Reduction of BCR-ABL1 mutant clones after discontinuation of TKI therapy

Karolien Beel; Ann Janssens; Gregor Verhoef; Peter Vandenberghe

doi:10.1016/j.leukres.2009.04.021

Reduction of BCR-ABL1 mutant clones after discontinuation of TKI therapy

Leuk Res. 2009 Dec;33(12):1703-5. doi: 10.1016/j.leukres.2009.04.021. Epub 2009 May 19.

Authors

Karolien Beel¹, Ann Janssens, Gregor Verhoef, Peter Vandenberghe

Affiliation

¹ Center for Human Genetics, University Hospitals Leuven, Herestraat 49, 3000 Leuven, Belgium.

PMID: 19457553
DOI: 10.1016/j.leukres.2009.04.021

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

Research Support, Non-U.S. Gov't

MeSH terms

Antineoplastic Agents / therapeutic use*
Drug Administration Schedule
Fusion Proteins, bcr-abl / antagonists & inhibitors
Fusion Proteins, bcr-abl / genetics*
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics*
Mutation*
Protein Kinase Inhibitors / administration & dosage
Protein Kinase Inhibitors / therapeutic use*
Protein-Tyrosine Kinases / antagonists & inhibitors
Protein-Tyrosine Kinases / genetics*

Substances

Antineoplastic Agents
Protein Kinase Inhibitors
Protein-Tyrosine Kinases
Fusion Proteins, bcr-abl