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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Dec 15, 2015; 7(12): 455-465
Published online Dec 15, 2015. doi: 10.4251/wjgo.v7.i12.455
Helicobacter pylori in gastric carcinogenesis
Hyo Jun Ahn, Dong Soo Lee
Hyo Jun Ahn, Dong Soo Lee, Division of Gastroenterology, Department of Internal Medicine, College of Medicine, Daejeon St. Mary’s Hospital, the Catholic University of Korea, Daejeon 301-723, South Korea
Author contributions: Ahn HJ and Lee DS equally contributed to this paper with conception and design of the study, literature review and analysis, drafting and critical revision and editing, and final approval of the final version.
Conflict-of-interest statement: The authors have no conflict of interest related to the manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dong Soo Lee, MD, PhD, Division of Gastroenterology, Department of Internal Medicine, College of Medicine, Daejeon St. Mary’s Hospital, the Catholic University of Korea, Daeheung-ro 64, Jung-gu, Daejeon 301-723, South Korea. endoscope@hanmail.net
Telephone: +82-42-2209294
Received: June 27, 2015
Peer-review started: June 27, 2015
First decision: July 25, 2015
Revised: October 10, 2015
Accepted: November 3, 2015
Article in press: November 4, 2015
Published online: December 15, 2015
Processing time: 170 Days and 11.1 Hours
Abstract

Gastric cancer still is a major concern as the third most common cancer worldwide, despite declining rates of incidence in many Western countries. Helicobacter pylori (H. pylori) is the major cause of gastric carcinogenesis, and its infection insults gastric mucosa leading to the occurrence of atrophic gastritis which progress to intestinal metaplasia, dysplasia, early gastric cancer, and advanced gastric cancer consequently. This review focuses on multiple factors including microbial virulence factors, host genetic factors, and environmental factors, which can heighten the chance of occurrence of gastric adenocarcinoma due to H. pylori infection. Bacterial virulence factors are key components in controlling the immune response associated with the induction of carcinogenesis, and cagA and vacA are the most well-known pathogenic factors. Host genetic polymorphisms contribute to regulating the inflammatory response to H. pylori and will become increasingly important with advancing techniques. Environmental factors such as high salt and smoking may also play a role in gastric carcinogenesis. It is important to understand the virulence factors, host genetic factors, and environmental factors interacting in the multistep process of gastric carcinogenesis. To conclude, prevention via H. pylori eradication and controlling environmental factors such as diet, smoking, and alcohol is an important strategy to avoid H. pylori-associated gastric carcinogenesis.

Keywords: Helicobacter pylori; Gastric cancer

Core tip:Helicobacter pylori (H. pylori) is an important etiologic agent in gastric carcinogenesis. Here, we summarize not only recently investigated mechanisms of virulence factors, host genetic factors, and environmental factors, but also potential prevention. The best preventive methods in H. pylori-induced carcinogenesis may be achieved through H. pylori eradication, dietary, or lifestyle modifications, as well as a better understanding of molecular pathogenesis.