Chronic myeloid leukemia in the tyrosine kinase inhibitor era: what is the "best" therapy?

Current Oncology Reports
Meetu AgrawalJorge Cortes

Abstract

The introduction of imatinib mesylate, a Bcr-Abl1 tyrosine kinase inhibitor (TKI), has revolutionized the treatment of chronic myeloid leukemia (CML). By directly targeting the Bcr-Abl kinase, imatinib leads to durable cytogenetic remissions and in turn improved survival. However, many patients with CML develop resistance, fail to respond, or become intolerant to imatinib due to side effects. This has spurred interest in developing second-generation TKIs to overcome the mechanisms of resistance that lead to treatment failure, specifically Bcr-Abl1 kinase domain mutations. Two second-generation TKIs, nilotinib and dasatinib, are approved for the treatment of CML after imatinib failure or intolerance. Unfortunately, many patients fail subsequent treatment with these agents, as they can develop highly resistant mutations such as T315I. Various other strategies are now in use to optimize the treatment of CML, including dose optimization of imatinib, combination therapy, upfront use of second-generation TKIs, and use of maintenance therapy with interferon-alpha and vaccines. This review highlights progress made in the treatment of CML in the past year.

References

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Citations

Nov 26, 2010·Frontiers of Medicine in China·Ying-Li WuGuo-Qiang Chen
Feb 18, 2011·Journal of Interferon & Cytokine Research : the Official Journal of the International Society for Interferon and Cytokine Research·Ben X WangEleanor N Fish
Feb 9, 2011·Leukemia & Lymphoma·Nicholas J Donato, Luke F Peterson
Dec 21, 2012·British Journal of Haematology·Eran EyalNinette Amariglio
Mar 11, 2011·Blood·Jean-Jacques KiladjianRonald Hoffman
Aug 10, 2012·Experimental Biology and Medicine·Pilar SanchoAna Isabel García-Pérez

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