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Diana J. Griffith
Researcher at Oregon Health & Science University
Publications - 19
Citations - 6356
Diana J. Griffith is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: PDGFRA & Receptor tyrosine kinase. The author has an hindex of 15, co-authored 19 publications receiving 6039 citations. Previous affiliations of Diana J. Griffith include Portland VA Medical Center & United States Department of Veterans Affairs.
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Journal ArticleDOI
PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors
Michael Heinrich,Christopher L. Corless,Anette Duensing,Laura McGreevey,Chang Jie Chen,Nora E. Joseph,Samuel Singer,Diana J. Griffith,Andrea Haley,Ajia Town,George D. Demetri,Christopher D.M. Fletcher,Jonathan A. Fletcher,Jonathan A. Fletcher +13 more
TL;DR: Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression, suggesting KIT and PDGFra mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs.
Journal ArticleDOI
Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor.
Michael Heinrich,Diana J. Griffith,Brian J. Druker,Cecily L. Wait,Kristen A. Ott,Amy J. Zigler +5 more
TL;DR: Findings show that STI 571 selectively inhibits c-kit tyrosine kinase activity and downstream activation of target proteins involved in cellular proliferation and survival.
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PDGFRA Mutations in Gastrointestinal Stromal Tumors: Frequency, Spectrum and In Vitro Sensitivity to Imatinib
Christopher L. Corless,Arin Schroeder,Diana J. Griffith,Ajia Town,Laura McGreevey,Patina Harrell,Sharon Shiraga,Troy Bainbridge,Jason Morich,Michael Heinrich +9 more
TL;DR: It is suggested that more than one third of GISTs with PDGFRA mutations may respond to imatinib and that mutation screening may be helpful in the management of these tumors.
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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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Dasatinib (BMS-354825), a dual SRC/ABL kinase inhibitor, inhibits the kinase activity of wild-type, juxtamembrane, and activation loop mutant KIT isoforms associated with human malignancies.
Marcus M Schittenhelm,Sharon Shiraga,Sharon Shiraga,Arin Schroeder,Arin Schroeder,Amie S. Corbin,Diana J. Griffith,Diana J. Griffith,Francis Y. Lee,Carsten Bokemeyer,Michael W. Deininger,Brian J. Druker,Michael Heinrich +12 more
TL;DR: It is reported that dasatinib potently inhibits WT KIT and juxtamembrane domain mutant KIT autophosphorylation and KIT-dependent activation of downstream pathways important for cell viability and cell survival, such as Ras/mitogen-activated protein kinase, phosphoinositide 3-kinase/Akt, and Janus-activated kinase/signal transducers and activators of transcription.