Source
Department of Haematology, The Hammersmith Hospital, London, UK. d.milojkovic@imperial.ac.uk
Abstract
PURPOSE OF REVIEW:
To revise the current goals of therapy of chronic myeloid leukaemia and to incorporate the influence of the underlying chronic myeloid leukaemia biology on directing therapeutic management.
RECENT FINDINGS:
The management of chronic myeloid leukaemia has been revolutionized by targeted molecular therapy that inhibits the ABL kinase activity of the BCR-ABL gene. The achievement of a major molecular response with the first tyrosine kinase inhibitor to be introduced into clinical practice, imatinib, is a focus of therapeutic regimens. Second-generation tyrosine kinase inhibitors are available that have more potent effects than imatinib, and have activity against imatinib-resistant subclones. Strategies to overcome the restoration of BCR-ABL signalling and subsequent resistance to therapy include imatinib dose escalation, a more potent tyrosine kinase inhibitor, as well as non-BCR-ABL-dependent approaches and agents in clinical development.
SUMMARY:
Therapeutic advances in chronic myeloid leukaemia continue to circumvent the challenges of drug resistance and the minimal residual leukaemic burden providing effective strategies for future therapy.