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. 2013 Mar;1(1):9-18.
doi: 10.1007/s40139-013-0009-8.

Helicobacter, Inflammation, and Gastric Cancer

Antonia R Sepulveda

Helicobacter, Inflammation, and Gastric Cancer

Antonia R Sepulveda. Curr Pathobiol Rep. 2013 Mar.

Abstract

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. Mutation of the epithelial cell genome, a hallmark of cancer, was 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.

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

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Conflict of interest statement

Disclosure No potential conflicts of interest relevant to this article were reported.

Figures

Figure 1
Figure 1
H. pylori virulence factors and inflammation mechanisms leading to gastric cancer.
See this image and copyright information in PMC

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