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- W2023953669 abstract "Chronic myelogenous leukemia (CML) is a disorder of hematopoietic stem cells that results from the Philadelphia chromosome (Ph) created through translocation of human chromosomes 9 and 22. The resulting Bcr-Abl fusion protein has constitutively high tyrosine kinase activity that causes transformation of hematopoietic stem cells. Imatinib mesylate (IM) was developed as a specific Bcr-Abl kinase inhibitor and is efficacious in treating Ph-chromosome-positive (Ph+) leukemias such as CML and Ph+ acute lymphoblastic leukemia (ALL). Within a few years of its introduction to the clinic, IM has dramatically altered the first-line therapy for CML. Although most newly diagnosed CML patients in the chronic phase (CP) achieved durable responses when treated with IM, resistance to IM has become a major problem in patients with advanced-stage disease. The most important mechanism of IM resistance are point mutations within the Abl kinase domain; therefore, there is an urgent need for novel agents that can inhibit mutated Bcr-Abl. In this review, we describe novel Bcr-Abl tyrosine kinase inhibitors, the so-called “Super Gleevec” inhibitors. Drug Dev Res 69:398–406, 2008. © 2008 Wiley-Liss, Inc." @default.
- W2023953669 created "2016-06-24" @default.
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- W2023953669 date "2008-11-01" @default.
- W2023953669 modified "2023-10-05" @default.
- W2023953669 title "Novel agents to override imatinib resistance mechanisms" @default.
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- W2023953669 doi "https://doi.org/10.1002/ddr.20271" @default.
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