Epstein-Barr Virus and Human Cancer

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(l) We demonstrated that EBV associated gastric carcinomas (EBV aGC) represent a clonal proliferation even in gastric mucosa at very early stages of the development. The carcinomas accompany with multiple carcinomas infected with EBV.(2) We defined that EBV aGC develops in front of chronic atrophic gastritis and associates closely with the gastric mucosa border which is the place for remodel of tubular structures.(3) We found a new type of EBV aGC which EBV infection is restricted in a small portion of the carcinoma. Two EBV infected cell lines were established from the cancerous and non-cancerous portions, respectively.(4) We re-evaluated that nasal T/NK cell lymphomas were originated from NK cells and defined the EBV latency type 2 infection in the cells.(5) We demonstrated that lethal midline granuloma (rhintis gangrenosa progressiva) is originated from NK or T cells and established the cell lines which have the characters of the lymphoma. The all cell lines were EBV positive NK cells and had the abnormality of chromosom 6 accompanied with a deletion of the long arm.(6) We defined the difference of escaping to cytotoxic T-cell mediated immune surveillance mechanisms between pyothorax-associated lymphoma and nasal natural killer-cell lymphoma.(7) We characterized EBNA-LP and defined the expression in cytoplasm and the co-localization with a cellular regulating factor HAX-1 and homo-dimelization of EBNA-LP.(8) We analyzed that the C-terminal regions of LMP-l is critical for the regulation of apoptosis and BHRFinhibits the apoptosis with TRAIL by suppression of caspase 8 activity.