ERROR 1
ERROR 1
ERROR 2
ERROR 2
ERROR 2
ERROR 2
ERROR 2
Password and Confirm password must match.
If you have an ACS member number, please enter it here so we can link this account to your membership. (optional)
ERROR 2
ACS values your privacy. By submitting your information, you are gaining access to C&EN and subscribing to our weekly newsletter. We use the information you provide to make your reading experience better, and we will never sell your data to third party members.
The cancer’s name—chronic myeloid leukemia—points to its lingering nature. Many patients with CML live long lives by taking a drug called imatinib. The treatment keeps the cancer in check but does not cure it. Researchers have long suspected that a pool of cancerous stem cells evade this treatment by being quiescent—hibernating to avoid the drug. Now, researchers led by Stéphane Prost of the Institute of Emerging Diseases & Innovative Therapies, in France, and Philippe Leboulch at Harvard Medical School may have found a way to beat those quiescent cancerous cells (Nature 2015, DOI: 10.1038/nature15248). Their trick is to interfere with a cellular pathway that allows the cancerous stem cells to remain quiescent. The team knew that the diabetes drug pioglitazone prods cells out of hibernation, and they speculated that pushing all the stem cells out of quiescence would allow imatinib to finish off the cancer. The strategy seems to have worked. In the three CML patients to whom the team gave imatinib and pioglitazone, the cancer did not return. The team is now pursuing a clinical trial for the combination therapy.
Join the conversation
Contact the reporter
Submit a Letter to the Editor for publication
Engage with us on X