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

Author:

Langabeer Stephen E.1ORCID,Macleod Stuart2,Bhreathnach Úna1,Fadalla Kamal2

Affiliation:

1. Cancer Molecular Diagnostics, St. James’s Hospital, Dublin D08W9RT, Ireland

2. Department of Haematology, St. Vincent’s University Hospital, Dublin D04T6F4, Ireland

Abstract

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.

Publisher

Hindawi Limited

Subject

Cell Biology,Developmental Biology,Embryology,Anatomy

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