Activating mutations in CSF1R and additional receptor tyrosine kinases in histiocytic neoplasms.
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ABSTRACT:
SUBMITTER: Durham BH
PROVIDER: S-EPMC6898787 | biostudies-literature | 2019 Dec
REPOSITORIES: biostudies-literature
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]
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