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

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

Research output: Contribution to journalArticle

86 Citations (Scopus)

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

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Leukemia, Neutrophilic, Chronic
Granulocyte Colony-Stimulating Factor Receptors
Janus Kinase 2
Emitter coupled logic circuits
Protein-Tyrosine Kinases
Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative
Phosphotransferases
Chemical activation
Mutation Rate
Therapeutics
Neoplasms
Genetics

ASJC Scopus subject areas

  • Hematology
  • Biochemistry
  • Cell Biology
  • Immunology

Cite this

The new genetics of chronic neutrophilic leukemia and atypical CML : Implications for diagnosis and treatment. / Gotlib, Jason; Maxson, Julia; George, Tracy I.; Tyner, Jeffrey.

In: Blood, Vol. 122, No. 10, 05.09.2013, p. 1707-1711.

Research output: Contribution to journalArticle

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