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.
复制标题
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
复制
发表时间:
2006
影响因子:
6.4
通讯作者:
Muñoz,Nubia
中科院分区:
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
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.