D. Griffith

发表

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.

C. Bokemeyer, B. Druker, M. Heinrich, 2006, Cancer research.

Primary and secondary kinase genotypes correlate with the biological and clinical activity of sunitinib in imatinib-resistant gastrointestinal stromal tumor.

C. Antonescu, J. Fletcher, G. Demetri, 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

Inhibition of c-kit receptor tyrosine kinase activity by STI 571, a selective tyrosine kinase inhibitor.

B. Druker, M. Heinrich, D. Griffith, 2000, Blood.

Posttranscriptional cell cycle-dependent regulation of human FANCC expression.

M. Montalto, M. Heinrich, D. Griffith, 2000, Blood.

The Multitargeted Receptor Tyrosine Kinase Inhibitor Linifanib (ABT-869) Induces Apoptosis through an Akt and Glycogen Synthase Kinase 3β–Dependent Pathway

K. Glaser, M. Heinrich, D. Griffith, 2011, Molecular Cancer Therapeutics.

The effect of crenolanib (CP-868596) on phosphorylation of the imatinib-resistant D842V PDGFRA activating mutation associated with advanced gastrointestinal stromal tumors.

M. Heinrich, D. Griffith, A. McKinley, 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

KIT mutations are common in testicular seminomas.

O. Cummings, J. Fletcher, M. Heinrich, 2004, The American journal of pathology.

FLT3 K663Q is a novel AML-associated oncogenic kinase: determination of biochemical properties and sensitivity to Sunitinib (SU11248)

R. Braziel, M. Heinrich, M. Schittenhelm, 2006, Leukemia.

PDGFRA Activating Mutations in Gastrointestinal Stromal Tumors

Samuel Singer, Jonathan A. Fletcher, J. Fletcher, 2003, Science.

A Functional Genomics Approach to Kaposi's Sarcoma

B. Druker, A. Moses, K. Früh, 2002, Annals of the New York Academy of Sciences.

Kaposi's Sarcoma-Associated Herpesvirus-Induced Upregulation of the c-kit Proto-Oncogene, as Identified by Gene Expression Profiling, Is Essential for the Transformation of Endothelial Cells

B. Druker, A. Moses, K. Früh, 2002, Journal of Virology.

PDGFRA mutations in gastrointestinal stromal tumors: frequency, spectrum and in vitro sensitivity to imatinib.

M. Heinrich, C. Corless, Sharon Shiraga, 2005, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

receptor tyrosine kinase SU5416 and SU5614 inhibit kinase activity of wild-type and mutant FLT3

G. Mcmahon, M. Heinrich, D. Griffith, 2013 .

SU5416 and SU5614 inhibit kinase activity of wild-type and mutant FLT3 receptor tyrosine kinase.

G. Mcmahon, M. Heinrich, D. Griffith, 2002, Blood.

SU 5416 and SU 5614 inhibit kinase activity of wild-type and mutant FLT 3 receptor tyrosine kinase

G. Mcmahon, M. Heinrich, D. Griffith, 2002 .

Crenolanib Inhibits the Drug-Resistant PDGFRA D842V Mutation Associated with Imatinib-Resistant Gastrointestinal Stromal Tumors

M. Heinrich, M. Debiec‐Rychter, D. Griffith, 2012, Clinical Cancer Research.

Sorafenib Inhibits Many Kinase Mutations Associated with Drug-Resistant Gastrointestinal Stromal Tumors

J. Fletcher, M. Heinrich, D. Griffith, 2012, Molecular Cancer Therapeutics.

Co-transduction of cDNAs for c-kit and steel factor into single CD34+ cord blood cells further enhances the growth of erythroid and multipotential progenitors.

M. Dai, M. Heinrich, D. Griffith, 2000, Journal of hematotherapy & stem cell research.

Combination Therapy for KIT-Mutant Mast Cells: Targeting Constitutive NFAT and KIT Activity

Janice Patterson, M. Heinrich, D. Griffith, 2014, Molecular Cancer Therapeutics.

Inhibition of HSP90 by AT13387 Delays the Emergence of Resistance to BRAF Inhibitors and Overcomes Resistance to Dual BRAF and MEK Inhibition in Melanoma Models

Kristina M. Ilieva, V. Petrenko, V. Sondak, 2014, Molecular Cancer Therapeutics.