Article
Concurrent inhibition of oncogenic and wild-type RAS-GTP for cancer therapy.
Nature - 1 May 2024
Holderfield Matthew, Lee Bianca J, Jiang Jingjing, Tomlinson Aidan, Seamon Kyle J, Mira Alessia, Patrucco Enrico, Goodhart Grace, Dilly Julien, Gindin Yevgeniy, Dinglasan Nuntana, Wang Yingyun, Lai Lick Pui, Cai Shurui, Jiang Lingyan, Nasholm Nicole, Shifrin Nataliya, Blaj Cristina, Shah Harshit, Evans James W, Montazer Nilufar, Lai Oliver, Shi Jade, Ahler Ethan, Quintana Elsa, Chang Stephanie, Salvador Anthony, Marquez Abby, Cregg Jim, Liu Yang, Milin Anthony, Chen Anqi, Ziv Tamar Bar, Parsons Dylan, Knox John E, Klomp Jennifer E, Roth Jennifer, Rees Matthew, Ronan Melissa, Cuevas-Navarro Antonio, Hu Feng, Lito Piro, Santamaria David, Aguirre Andrew J, Waters Andrew M, Der Channing J, Ambrogio Chiara, Wang Zhengping, Gill Adrian L, Koltun Elena S, Smith Jacqueline A M, Wildes David, Singh Mallika
Abstract excerpt
RAS oncogenes (collectively NRAS, HRAS and especially KRAS) are among the most frequently mutated genes in cancer, with common driver mutations occurring at codons 12, 13 and 611. Small molecule inhibitors of the KRAS(G12C) oncoprotein have demonstrated clinical efficacy in patients with multiple cancer types and have led to regulatory approvals for the treatment of non-small cell lung cancer2,3. Nevertheless,...
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