• Blood · Sep 2013

    Review

    The new genetics of chronic neutrophilic leukemia and atypical CML: implications for diagnosis and treatment.

    • Jason Gotlib, Julia E Maxson, Tracy I George, and Jeffrey W Tyner.
    • Division of Hematology, Department of Medicine, Stanford University School of Medicine/Stanford Cancer Institute, Stanford, CA 94305-5821, USA. jason.gotlib@stanford.edu
    • Blood. 2013 Sep 5;122(10):1707-11.

    AbstractAlthough activation of tyrosine kinase pathways is a shared theme among myeloproliferative neoplasms, the pathogenetic basis of chronic neutrophilic leukemia (CNL) has remained elusive. Recently, we identified high-frequency oncogenic mutations in the granulocyte-colony stimulating factor receptor (CSF3R) in CNL and in some patients with atypical chronic myeloid leukemia. Inhibition of Janus kinase 2 or SRC kinase signaling downstream of mutated CSF3R is feasible and should be explored therapeutically. Herein, we discuss the potential impact of these findings for the classification and treatment of these disorders.

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