Helicobacter pylori and the molecular pathogenesis of intestinal-type gastric carcinoma

Abstract

Gastric carcinoma is an inflammation-related cancer caused by long-term infection with the human bacterial pathogen, Helicobacter pylori. The pattern of acute-on-chronic inflammation causes progressive mucosal damage which may result in atrophy with metaplastic epithelia and eventually gastric cancer. Recently, it has been recognized that H. pylori can also cause genetic instability such as double-stranded DNA breaks and can produce gene activation and silencing via epigenetic pathways. As genetic instability is the hallmark of cancer, we highlight recent progress in understanding the gastric carcinogenesis in relation to H. pylori-related inflammation, H. pylori-induced double-stranded DNA breakage and aberrant gene expression as well as the mechanisms and role of H. pylori-associated epigenetic change in gene expression.

Keywords: DNA breakage; Helicobacter pylori; epigenetic gene expression changes; food intake; genome instabilities; inflammations; intestinal-type gastric cancers; virulence factors.