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Abstract
Chronic myeloid leukemia (CML) is a malignant disease induced by the oncogenic signal of the BCRABL transcript resulting from the translocation between chromosome 9 and 22, t (9:22). This genetic alteration evoked the development of imatinib, a tyrosine kinas inhibitor (TKI) targeting BCR-ABL tyrosine kinase. This drug showed higher activity with durable response compared with conventional interferon therapy and became a standard therapy for newly diagnosed CML patients. Dasatinib and nilotinib, the next generation TKIs are used for patients with chronic phase CML as first line therapy as well after finding that these drugs exert faster and deeper response than imatinib. Resistance and intolerance to BCR-ABL TKIs are the obstacles to managing patients. Substantial new drugs are developed for targeting mutations resistant to BCR-ABL TKIs. More concern is paid to long-term management of patients showing complications when taking these drugs, and eventually stopping drugs in selected patient populations are being evaluated.
References
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