Journal
JOURNAL OF PATHOLOGY
Volume 240, Issue 3, Pages 282-290Publisher
WILEY
DOI: 10.1002/path.4775
Keywords
NTRK3 fusion; Spitz tumour; melanoma; kinase inhibitor; Spitz naevus; atypical Spitz tumour; spitzoid melanoma; oncogene; genetics
Funding
- NCI NIH HHS [P01 CA025874] Funding Source: Medline
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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 C1 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. Copyright (c) 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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