title: Helicobacter, Inflammation, and Gastric Cancer.
abstract: Helicobacter pyloriinfection leads to long-lasting chronic inflammation and represents the most common risk factor underlying gastric cancer. Recently, new insights into the mechanisms through whichH. pyloriand mucosal inflammation lead to cancer development have emerged.H. pylorivirulence factors, in particular specificCagAgenotypes, represent main factors in gastric cancer, inducing altered intracellular signaling in epithelial cells. The chronic nature ofH. pyloriinfection appears to relate to the VacA virulence factor and Th17/Treg mechanisms. A role ofH. pyloriinfection in epigenetic and microRNA deregulation has been shown. Mutation of the epithelial cell genome, a hallmark of cancer, was demonstrated to accumulate inH. pyloriinfected stomach partly due to inadequate DNA repair. Gastric stem cells were shown to be targets of oxidative injury in the Helicobacter-inflammatory milieu. Recent advances emphasizing the contribution of bacterial factors, inflammatory mediators, and the host epithelial response in gastric carcinogenesis are reviewed.
authors.forename: Antonia R
authors.initials: AR
authors.lastname: Sepulveda
keywords: DNA repair; Gastric cancer; H. pylori; Helicobacter; Inflammation; Mutation; Pathobiology; Stem cells