereanalysed with a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method.Results: The frequencies of IL-1B +3954 A1A1, A1A2 and A2A2 genotypes in healthy individuals were 26.4, 66and 7.6 %, respectively. However, in gastric cancer patients, A1A1, A1A2 and A2A2 with 4.1, 51 and 44.9% wereobserved (p<0.05). Conclusions: The findings of our results show a positive association between the IL-1B+3954genotype distribution and the risk of gastric cancer disease in the Iranian population.     

Association between C1019T polymorphism in the connexin 37 gene and Helicobacter pylori infection in patients with gastric cancer

Objective: To investigate the association between the connexin 37 C1019T polymorphism and Helicobacterpylori infection in patients with gastric cancer. Methods: 388 patients with gastric cancer (GC), 204 with chronicsuperficial gastritis (CSG) were studied. H. pylori was detected by gastric mucosal biopsies biopsy dyeing method.Connexin 37 gene polymorphism 1019 site genotypes were determined by gene sequencing technology. Genotypesand alleles frequencies were compared. Results: (1) Connexin37 gene 1019 site distribution frequency (CC type,TC type, TT type) in the CSG group was 18.1%, 45.1% and 36.8%; in the stomach cancer group it was 35.1%,45.9% and 19.%, conforming to the Hardy-Weinberg euilibrium. (2) In comparison with CSG group, thefrequency of Connexin37 C allele was higher in the gastric cancer group (58.0% vs 40.7%, OR = 2.01, 95%CI =1.58-2.57, P < 0.01). The prevalence of gastric cancer risk was significantly increased in the carriers of C allele(CC+TC) than in TT homozygote (OR = 2.47, 5%CI = 1.68- 3.610. (3) Gastric cancer patients complicated withHp infection 211 cases, gastric cancer group of the male patients with HP positive patients with 187 cases, 40cases of female patients with negative patients, 24 cases were HP positive, negative in 137 cases, control groupmale patients, 28 cases were Hp positive, negative in 95 patients, female patients with Hp positive 6 cases, 75cases were negative. On hierarchical analysis, the male group OR value was 15.9 (95%CI to 9.22-27.3), and thefemale OR was 2.19 (95%CI 0.88-5.59), indicating a greater contribution in males (P <0.01). After eliminationof gender effects, positive HP and gastric cancer were closely related (OR 8.82, 95% CI: 5.45-14.3). (4) Thedistribution frequency of C allele in patients with Hp infection was much higher than that in Hp negative casesin the GC group (64.5% vs 47.0%, OR = 2.05, 95%CI = 1.54-2.74, P < 0.01). Compared with TT homozygotes,(CC+TC) genotype prevalence of gastric cancer risk increased significantly (OR = 2.96, 5%CI = 1.76-2.99 ).Conclusion: The T allele in the connexin37 gene might not only be associated with gastric cancer but also withH. pylori infection.     

Genetic factors involved in the development of Helicobacter pylori-related gastric cancer

Developmental process to gastric cancer by Helicobacter pylori infection consists of three steps: (1) H. pylori infection; (2) gastric atrophy development; and (3) carcinogenesis. In each step, genetic traits may influence the process, interacting with lifestyle. In the step of H. pylori infection, two lines of genetic polymorphisms were assumed: one influencing gastric acid inhibition interacting with smoking, and the other concerning innate immune response attenuation. The former includes functional polymorphisms of IL-1B (C-31T or tightly linked T-511C), and TNF-A (T-1031C and C-857T), and the latter possibly includes NQO1 C609T. In the step to gastric atrophy, polymorphisms pertaining to the signal transduction from cytotoxin-associated gene A (PTPN11 A/G at intron 3) and to T-cell responses (IL-2 T-330G and IL-13 C-1111T) were hypothesized. There are a limited number of epidemiological genotype studies on the final step of literal carcinogenesis, potentially interacting with smoking, a low vegetable and fruit intake, and salty foods, the well-documented risk factors. In past case-control studies on the associations between genotype and gastric cancer risk, the cases consisted of H. pylori-related and unrelated gastric cancer patients and the controls consisted of individuals including the uninfected (H. pylori unexposed and exposed) and the infected with and without gastric atrophy. Accordingly, it was not clear whether the observed risk was for H. pylori-related or -unrelated gastric cancer, nor which step was involved in the observed associations even when nearly all cases were H. pylori-related. In order to elucidate the genetic traits of H. pylori-related gastric cancer, stepwise evaluation will be required.     

幽门螺杆菌感染与胃部疾病的相关性

[目的]探讨幽门螺杆菌（Hp）感染在胃癌发生发展中的作用。[方法]选择2009年1月至2012年12月经胃镜检查病理确诊胃部疾病439例患者,其中慢性浅表性胃炎163例、慢性萎缩性胃炎64例、胃食管反流病47例、胃溃疡79例、十二指肠溃疡54例、胃不典型增生12例和胃癌20例。采用C14呼气实验和快速尿素酶法,二项任意一项阳性均被诊断胃Hp阳性。[结果]胃部疾病439例患者中Hp阳性219例,阳性率为49．89％。胃癌患者的Hp阳性率比慢性胃炎患者Hp阳性率高（65．00％VS43．17％,χ^2=3．850,P=0．043）,也比胃食管反流病患者Hp阳性率高（65．00％vs34．04％,χ^2=5．477,19=0．019）,但与胃、十二指肠溃疡患者比较Hp阳性率无统计学差异（65．00％V863．91％,χ^2=0．009,／9=0．925）。60岁以下者,随年龄增长Hp感染率逐渐升高。[结论]胃幽门螺杆菌感染与胃溃疡、不典型增生和胃癌的发生有着密切的关系,幽门螺杆菌感染是胃癌的危险因素。根除Hp感染治疗可能有助于降低胃癌发生的风险。     

Gastric cancer risk in a Mexican population: role of Helicobacter pylori CagA positive infection and polymorphisms in interleukin-1 and -10 genes

Several polymorphisms of the IL1B and IL10 gene promoters have been reported to be associated with gastric cancer risk in Caucasians. However, studies in other populations have shown differing results. We aimed to test for associations between polymorphisms in IL1B (-31 and +3954), IL10-592 and IL1RN variable number of tandem repeats (VNTR) and risk of gastric cancer in a Mexican population. DNA was extracted from sera of 183 gastric adenocarcinoma patients and 377 controls. The IL1B-31, IL1B+3954 and IL10-592 biallelic polymorphisms were discriminated using 5' Nuclease (TaqMan) assays and Pyrosequencing. The IL1RN penta-allelic VNTR polymorphism was genotyped using PCR followed by GeneScan analysis. A significant interaction was found between IL1B-31 and CagA status for the risk of intestinal-type gastric cancer (p = 0.023). Among CagA positive subjects, those with IL1B-31CC genotype had an increased risk of intestinal-type gastric cancer (OR 3.19, 95%CI = 1.05-9.68), compared to carriers of IL1B-31TT genotype. In contrast, among CagA negative subjects, no significant association of IL1B-31CC genotype with gastric cancer was observed. The IL10-592CC genotype was associated with more than doubling of the risk of the intestinal-type gastric cancer (OR, 2.20, 95%CI = 1.04-4.65). A nonsignificantly increased risk for intestinal-type gastric cancer was found in IL1RN*2 carriers (OR 1.49, 95%CI = 0.89-2.50). None of these polymorphisms was significantly related to the risk of diffuse-type gastric cancer. No significant association was found between risk of gastric cancer and the IL1B+3954 polymorphism. Individuals carrying 2 or more of the risk-associated alleles (IL1B-31C, IL1RN *2 and IL10-592C) were at increased risk for intestinal-type gastric cancer, compared to those with 0 or 1 risk-associated allele. The risk from multiple risk-associated alleles was especially high in subjects infected with CagA positive H. pylori. Our results support the identification of the IL1B-31 promoter polymorphism as a useful marker for risk of intestinal type gastric cancer in persons with CagA positive H. pylori infections.