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BCR-ABL signaling

A new STATus in CML

Nature Chemical Biology volume 8, pages 228–229 (2012)Cite this article

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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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Figure 1: Schematic representation of STAT5 activation in normal hematopoietic stem cell and in Ph+ CML.

Katie Vicari

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  1. Doriano Fabbro is at the Novartis Institute for Biomedical Research, Basel, Switzerland.,

    Doriano Fabbro

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  1. Doriano Fabbro
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Correspondence to Doriano Fabbro.

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The author declares no competing financial interests.

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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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