| Literature DB >> 27477320 |
Iwei Yeh1,2,3, Meng Kian Tee4,5, Thomas Botton4,5, A Hunter Shain4,5, Alyssa J Sparatta4,5, Alexander Gagnon4,6,5, Swapna S Vemula4,6,5, Maria C Garrido4,5, Kenji Nakamaru7, Takeshi Isoyama8, Timothy H McCalmont4,6,5, Philip E LeBoit4,6,5, Boris C Bastian9,10,11.
Abstract
Oncogenic fusions in TRK family receptor tyrosine kinases have been identified in several cancers and can serve as therapeutic targets. We identified ETV6-NTRK3, MYO5A-NTRK3 and MYH9-NTRK3 fusions in Spitz tumours, and demonstrated that NTRK3 fusions constitutively activate the mitogen-activated protein kinase, phosphoinositide 3-kinase and phospholipase Cγ1 pathways in melanocytes. This signalling was inhibited by DS-6051a, a small-molecule inhibitor of NTRK1/2/3 and ROS1. NTRK3 fusions expand the range of oncogenic kinase fusions in melanocytic neoplasms and offer targets for a small subset of melanomas for which no targeted options currently exist.Entities:
Keywords: NTRK3 fusion; Spitz naevus; Spitz tumour; atypical Spitz tumour; genetics; kinase inhibitor; melanoma; oncogene; spitzoid melanoma
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Year: 2016 PMID： 27477320 PMCID： PMC5071153 DOI： 10.1002/path.4775
Source DB: PubMed Journal: J Pathol ISSN： 0022-3417 Impact factor: 7.996