Mechanisms of primary and secondary resistance to imatinib in chronic myeloid leukemia

Alfonso Quintás-Cardama, Hagop M. Kantarjian, Jorge E. Cortes

Research output: Contribution to journalReview article

160 Scopus citations

Abstract

Background: Although the vast majority of patients with chronic myeloid leukemia (CML) respond to the tyrosine kinase inhibitor (TKI) imatinib mesylate, resistance might occur de novo or during treatment. Methods: The authors reviewed the known mechanisms of primary and secondary resistance to imatinib and other TKIs used in the management of CML. Results: Mutations within the kinase domain of BCR-ABLI account for 30% to 40% of cases of imatinib resistance. Other mechanisms include BCR-ABLI amplification, overexpression of the SRC family of kinases, and pharmacokinetic and pharmacodynamic factors. Conclusions: Although not all resistance mechanisms have been identified and understood, several agents based on the known mechanisms have already been designed and developed and are beginning clinical trials.

Original languageEnglish (US)
Pages (from-to)122-131
Number of pages10
JournalCancer Control
Volume16
Issue number2
DOIs
StatePublished - Apr 2009
Externally publishedYes

ASJC Scopus subject areas

  • Hematology
  • Oncology

Fingerprint Dive into the research topics of 'Mechanisms of primary and secondary resistance to imatinib in chronic myeloid leukemia'. Together they form a unique fingerprint.

  • Cite this