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Resistance looms for KRASG12C inhibitors

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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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Fig. 1: The disparate responses to KRAS inhibitors in lung cancer.

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Authors and Affiliations

  1. Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA

    Aaron N. Hata

  2. Novartis Institutes of Biomedical Research, Cambridge, MA, USA

    Alice T. Shaw

Authors
  1. Aaron N. Hata
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  2. Alice T. Shaw
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Correspondence to Aaron N. Hata or Alice T. Shaw.

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Competing interests

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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