Esptein-Barr Virus Related Protein Expression and Clinicopathological Findings in Epstein-Barr Virus Genome Positive Gastric Carcinomas

This study has been carried out rate of Epstein-Barr virus (EBV) positive gastric carcinomas, these have been known frequency of EBV infection in gastric carcinoma with lymphoid stroma (GCLS) that has marked lymphocytic infiltration around the tumor and stroma in the medullary poorly differentiated adenocarcinoma. And has been undertaken significance of EBV infection and carcinogenesis of EBV for latent gene protein EBNA2 and LMP1 expression and characterized clinicopathological findings in EBV positive gastric carcinomas, and classified EBV positive gastric carcinoma in EBV related neoplasma. Additionally, relationship between EBV infection and lymphcytic infiltration of gastric carcinomas. The subjects consisted of three groups, 10 cases were GCLS, 14 cases were marked lymphocytic infiltration except for GCLS, and 300 cases were none or few lymphocytic infiltration. EBV positive cases were 8 to 10 (80.0%) in GCLS, 8 of 14 (57.1%) in lymphocytic infiltration group, and 23 of 300 (7.7%) in nonlymphocytic infiltration group. GCLS and lymphocytic infiltration group were frequent related of EBV positive gastric carcinomas that were lower lymph nodes involvement than non-lymphocytic infiltration group. EBV expression was early gastric carcinoma and positive reaction was observed in the nucli of almost all neoplastic cells, and these infection were monoclonal multiplication, but EBNA2 and LMP1 were not detect in all EBV positive cases. EBV positive gastric carcinomas were in Burkitt's lymphoma group (EBNA2-, LMP1-) or nasopharyngeal carcinoma group (EBNA2-, LMP1+/-). Our result suggest that EBV has inactivity and unability of permanent multiply in cancerous cells, but EBV infection occurred early oncogenesis and EBV infected cancerous cells include a faciling for escaping immunoreaction, for example the lymphocystic immunoreaction, and has been kept long term the latent infection and these phenomenon may be add to carcinogenesis of gastric carcinoma.