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• W3013112801 abstract "Oncogenic RAS proteins, which are mutated in approximately 24% of all human cancers, have earned a well-deserved reputation as being undruggable. However, several studies have challenged that reputation. With the first small molecules that directly target one oncogenic RAS mutant (G12C) undergoing clinical evaluation, there have been substantial advances in finding anti-RAS therapeutic strategies. Furthermore, new insights have come from the growing appreciation that neither all RAS proteins (HRAS, NRAS, and KRAS4A/KRAS4B) nor all oncogenic RAS mutations (such as at residues Gly12, Gly13, and Gln61) have the same impact on RAS signaling and function. The role of the nonmutated, wild-type RAS proteins in the context of mutant RAS is increasingly considered to be targetable, with reports of strategies that directly disrupt either the RAS interaction with activating guanine nucleotide exchange factors (GEFs) or receptor tyrosine kinase-mediated and GEF-dependent RAS activation (such as by targeting the scaffolding phosphatase SHP2). Last, the development of agents that target downstream effectors of RAS signaling has advanced substantially. In this review, we highlight some important trends in the targeting of RAS proteins in cancer." @default.
• W3013112801 created "2020-04-03" @default.
• W3013112801 creator A5005237041 @default.
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• W3013112801 date "2020-03-24" @default.
• W3013112801 modified "2023-10-16" @default.
• W3013112801 title "RAS, wanted dead or alive: Advances in targeting RAS mutant cancers" @default.
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• W3013112801 doi "https://doi.org/10.1126/scisignal.aay6013" @default.
• W3013112801 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7393681" @default.
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• W3013112801 hasPublicationYear "2020" @default.
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