Eradication of Helicobacter pylori decreases the expression of p53 and c-Myc oncogenes

Abstract 

Background and study aims

Although it is fairly well accepted that Helicobacter pylori infection (H. pylori) plays a significant role in causing gastric cancer, the exact mechanisms involved in its pathogenesis are unclear and there is controversial data about the state of chronic gastritis and the precancerous lesion after treatment of H. pylori. This study was designed to investigate the relationship between H. pylori infection, the activity of chronic gastritis and oncogenes before and after treatment of H. pylori.

Patients and methods

Fifty-five of chronic gastritis cases were studied for H. pylori, activity of chronic gastritis, p53 and c-Myc expression. Positive H. pylori cases were re-evaluated again for the activity of gastritis, expression of p53 and c-Myc after treatment (6 months later).

Results

Forty-five cases were positive for H. pylori. The activity of chronic gastritis correlated with H. pylori infection. p53 and c-Myc expression correlated positively with the grade of chronic gastritis. After treatment of H. pylori, the activity of gastritis decreased and the expression of both p53 and c-Myc decreased.

Conclusion

H. pylori infection in the gastric mucosa may be implicated in the pathway of gastric carcinogenesis. It seems that H. pylori infection is responsible for early genomic instability even before any neoplastic changes and its eradication can reverse the sequence of inflammation and related atrophy, metaplasia, and genomic instability and, thus, may prevent gastric cancer development.

Keywords: Helicobacter pylori, Chronic gastritis, Intestinal metaplasia, p53, c-Myc