Activating mutations in CSF1R and additional receptor tyrosine kinases in histiocytic neoplasms.
case_series · Level IV
Where this comes from
- Record sourced from PubMed, PMID 31768065.
- Also identified by DOI 10.1038/s41591-019-0653-6 and PMC identifier 6898787.
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Abstract
Histiocytoses are clonal hematopoietic disorders frequently driven by mutations mapping to the BRAF and MEK1 and MEK2 kinases. Currently, however, the developmental origins of histiocytoses in patients are not well understood, and clinically meaningful therapeutic targets outside of BRAF and MEK are undefined. In this study, we uncovered activating mutations in CSF1R and rearrangements in RET and ALK that conferred dramatic responses to selective inhibition of RET (selpercatinib) and crizotinib, respectively, in patients with histiocytosis.
Medical subject headings
- Anaplastic Lymphoma Kinase
- Histiocytosis
- Proto-Oncogene Proteins c-ret
- Receptors, Granulocyte-Macrophage Colony-Stimulating Factor