Chronic myeloid leukemia (CML) is the first cancer in which a genetic alteration was proven to be of pathogenic significance and is considered a disease model for oncogene addiction, targeted therapy, and cancer stem cells (CSCs). The introduction of tyrosine kinase inhibitors (TKIs) resulted in dramatic improvement in response and survival for patients with CML in chronic phase (CP); however, CSCs are spared by TKIs. In this article, we review the role of CSCs in CML in CP, their persistence following TKI treatment, and current approaches to target this population in an attempt to achieve disease cure.
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