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
PAX8-PPARγ1 Fusion in Oncogene Human Thyroid Carcinoma
Todd G. Kroll,Pasha Sarraf,Lorenza Pecciarini,Chang-Jie Chen,Elisabetta Mueller,Bruce M. Spiegelman,Jonathan A. Fletcher,Jonathan A. Fletcher,Jonathan A. Fletcher +8 more
TL;DR: T(2;3)(q13;p25), a translocation identified in a subset of human thyroid follicular carcinomas, results in fusion of the DNA binding domains of the thyroid transcription factor PAX8 to domains A to F of the peroxisome proliferator–activated receptor (PPAR) γ1.
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STI571 inactivation of the gastrointestinal stromal tumor c-KIT oncoprotein: biological and clinical implications
David A. Tuveson,Nicholas A. Willis,Tyler Jacks,Tyler Jacks,James D. Griffin,Samuel Singer,Christopher D.M. Fletcher,Jonathan A. Fletcher,George D. Demetri +8 more
TL;DR: Cell-culture-based studies support an important role for c-KIT signaling in GIST and suggest therapeutic potential for STI571 in patients afflicted by this chemoresistant tumor.
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Terminal differentiation of human liposarcoma cells induced by ligands for peroxisome proliferator-activated receptor γ and the retinoid X receptor
Peter Tontonoz,Samuel Singer,Barry M. Forman,Pasha Sarraf,Jonathan A. Fletcher,Christopher D.M. Fletcher,Regina P. Brun,Elisabetta Mueller,Soner Altiok,Heather Oppenheim,Ronald M. Evans,Bruce M. Spiegelman +11 more
TL;DR: PPAR gamma ligands such as thiazolidinediones and RXR-specific retinoids may be useful therapeutic agents for the treatment of liposarcoma, suggesting that the differentiation block in these cells can be overcome by maximal activation of the PPAR pathway.
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Primary and Secondary Kinase Genotypes Correlate With the Biological and Clinical Activity of Sunitinib in Imatinib-Resistant Gastrointestinal Stromal Tumor
Michael Heinrich,Robert G. Maki,Christopher L. Corless,Cristina R. Antonescu,Amy Harlow,Diana J. Griffith,Ajia Town,Arin McKinley,Wen-Bin Ou,Jonathan A. Fletcher,Christopher D.M. Fletcher,Xin Huang,Darrel P. Cohen,Charles M. Baum,George D. Demetri +14 more
TL;DR: The clinical activity of sunitinib after imatinib failure is significantly influenced by both primary and secondary mutations in the predominant pathogenic kinases, which has implications for optimization of the treatment of patients with GIST.
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NPAT links cyclin E-Cdk2 to the regulation of replication-dependent histone gene transcription.
Jiyong Zhao,Jiyong Zhao,Brian K. Kennedy,Brandon D. Lawrence,David A. Barbie,A. Gregory Matera,Jonathan A. Fletcher,Ed Harlow +7 more
TL;DR: It is demonstrated that NPAT activates histone gene transcription and that this activation is dependent on the promoter elements (SSCSs) previously proposed to mediate cell cycle-dependent transcription.