| [ Summary ] |
The Epstein-Barr virus(EBV) is a DNA tumor virus, which is detected in 10% of all cases of gastric carcinoma(GC). Analysis of EBV-positive GC biopsies indicates that the carcinomas are formed by monoclonal proliferation of EBV-infected single cells. These findings suggest that EBV plays an important role in the development of EBV-positive GCs. EBV maintains latent infections in cancer cells, and the infected cells express only specific latent genes, such as EBV determined nuclear antigens(EBNA1), EBV-encoded small RNA (EBER), and BamHI-A rightward transcripts(BARTs). In some cases, latent membrane protein 2A(LMP2A) and BamHI-A rightward frame 1(BARFI) are also expressed. Epithelial cells are refractory to EBV infection in vitro. This has hampered the study of the role of EBV on epithelioid malignancies. We have overcome this difficulty through the use of recombinant EBV carrying a selectable marker gene, and have established in vitro models of EBV infection of epithelial cells. The established cell clones expressed EBV genes which were identical to those expressed in EBV-positive GCs, and showed accelerated malignant properties including increase of growth rate and growth in soft agarose. In addition, primary gastric epithelial cells were immortalized by EBV infection. Here in, we introduce our findings concerning the role of EBV on EBV-positive GC, and summarize recent reports on the functions of each EBV gene expressed in EBV-positive GCs. We also discuss the molecular mechanisms of EBV-mediated epithelioid malignancies. |