Published online Sep 28, 2014. doi: 10.3748/wjg.v20.i36.12860
Revised: March 12, 2014
Accepted: May 29, 2014
Published online: September 28, 2014
Processing time: 308 Days and 19.4 Hours
Gastric cancer is one of the most frequent neoplasms and a main cause of death worldwide, especially in China and Japan. Numerous epidemiological, animal and experimental studies support a positive association between chronic Helicobacter pylori (H. pylori) infection and the development of gastric cancer. However, the exact mechanism whereby H. pylori causes gastric carcinogenesis remains unclear. It has been demonstrated that expression of cyclooxygenase-2 (COX-2) is elevated in gastric carcinomas and in their precursor lesions. In this review, we present the latest clinical and experimental evidence showing the role of gastrin and COX-2 in H. pylori-infected patients and their possible association with gastric cancer risk.
Core tip:Helicobacter pylori (H. pylori) is one of the most common pathogens, infecting approximately half of the world’s population. It is well known that H. pylori infection has been associated with an elevated risk of developing gastric carcinoma. In this review, we present the latest clinical and experimental evidence showing the role of gastrin and cyclooxygenase-2 in H. pylori-infected patients and their possible association with gastric cancer risk.