He Bangshun, Xu Tao, Pan Bei, Pan Yuqin, Wang Xuhong, Dong Jingwu, Sun Huiling, Xu Xueni, Liu Xiangxiang, Wang Shukui
1General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, 68 Changle Road, Nanjing, 210006 China.
2Helicobacter pylori Research Key Laboratory, Nanjing Medical University, Nanjing, 210000 China.
Cancer Cell Int. 2018 Nov 20;18:191. doi: 10.1186/s12935-018-0682-0. eCollection 2018.
()-induced gastric cancer is an intricate progression of immune response against infection. IL-16, TGF-β1 and TLR4 pathways were the mediators involved in the immune response. We hypothesized that genetic variations in genes of these pathways have potential susceptibility to gastric cancer risk, and predict clinical outcomes of patients.
To investigate the susceptibility and prognostic value of genetic variations of -, and pathways to gastric cancer, we performed a case-control study combined a retrospective study in a Chinese population. Genotyping for all polymorphisms was based on the Sequenom's MassARRAY platform, and infection was determined by using an immunogold testing kit.
We found rs10512263 CC genotype was found to be a decreased risk of gastric cancer (CC vs. TT: adjusted OR = 0.54, 95% CI 0.31-0.97); however, rs334348 GG genotype was associated with increased risk of gastric cancer (GG vs. AA: adjusted OR = 1.51, 95% CI 1.05-2.18). We found that carriers harboring rs1927911 A allele (GA/AA) or rs10512263 C allele (CT/CC) have unfavorable survival time than none carriers (rs1927911: GA/AA vs. GG: adjusted HR = 1.27, 95% CI 1.00-1.63; rs10512263: CT/CC vs. TT: adjusted HR = 1.29, 95% CI 1.02-1.63) and that individuals harboring both two minor alleles (rs1927911 GA/AA and rs10512263 CT/CC) suffered a significant unfavorable survival (adjusted HR = 1.64, 95% CI 1.17-2.31).
In short, we concluded that two polymorphisms (rs334348, rs10512263) in were associated with risk of gastric cancer, and that rs1927911 and rs10512263 were associated with clinical outcomes of gastric cancer patients.
（）诱发的胃癌是针对感染的免疫反应的复杂进展。白细胞介素-16、转化生长因子-β1和Toll样受体4途径是参与免疫反应的介质。我们假设这些途径基因的遗传变异对胃癌风险具有潜在易感性，并可预测患者的临床结局。
为了研究、和途径的遗传变异对胃癌的易感性和预后价值，我们在中国人群中进行了一项病例对照研究并结合一项回顾性研究。所有多态性的基因分型基于Sequenom的MassARRAY平台，感染情况通过免疫金检测试剂盒确定。
我们发现rs10512263 CC基因型胃癌风险降低（CC与TT相比：校正比值比=0.54，95%可信区间0.31-0.97）；然而，rs334348 GG基因型与胃癌风险增加相关（GG与AA相比：校正比值比=1.51，95%可信区间1.05-2.18）。我们发现携带rs1927911 A等位基因（GA/AA）或rs10512263 C等位基因（CT/CC）的携带者生存时间比非携带者差（rs1927911：GA/AA与GG相比：校正风险比=1.27，95%可信区间1.00-1.63；rs10512263：CT/CC与TT相比：校正风险比=1.29，95%可信区间1.02-1.63），并且同时携带两个次要等位基因（rs1927911 GA/AA和rs10512263 CT/CC）的个体生存明显较差（校正风险比=1.64，95%可信区间1.17-2.31）。
简而言之，我们得出结论，中的两个多态性（rs334348、rs10512263）与胃癌风险相关，并且rs1927911和rs10512263与胃癌患者的临床结局相关。
