Abstract
Casein kinase II (CK2) promotes cell cycle progression and cellular proliferation in leukemia. Overexpression of CK2 results in the development of high-risk leukemia, that is resistant to chemotherapy. The mechanism by which CK2 promotes cellular proliferation and malignant transformation is unknown. Our published data showed that CK2 phosphorylates the Ikaros tumor suppressor protein, which results in loss of its function as a transcriptional repressor. To determine the therapeutic efficacy of CK2 inhibitors, we tested their effect on Ikaros tumor suppressor function in vitro in human pre-B acute lymphoblastic leukemia (ALL) and in vivo using a preclinical human-mouse pre-B ALL xenograft model.
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