W
William Luther
Researcher at Harvard University
Publications - 8
Citations - 1308
William Luther is an academic researcher from Harvard University. The author has contributed to research in topics: Anaplastic lymphoma kinase & Neuroblastoma. The author has an hindex of 6, co-authored 7 publications receiving 1188 citations.
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Journal ArticleDOI
Activating mutations in ALK provide a therapeutic target in neuroblastoma
Rani E. George,Takaomi Sanda,Megan Hanna,Stefan Fröhling,William Luther,Jianming Zhang,Yebin Ahn,Wenjun Zhou,Wendy B. London,Patrick McGrady,Liquan Xue,Sergey Zozulya,Vlad Edward Gregor,Thomas R. Webb,Nathanael S. Gray,D. Gary Gilliland,Lisa Diller,Heidi Greulich,Stephan W. Morris,Matthew Meyerson,A. Thomas Look +20 more
TL;DR: In this paper, the authors reported the detection of previously unknown mutations in the ALK gene, which encodes a receptor tyrosine kinase, in 8% of primary neuroblastomas.
Journal ArticleDOI
The ALK(F1174L) mutation potentiates the oncogenic activity of MYCN in neuroblastoma.
Teeara Berry,William Luther,Namrata Bhatnagar,Yann Jamin,Evon Poon,Takaomi Sanda,De-Sheng Pei,Bandana Sharma,Winston R. Vetharoy,Albert Hallsworth,Zai Ahmad,Karen Barker,Lisa A. Moreau,Hannah Webber,Wenchao Wang,Qingsong Liu,Antonio R. Perez-Atayde,Scott J. Rodig,Nai-Kong V. Cheung,Florence I. Raynaud,Bengt Hallberg,Simon P. Robinson,Nathanael S. Gray,Andrew D.J. Pearson,Andrew D.J. Pearson,Suzanne A. Eccles,Louis Chesler,Louis Chesler,Rani E. George +28 more
TL;DR: Combined treatment with the ATP-competitive mTOR inhibitor Torin2 overcame the resistance of ALK(F1174L)/MYCN tumors to crizotinib and suggested a strategy for improving targeted therapy for ALK-positive neuroblastoma.
Journal ArticleDOI
ALK inhibitor resistance in ALK(F1174L)-driven neuroblastoma is associated with AXL activation and induction of EMT.
David Debruyne,Namrata Bhatnagar,Bandana Sharma,William Luther,Nathan Moore,Cheung Nk,Nathanael S. Gray,Rani E. George +7 more
TL;DR: In this article, the diaminopyrimidine TAE684 and its derivative ceritinib (LDK378), which are structurally distinct from crizotinib-resistant ALKF1174L mutation arises de novo in neuroblastoma (NB) and is acquired in ALK translocation driven cancers, lending impetus to the development of novel anaplastic lymphoma kinase (ALK) inhibitors with different modes of action.
Journal ArticleDOI
Distinct neuroblastoma-associated alterations of PHOX2B impair sympathetic neuronal differentiation in zebrafish models.
De-Sheng Pei,William Luther,Wenchao Wang,Barry H. Paw,Barry H. Paw,Rodney A. Stewart,Rani E. George +6 more
TL;DR: In this paper, the authors used zebrafish models to study the functional consequences of aberrant PHOX2B expression in the cells of the developing sympathetic nervous system, showing that PHox2b deficiency uncouples this autoregulatory mechanism, leading to inhibition of sympathetic neuron differentiation.
Journal ArticleDOI
Discovery of 3,5-Diamino-1,2,4-triazole Ureas as Potent Anaplastic Lymphoma Kinase Inhibitors
Xianming Deng,Jinhua Wang,Jianming Zhang,Taebo Sim,Nam Doo Kim,Takaaki Sasaki,William Luther,Rani E. George,Pasi A. Jänne,Nathanael S. Gray +9 more
TL;DR: A series of novel 3,5-diamino-1,2,4-triazole benzyl ureas was identified as having potent anaplastic lymphoma kinase (ALK) inhibition exemplified by 15a, 20a, and 23a, which exhibited antiproliferative IC50 values of 70, 40, and 20 nM in Tel-ALK transformed Ba/F3 cells, respectively.