Abstract
Epstein–Barr virus (EBV) was first identified in malignant Burkitt lymphoma cells in 1964. Since then, EBV has been associated with a number of other malignancies of either lymphocytic origin, including both B cell and NK/T cell cancers, or epithelial origin, predominantlynasopharyngeal and gastric cancers. While a complete understanding of the relationship between EBV-mediated cellular transformation and the oncogenic events that lead to uncontrolled malignant cell growth remains to be determined for a number of these cancers, it is clear in all of these settings that a breakdown in the immune surveillance of virally infected cells contributes to the survival of EBV-bearing malignant cells.
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