Abstract
Chemotherapy-resistant cancer stem cells make it hard to cure many forms of the disease. Repositioning an existing drug to tackle this problem could significantly improve treatment for one form of leukaemia. See Letter p.380 Chronic myeloid leukaemia (CML) is in many cases driven by the BCR-ABL translocation which leads to constitutive activation of the ABL kinase. This has led to good clinical results with ABL kinase inhibitors such as imatinib. However, resistance emerges in many patients, which has been attributed to the inherent resistance of quiescent CML stem cells. Stephane Prost et al. now demonstrate that pioglitazone — a glitazone antidiabetic that acts via the nuclear receptor PPARγ — can reduce the pool of CML stem cells and in combination with imatinib achieve lasting effects in CML patients.
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