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Cancer Control. 2009 Apr;16(2):122-31.

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

Author information

1
Department of Leukemia at The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. aquintas@mdanderson.org

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.

PMID:
19337198
DOI:
10.1177/107327480901600204
[Indexed for MEDLINE]

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