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A two-pronged attack on chronic myeloid leukaemia Embargo London: Wednesday 02 September 2015 18:00 (BST) New York: Wednesday 02 September 2015 13:00 (EDT) Tokyo: Thursday 03 September 2015 02:00 (JST) Sydney: Thursday 03 September 2015 03:00 (AEST) A combination therapy approach that could improve treatment of chronic myeloid leukaemia (CML) is reported in a study published in Nature this week. Long-lasting therapeutic effects were observed in three patients with CML who were temporarily given antidiabetic drugs known as glitazones in addition to imatinib (a drug commonly used to treat CML). The study demonstrates the potential of this combination therapy for CML, although further clinical testing is needed. CML is a cancer of the white blood cells for which there is currently no cure. Imatinib and other tyrosine kinase inhibitors (TKIs) have improved outcomes for patients with this cancer, but leukaemia stem cells, which are thought to be responsible for initiating and developing leukaemia, can develop resistance to TKIs. This resistance seems to result from the presence of dormant (quiescent), drug-resistant leukaemia stem cells. Philippe Leboulch and colleagues describe the molecular pathway leading to quiescence in leukaemia stem cells. They show that glitazones can block this pathway, reduce the pool of CML stem cells and, in combination with imatinib, achieve therapeutic effects that lasted for months to years when tested on three patients with CML. With this combined therapy, patients remained disease free for up to 4.7 years after withdrawal from the glitazones. Additional clinical trials that are currently underway could help to further develop these results and to assess the potential of such combination therapies for CML. Article and author details 1. Erosion of the chronic myeloid leukaemia stem cell pool by PPAR agonists Corresponding Author Philippe Leboulch CEA, Fontenay-aux-Roses, France, and Harvard Medical School, Boston, MA, USA Tel: +33 6 48 37 76 79; E-mail: [email protected] N&V Author Tessa Holyoake University of Glasgow, UK Tel: +44 141 3017880; E-mail: [email protected] DOI 10.1038/nature15248 Online paper* http://nature.com/articles/doi:10.1038/nature15248 * Please link to the article in online versions of your report (the URL will go live after the embargo ends).
