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Chronic myelogenous leukemia (CML) is caused by chromosomal translocation that creates a fused gene; this gene produces an oncoprotein, BCR-ABL. Targeting this protein with imatinib (Gleevec) and other tyrosine kinase inhibitors (TKIs) produces dramatic clinical improvement in many patients — but few cures. Many experts believe that cures are prevented because dormant (nonreplicating) cancer stem cells are not killed by TKIs and thereby sustain disease.
A French team reports that a molecular pathway, triggered by activation of peroxisome proliferator-activated receptor gamma (PPARγ), causes fewer cancer stem cells to remain dormant, thereby rendering them more vulnerable to treatment. The team added the PPARγ-activating drug pioglitazone, wh…