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Diverse alterations associated with resistance to KRAS(G12C) inhibition
Open accessAbstract
Inactive state-selective KRAS(G12C) inhibitors 1-8 demonstrate a 30-40% response rate and result in approximately 6-month median progression-free survival in patients with lung cancer 9. The genetic basis for resistance to these first-in-class mutant GTPase inhibitors remains under investigation. Here we evaluated matched pre-treatment and post-treatment specimens from 43 patients treated with the KRAS(G12C) inhibitor sotorasib. Multiple treatment-emergent alterations were observed across 27 patients, including alterations in KRAS, NRAS, BRAF, EGFR, FGFR2, MYC and other genes. In preclinical patient-derived xenograft and cell line models, resistance to KRAS(G12C) inhibition was associated with low allele frequency hotspot mutations in KRAS(G12V or G13D), NRAS(Q61K or G13R), MRAS(Q71R) and/or BRAF(G596R), mirroring observations in patients. Single-cell sequencing in an isogenic lineage identified secondary RAS and/or BRAF mutations in the same cells as KRAS(G12C), where they bypassed inhibition without affecting target inactivation. Genetic or pharmacological targeting of ERK signalling intermediates enhanced the antiproliferative effect of G12C inhibitor treatment in models with acquired RAS or BRAF mutations. Our study thus suggests a heterogenous pattern of resistance with multiple subclonal events emerging during G12C inhibitor treatment. A subset of patients in our cohort acquired oncogenic KRAS, NRAS or BRAF mutations, and resistance in this setting may be delayed by co-targeting of ERK signalling intermediates. These findings merit broader evaluation in prospective clinical trials.
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“The discovery of KRAS G12C inhibitors raises great excitement; nevertheless, intrinsic and acquired resistance to sotorasib and adagrasib has been reported in preclinical studies and clinical trials (8–10).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [9]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“It is believed that this resistance can arise from a variety of mechanisms, including the emergence of additional mutations in KRAS or other genes involved in the RAS pathway, non-mutational activation of bypass signaling pathways such as the MAPK or PI3K pathways, and diverse remodeling of the tumor microenvironment (8–10).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [9]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Acquired mutations of NRAS, BRAF, RTK, and MYC were also found in patients treated with sotorasib or adagrasib monotherapy [49, 51, 53, 54].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [51]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Amplifications or gene fusions of MET, EGFR, FGFR2, FGFR3, and ALK have been detected in patients with acquired resistance to sotorasib and adagrasib monotherapy [49, 51].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [51]
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In the citing paper
“Expression of the identified KRAS mutants was sufficient to confer resistance to KRAS G12C inhibitors in KRAS G12C cancer cells [49, 51, 60].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [51]
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In the citing paper
“Therapeutic pressure from KRAS inhibition can rapidly reshape tumor clonal architecture [35,36,47,81].”
From Precision Targeting of KRAS-Mutant Cancers: Beyond G12C Toward G12D and Pan-RAS Therapeutic Strategies (2026) · cites this paper as [36]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Combination strategies targeting KRAS G12C and upstream regulators or downstream effectors of the RAS signaling have been extensively explored to overcome resistance to sotorasib or adagrasib (9–12, 56).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [9]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Cells containing mutations conferring KRASi resistance are frequently clonally or subclonally selected and can come to dominate much of the tumor post-relapse [62,68,97].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Interestingly, some of the treatment-emergent KRAS secondary mutations that are not commonly observed in primary tumors, such as KRAS V8L and KRAS V14I, arise in patients who are relatively responsive to sotorasib (as defined by RECIST scores ≤ 30) [97].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In patient tumors with KRAS G12C that were analyzed post-sotorasib treatment, 14% of tumors displayed an additional or alternative point mutation in KRAS [97].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Point mutations in the KRAS gene included G12D/F/R/V/W, which prevent covalent interactions with mutant cysteine, as well as V8L, G13D, V14I, Q61H, H95D/Q/R, Y96C, and Y96D [62,97,102,103].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Many of the novel mutations were observed at low subclonal frequencies, contributing to tumor heterogeneity [97,103].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“CRISPR screens specifically investigating sotorasib resistance identified and validated ERK1/2, SHOC2, NRAS, CRAF, and BRAF as vulnerable targets that were synthetically lethal with KRAS inhibition [97].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The downstream effectors of KRAS signaling that were mutated post-KRAS inhibition included activating lesions in PIK3CA, MEK1, BRAF, and RAF1 [51,68,97,112].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“These included ALK, APC, CDKN2A/B, CTNNB1, IDH1/2, KEAP1, MET, MYC, NRAS, PTCH1, PTEN, RB1, RET, RICTOR, SMARCA4, and TP53 [50,97,102].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Multiple mechanisms of acquired resistance have been identified, which largely converge on re-activation of the RAS pathway or alternatively activate parallel signaling pathways such as the PI3K/mTOR pathway10–14.”
From Combined inhibition of KRASG12C and mTORC1 kinase is synergistic in non-small cell lung cancer (2024) · cites this paper as [14]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“We and others have recently described mechanisms of acquired resistance in patients with lung and colorectal cancer (CRC) treated with KRASG12C inhibitors, including mutations in KRAS or other RTK–RAS–MAPK pathway effectors, adaptive signaling alterations, and histologic transformation to drug-resistant cell states (14, 18–24).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [19]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Recent studies using preclinical models have indicated that acquired resistance to KRASG12C inhibition may be mediated by the activation of multiple receptor tyrosine kinase (RTK) regulators, including epidermal growth factor receptor (EGFR), fibroblast growth factor receptor (FGFR), insulin-like growth factor 1 receptor (IGF1R), human epidermal growth factor 2 (HER2), and Src homology 2 domain-”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Vertical reactivation of the RAS pathway elements has been observed in most samples collected from patients who developed resistance to KRASG12C inhibitors.4,8,20,21”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“One major route leading to such recovery of RAS activity is the activation of RTKs through either genetic (e.g., gene amplification or fusion) or non-genetic mechanisms.2,4,5,6,7,8,22,23,24,25”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“A genome-wide CRISPR screen revealed that the adenosine triphosphate binding cassette transporter ABCC1 mediates MRTX849 resistance.”
From SRC kinase drives multidrug resistance induced by KRAS-G12C inhibition (2024) · cites this paper as [14]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This screen identified ABCC1 as a top-ranked gene whose disruption could reverse resistance to the G12Ci AMG510 (Fig. 2F).”
From SRC kinase drives multidrug resistance induced by KRAS-G12C inhibition (2024) · cites this paper as [14]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Genetic alterations, especially secondary RAS mutations, have been identified as one of the most common mechanisms of acquired resistance to KRAS inhibitors in patients [49, 51–55].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [51]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“However, clinical efficacy remains limited by intrinsic and acquired resistance, adaptive pathway reactivation, and tumor heterogeneity.”
From Precision Targeting of KRAS-Mutant Cancers: Beyond G12C Toward G12D and Pan-RAS Therapeutic Strategies (2026) · cites this paper as [36]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The co-evolution of multiple putative drug-resistance mechanisms within the same tumors mirrors observations in human samples whereby multiple distinct mechanisms have been observed within the same patients (14, 18, 19).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [19]
The cited source says what the claim attributes to it.
In the citing paper
“Although this is an important milestone in precision oncology, G12Ci treatments are facing challenges due to the emerging development of drug resistance (13, 14).”
From SRC kinase drives multidrug resistance induced by KRAS-G12C inhibition (2024) · cites this paper as [14]
The cited source says what the claim attributes to it.
In the citing paper
“Analysis of matched pre- and post-treatment specimens from 43 (36 NSCLC, 3 CRC, and 4 other) sotorasib-treated patients revealed treatment-induced genetic alterations in 27 patients, including 4 with secondary KRAS mutations (G12D, G12V, G12F, V8L) and 3 with copy-number gains of KRAS [51].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [51]
The cited source says what the claim attributes to it.
In the citing paper
“Long-term culture in high-dose adagrasib (10 × IC50) was used to generate adagrasib-resistant NCI-H358 cells (NCI-H358R), which were confirmed to retain KRASG12C and did not acquire any mutations associated with resistance in patients9,11 (Supplementary Table 10).”
From Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance (2024) · cites this paper as [11]
The cited source says what the claim attributes to it.
In the citing paper
“In a study of sotorasib-treated patients, 7% of patients in the study developed KRAS G12C amplifications [97].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
The cited source says what the claim attributes to it.
In the citing paper
“Time courses of G12C-mutant cell lines treated with increasing doses of G12C inhibitors demonstrated that the population frequency of rare resistance mutations increased over time [97].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
The cited source says what the claim attributes to it.
In the citing paper
“While previous studies have characterized acquired resistance to KRASG12C inhibition and identified causal mutations and non-genetic mechanisms including RTK activation and epithelial-to-mesenchymal transition11–14,35, the mechanisms underlying differential sensitivity to KRASG12C inhibition are less well understood.”
From Combined inhibition of KRASG12C and mTORC1 kinase is synergistic in non-small cell lung cancer (2024) · cites this paper as [14]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Previous reports have shown that PIK3CA mutations can confer acquired resistance to KRAS G12C inhibitor and KRAS G12C inhibitor–cetuximab combination therapy in patients with NSCLC and CRC34–36.”
From Mechanisms of KRAS inhibitor resistance in KRAS-mutant colorectal cancer harboring Her2 amplification and aberrant KRAS localization (2025) · cites this paper as [34]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“sgRNAs against CAB39, DUSP4, and NRBP1 were enriched in sotorasib-resistant cells, suggesting that their loss confers a selective advantage during treatment [97].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [97]
Experimental — accuracy not yet measuredIn the citing paper
“Nonetheless, there remains an ongoing need for improved clinical outcomes (21), especially since emerging data indicate multiple mechanisms of acquired resistance in patients treated with sotorasib or adagrasib (22–24), many of which involve RAS pathway reactivation.”
In the citing paper
“Despite this success, disease progression occurs in many patients4,5,7, with development of resistance to KRASG12Ci recapitulated in preclinical studies9–11.”
From Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance (2024) · cites this paper as [11]
In the citing paper
“Transcriptomic analysis of tumors explanted at the end of study, however, did not identify secondary KRAS mutations, increased KRAS expression, or genomic aberrations, previously reported in tumors with acquired resistance to KRASG12Ci (refs. 9,11) (Supplementary Table 12).”
From Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance (2024) · cites this paper as [11]
In the citing paper
“Many of the aforementioned mutations were detected only at low frequencies and only in approximately half of patients relapsing on KRASG12Ci (ref. 11).”
From Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance (2024) · cites this paper as [11]
In the citing paper
“activating mutations in MRAS (Q71R) have been reported at low allelic frequency in KRASG12Ci-resistant NSCLC cell lines11.”
From Co-targeting SOS1 enhances the antitumor effects of KRASG12C inhibitors by addressing intrinsic and acquired resistance (2024) · cites this paper as [11]
In the citing paper
“Pan-KRAS drugs would have advantages versus mutant-selective KRAS drugs in heterogeneous cancers driven by multiple KRAS alterations at baseline or upon development of acquired resistance due to secondary KRAS on-target alterations when compared to mutant-selective inhibitors (Fig. 3), with first examples emerging in the clinic (64–66).”
From Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants (2022) · cites this paper as [66]
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Self-citationAdeno-to-squamous transition drives resistance to KRAS inhibition in LKB1 mutant lung cancer
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“Genome-wide CRISPR screens in untreated KRAS-mutant, NRAS-mutant, and wild-type cell lines identified several classes of synthetic lethalities with mutant KRAS.”
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Targeting KRAS in Pancreatic Ductal Adenocarcinoma: The Long Road to Cure
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Hippo Signaling at the Hallmarks of Cancer and Drug Resistance
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Pharmacological restoration of GTP hydrolysis by mutant RAS
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Self-citationMore to the RAS Story: KRAS G12C Inhibition, Resistance Mechanisms, and Moving Beyond KRAS G12C
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Self-citationCombined inhibition of KRASG12C and mTORC1 kinase is synergistic in non-small cell lung cancer
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“…G12C inhibition and identi fi ed causal mutations and non-genetic mechanisms including RTK activation and epithelial-to-mesenchymal transition 11 – 14, 35 , the mechanisms underlying differential sensitivity to KRAS We, therefore, tested whether inhibitors of individual components of the PI3K…”
BackgroundEmerging Pharmacotherapeutic Strategies to Overcome Undruggable Proteins in Cancer
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Metadata
- Authors
- Zhao, Y., Murciano-Goroff, Y. R., Xue, J. Y., Ang, A., Lucas, J., Mai, T. T., Da Cruz Paula, A. F., Saiki, A. Y., Mohn, D., Achanta, P., Sisk, A. E., Arora, K. S., Roy, R. S., Kim, D., Li, C., Lim, L. P., Li, M., Bahr, A., Loomis, B. R., de Stanchina, E., Reis-Filho, J. S., Weigelt, B., Berger, M., Riely, G., Arbour, K. C., Lipford, J. R., Li, B. T., & Lito, P.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Amgen (United States) (US)
- Corresponding author
- Lito, Piro
- ORCID
- Venue
- Nature
- Published
- 2021-11-10
- Volume
- 599
- Issue
- 7886
- Pages
- 679-683
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC8887821
- OpenAlex
- W3212888956
- Cited by
- 479
- References
- 31
- Citations by year
- 2026: 95 · 2025: 90 · 2024: 127 · 2023: 99 · 2022: 65 · 2021: 3
- FWCI
- 47.87
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health (UL1TR000457, U54OD020355, UL1TR001873)
- National Cancer Institute (R01CA230267, K08CA191082, R01CA087486, F30CA232549, P50CA247749, P30CA008748, R01CA230745)
- National Institute of General Medical Sciences (T32GM007739)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- KRAS G12C inhibitors, sotorasib, acquired drug resistance, lung cancer, RAS mutations, BRAF mutation, ERK signaling, subclonal evolution, patient-derived xenografts, single-cell sequencing, KRAS G12V, NRAS Q61K, FGFR2, EGFR, c-Myc
- MeSH terms
- Acetonitriles, Animals, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Cell Line, Female, Humans, Membrane Proteins, Mutation, Neoplasms, Piperazines, Pyridines, Pyrimidines, Cohort Studies, Proto-Oncogene Proteins p21(ras), Drug Resistance, Neoplasm, GTP Phosphohydrolases, MAP Kinase Signaling System, Xenograft Model Antitumor Assays, Extracellular Signal-Regulated MAP Kinases, Proto-Oncogene Proteins B-raf, Mice
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