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RAS genes are mutated in more than 30 percent of human cancers and represent one of the most sought-after cancer targets for drug developers. However, this goal has been elusive because of the absence of any drug-binding pockets in the mutant RAS protein. A new study published in the April 20 issue of the journal Cell by researchers at the Icahn School of Medicine at Mount Sinai led by E. Premkumar Reddy, PhD, has identified a new mechanism for targeting this important cancer gene.
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