Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain Mutation

Acquired resistance to tyrosine kinase inhibitors (TKIs) remains a therapeutic challenge in the treatment of chronic myeloid leukemia (CML). The most studied reason for TKI resistance is the acquisition of mutations within the BCR::ABL1 tyrosine kinase domain (KDM) and of which the majority of which...

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Bibliographic Details
Main Authors: Stephen E. Langabeer, Stuart Macleod, Úna Bhreathnach, Kamal Fadalla
Format: Article
Language:English
Published: Hindawi Limited 2023-01-01
Series:Case Reports in Hematology
Online Access:http://dx.doi.org/10.1155/2023/6673144
Description
Summary:Acquired resistance to tyrosine kinase inhibitors (TKIs) remains a therapeutic challenge in the treatment of chronic myeloid leukemia (CML). The most studied reason for TKI resistance is the acquisition of mutations within the BCR::ABL1 tyrosine kinase domain (KDM) and of which the majority of which occur at seven codons within this region. A case of CML is described in which presence of a rare D363G BCR::ABL1 KDM resulted in a suboptimal response to frontline imatinib. Switching to dasatinib resulted in achieving a sustained major molecular response that was maintained after a subsequent switch to bosutinib due to the side effects. Reporting of such cases is important for the future management of any CML patients with this rare mutation.
ISSN:2090-6579