Scientists have solved the structure of an important complex of RAS-pathway proteins, explaining how known mutations lead to disease and suggesting potential new binding sites for cancer drugs.
In explaining why mutations in the gene TP53 tend to cluster in “hot spots,” a new study lays the groundwork for ability to identify the function of any mutation in any cancer gene.
John Doench, associate director of the Genetic Perturbation Platform (GPP) and institute scientist at the Broad Institute, and Ruth Hanna, research associate in GPP, discuss how the CRISPR system has revolutionized studies of gene function.