Bad-deficient mice develop diffuse large B cell lymphoma

Ann M. Ranger, Jiping Zha, Hisashi Harada, Sandeep Robert Datta, Nika N. Danial, Andrew P. Gilmore, Jeffery L. Kutok, Michelle M. Le Beau, Michael E. Greenberg, Stanley J. Korsmeyer

    Research output: Contribution to journalArticlepeer-review


    The proapoptotic activity of the "BH3-only" molecule BAD can be differentially regulated by survival factor signaling. Bad-deficient mice lacking both BAD long and BAD short proteins proved viable, and most cell types appeared to develop normally. BAD did not exclusively account for cell death after withdrawal of survival factors, but it was an intermediate for epidermal growth factor- or insulin-like growth factor I-countered apoptosis, consistent with a "sensitizing" BH3-only molecule. Lymphocytes developed normally with no premalignant hyperplasia, but they displayed subtle abnormalities in proliferation and IgG production. Despite the minimal phenotype, Bad-deficient mice progressed, with aging, to diffuse large B cell lymphoma of germinal center origin. Exposure of Bad-null mice to sublethal γ-irradiation resulted in an increased incidence of pre-T cell and pro-/pre-B cell lymphoblastic leukemia/lymphoma. Thus, proapoptotic BAD suppresses tumorigenesis in the lymphocyte lineage.
    Original languageEnglish
    Pages (from-to)9324-9329
    Number of pages5
    JournalProceedings of the National Academy of Sciences of the United States of America
    Issue number16
    Publication statusPublished - 5 Aug 2003


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