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Activating mutations in CSF1R and additional receptor tyrosine kinases in histiocytic neoplasms.
Nature Medicine ( IF 82.9 ) Pub Date : 2019-11-25 , DOI: 10.1038/s41591-019-0653-6 Benjamin H Durham 1, 2 , Estibaliz Lopez Rodrigo 3, 4 , Jennifer Picarsic 5, 6 , David Abramson 7 , Veronica Rotemberg 8 , Steven De Munck 9, 10 , Erwin Pannecoucke 9, 10 , Sydney X Lu 1 , Alessandro Pastore 1 , Akihide Yoshimi 1 , Diana Mandelker 2 , Ozge Ceyhan-Birsoy 2 , Gary A Ulaner 11 , Michael Walsh 3 , Mariko Yabe 2 , Kseniya Petrova-Drus 2 , Maria E Arcila 2 , Marc Ladanyi 1, 2 , David B Solit 1 , Michael F Berger 1, 2 , David M Hyman 12 , Mario E Lacouture 8 , Caroline Erickson 1 , Ruth Saganty 1 , Michelle Ki 1 , Ira J Dunkel 3 , Vicente Santa-María López 13 , Jaume Mora 13 , Julien Haroche 14 , Jean-Francois Emile 15 , Olivier Decaux 16 , Frederic Geissmann 4 , Savvas N Savvides 9, 10 , Alexander Drilon 12 , Eli L Diamond 17 , Omar Abdel-Wahab 1
Nature Medicine ( IF 82.9 ) Pub Date : 2019-11-25 , DOI: 10.1038/s41591-019-0653-6 Benjamin H Durham 1, 2 , Estibaliz Lopez Rodrigo 3, 4 , Jennifer Picarsic 5, 6 , David Abramson 7 , Veronica Rotemberg 8 , Steven De Munck 9, 10 , Erwin Pannecoucke 9, 10 , Sydney X Lu 1 , Alessandro Pastore 1 , Akihide Yoshimi 1 , Diana Mandelker 2 , Ozge Ceyhan-Birsoy 2 , Gary A Ulaner 11 , Michael Walsh 3 , Mariko Yabe 2 , Kseniya Petrova-Drus 2 , Maria E Arcila 2 , Marc Ladanyi 1, 2 , David B Solit 1 , Michael F Berger 1, 2 , David M Hyman 12 , Mario E Lacouture 8 , Caroline Erickson 1 , Ruth Saganty 1 , Michelle Ki 1 , Ira J Dunkel 3 , Vicente Santa-María López 13 , Jaume Mora 13 , Julien Haroche 14 , Jean-Francois Emile 15 , Olivier Decaux 16 , Frederic Geissmann 4 , Savvas N Savvides 9, 10 , Alexander Drilon 12 , Eli L Diamond 17 , Omar Abdel-Wahab 1
Affiliation
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.
中文翻译：
激活组织细胞肿瘤中 CSF1R 和其他受体酪氨酸激酶的突变。
组织细胞增多症是克隆性造血疾病，通常由映射到 BRAF 和 MEK1 和 MEK2 激酶的突变驱动。然而，目前，患者组织细胞增多症的发育起源尚不清楚，BRAF 和 MEK 之外的临床意义治疗靶点尚未确定。在这项研究中，我们发现了 CSF1R 的激活突变和 RET 和 ALK 的重排，它们分别赋予了组织细胞增多症患者对 RET（selpercatinib）和克唑替尼的选择性抑制的显着反应。
更新日期：2019-11-26
中文翻译：
激活组织细胞肿瘤中 CSF1R 和其他受体酪氨酸激酶的突变。
组织细胞增多症是克隆性造血疾病，通常由映射到 BRAF 和 MEK1 和 MEK2 激酶的突变驱动。然而，目前，患者组织细胞增多症的发育起源尚不清楚，BRAF 和 MEK 之外的临床意义治疗靶点尚未确定。在这项研究中，我们发现了 CSF1R 的激活突变和 RET 和 ALK 的重排，它们分别赋予了组织细胞增多症患者对 RET（selpercatinib）和克唑替尼的选择性抑制的显着反应。
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