Oncogenic CSF3R Mutations in Neutrophilic Leukemia
OHSU # 1855
Atypical chronic myelogenous leukemia (aCML) and chronic neutrophilic leukemia (CNL) are rare blood cancers with poor prognoses and no standard of care exists for these disorders. Patients are typically diagnosed using histological and cytogenetic techniques and few recurrent genetic mutations are associated with these disorders.
OHSU investigators have identified a number of mutations in the gene encoding the colony stimlulating factor 3 receptor (CSF3R) that are preferentially associated with aCML and CNL. Moreover, they have determined that cells harboring mutations resulting in a CSF3R membrane-proximal point mutation or a truncation of the cytoplasmic tail of CSF3R demonstrate differential sensitivities to JAK and SRC kinase inhibitors. For example, primary patient cells that express point mutations respond better to the JAK kinase inhibitor Ruxolitinib and those expressing truncation mutations respond better to the SFR/TNK2 inhibitor Dasatinib. This method can be used to diagnose distinct subgroups of CNL and aCML patients that have sensitivity to either SRC family kinase or JAK family kinase inhibitors.
This method distinguishes between different classes of CSF3R mutations (point mutations and truncation mutations) in patients with aCML or CNL and identifies informative treatment options for these patients based on the nature of the mutation.
U.S. patent application number 15/336,570, published as US/17/044625
Maxson et al., Oncogenic CSF3R Mutations in Chronic Neutrophilic Leukemia and Typical CML, N Engl J Med 2013; 368: 1781-1790
This technology is available for exclusive licensing.
- Jeffrey Tyner, SM.Knight Leukemia Center
- Julia Maxson, SM.Knight Hem/Onc CHM
- Brian Druker, SM.Knight Hem/Onc CHM
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Technology Development Manager