Abstract
Epstein-Barr virus (EBV), a causal agent for infectious mononucleosis, is recognised as a carcinogenic agent for man, providing a major risk factor for a number of malignancies, including B-cell (Burkitt’s, immuno-suppression-related and Hodgkin’s disease) and T-cell (sinonasal angiocentric) lymphomas, and poorly differentiated nasopharyngeal carcinoma. Over the past decade, although the data are less consistent, an association with a large number of other tumors has been identified, including many lymphoepithelial carcinomas. The expression pattern of EBV genes differs among the tumors, implying strong host cell control over viral gene expression; non-overlapping regions on the viral genome, specific for immortalization of either B-lymphocytes or epithelial cells in culture have been identified. Reports on tumor cells that initially possess, then lose EBV genetic information, point to a possible “hit and run” mechanism following on from viral infection, without significant loss of cell phenotype. As such an event may mimic tumor progression, identification of the initial pattern of viral gene expression, followed by alterations that result in genetic loss, should be a focus of research for the future, alongside new protocols for viral and/or tumor containment.
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Griffin, B.E. (1999). Epstein-Barr Virus and Malignant Diseases. In: Hortobagyi, G.N., Khayat, D. (eds) Progress in Anti-Cancer Chemotherapy. Progress in Anti-Cancer Chemotherapy, vol 3. Springer, Paris. https://doi.org/10.1007/978-2-8178-0918-2_14
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DOI: https://doi.org/10.1007/978-2-8178-0918-2_14
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