Tumours have many ways to dodge drug therapies, even those that are genetically targeted to attack them, two studies published today reveal. By uncovering these escape routes, researchers hope that therapies can be tailored to cut them off.
Both studies focus on lung cancers with genetic mutations that activate a protein called epidermal growth factor receptor (EGFR). Improper activation of this protein can lead to uncontrolled cell division, a hallmark of cancer. Two drugs — gefitinib (Iressa) and erlotinib (Tarceva) — block EGFR in tumours with activating mutations to prevent tumour growth. These drugs help most patients: about three quarters of those with EGFR-activating mutations respond well to gefitinib, for example. But the rest respond poorly, if at all, and no one knows why.