Genomic landscape of clinically acquired resistance alterations in patients treated with KRASG12C inhibitors

Acquired RAS/MAPK alterations are recurrent drivers of resistance to KRAS<sup>G12C</sup>i detected in CRC and, less frequently, in NSCLC. Preclinical data suggest that novel (K)RAS inhibitors may overcome many of these resistance alterations.

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Publication Details

Journal
Annals of Oncology
Published
2025-02-04
DOI
https://doi.org/10.1016/j.annonc.2025.01.020
Citations
28
Primary Topic
Protein Kinase Regulation and GTPase Signaling
Type
article
Field-Weighted Citation Impact
22.57

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article

Genomic landscape of clinically acquired resistance alterations in patients treated with KRASG12C inhibitors

Jakob M. Riedl, Scott Kopetz, Christine Megerdichian Parseghian, Haley Ellis et al.
28 citations
Annals of Oncology
Protein Kinase Regulation and GTPase Signaling
22.57
article

Genomic landscape of clinically acquired resistance alterations in patients treated with KRASG12C inhibitors

Jakob M. Riedl, Scott Kopetz, Christine Megerdichian Parseghian, Haley Ellis, Ferran Fece de la Cruz, Bryanna L. Norden, Ryan Bruce Corcoran, Leontios Pappas, Haley Barnes, Bennett Adam Caughey, A.R. Parikh, Preeti Patel, Rebecca S. Heist, Sara Ehnstrom, Samuel Jacob Klempner, Justin F. Gainor, W. Marston Linehan, Aaron N. Hata, Alvin A. Morales-Giron, Jonathan Kim, Hiroyuki Matsubara, H. Nakamura, Erich James Kushner, A Vakaris
article en
28 citations

Abstract

Acquired RAS/MAPK alterations are recurrent drivers of resistance to KRAS<sup>G12C</sup>i detected in CRC and, less frequently, in NSCLC. Preclinical data suggest that novel (K)RAS inhibitors may overcome many of these resistance alterations.

Annals of OncologyVol. 36(6)
Harvard University (US), Medical University of Graz (AT), University of Ulsan (KR), Massachusetts General Hospital (US), Center for Cancer Research (US)
Austrian Science Fund, National Institutes of Health, Stand Up To Cancer, National Cancer Institute
Openalex Percentile: Top 0%
Protein Kinase Regulation and GTPase Signaling
22.57
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