Abstract
The introduction of the tyrosine kinase inhibitor (TKI), imatinib, has had a significant impact in improving the long term survival prospects of patients with chronic myeloid leukaemia (CML). However, many patients develop resistance to imatinib, which has prompted the development of more potent TKIs and other new agents with different mechanisms of action. This article examines how TKIs work in CML, describes mutations that may develop to confer resistance and discusses
Original language | English |
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Pages (from-to) | 11-15 |
Number of pages | 5 |
Journal | British Oncology Pharmacy Association Bulletin |
Volume | 3 |
Publication status | Published - 2011 |