Abstract
In this letter we describe two case reports of CML patients with acquired mutations of the BCR-ABL1 kinase domain, in whom the mutant clone regressed and drug sensitivity was restored after temporary interruption of TKI. We believe that temporary interruption of an ATP-competitive tyrosine kinase inhibitor and switching to non-selective therapy can be a valid therapeutic option in CML patients. In addition, we highlight the potential of a flow cytometric CRKL phosphorylation assay to explore TKI sensitivity in CML cells ex vivo, and its correlation with clinical and haematological sensitivity or resistance.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents / therapeutic use*
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Drug Administration Schedule
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Fusion Proteins, bcr-abl / antagonists & inhibitors
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Fusion Proteins, bcr-abl / genetics*
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Humans
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*
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Mutation*
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Protein Kinase Inhibitors / administration & dosage
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Protein Kinase Inhibitors / therapeutic use*
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Protein-Tyrosine Kinases / antagonists & inhibitors
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Protein-Tyrosine Kinases / genetics*
Substances
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Antineoplastic Agents
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Protein Kinase Inhibitors
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Protein-Tyrosine Kinases
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Fusion Proteins, bcr-abl