A combination of genetic and pharmacological approaches using mouse leukemia models show that STAT5 phosphorylation is one of the major drivers of the proliferation of Philadelphia chromosome–positive (BCR-ABL-positive or Ph+) chronic myeloid leukemia. Once BCR-ABL expression has been established, JAK2 is required only for lymphoid cell transformation, not for the maintenance of the lymphoid or myeloid leukemia.
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Fabbro, D. A new STATus in CML. Nat Chem Biol 8, 228–229 (2012). https://doi.org/10.1038/nchembio.900
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DOI: https://doi.org/10.1038/nchembio.900
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Combination of the ABL kinase inhibitor imatinib with the Janus kinase 2 inhibitor TG101348 for targeting residual BCR-ABL-positive cells
Journal of Hematology & Oncology (2014)