Su1932 H. pylori Might Induce TGF-β1-Induced EMT by Way of cagE

Abstract

G A A b st ra ct s suppresses the development of MGC. To clarify the molecular changes due to H. pylori eradication, in this study, we evaluated differences in molecular alterations related to carcinogenesis in background mucosa of GC between H. pylori positive and negative patients. Materials and Methods: Seventy-seven consecutive patients who underwent ER for GC were enrolled. H. pylori status was analyzed in each patient by two methods: Giemsa staining and serum H. pylori-IgG antibody. Biopsy specimens were obtained from all cases, and DNA was extracted from intestinal metaplasia (IM), a precancerous lesion, via laser capture microdissection. Microsatellite instability (MSI) was evaluated at five loci based on the Bethesda panel; promoter methylation at hMLH1, E-cadherin, p16, and APC was assessed using methylation-specific polymerase chain reaction. Reactivity of monoclonal antibody for colonic phenotype (mAb Das-1) to IM was also evaluated by an immunoperoxidase assay. Results: H. pylori status was negative in 32 of 77 participants (41.6%). The incidence of MSI and hypermethylation at hMLH1, E-cadherin, p16, and APC genes in IM for H. pylori positive and negative patients, respectively, were 47.6%, 23.7%, 10.5% and 56.1% and 36.7%, 6.7%, 3.4%, 38.7% and 35.5%. There were no significant differences in molecular alterations between H. pylori positive and negative cases. mAb Das-1 reactivity to IM was 70.5% in H. pylori positive and 71.0% in H. pylori negative patients, demonstrating no significant difference. Conclusions: Early GC occurs frequently even in H. pylori negative patients. There were no significant differences in molecular alterations in IM between H. pylori positive and negative patients, suggesting that H. pylori eradication may not change the course of molecular alterations in background mucosa once GC has occured in the stomach.