Cancer Researchers Use Evolution to Target Drug Resistance

New therapeutic approaches in oncology aim to manipulate or block cancer’s adaptation to treatment.

Written byCatherine Offord
| 20 min read

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ABOVE: © Lucy Reading-IkKanda

In the early 2000s, back when biologist Olivia Rossanese worked as an investigator at GlaxoSmithKline, fighting cancer was an exercise in brute force. Researchers at the company had set their sights on developing inhibitors of B-Raf, a protein kinase involved in cell signaling that becomes dysfunctional in many cancers, and “what we were thinking was that we needed to hit this . . . protein so hard,” says Rossanese. “You had to inhibit it 99.999 percent to shut down the signaling pathway.”

In 2008, Rossanese and her GSK colleagues discovered just the sort of compound they were after: a small molecule, dabrafenib, that potently inhibited B-Raf and showed striking effects in melanoma patients with certain mutations in the BRAF gene. With dabrafenib, says Rossanese, “we see really amazing responses, and melanomas go away.” The drug was approved by the US Food and Drug Administration (FDA) in ...

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Meet the Author

  • After undergraduate research with spiders at the University of Oxford and graduate research with ants at Princeton University, Catherine left arthropods and academia to become a science journalist. She has worked in various guises at The Scientist since 2016. As Senior Editor, she wrote articles for the online and print publications, and edited the magazine’s Notebook, Careers, and Bio Business sections. She reports on subjects ranging from cellular and molecular biology to research misconduct and science policy. Find more of her work at her website.

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