Expanding the RAS-verse: Novel Inhibitors, Emergent Dependencies, Fresh Opportunities in RAS -Mutant NSCLC

Summary:

In this issue, two studies establish KRASG13C as a directly targetable oncoprotein in non–small cell lung cancer (NSCLC) while revealing distinct dependence of codon 13–mutant NSCLC on wild-type (WT) RAS and enhanced sensitivity to standard-of-care chemotherapy. A third study highlights rewired oncogenic signaling through WT RAS as a therapeutically tractable mechanism of resistance to KRASG12C inhibitors in the context of acquired oncogenic kinase fusions.

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