Helicobacter, Inflammation, and Gastric Cancer

Document Type

Journal Article

Publication Date

3-1-2013

Journal

Current Pathobiology Reports

Volume

1

Issue

1

DOI

10.1007/s40139-013-0009-8

Keywords

DNA repair; Gastric cancer; H. pylori; Helicobacter; Inflammation; Mutation; Pathobiology; Stem cells

Abstract

© 2013, Springer Science+Business Media New York. Helicobacter pylori infection leads to long-lasting chronic inflammation and represents the most common risk factor underlying gastric cancer. Recently, new insights into the mechanisms through which H. pylori and mucosal inflammation lead to cancer development have emerged. H. pylori virulence factors, in particular specific CagA genotypes, represent main factors in gastric cancer, inducing altered intracellular signaling in epithelial cells. The chronic nature of H. pylori infection appears to relate to the VacA virulence factor and Th17/Treg mechanisms. A role of H. pylori infection in epigenetic and microRNA deregulation has been shown. Mutations of the epithelial cell genome, a hallmark of cancer, were demonstrated to accumulate in H. pylori infected 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.

This document is currently not available here.

Share

COinS