Host-bacterial interaction in the development of gastric precancerous lesions in a high risk population for gastric cancer in Venezuela.

Host-bacterial interaction in the development of gastric precancerous lesions in a high risk population for gastric cancer in Venezuela.
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委内瑞拉胃癌高危人群胃癌前病变发展中宿主与细菌的相互作用。

DOI:
10.1002/ijc.21979
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发表时间:
2006
影响因子:
6.4
通讯作者:
Muñoz,Nubia
Muñoz,Nubia
中科院分区:
医学1区
文献类型:
--
作者:
Kato,Ikuko;vanDoorn,Leen-Jan;Canzian,Federico;Plummer,Martyn;Franceschi,Silvia;Vivas,Jorge;Lopez,Gladys;Lu,Yanhui;Gioia-Patricola,Lydie;Severson,RichardK;Schwartz,AnnG;Muñoz,Nubia

文献摘要

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幽门螺杆菌(HP)感染影响世界上超过50%的人口。在胃癌高危人群中,其患病率超过90%,但感染的临床结局高度可变,因此除了细菌因素外,宿主遗传因素也在其结局中发挥作用。在这项研究中,我们研究了已知在HP感染的胃粘膜中过表达的几种促炎细胞因子的常见功能遗传多态性对不同阶段胃癌前病变风险的影响。通过多项logistic回归分析,估计了2,033名委内瑞拉受试者中萎缩性胃炎、肠上皮化生和异型增生的比值比(OR)和95%置信区间(CI)。IL 8 - 251 A等位基因对异型增生的患病率有显著影响(p= 0.021)。与TT基因型相比,杂合子与A等位基因相关的OR为1.34(95%CI:0.82-2.18),纯合子为2.00(95%CI:1.13-3.56)。此外,A-等位基因的数量与HPcagA基因型之间存在统计学显著的相互作用(p= 0.009),表明A-等位基因仅在存在HPcagA时增加发育不良的风险。本组AA基因型与TT基因型的OR值为3.22(95%CI:1.60-6.52)。与研究的其他促炎细胞因子无关,即,IL 1 β、IL 6、单核细胞趋化蛋白1(MCP 1)和TNFα,或与其他阶段的癌前病变。本研究提供了重要的证据表明宿主-细菌相互作用在胃癌前病变的发展。© 2006 Wiley利斯公司
Helicobacter pylori(HP) infection affects over 50% of the world's population. The prevalence is over 90% in populations at high risk for gastric cancer, but clinical outcomes of the infection are highly variable and thus host genetic factors have been suggested to play a role in its outcomes in addition to bacterial factors. In this study, we examined the effects of common functional genetic polymorphisms of several proinflammatory cytokines known to be overexpressed in HP‐infected gastric mucosa on the risk of various stages of gastric premalignant lesions. The odds ratios (ORs) and 95% confidence intervals (CI) for atrophic gastritis, intestinal metaplasia and dysplasia were estimated by multinominal logistic regression analysis among 2,033 Venezuelan subjects. There was a significant effect ofIL8‐251A allele on the prevalence of dysplasia (p= 0.021). The OR associated with the A‐allele was 1.34 (95% CI: 0.82–2.18) for heterozygotes and 2.00 (95% CI: 1.13–3.56) for homozygotes, compared with the TT genotype. Furthermore, there was a statistically significant interaction between the number of A‐alleles and HPcagA genotype (p= 0.009), suggesting that the A‐allele increased the risk of dysplasia only whencagA was present. The OR for the AA compared with TT genotype was 3.22 (95% CI: 1.60–6.52) in this group. There were no associations with other proinflammatory cytokines studied, i.e., IL1β, IL6, monocyte chemoattractant protein 1 (MCP1) and TNFα, or with other stages of premalignant lesions. The present study provides important evidence suggesting host–bacterial interactions in the development of gastric precancerous lesions. © 2006 Wiley‐Liss, Inc.