Abstract
Mutations within the ABL kinase domain and overexpression of SRC family kinases have been identified among the known mechanisms of resistance to imatinib in chronic myeloid leukemia (CML). The development of agents with dual inhibitory activity against SRC and ABL kinases is one approach to overcome imatinib resistance. One such agent, dasatinib (formerly BMS-354825), is approximately 300-fold more potent against BCR-ABL than imatinib, and is active against all tested ABL mutant isoforms, except for T315I. Dasatinib has demonstrated high efficacy in Phase I and II studies in patients with CML following failure of imatinib therapy. Studies exploring the efficacy of dasatinib as front-line therapy in patients with BCR-ABL-expressing hematologic malignancies are underway.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 655-665 |
| Number of pages | 11 |
| Journal | Future Oncology |
| Volume | 2 |
| Issue number | 6 |
| DOIs | |
| State | Published - Dec 2006 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- BCR-ABL
- Chronic myeloid leukemia
- Dasatinib
- Resistance
- SRC
- Tyrosine kinase inhibitor
ASJC Scopus subject areas
- Oncology
- Cancer Research
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