Cited research Cancer Cell 18, 74–87 (2010)

The primary therapy for chronic myeloid leukaemia (CML), a blood cancer, is the drug Gleevec (imatinib mesylate), which targets a protein thought to be causative in the disease. But many patients relapse when treatment is stopped. To find additional drug targets, James DeGregori at the University of Colorado School of Medicine in Aurora and his colleagues looked for genes essential to keeping CML cells alive.

They found that a gene-regulating protein, NFAT, helped CML cells to survive even during treatment with Gleevec or similar drugs. Moreover, cyclosporin, a drug widely used to suppress the immune system, blocked NFAT's effects in mice, and might help patients if combined with current therapies.