| First Author | Ontiveros EP | Year | 2014 |
| Journal | Leuk Lymphoma | Volume | 55 |
| Issue | 12 | Pages | 2917-23 |
| PubMed ID | 24605938 | Mgi Jnum | J:326984 |
| Mgi Id | MGI:7327458 | Doi | 10.3109/10428194.2014.900762 |
| Citation | Ontiveros EP, et al. (2014) A new model of LMP1-MYC interaction in B cell lymphoma. Leuk Lymphoma 55(12):2917-23 |
| abstractText | Epstein-Barr virus (EBV) is associated with aggressive B cell lymphomas (BCLs). Latent membrane protein 1 (LMP1) of EBV is an oncogenic protein required for EBV B cell transformation. However, LMP1 is a weak oncogene in mice. Mice expressing Myc inserted 5' of the Emu enhancer (iMyc(Emu)), mimicking the t(8;14) translocation of endemic Burkitt lymphoma, develop delayed onset BCLs. To investigate potential cooperation between LMP1 and oncogenic MYC, we produced mice expressing the LMP1 signaling domain via a hybrid CD40-LMP1 transgene (mCD40-LMP1), and the dysregulated MYC protein of aggressive EBV+ BCLs. mCD40-LMP1/iMyc(Emu) mice trended toward earlier BCL onset. BCLs from mCD40-LMP1/iMyc(Emu) mice expressed LMP1 and were transplantable into immunocompetent recipients. iMyc(Emu) and mCD40-LMP1/iMyc(Emu) mice developed BCLs with similar immunophenotypes. LMP1 signaling was intact in BCLs as shown by inducible interleukin-6. Additionally, LMP1 signaling to tumor cells induced the two isoforms of Pim1, a constitutively active prosurvival kinase implicated in lymphomagenesis. |
