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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| Format: | Article |
| Language: | English |
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Wiley
2023-01-01
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| Series: | Case Reports in Hematology |
| Online Access: | http://dx.doi.org/10.1155/2023/6673144 |
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| _version_ | 1832547911082180608 |
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| author | Stephen E. Langabeer Stuart Macleod Úna Bhreathnach Kamal Fadalla |
| author_facet | Stephen E. Langabeer Stuart Macleod Úna Bhreathnach Kamal Fadalla |
| author_sort | Stephen E. Langabeer |
| collection | DOAJ |
| 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. |
| format | Article |
| id | doaj-art-45cfd3120dc54aeb8d83cad8344691e7 |
| institution | Kabale University |
| issn | 2090-6579 |
| language | English |
| publishDate | 2023-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Case Reports in Hematology |
| spelling | doaj-art-45cfd3120dc54aeb8d83cad8344691e72025-02-03T06:42:49ZengWileyCase Reports in Hematology2090-65792023-01-01202310.1155/2023/6673144Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain MutationStephen E. Langabeer0Stuart Macleod1Úna Bhreathnach2Kamal Fadalla3Cancer Molecular DiagnosticsDepartment of HaematologyCancer Molecular DiagnosticsDepartment of HaematologyAcquired 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.http://dx.doi.org/10.1155/2023/6673144 |
| spellingShingle | Stephen E. Langabeer Stuart Macleod Úna Bhreathnach Kamal Fadalla Imatinib Resistance in Chronic Myeloid Leukemia Associated with a D363G BCR::ABL1 Kinase Domain Mutation Case Reports in Hematology |
| 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 |
| url | http://dx.doi.org/10.1155/2023/6673144 |
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