Considering that EBV-associated GCs show global CpG island methylation, our findings suggest that EBV infection allows the gastric mucosa to escape from aberrant methylation of hMLH1 and induces a malignant pathway independent of MSI.
Taken together, loss of ARID1A may be an early change in carcinogenesis and may precede EBV infection in gastric epithelial cells, while loss of ARID1A promotes cancer progression in gastric cancer cells without EBV infection or loss of MLH1 expression.
To verify the methylation status of CDH1, DAPK, COX2, hMLH1 and CDKN2A genes and to evaluate their association with Helicobacter pylori (H. pylori)-cagA(+) and Epstein Barr virus (EBV) infections in gastric adenocarcinomas.