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The Journal of Clinical Investigation|August 3, 2004
Novel mode of action of c-kit tyrosine kinase inhibitors leading to NK cell-dependent antitumor effectsChristophe Borg, Magali Terme, Julien Taïeb, et al.
Science Translational Medicine|November 3, 2017
A precision therapy against cancers driven by KIT/PDGFRA mutationsErica K Evans, Alexandra K Gardino, Joseph L Kim, et al.
Nature Communications|March 9, 2017
MAX inactivation is an early event in GIST development that regulates p16 and cell proliferationInga-Marie Schaefer, Yuexiang Wang, Cher-Wei Liang, et al.
Cancer Cell|September 24, 2019
Combining the Allosteric Inhibitor Asciminib with Ponatinib Suppresses Emergence of and Restores Efficacy against Highly Resistant BCR-ABL1 MutantsChristopher A Eide, Matthew S Zabriskie, Samantha L Savage Stevens, et al.
Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology|February 26, 2024
KIT ATP-Binding Pocket/Activation Loop Mutations in GI Stromal Tumor: Emerging Mechanisms of Kinase Inhibitor EscapeThomas Mühlenberg, Johanna Falkenhorst, Tom Schulz, et al.
European Journal of Cancer (Oxford, England : 1990)|August 20, 2023
Patient-reported outcomes and tolerability in patients receiving ripretinib versus sunitinib after treatment with imatinib in INTRIGUE, a phase 3, open-label studyHans Gelderblom, Robin L Jones, Jean-Yves Blay, et al.
Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology|June 19, 2013
Imatinib for melanomas harboring mutationally activated or amplified KIT arising on mucosal, acral, and chronically sun-damaged skinF Stephen Hodi, Christopher L Corless, Anita Giobbie-Hurder, et al.
Nature Medicine|January 5, 2024
Ripretinib versus sunitinib in gastrointestinal stromal tumor: ctDNA biomarker analysis of the phase 3 INTRIGUE trialMichael C Heinrich, Robin L Jones, Suzanne George, et al.
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