Targeting ABL and SRC kinases in chronic myeloid leukemia: Experience with dasatinib

Alfonso Quintás-Cardama, Hagop Kantarjian, Jorge Cortes

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


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 languageEnglish (US)
Pages (from-to)655-665
Number of pages11
JournalFuture Oncology
Issue number6
StatePublished - Dec 2006
Externally publishedYes


  • Chronic myeloid leukemia
  • Dasatinib
  • Resistance
  • SRC
  • Tyrosine kinase inhibitor

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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