Promoter Methylation Status of P53 and E-Cadherin Genes in Gastric Cancer and its Association with Epstein-Barr Virus and Helicobacter Pylori Infections

Abstract

Objectives: Gastric cancer is one of the leading causes of morbidity and mortality worldwide. As in other cancers, the development and progression of gastric cancer has been attributed to many factors, including infection with Helicobacter pylori (H. pylori) and Epstein-Barr virus (EBV), genetic alterations, and epigenetic silencing due to aberrant methylation of tumor suppressor genes. The purpose of this work is to analyze the promoter methylation status of P53 (TP53) and E-cadherin (CDH1) genes and its association with EBV and H. pylori infections in the gastric cancer patients of Grand Casablanca. Methods: In this study, a total of 50 gastric cancer patients were recruited. Methylation in tumor tissues was detected by methylation-specific PCR (MSP), and the clinical relevance was statistically analyzed. Results: Results revealed a methylation of TP53 promoter observed in 36% of gastric carcinoma cases, which was significantly higher than adjacent normal tissue [p?0.0001]. While no methylation of CDH1 promoter was observed. Furthermore, the frequency of TP53 promoter methylation was significantly different with intestinal and diffuse types of gastric cancer [22.3% vs 77.7%; <0.05]. Moreover cases with EBV infection had higher frequencies of TP53 methylation [p<0.05], while no significant correlation between H. pylori and TP53 methylation was observed. Conclusion: Thus; the present data suggest a vital role of epigenetic alteration of TP53 in the causation and development of gastric cancer, especially Epstein-Barr virus-associated gastric cancer in our population. Keywords: Epstein-Barr virus, CDH1, gastric cancer, methylation, TP53, helicobacter pylori