The roots of resistance

摘要

A promising new cancer drug called PLX4032 made waves earlier this year for its success against the deadly cancer melanoma. The results of a clinical trial were dramatic, with some patients emerging nearly cancer-free. But for most, the drug stopped working about seven months after therapy began, and the tumours returned. This week, two follow-up studies reveal why PLX4032 fails and how tumours' resistance to it might be overcome.rnAbout half of patients with melanoma have a mutated version of the B-RAF protein, which is thought to help trigger the growth of tumour cells. PLX4032 was designed by Plexxikon, a pharmaceutical company in Berkeley, California, to selectively inhibit it. In one study, PLX4032 shrank tumours in 24 of 32 patients with B-RAF mutations. But tumours often evolve ways to evade treatment, and this was no exception.