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

Jason Gotlib, Julia E. Maxson, Tracy I. George, Jeffrey W. Tyner

Research output: Contribution to journalArticle

98 Scopus citations

Abstract

Although 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.

Original languageEnglish (US)
Pages (from-to)1707-1711
Number of pages5
JournalBlood
Volume122
Issue number10
DOIs
StatePublished - Sep 5 2013

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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