Cells develop a heterogeneous response to KRAS inhibitors, bypassing their anti-growth effects by producing more of the protein that does not bind the inhibitor.
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A.N.H. has received research funding from Amgen, Pfizer, Roche/Genentech, Eli Lilly, Novartis and Relay Therapeutics. A.T.S. has served as a compensated consultant or received honoraria from Achilles, Archer, ARIAD, Bayer, Blueprint Medicines, Chugai, Daiichi Sankyo, EMD Serono, Foundation Medicine, Genentech/Roche, Guardant, Ignyta, KSQ Therapeutics, LOXO, Natera, Novartis, Pfizer, Servier, Syros, Taiho Pharmaceutical, Takeda and TP Therapeutics; has received research (institutional) funding from Daiichi Sankyo, Ignyta, Novartis, Pfizer, Roche/Genentech and TP Therapeutics; has served on the Board of Directors of Syros Pharmaceuticals; and is currently an employee of Novartis.
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Hata, A.N., Shaw, A.T. Resistance looms for KRASG12C inhibitors. Nat Med 26, 169–170 (2020). https://doi.org/10.1038/s41591-020-0765-z
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DOI: https://doi.org/10.1038/s41591-020-0765-z
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