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首页> 外文期刊>Radiology and Oncology >The influence of cytokine gene polymorphisms on the risk of developing gastric cancer in patients with Helicobacter pylori infection
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The influence of cytokine gene polymorphisms on the risk of developing gastric cancer in patients with Helicobacter pylori infection

机译：细胞因子基因多态性对幽门螺杆菌感染患者发生胃癌风险的影响

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Background. Helicobacter pylori infection is the main cause of gastric cancer. The disease progression is influenced by the host inflammatory responses, and cytokine single nucleotide polymorphisms (SNPs) may have a role in the course of the disease. The aim of our study was to investigate proinflammatory cytokine polymorphisms, previously associated with the development of gastric cancer, in a Slovenian population.Patients and methods. In total 318 patients and controls were selected for the study and divided into three groups: (i) patients with gastric cancer (n = 58), (ii) patients with chronic gastritis (n = 60) and (iii) healthy control group (n = 200). H. pylori infection in patient groups was determined by serology, histology and culture. Four proinflammatory gene polymorphisms were determined (IL-1?2, IL-1r?±, TNF-?±, TLR-4) in all subjects.Results. We found a statistically significant difference between males and females for the groups (p = 0.025). Odds ratio (OR) for gastric cancer risk for females was 0.557 (95% confidence interval [CI]: 0.233a€?1.329) and for chronic gastritis 2.073 (95% CI: 1.005a€?4.277). IL-1B-511*T/T homozygous allele for cancer group had OR = 2.349 (95% CI: 0.583a€?9.462), heterozygous IL-1B-511*T had OR = 1.470 (95% CI: 0.583a€?3.709) and heterozygotes in TNF-A-308 genotype for chronic gastritis had OR = 1.402 (95% CI: 0.626a€?3.139). Other alleles had OR less than 1.Conclusions. We could not prove association between gastric cancer and chronic gastritis due to H. pylori in any cytokine SNPs studied in Slovenian population. Other SNPs might be responsible besides infection with H. pylori for the progression from atrophy to neoplastic transformation.
机译：背景。幽门螺杆菌感染是胃癌的主要原因。疾病的进展受宿主炎症反应的影响，细胞因子单核苷酸多态性（SNP）可能在疾病过程中起作用。我们研究的目的是调查斯洛文尼亚人群中以前与胃癌的发展有关的促炎细胞因子多态性。患者和方法。总共318名患者和对照组被选为研究对象，分为三组：（i）胃癌患者（n = 58），（ii）慢性胃炎患者（n = 60）和（iii）健康对照组（ n = 200）。通过血清学，组织学和培养确定患者组中的幽门螺杆菌感染。在所有受试者中确定了四个促炎基因多态性（IL-1？2，IL-1r？±，TNF-？±，TLR-4）。我们发现两组之间的男性和女性之间在统计学上有显着差异（p = 0.025）。女性患胃癌的几率（OR）为0.557（95％可信区间[CI]：0.233a？1.329）和慢性胃炎2.073（95％CI：1.005a？4.277）。癌症组的IL-1B-511 * T / T纯合等位基因OR = 2.349（95％CI：0.583a？9.462），杂合性IL-1B-511 * T具有OR = 1.470（95％CI：0.583a€）慢性胃炎的TNF-A-308基因型中的杂合子（OR = 3.709）OR = 1.402（95％CI：0.626a = 3.139）。其他等位基因的OR小于1。在斯洛文尼亚人群中研究的任何细胞因子SNP中，我们都无法证明由于幽门螺杆菌引起的胃癌与慢性胃炎之间的关联。除感染幽门螺杆菌外，其他SNP可能还负责从萎缩到肿瘤转化的进程。

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