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Clinical Pharmacokinetics of Imatinib
Clinical Pharmacokinetics, 2005Imatinib is a potent and selective inhibitor of the protein tyrosine kinase Bcr-Abl, platelet-derived growth factor receptors (PDGFRalpha and PDGFRbeta) and KIT. Imatinib is approved for the treatment of chronic myeloid leukaemia (CML) and gastrointestinal stromal tumour (GIST), which have dysregulated activity of an imatinib-sensitive kinase as the ...
Peter Lloyd, Bin Peng, Horst Schran
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Pharmacology of imatinib (STI571)
European Journal of Cancer, 2002Deregulation of protein kinase activity has been shown to play a central role in the pathogenesis of human cancer. The molecular pathogenesis of chronic myelogenous leukemia (CML) in particular, depends on formation of the bcr-abl oncogene, leading to constitutive expression of the tyrosine kinase fusion protein, Bcr-Abl.
Elisabeth Buchdunger +2 more
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Nature Reviews Clinical Oncology, 2011
Imatinib is an anticancer therapy that acts as a tyrosine kinase inhibitor of the BCR–ABL oncoprotein, as well as c-Kit and the platelet-derived growth factor receptor. This targeted therapy is the standard of care for adults newly diagnosed with chronic myeloid leukemia (CML) in the chronic phase and has demonstrated efficacy in patients with ...
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Imatinib is an anticancer therapy that acts as a tyrosine kinase inhibitor of the BCR–ABL oncoprotein, as well as c-Kit and the platelet-derived growth factor receptor. This targeted therapy is the standard of care for adults newly diagnosed with chronic myeloid leukemia (CML) in the chronic phase and has demonstrated efficacy in patients with ...
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Blood, 2005
Abstract Chronic myelogenous leukemia (CML) and Philadelphia chromosome positive (Ph+) acute lymphoblastic leukemia (ALL) are caused by the Bcr-Abl tyrosine kinase oncogene. The Abl inhibitor imatinib is an effective, frontline therapy for early, chronic phase CML. However, accelerated or blast crisis phase CML and Ph+ ALL patients often
Ellen Weisberg, James D. Griffin
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Abstract Chronic myelogenous leukemia (CML) and Philadelphia chromosome positive (Ph+) acute lymphoblastic leukemia (ALL) are caused by the Bcr-Abl tyrosine kinase oncogene. The Abl inhibitor imatinib is an effective, frontline therapy for early, chronic phase CML. However, accelerated or blast crisis phase CML and Ph+ ALL patients often
Ellen Weisberg, James D. Griffin
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Imatinib is receptive to a collaboration
Blood, 2011Before the introduction of imatinib, biologic therapy with IFN-α was the most promising treatment option for CML because it induced durable remissions in a subset of chronic-phase patients. 1 However, because of its toxicity as well as its limited and unpredictable efficacy, IFN-α therapy has been displaced by Bcr-Abl kinase inhibitors, which have ...
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2017
Imatinib mesylate (Gleevec, Glivec, Novartis) is a selective inhibitor of ABL, ARG, KIT, PDGFR, and some oncogenic forms, most notably BCR-ABL. Accelerated approval was initially granted by the Food and Drug Administration (FDA) in 2001 for the treatment of Ph+CML after the failure of IFNα therapy. Approval was extended later that year to pediatric CML
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Imatinib mesylate (Gleevec, Glivec, Novartis) is a selective inhibitor of ABL, ARG, KIT, PDGFR, and some oncogenic forms, most notably BCR-ABL. Accelerated approval was initially granted by the Food and Drug Administration (FDA) in 2001 for the treatment of Ph+CML after the failure of IFNα therapy. Approval was extended later that year to pediatric CML
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New England Journal of Medicine, 2017
The initial successes of combination chemotherapy were stunning. Childhood acute leukemia, several forms of lymphoma, and testicular cancer all became largely curable malignant conditions. Adjuvant chemotherapy led to dramatically longer survival among persons with breast cancer.
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The initial successes of combination chemotherapy were stunning. Childhood acute leukemia, several forms of lymphoma, and testicular cancer all became largely curable malignant conditions. Adjuvant chemotherapy led to dramatically longer survival among persons with breast cancer.
openaire +3 more sources