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Typically, when scientists discover a cancer-causing mutation, the goal is to develop a molecule that blocks the protein produced by the mutated gene. But for cancers driven by mutations in the KRAS gene—which include non-small cell lung, colorectal, and pancreatic cancers—this path to drug development has long been thwarted. The mutated KRAS gene encodes for a protein that releases continuous “grow” signals, causing cells to proliferate uncontrollably. For 40 years, this mutant protein was considered “undruggable,” its surface too smooth for a therapeutic molecule to bind. Then, after screening nearly 500 different molecules, a team at the University of California, San Francisco (led by Kevan M. Shokat, PhD, mentor to several Damon Runyon Fellows and former Damon Runyon-Rachleff Innovation Award Committee Member) discovered one that locks into a hidden crevice in the protein, stopping its activity. Even better, this hidden crevice only exists in the mutant version of the protein, meaning the molecule only targets cancerous cells—sparing healthy cells.
