| Literature DB >> 24605938 |
Evelena P Ontiveros1, Ahmad Halwani, Laura L Stunz, Natalie Kamberos, Alicia K Olivier, Siegfried Janz, Gail A Bishop.
Abstract
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 Eμ enhancer (iMyc(Eμ)), 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(Eμ) mice trended toward earlier BCL onset. BCLs from mCD40-LMP1/iMyc(Eμ) mice expressed LMP1 and were transplantable into immunocompetent recipients. iMyc(Eμ) and mCD40-LMP1/iMyc(Eμ) 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.Entities:
Keywords: LMP1; MYC; lymphoma
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Year: 2014 PMID： 24605938 PMCID： PMC4207734 DOI： 10.3109/10428194.2014.900762
Source DB: PubMed Journal: Leuk Lymphoma ISSN： 1026-8022