Helicobacter pylori-associated Chronic Atrophic Gastritis and Progression of Gastric Carcinogenesis

Abstract

Chronic inflammation due to a Helicobacter pylori (H. pylori) infection is a representative cause of gastric cancer that can promote gastric carcinogenesis by abnormally activating immune cells and increasing the inflammatory cytokines levels. H. pylori infections directly cause DNA double-strand breaks in gastric epithelial cells and genetic damage by increasing the enzymatic activity of cytidine deaminase. Eventually, gastric cancer is induced through dysplasia. Hypermethylation of tumor suppressor genes is an important cause of gastric cancer because of a H. pylori infection. In addition, the changes in gastric microbiota and the mucosal inflammatory changes associated with a co-infection with the Epstein-Barr virus are associated with gastric cancer development. DNA damage induced by H. pylori and the subsequent responses of gastric stem cells have implications for gastric carcinogenesis. Although the pathogenesis of H. pylori has been established, many uncertainties remain, requiring more study.

Keywords: Gastric cancer; Helicobacter pylori; Inflammation.

Fig. 1

Metachronous gastric cancer after Helicobacter pylori eradication. (A) A 2.0 cm elevated mucosal lesion with a central depression (arrow) is identified on the anterior wall of the proximal antrum on the initial endoscopy. After endoscopic submucosal dissection, successful Helicobacter pylori is performed. (B) After six years of endoscopic treatment, surveillance endoscopy shows a surgical scar on the anterior wall of the proximal antrum. A 1.4 cm elevated mucosal lesion with central depression is shown on the greater curvature side of the high body. It is a metachronous lesion.