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A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia AML or not amenable to conventional therapy for the disease
W. Fiedler, H. Serve, H. Dohner, M. Schwittay, O. G. Ottmann, A. M. O'Farrell, C. L. Bello, R. Allred, W. C. Manning, J. M. Cherrington, S. G. Louie, W. Hong, N. M. Brega, G. Massimini, P. Scigalla, W. E. Berdel, and D. K. Hossfeld Blood 105(3):986-993 (2005)
to & 3 Acute Aged Clearance Endothelial Factor Female Follow-Up Genotype Growth Human Humans Hypertension Indoles Kinase Kinases Leukemia Lung Male Metabolic Middle Mutation Myeloid Pharmacokinetics Platelet-Derived Protein-Tyrosine Proteins Proto-Oncogene Pyrroles Rate Receptor Receptors Research SU11248 Studies Tyrosine Vascular analysis antagonists cells drug fms-Like genetics inhibitors protein response therapeutic therapy toxicity use by kanefendt on Feb 5, 2010, 11:28 AM
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Overexpression and constitutive activation of FLT3 induces STAT5 activation in primary acute myeloid leukemia blast cells
K. Spiekermann, K. Bagrintseva, R. Schwab, K. Schmieja, and W. Hiddemann Clin.Cancer Res. 9(6):2140-2150 (2003)
to 3 Acid Activation Acute Amino Cell DNA-Binding Data Enzyme Factor Human Humans Indoles Kinase Kinases Leukemia Milk Mitogen-Activated Molecular Mutation Myeloid Neoplastic Phenotype Phosphorylation Protein Protein-Tyrosine Proteins Proto-Oncogene Receptor Research STAT3 STAT5 Sequence Trans-Activators Transcription Transformation Tyrosine cells fms-Like metabolism pathology pharmacology physiology protein response therapy by kanefendt on Feb 5, 2010, 11:28 AM
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