Unknown

Dataset Information

0

Activating mutations in CSF1R and additional receptor tyrosine kinases in histiocytic neoplasms.

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.

SUBMITTER: Durham BH 

PROVIDER: S-EPMC6898787 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

Json Xml
altmetric image

Publications

Activating mutations in CSF1R and additional receptor tyrosine kinases in histiocytic neoplasms.

Durham Benjamin H BH   Lopez Rodrigo Estibaliz E   Picarsic Jennifer J   Abramson David D   Rotemberg Veronica V   De Munck Steven S   Pannecoucke Erwin E   Lu Sydney X SX   Pastore Alessandro A   Yoshimi Akihide A   Mandelker Diana D   Ceyhan-Birsoy Ozge O   Ulaner Gary A GA   Walsh Michael M   Yabe Mariko M   Petrova-Drus Kseniya K   Arcila Maria E ME   Ladanyi Marc M   Solit David B DB   Berger Michael F MF   Hyman David M DM   Lacouture Mario E ME   Erickson Caroline C   Saganty Ruth R   Ki Michelle M   Dunkel Ira J IJ   Santa-María López Vicente V   Mora Jaume J   Haroche Julien J   Emile Jean-Francois JF   Decaux Olivier O   Geissmann Frederic F   Savvides Savvas N SN   Drilon Alexander A   Diamond Eli L EL   Abdel-Wahab Omar O  

Nature medicine 20191125 12

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,  ...[more]

Similar Datasets

Transcriptomics Constitutively activating MEK1 mutations drive treatment refractory histiocytic neoplasms but confer response to ERK inhibition
2024-09-03 | GSE268618 | GEO
Unknown Oncogenic potential is related to activating effect of cancer single and double somatic mutations in receptor tyrosine kinases.
| S-EPMC3465464 | biostudies-literature
Unknown Sequence survey of receptor tyrosine kinases reveals mutations in glioblastomas.
| S-EPMC1242336 | biostudies-literature
Unknown Activating Mutations in PTPN11 and KRAS in Canine Histiocytic Sarcomas.
| S-EPMC6678586 | biostudies-literature
Unknown Gatekeeper mutations activate FGF receptor tyrosine kinases by destabilizing the autoinhibited state.
| S-EPMC9974468 | biostudies-literature
Unknown Cell signaling by receptor tyrosine kinases.
| S-EPMC2914105 | biostudies-literature
Unknown Receptor tyrosine kinases in kidney development.
| S-EPMC3100575 | biostudies-literature
Unknown Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms.
| S-EPMC4744547 | biostudies-literature
Unknown Prognostic factors for histiocytic and dendritic cell neoplasms.
| S-EPMC5716762 | biostudies-literature
Transcriptomics Recurrent activating STAT5B N642H mutations in myeloid neoplasms with eosinophilia
2019-01-12 | E-MTAB-7492 | biostudies-arrayexpress