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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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Autores principales: Langabeer, Stephen E., Macleod, Stuart, Bhreathnach, Úna, Fadalla, Kamal
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10139808/
https://www.ncbi.nlm.nih.gov/pubmed/37123466
http://dx.doi.org/10.1155/2023/6673144
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author Langabeer, Stephen E.
Macleod, Stuart
Bhreathnach, Úna
Fadalla, Kamal
author_facet Langabeer, Stephen E.
Macleod, Stuart
Bhreathnach, Úna
Fadalla, Kamal
author_sort Langabeer, Stephen E.
collection PubMed
description 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.
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spelling pubmed-101398082023-04-28 Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain Mutation Langabeer, Stephen E. Macleod, Stuart Bhreathnach, Úna Fadalla, Kamal Case Rep Hematol Case Report 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. Hindawi 2023-04-20 /pmc/articles/PMC10139808/ /pubmed/37123466 http://dx.doi.org/10.1155/2023/6673144 Text en Copyright © 2023 Stephen E. Langabeer et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Case Report
Langabeer, Stephen E.
Macleod, Stuart
Bhreathnach, Úna
Fadalla, Kamal
Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain Mutation
title Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain Mutation
title_full Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain Mutation
title_fullStr Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain Mutation
title_full_unstemmed Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain Mutation
title_short Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain Mutation
title_sort imatinib resistance in chronic myeloid leukemia associated with a d363g bcr::abl1 kinase domain mutation
topic Case Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10139808/
https://www.ncbi.nlm.nih.gov/pubmed/37123466
http://dx.doi.org/10.1155/2023/6673144
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