Results 291 to 300 of about 87,925 (315)
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Seminars in Hematology, 2003
Imatinib (Gleevec), a highly effective specific tyrosine kinase inhibitor, demonstrates a better side effect profile than interferon-alpha (IFN), which impairs patients' quality of life (QoL). This phase III international study evaluated QoL outcomes in 1,106 newly diagnosed patients with chronic-phase chronic myeloid leukemia (CML) who were randomized
Elizabeth A. Hahn +1 more
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Imatinib (Gleevec), a highly effective specific tyrosine kinase inhibitor, demonstrates a better side effect profile than interferon-alpha (IFN), which impairs patients' quality of life (QoL). This phase III international study evaluated QoL outcomes in 1,106 newly diagnosed patients with chronic-phase chronic myeloid leukemia (CML) who were randomized
Elizabeth A. Hahn +1 more
openaire +3 more sources
Adjuvant Imatinib for High-Risk GI Stromal Tumor: Analysis of a Randomized Trial.
Journal of Clinical Oncology, 2016PURPOSE Three years of adjuvant imatinib therapy are recommended for patients with GI stromal tumor (GIST) with high-risk features, according to survival findings in the Scandinavian Sarcoma Group XVIII/AIO (Arbeitsgemeinschaft Internistische Onkologie ...
H. Joensuu +18 more
semanticscholar +1 more source
2009
Imatinib mesylate (Gleevec, Glivec [Novartis, Basel, Switzerland], formerly referred to as STI571 or CGP57148B) represents the paradigm of a new class of anticancer agents, so-called small molecules. They have a high selectivity against a specific molecular target known to be the cause for the establishment and maintenance of the malignant phenotype ...
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Imatinib mesylate (Gleevec, Glivec [Novartis, Basel, Switzerland], formerly referred to as STI571 or CGP57148B) represents the paradigm of a new class of anticancer agents, so-called small molecules. They have a high selectivity against a specific molecular target known to be the cause for the establishment and maintenance of the malignant phenotype ...
openaire +5 more sources
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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The development and application of imatinib
Expert Opinion on Drug Safety, 2005The hallmark characteristics of cancer include an unrestrained proliferation involving activation of growth signals, loss of negative regulation and dysfunctional apoptotic pathways. Targeting abnormal cell signalling pathways should provide a more selective approach to cancer treatment than conventional cytotoxic chemotherapy. Tyrosine kinases play an
Ian Judson, Robin L. Jones
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Pharmacology and pharmacokinetics of imatinib in pediatric patients
Expert Review of Clinical Pharmacology, 2018Introduction: The tyrosine kinase inhibitor (TKI) imatinib was rationally designed to target BCR-ABL1 which is constitutively activated in chronic myeloid leukemia (CML).
M. Suttorp +4 more
semanticscholar +1 more source
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 treatment and Aβ42 in humans
Alzheimer's & Dementia, 2013AbstractBackgroundThe first‐line treatment in chronic myeloid leukemia (CML), imatinib, has been shown to decrease the production of amyloid‐β (Aβ) in vitro and in animal studies. However, whether imatinib has this effect in humans is not known.MethodsPlasma levels of Aβ42 were analyzed in sequential samples from CML patients treated with imatinib (n =
Bob Olsson +9 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 ...
openaire +3 more sources