Abstract
Cancer Therapy Unlike most colorectal cancer patients with mutations in the KRAS gene, those with the Gly13→Asp (G13D) mutation respond to blockade of epidermal growth factor receptor (EGFR). Using a systems biology approach, McFall et al. showed that EGFR-mediated activation of wild-type KRAS depended on whether the mutant KRAS inhibited the tumor suppressor neurofibromin 1 (NF1). Because the KRAS G13D mutant did not inhibit NF1, EGFR signaling still activated wild-type KRAS in KRAS G13D cells and drove tumor growth. These findings underscore how precision medicine could benefit from a systems-level analysis of patients. Sci. Signal. 12 , eaaw8288 (2019).
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