Background: The Epstein-Barr virus (EBV) has been detected in lymphoepithelioma of the nasopharynx and lymphoepithelioma-like carcinomas in various organs. Ten percent of gastric carcinomas, including lymphepithelioma-like carcinoma and adenocarcinoma, are associated with EBV infection. The p16 protein is a cyclin-dependent kinase (CDK) inhibitor that decelerates the cell cycle, inactivating the CDKs that phosphorylate retinoblastoma (Rb) protein.
Materials and methods: To clarify the relationship between p16 overexpression and EBV-associated gastric carcinomas, immunohistochemical analysis of p16 and detection of EBV by in situ hybridization were performed on 238 formalin-fixed and paraffin-embedded samples of gastric carcinomas.
Results: The non-expression of p16 protein in EBV-positive and -negative carcinoma was 81.5% (53 out of 65 samples) and 26.6% (46 out of 173 samples), respectively (p < 0.001).
Conclusion: We suggest that the carcinogenesis of EBV-associated gastric cancers may be closely associated with a p16 abnormality.