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

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.

• Authors: Jason Gotlib, Julia E Maxson, Tracy I George, Jeffrey W Tyner
• Journal: Blood (Blood) Vol. 122 Issue 10 Pg. 1707-11 (Sep 05 2013) ISSN: 1528-0020 [Electronic] United States
• PMID: 23896413 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Nuclear Proteins
• Receptors, Granulocyte Colony-Stimulating Factor

Topics

• Humans
• Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative (diagnosis, genetics, pathology, therapy)
• Leukemia, Neutrophilic, Chronic (diagnosis, genetics, pathology, therapy)
• Mutation (genetics)
• Nuclear Proteins (genetics)
• Receptors, Granulocyte Colony-Stimulating Factor (genetics)