The LCR of EBV makes Burkitt's lymphoma endemic.

The spectacular ability of Epstein-Barr virus (EBV) to immortalize and morphologically transform human B cells in vitro to lymphoblastoid cell lines (LCLs) is central to most molecular models of viral oncogenesis. However, binding of transcription factor and oncoprotein c-Myc to the major locus control region (LCR) of the viral genome directs us to an alternative model for the origin of Burkitt's lymphoma (BL). In this model, improved nuclear maintenance of the viral genome and the continuous expression of anti-apoptotic functions in B cells exhibiting class I EBV latency contribute to the generation of BL, without any detour through EBV nuclear antigen (EBNA) 2-driven B-cell immortalization (also called class III latency).