NTRK3 kinase fusions in Spitz tumours

被引：119
作者：
Yeh, Iwei [1 ,2 ,3 ]
Tee, Meng Kian [1 ,3 ]
Botton, Thomas [1 ,3 ]
Shain, A. Hunter [1 ,3 ]
Sparatta, Alyssa J. [1 ,3 ]
Gagnon, Alexander [1 ,2 ,3 ]
Vemula, Swapna S. [1 ,2 ,3 ]
Garrido, Maria C. [1 ,3 ]
Nakamaru, Kenji [4 ]
Isoyama, Takeshi [5 ]
McCalmont, Timothy H. [1 ,2 ,3 ]
LeBoit, Philip E. [1 ,2 ,3 ]
Bastian, Boris C. [1 ,2 ,3 ]
机构：
[1] Univ Calif San Francisco, Dept Dermatol, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94140 USA
[3] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA
[4] Daiichi Sankyo Co Ltd, Translat Res & Clin Pharmacol, Tokyo, Japan
[5] Daiichi Sankyo Co Ltd, Oncol Labs, Tokyo, Japan
来源：
JOURNAL OF PATHOLOGY | 2016年 / 240卷 / 03期
关键词：
NTRK3; fusion; Spitz tumour; melanoma; kinase inhibitor; Spitz naevus; atypical Spitz tumour; spitzoid melanoma; oncogene; genetics; BURROWS-WHEELER TRANSFORM; ETV6-NTRK3 GENE FUSION; CONGENITAL FIBROSARCOMA; SEQUENCING DATA; UVEAL MELANOMA; READ ALIGNMENT; MUTATIONS; CANCER; REARRANGEMENTS; LANDSCAPE;
D O I：
10.1002/path.4775
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
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.
引用
收藏
页码：282 / 290
页数：9
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