Conclusions

Imatinib targets the tyrosine kinase activity of Bcr-Abl and is a breakthrough therapy that has dramatically altered the treatment of CML. Decreased efficacy of imatinib is often due to the emergence of clones expressing mutant forms of Bcr-Abl with reduced sensitivity to imatinib. The clinical importance of imatinib resistance and increased understanding of the structure of Abl and the molecular basis for resistance have resulted in the development of new agents active against Bcr-Abl mutants. Results from phase I and II clinical trials have demonstrated that nilotinib was effective and safe in patients with imatinib-resistant CML. Nilo-tinib may also be useful in the treatment of other conditions, such as chronic myel-monocytic leukemia, hypereosinophilic syndrome, systemic mastocytosis, or GIST.

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