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

Meetu Agrawal, Ravin J. Garg, Hagop Kantarjian, Jorge Cortes

Research output: Contribution to journalReview articlepeer-review

26 Scopus citations

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-α and vaccines. This review highlights progress made in the treatment of CML in the past year.

Original languageEnglish (US)
Pages (from-to)302-313
Number of pages12
JournalCurrent Oncology Reports
Volume12
Issue number5
DOIs
StatePublished - Sep 1 2010
Externally publishedYes

Keywords

  • Chronic myeloid leukemia
  • Dasatinib
  • Imatinib
  • Nilotinib

ASJC Scopus subject areas

  • Oncology

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