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- W144098340 endingPage "74" @default.
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- W144098340 abstract "The Bcr-Abl tyrosine kinase inhibitor imatinib mesylate launched the era of molecular targeted therapy and constitutes a milestone in oncology history. However, despite impressive cytogenetic response rates achieved with this agent in patients with chronic myelogenous leukemia (CML) in chronic phase, those with advanced-stage CML frequently obtain more modest responses that are in many instances of short duration. Several mechanisms of resistance to imatinib have been described among patients that develop clinical resistance to imatinib. Point mutations in the Bcr-Abl kinase domain that impair the ability of imatinib to inhibit the kinase activity represent the leading cause of resistance. Several approaches are being pursued to overcome these mutations. In addition, many other protein kinases implicated in signaling transduction downstream Bcr-Abl play critical roles in the pathogenesis of CML, thus representing potential therapeutic targets. Multiple compounds are being screened to identify inhibitors of these kinases. This article focuses on the current state of development of new kinase inhibitors for the therapy of CML." @default.
- W144098340 created "2016-06-24" @default.
- W144098340 creator A5015101485 @default.
- W144098340 creator A5019337932 @default.
- W144098340 date "2006-05-01" @default.
- W144098340 modified "2023-10-15" @default.
- W144098340 title "Kinase inhibitors in chronic myelogenous leukemia." @default.
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- W144098340 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16728945" @default.
- W144098340 hasPublicationYear "2006" @default.
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