| First Author | Bultema R | Year | 2009 |
| Journal | Oncogene | Volume | 28 |
| Issue | 11 | Pages | 1471-6 |
| PubMed ID | 19182823 | Mgi Jnum | J:147588 |
| Mgi Id | MGI:3841517 | Doi | 10.1038/onc.2008.492 |
| Citation | Bultema R, et al. (2009) Epstein-Barr virus LMP2A accelerates MYC-induced lymphomagenesis. Oncogene 28(11):1471-6 |
| abstractText | Despite the identification of Epstein-Barr virus (EBV) in tumors of Burkitt's lymphoma (BL) over 40 years ago, the exact contribution of EBV to BL is undefined. EBV encodes for multiple proteins in latent B cells that affect B cell survival and activation. One such protein, latent membrane protein 2A (LMP2A), protects B cells from numerous pro-apoptotic stimuli. Therefore, we tested whether LMP2A protects B cells from apoptosis induced by aberrant c-MYC expression that precedes and dominates BL. We crossed LMP2A-transgenic mice (LMP2A-Tg), in which all B cells express LMP2A, to a transgenic mouse that expresses a BL translocation of myc (lambda-MYC-Tg mice). LMP2A promotes proliferation and protects B cells from MYC-induced apoptosis in lambda-MYC-Tg mice. LMP2A also accelerates the development of lymphoma in LMP2A/lambda-MYC-Tg mice. Finally, LMP2A increases the expression of Bcl-X(L) in both pre-tumor B cells and tumor cells, suggesting a mechanism for LMP2A-mediated B cell survival in the presence of MYC. These results support a hypothesis that EBV LMP2A promotes tumor development by protecting pre-tumor B cells that would normally apoptose after the c-myc translocation. |
