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- W2064109729 abstract "Development of drug resistance to imatinib mesylate in chronic myeloid leukemia (CML) patients is often accompanied by selection of point mutations in the kinase domain (KD) of the Bcr-Abl oncoprotein, where imatinib binds. Several second-generation tyrosine kinase inhibitors (TKIs) have been designed rationally so as to enhance potency and retain the ability to bind mutated forms of Bcr-Abl. Since the preclinical phase of their development, most of these inhibitors have been tested in in vitro studies to assess their half maximal inhibitory concentration (IC₅₀) for unmutated and mutated Bcr-Abl-that is, the drug concentration required to inhibit the cell proliferation or the phosphorylation processes driven by either the unmutated or the mutated forms of the kinase. A number of such studies have been published, and now that two inhibitors-dasatinib and nilotinib-are available for the treatment of imatinib-resistant cases, it is tempting for clinicians to reason on the IC₅₀ values to guess, case by case, which one will work best in patients harboring specific Bcr-Abl KD mutations. Here, we discuss the pros and cons of using this approach in TKI selection." @default.
- W2064109729 created "2016-06-24" @default.
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- W2064109729 date "2011-05-31" @default.
- W2064109729 modified "2023-10-02" @default.
- W2064109729 title "Choosing the Best Second-Line Tyrosine Kinase Inhibitor in Imatinib-Resistant Chronic Myeloid Leukemia Patients Harboring Bcr-Abl Kinase Domain Mutations: How Reliable Is the IC50?" @default.
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- W2064109729 doi "https://doi.org/10.1634/theoncologist.2010-0388" @default.
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