Chemoprevention of gastric cancer byHelicobacter pylorieradication and its underlying mechanism

摘要: The cascade of gastric cancer, a leading cause cancer incidence and mortality, is multifactorial. Helicobacter pylori (HP) infection plays major role in (GC), there has been an accumulation data regarding the chemopreventive effect HP eradication. However, it remains unclear how causes GC eradication prevents GC. To clarify this issue, following approaches were performed review article. First, HP-induced atrophic gastritis (AG) intestinal metaplasia (IM) provoke development shown, followed by long takes to induce reversible change AG IM. Second, epigenetic studies PTPN6, MOS, DCC, CRK, VAV1 noncancerous specimens terms status. Among these genes, MOS was found be possible surrogate marker for development. decreased aberrant DNA methylation gene-specific manner, played metachronous neoplasms. Third, transforming growth factor-β1 (TGF-β1) TGF-β1-induced epithelial-mesenchymal transition (EMT) markers investigated mucosa. triggered EMT pathway caused emergence stem cells, such as CD44v8-10. When eradicated, two pathways inhibited. Finally, 2222 cohort study showed that significantly risk noncardiac Taken together, effective primary prevention method, its underlying mechanism includes reversibility IM, methylation, EMT, cells.