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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Humans
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Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / diagnosis*
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Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics*
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Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / pathology
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Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / therapy
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Leukemia, Neutrophilic, Chronic / diagnosis*
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Leukemia, Neutrophilic, Chronic / genetics*
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Leukemia, Neutrophilic, Chronic / pathology
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Leukemia, Neutrophilic, Chronic / therapy
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Mutation / genetics
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Nuclear Proteins / genetics
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Receptors, Granulocyte Colony-Stimulating Factor / genetics
Substances
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Nuclear Proteins
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Receptors, Granulocyte Colony-Stimulating Factor