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    Critical B-lymphoid cell intrinsic role of endogenous MCL-1 in c-MYC-induced lymphomagenesis

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    Author
    Grabow, S; Kelly, GL; Delbridge, ARD; Kelly, PN; Bouillet, P; Adams, JM; Strasser, A
    Date
    2016-03-01
    Source Title
    Cell Death and Disease
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Bouillet, Philippe; Grabow, Stephanie; Delbridge, Alex; Kelly, Gemma; Strasser, Andreas; Adams, Jerry
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Grabow, S., Kelly, G. L., Delbridge, A. R. D., Kelly, P. N., Bouillet, P., Adams, J. M. & Strasser, A. (2016). Critical B-lymphoid cell intrinsic role of endogenous MCL-1 in c-MYC-induced lymphomagenesis. CELL DEATH & DISEASE, 7 (3), https://doi.org/10.1038/cddis.2016.43.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/260233
    DOI
    10.1038/cddis.2016.43
    Abstract
    Evasion of apoptosis is critical for tumorigenesis, and sustained survival of nascent neoplastic cells may depend upon the endogenous levels of pro-survival BCL-2 family members. Indeed, previous studies using gene-targeted mice revealed that BCL-XL, but surprisingly not BCL-2, is critical for the development of c-MYC-induced pre-B/B lymphomas. However, it remains unclear whether another pro-survival BCL-2 relative contributes to their development. MCL-1 is an intriguing candidate, because it is required for cell survival during early B-lymphocyte differentiation. It is expressed abnormally high in several types of human B-cell lymphomas and is implicated in their resistance to chemotherapy. To test the B-cell intrinsic requirement for endogenous MCL-1 in lymphoma development, we conditionally deleted Mcl-1 in B-lymphoid cells of Eμ-Myc transgenic mice. We found that MCL-1 loss in early B-lymphoid progenitors delayed MYC-driven lymphomagenesis. Moreover, the lymphomas that arose when MCL-1 levels were diminished appeared to have been selected for reduced levels of BIM and/or increased levels of BCL-XL. These results underscore the importance of MCL-1 in lymphoma development and show that alterations in the levels of other cell death regulators can compensate for deficiencies in MCL-1 expression.

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