Reduction of BCR-ABL1 mutant clones after discontinuation of TKI therapy.
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.
Beel
Karolien
K
Center for Human Genetics, University Hospitals Leuven, Herestraat 49, 3000 Leuven, Belgium.
Janssens
Ann
A
Verhoef
Gregor
G
Vandenberghe
Peter
P
D000970:Antineoplastic Agents / Q000627:therapeutic use*; D004334:Drug Administration Schedule; D016044:Fusion Proteins, bcr-abl / Q000037:antagonists & inhibitors / Q000235:genetics*; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy / Q000235:genetics*; D009154:Mutation; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000235:genetics*
D000970:Antineoplastic Agents; D047428:Protein Kinase Inhibitors; D011505:Protein-Tyrosine Kinases; D016044:Fusion Proteins, bcr-abl