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Review
. 2017 Aug 3;18(8):1699.
doi: 10.3390/ijms18081699.

Prevention of Gastric Cancer: Eradication of Helicobacter Pylori and Beyond

Affiliations
Review

Prevention of Gastric Cancer: Eradication of Helicobacter Pylori and Beyond

Tetsuya Tsukamoto et al. Int J Mol Sci. .

Abstract

Although its prevalence is declining, gastric cancer remains a significant public health issue. The bacterium Helicobacter pylori is known to colonize the human stomach and induce chronic atrophic gastritis, intestinal metaplasia, and gastric cancer. Results using a Mongolian gerbil model revealed that H. pylori infection increased the incidence of carcinogen-induced adenocarcinoma, whereas curative treatment of H. pylori significantly lowered cancer incidence. Furthermore, some epidemiological studies have shown that eradication of H. pylori reduces the development of metachronous cancer in humans. However, other reports have warned that human cases of atrophic metaplastic gastritis are already at risk for gastric cancer development, even after eradication of these bacteria. In this article, we discuss the effectiveness of H. pylori eradication and the morphological changes that occur in gastric dysplasia/cancer lesions. We further assess the control of gastric cancer using various chemopreventive agents.

Keywords: Helicobacter pylori; chemoprevention; chronic atrophic gastritis; eradication; intestinal metaplasia.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Gastric inflammation before and after eradication of Helicobacter pylori. (A) Neutrophil inflammation before H. pylori eradication; (B) edematous stroma after H. pylori eradication. Hematoxylin-Eosin (HE) staining. Original magnification, 400× (A,B).
Figure 2
Figure 2
Gastric dysplasia (intramucosal adenocarcinoma) before and after eradication of Helicobacter pylori. (A,B) Dysplasia proliferating to the surface of the mucosa in an H. pylori-positive specimen (*). (C,D) Regression of dysplasia, localized beneath the normal surface epithelium in an H. pylori-negative specimen (**). HE staining (A,B) and Ki-67 immunostaining (C,D). Original magnification, 100×.
Figure 3
Figure 3
Schematic view of gastric dysplasia (intramucosal adenocarcinoma) before and after eradication of Helicobacter pylori (H. pylori). Normal glands have proliferating cells in the lower narrow region (left). H. pylori infection widens proliferating zone in the normal glands (middle, blue line). Gastric dysplasia shows expanding proliferation with H. pylori infection and inflammation (middle, orange line). The tumor is shown around the proliferative zone (right, orange line) with subsequent regression at the top and bottom regions that are then occupied by adjacent normal epithelia (right, blue line) after eradication.

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