Dasatinib overrides imatinib resistance mediated by the F359I residue mutation in two patients with chronic myeloid leukemia.
| Autor: | Serpa M; Department of Hematology, Faculty of Medicine, University of São Paulo, Brazil., Sanabani SS, Dorlhiac-Llacer PE, Nardinelli L, de Barros Ferreira P, Martins TF, Seguro F, Bendit I |
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| Jazyk: | angličtina |
| Zdroj: | Acta haematologica [Acta Haematol] 2012; Vol. 127 (1), pp. 56-9. Date of Electronic Publication: 2011 Nov 17. |
| DOI: | 10.1159/000333092 |
| Abstrakt: | Despite the beneficial effects of imatinib mesylate, some patients may either not respond or respond suboptimally. Here, we report two chronic myelogenous leukemia patients; one had a suboptimal response according to European LeukemiaNet criteria (a major molecular response was not achieved after 18 months of standard-dose imatinib therapy) and the other had failure with a standard dose of imatinib. At the time of the suboptimal response in patient 1 and the failure in patient 2, we were able to detect the F359I mutation in the BCR-ABL tyrosine kinase domain using DNA sequencing in both patients. Therefore, it was decided to change the therapeutic regimen to dasatinib at a dose of 100 mg once daily in both patients. This change resulted in the achievement of complete cytogenetic remission in patient 1 after 4 months and a major molecular response within 2 and 3 months in both patients. Detection of the F359I mutation in our two cases likely explains the suboptimal response to imatinib in case 1 and the failure in case 2. This implies that in such cases dasatinib should be considered to effectively suppress the mutated clones. (Copyright © 2011 S. Karger AG, Basel.) |
| Databáze: | MEDLINE |
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