J
Jonathan A. Fletcher
Researcher at Brigham and Women's Hospital
Publications - 426
Citations - 57627
Jonathan A. Fletcher is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: GiST & PDGFRA. The author has an hindex of 109, co-authored 413 publications receiving 53642 citations. Previous affiliations of Jonathan A. Fletcher include Albany Medical College & Oregon Health & Science University.
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Journal ArticleDOI
Comparison between the in vitro intrinsic radiation sensitivity of human soft tissue sarcoma and breast cancer cell lines.
Wlodzimierz Ruka,Alphonse G. Taghian,Danielle Gioioso,Jonathan A. Fletcher,Frederick Preffer,Herman D. Suit +5 more
TL;DR: The data presented here do not support the view that cells of sarcomas show unusual radiation resistance, and to the extent that the in vitro determined cellular radiation sensitivity reflects the tumor response in vivo, the success rate for radiation applied against sarcoma and breast carcinoma of comparable size could be similar.
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Genome-Wide Functional Screening Identifies CDC37 as a Crucial HSP90-cofactor for KIT Oncogenic Expression in Gastrointestinal Stromal Tumors
Adrián Mariño-Enríquez,Wen-Bin Ou,Glenn S. Cowley,Biao Luo,Anneliene H. Jonker,Mark Mayeda,Michael Okamoto,Grant Eilers,Jeffrey T. Czaplinski,Ewa Sicinska,Yuexiang Wang,Takahiro Taguchi,George D. Demetri,David E. Root,Jonathan A. Fletcher +14 more
TL;DR: CDC37 targeting is expected to be selective for KIT/PDGFRA and a subset of other HSP90 clients, and thereby represents a promising strategy for inactivating the myriad KIT or PDGFRA oncoproteins in TKI-resistant GIST patients.
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Cystic neuroblastoma: emphasis on gene expression, morphology, and pathogenesis.
Harry P.W. Kozakewich,Antonio R. Perez-Atayde,Michael J. Donovan,Jonathan A. Fletcher,Judy A. Estroff,Robert C. Shamberger,Lisa Diller +6 more
TL;DR: Although the complete natural history of CN is not fully defined, the experience suggests that some tumors progress in size, whereas others may spontaneously regress or mature.
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Genomic aberrations in cell cycle genes predict progression of KIT -mutant gastrointestinal stromal tumors (GISTs).
Michael Heinrich,Janice Patterson,Carol Beadling,Yuexiang Wang,Maria Debiec-Rychter,Barbara Dewaele,Christopher L. Corless,Anette Duensing,Chandrajit P. Raut,Brian P. Rubin,Tamas Ordog,Matt van de Rijn,Jerry Call,Thomas Mühlenberg,Jonathan A. Fletcher,Sebastian Bauer +15 more
TL;DR: It is demonstrated that genomic events targeting cell cycle-related genes are associated with GIST progression to malignant disease and a model for molecular pathogenesis of malignant GIST is proposed.
Journal ArticleDOI
Mutational inactivation of mTORC1 repressor gene DEPDC5 in human gastrointestinal stromal tumors.
Yuzhi Pang,Feifei Xie,Hui Cao,Chunmeng Wang,Meijun Zhu,Xiaoxiao Liu,Xiaojing Lu,Tao Huang,Yanying Shen,Ke Li,Xiaona Jia,Zhang Li,Xufen Zheng,Simin Wang,Yi He,Linhui Wang,Jonathan A. Fletcher,Yuexiang Wang +17 more
TL;DR: The findings of recurrent genomic alterations validate the DEPDC5 as a bona fide tumor suppressor contributing to GIST progression and a biologically relevant target of the frequent chromosome 22q deletions.