Published online Feb 15, 2016. doi: 10.4291/wjgp.v7.i1.97
Peer-review started: May 5, 2015
First decision: July 27, 2015
Revised: September 18, 2015
Accepted: November 3, 2015
Article in press: November 4, 2015
Published online: February 15, 2016
Processing time: 278 Days and 11.9 Hours
Gastric cancer (GC) is one of the most common carcinoma and the second leading cause of cancer-related deaths worldwide. Helicobacter pylori (H. pylori) infection causes a series of precancerous lesions like gastritis, atrophy, intestinal metaplasia and dysplasia, and is the strongest known risk factor for GC, as supported by epidemiological, preclinical and clinical studies. However, the mechanism of H. pylori developing gastric carcinoma has not been well defined. Among infected individuals, approximately 10% develop severe gastric lesions such as peptic ulcer disease, 1%-3% progresses to GC. The outcomes of H. pylori infection are determined by bacterial virulence, genetic polymorphism of hosts as well as environmental factors. It is important to gain further understanding of the pathogenesis of H. pylori infection for developing more effective treatments for this common but deadly malignancy. The recent findings on the bacterial virulence factors, effects of H. pylori on epithelial cells, genetic polymorphism of both the bacterium and its host, and the environmental factors for GC are discussed with focus on the role of H. pylori in gastric carcinogenesis in this review.
Core tip: It is important to gain further understanding of the pathogenesis of Helicobacter pylori (H. pylori) infection for developing more effective treatments for this common but deadly malignancy. The recent findings on the bacterial virulence factors, effects of H. pylori on epithelial cells, genetic polymorphism of both the bacterium and its host, and the environmental factors for gastric cancer are discussed with focus on the role of H. pylori in gastric carcinogenesis in this review.