Ever since the approval of Gleevec in 2001, a cancer-cell-specific drug used to treat chronic myelogenous leukemia (CML), the field of cancer therapeutics has been rushing full speed into the era of so-called “targeted” medicines. The challenge of developing these medicines, which spare normal cells because they are designed to kill only cancer cells, has been complicated by the recognition that resistance to even targeted therapies can develop. In the case of Gleevec, for example, which disables the BCR-ABL1 protein that causes CML, resistance has become a growing problem. Currently, physicians estimate that 5 percent to 10 percent of patients who begin treatment in the chronic phase of their disease will develop resistance to Gleevec; and if treatment is begun at more advanced stages of CML, this percentage is much higher.Now researchers at the Abramson Cancer Center of the University of Pennsylvania have found a way around this problem. By disabling a BCR-ABL1-associated enzyme called Lyn kinase, they have induced cell death in drug-resistant CML cells taken from CML patients. Normal blood cells do not appear to be harmed by this approach because they are not so dependent on the Lyn kinase as CML cells. The Lyn kinase is therefore a good candidate for a targeted therapy.
