The DOI matches its Crossref record; 30 of the 31 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The 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 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]
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
“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]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Trimmomatic: a flexible trimmer for Illumina sequence data
Bolger, A. M., Lohse, M., & Usadel, B. (2014) · Bioinformatics · doi:10.1093/bioinformatics/btu170 · Cited by 65,548
The Sequence Alignment/Map format and SAMtools
Li, H., Handsaker, B., Wysoker, A., Fennell, T., Ruan, J., Homer, N., Marth, G., Abecasis, G., Durbin, R., & 1000 Genome Project Data Processing Subgroup (2009) · Bioinformatics · doi:10.1093/bioinformatics/btp352 · Cited by 62,041
The Genome Analysis Toolkit: A MapReduce framework for analyzing next-generation DNA sequencing data
McKenna, A., Hanna, M., Banks, E., Sivachenko, A., Cibulskis, K., Kernytsky, A., Garimella, K., Altshuler, D., Gabriel, S., Daly, M., et al. (2010) · Genome Research · doi:10.1101/gr.107524.110 · Cited by 27,895
Ultrafast and memory-efficient alignment of short DNA sequences to the human genome.
Langmead, B., Trapnell, C., Pop, M., & Salzberg, S. L. (2009) · Genome Biology · doi:10.1186/gb-2009-10-3-r25 · Cited by 21,849
Kim, D., Pertea, G., Trapnell, C., Pimentel, H., Kelley, R., & Salzberg, S. L. (2013) · Genome Biology · doi:10.1186/gb-2013-14-4-r36 · Cited by 12,668
Self-citationComprehensive molecular profiling of lung adenocarcinoma
The Cancer Genome Atlas Research Network (2014) · Nature · doi:10.1038/nature13385 · Cited by 5,732
Zehir, A., Benayed, R., Shah, R. H., Syed, A., Middha, S., Kim, H. R., Srinivasan, P., Gao, J., Chakravarty, D., Devlin, S. M., et al. (2017) · Nature Medicine · doi:10.1038/nm.4333 · Cited by 3,380
Self-citationK-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions
Ostrem, J. M., Peters, U., Sos, M. L., Wells, J. A., & Shokat, K. M. (2013) · Nature · doi:10.1038/nature12796 · Cited by 2,557
The Clinical KRAS(G12C) Inhibitor AMG 510 Drives Anti-Tumour Immunity
Canon, J., Rex, K., Saiki, A. Y., Mohr, C., Cooke, K., Bagal, D., Gaida, K., Holt, T., Knutson, C. G., Koppada, N., et al. (2019) · Nature · doi:10.1038/s41586-019-1694-1 · Cited by 2,277
Self-citationMemorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets (MSK-IMPACT)
Cheng, D. T., Mitchell, T. N., Zehir, A., Shah, R. H., Benayed, R., Syed, A., Chandramohan, R., Liu, Z. Y., Won, H. H., Scott, S. N., et al. (2015) · The Journal of Molecular Diagnostics · doi:10.1016/j.jmoldx.2014.12.006 · Cited by 2,119
Self-citation
Cited by
Sorted by citations
Items 301–400 of 476
Maso, L., Mosure, S. A., Rodriguez‐Aponte, S. A., Pizzo, A., Mensah, D. N., Southard, M., Sze, S., Ahmed, T., Vash, B., Hattori, T., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-66132-w · Cited by 3
Systematic and precise interventions for KRAS-mutant cancers
Liang, J., Wu, J., Zhang, Y., Wang, H., Zheng, Y., & He, Q. (2026) · Experimental Hematology and Oncology · doi:10.1186/s40164-026-00763-7 · Cited by 4
Martín, A., García-Pérez, I. M., José, S. S., Rojo, P., Riego‐Mejías, C., Teodósio, C., Barbosa, B. M. G., Sánchez, C., Folch-I-Casanovas, I., Odena, M. A., et al. (2026) · Cancer Research · doi:10.1158/0008-5472.can-25-5172 · Cited by 3
Alejandre, C., Calle-Espinosa, J., & Iranzo, J. (2024) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1012081 · Cited by 3
Cregg, J., Edwards, A. V., Tomlinson, A. C. A., Gill, A. L., & Koltun, E. S. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21861-3.00011-5 · Cited by 3
Intratumor heterogeneity in KRAS signaling shapes treatment resistance
Petrenko, O., Kirillov, V., D’Amico, S., & Reich, N. C. (2024) · iScience · doi:10.1016/j.isci.2024.111662 · Cited by 3
Patel, H. V., Smith, A. E., Chan, S., Gasendo, J. G., Jombik, A., Greer, J. E., Samantaray, T., Kessler, L. V., Mitra, A., Zhu, X., et al. (2026) · Cancer Research · doi:10.1158/0008-5472.can-25-2764 · Cited by 3
Identifying genes associated with resistance to KRAS G12C inhibitors via machine learning methods
Lin, X., Ma, Q., Chen, L., Guo, W., Huang, Z., Huang, T., & Cai, Y. (2023) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2023.130484 · Cited by 3
Insights into direct KRAS inhibition strategies for cancer treatment
Li, T., Gu, C., Zhou, C., Mao, C., Yang, K., Xu, J., Lu, T., & Chen, J. (2024) · Future Medicinal Chemistry · doi:10.1080/17568919.2024.2424149 · Cited by 3
Zhang, Z. (2024) · American Journal of Cancer Research · doi:10.62347/xebr7848 · Cited by 3
Song, Y., Wang, Y., Guan, A., Xue, J., Li, B., Huang, Z., Zheng, Z., Liang, N., Yang, Y., & Li, S. (2023) · Frontiers in Bioengineering and Biotechnology · doi:10.3389/fbioe.2023.1132940 · Cited by 3
Self-citationPatient-Derived-Xenografts in Mice: A Preclinical Platform for Cancer ResearchPreprint
Cocco, E., & de Stanchina, E. (2023) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a041381 · Cited by 3
Targeting Hyperactive Ras Signaling in Pediatric CancerPreprint
Levinson, A. L., Shannon, K., & Huang, B. J. (2024) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a041572 · Cited by 3
Meraz, I. M., Wu, S., Xu, Y., Gao, L., Feng, M., Ren, C., Song, R., Zhang, R., Wang, Q., Xi, Y., et al. (2025) · eLife · doi:10.7554/elife.106875.1 · Cited by 3
Zuo, G., Xu, H., Zhang, Y., Liu, Z., Tu, J., Gou, D., Fu, P., Huang, H., Ren, J., Hu, Y., et al. (2024) · Organic Process Research & Development · doi:10.1021/acs.oprd.4c00279 · Cited by 2
KRAS inhibitors in drug resistance and potential for combination therapy
Rathod, L. S., Sakle, N. S., & Mokale, S. N. (2024) · Tumori Journal · doi:10.1177/03008916241289206 · Cited by 3
Novel paradigms in KRAS targeting: Unveiling strategies to combat drug resistance
Luo, X., Zhou, F., Tang, Y., Liu, X., Xiao, R., Gu, M., Bai, J., Jiang, D., Yang, G., You, L., et al. (2025) · Chinese Medical Journal · doi:10.1097/cm9.0000000000003776 · Cited by 2
Self-citationPaula, A. D. C., Zhu, Y., Brown, D. N., Bhaloo, S. I., Pareja, F. G., Hoang, T. J., Green, H., Basili, T., Dopeso, H., Selenica, P., et al. (2025) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-25-1237 · Cited by 2
Self-citationHe, D., Zhu, Y., Zhong, J., Cai, H., Li, Y., Zhuang, W., He, Y., Xu, Y., Fan, L., Fei, K., et al. (2025) · Journal of the National Cancer Center · doi:10.1016/j.jncc.2025.11.003 · Cited by 2
Tumor suppressor genes and KRAS G12C inhibitor resistance in non-small cell lung cancer
Zhu, L., Jia, X., Xu, L., Chen, L., Fu, X., Yan, H., Ai, B., & Peng, S. (2025) · iScience · doi:10.1016/j.isci.2025.114429 · Cited by 2
Intrinsic resistance to RAS inhibitors is driven by dysregulation of KRAS degradation
Ivanišević, T., Ma, Y., Boxel, E. V., Magits, W., Lechat, B., Koçberber, Z., Willnow, P., Fendt, S., Velde, G. V., Sewduth, R. N., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-67109-5 · Cited by 2
Targeting HGF/MET and CXCL1/CXCR2 axes bypasses resistance to KRASG12C inhibitors in NSCLC
Cavazzoni, A., Mariano, M. P., Palladini, A., Digiacomo, G., Monica, S., Bonelli, M., Galetti, M., Pace, I., Roncarati, R., Giovannetti, E., et al. (2026) · Lung Cancer · doi:10.1016/j.lungcan.2026.108939 · Cited by 2
Devanahally, S., & Dubey, S. (2026) · Cancer Pathogenesis and Therapy · doi:10.1016/j.cpt.2026.02.001 · Cited by 2
Miyan, J., Vudatha, V., Cao, L., Zhang, P., Zheng, G., Zheng, L., Trevino, J., Zhou, D., & Khan, S. (2026) · Cancers · doi:10.3390/cancers18060920 · Cited by 2
Lin, W., Chen, Q., Yang, Y., Gao, Y., & He, J. (2026) · Experimental Hematology and Oncology · doi:10.1186/s40164-026-00797-x · Cited by 2
Robb, R. N., Ackermann, S. E., Degan, S. E., Taylor, K. E., Yang, R. Y., Marler, A. Z., Calvert, V. S., Pierobon, M., Lyons, S. P., Barker, N. K., et al. (2026) · Cancer Research Communications · doi:10.1158/2767-9764.crc-25-0731 · Cited by 2
Targeting Distinct Cell-Cycle Nodes Overcomes RAS Inhibitor Resistance
Kumarasamy, V. M., Wang, J., Yau, E. H., Abel, E. V., Witkiewicz, A. K., & Knudsen, E. S. (2026) · Cancer Research · doi:10.1158/0008-5472.can-26-1315 · Cited by 2
Ohana, J., Sandler, U., Devary, O. V., & Devary, Y. (2023) · Oncotarget · doi:10.18632/oncotarget.28467 · Cited by 2
Liu, B., Fink-Baldauf, I. M., Stuart, W. D., Jiang, C., Naren, A. P., Shi, D., Guo, M., Whitsett, J. A., & Maeda, Y. (2025) · Molecular Pharmaceutics · doi:10.1021/acs.molpharmaceut.5c00550 · Cited by 2
Megid, R., Ribeiro, G., Gomes, I. N. F., Laus, A. C., Leal, L. F., da Silva, L. S., Ariwoola, A.-B. A., Dias, J. M., Reis, R. M., & Oliveira, R. J. D. S. (2025) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2025.1537523 · Cited by 3
SYSMut: decoding the functional significance of rare somatic mutations in cancer
Khalighi, S., Joseph, P. L., Babu, D., Singh, S., LaFramboise, T., Guda, K., & Varadan, V. (2022) · Briefings in Bioinformatics · doi:10.1093/bib/bbac280 · Cited by 2
Decoding the proteostasis network in resistance to KRAS inhibitors
Song, X., Zhou, Z., & Westover, K. D. (2023) · The Innovation · doi:10.1016/j.xinn.2023.100526 · Cited by 2
Targeted Therapies for Pancreatic Cancer
Lee, M. S., & Pant, S. (2023) · Springer eBooks · doi:10.1007/978-3-031-38623-7_5 · Cited by 2
Inhibition of ULK1/2 and KRASG12C controls tumor growth in preclinical models of lung cancerPreprint
Ghazi, P. C., O’Toole, K. T., Boggaram, S. S., Scherzer, M. T., Silvis, M. R., Zhang, Y., Jagannathan‐Bogdan, M., Smith, B. D., Lozano, G., Flynn, D. L., et al. (2024) · eLife · doi:10.7554/elife.96992.2 · Cited by 1
Özakıncı, H., Desai, B., Kalos, D., Chen, D., Henry, M., Solanki, H. S., Boyle, T. A., Bittar, H. E. T., Nazario, G. S., Haura, E. B., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.12.17.628751 · Cited by 2
Genetic mechanisms of resistance to targeted KRAS inhibitionPreprint
Diaz, B. J., Kops, M. S., Bernardo, S., Schmidt, H., Grankowsky, E., Vega, A., Zhang, C., Bott, M. J., Skamagki, M., Tomlinson, A. C. A., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.08.04.668444 · Cited by 2
Adaptive Feedback Signaling Through the FAK/SRC Pathway Promotes KRAS G12C Inhibitor Resistance
Udagawa, H., Shibata, Y., Nilsson, M. B., Nishii, K., Robichaux, J. P., Galan-Cobo, A., He, J., Poteete, A., Qian, Y., Molkentine, D., et al. (2026) · Journal of Thoracic Oncology · doi:10.1016/j.jtho.2026.103991 · Cited by 1
Peng, S., Zhang, Y., Lin, X., Si, C., Van Horn, R. D., Dempsey, J. A., Goetz, E., Evans, R. J., Farber, A., Vandekopple, M. J., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-72650-y · Cited by 1
Addicted to proteostasis: How KRAS-driven cancers acquire resistance to clinical KRAS inhibitors
Klein, A. T., & Mendillo, M. L. (2023) · Cell chemical biology · doi:10.1016/j.chembiol.2023.10.007 · Cited by 1
Jean-Francois, F. L. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21861-3.00010-3 · Cited by 1
Discovery of JDQ443 (opnurasib)
Cotesta, S., & Zécri, F. J. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21861-3.00015-2 · Cited by 1
Tamayo, N. A., Wurz, R. P., & Lanman, B. A. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21861-3.00001-2 · Cited by 1
Targeting RAS for Cancer Treatment: What a Long, Strange Trip It's Been
Cox, A. D., & Der, C. J. (2025) · Annual Review of Cancer Biology · doi:10.1146/annurev-cancerbio-071024-082459 · Cited by 1
Spectral decomposition of human BCL2 bonded to a PROTAC
Nauta, W. J., de Graaf, C., Meul, Y., Vissenberg, K., Schoenaers, S., & Cunha, A. V. (2025) · The Journal of Chemical Physics · doi:10.1063/5.0288378 · Cited by 1
Miao, S., Sun, Y., Qu, Y., Zhu, L., Zhong, Z., & Meng, F. (2025) · Acta Biomaterialia · doi:10.1016/j.actbio.2025.12.045 · Cited by 1
Hamada, T., Yokoyama, S., Nakabayashi, R., Suzuki, Y., Morishita, S., Akahane, T., Matsuo, K., Kitazono, I., Furukawa, T., & Tanimoto, A. (2026) · Current Issues in Molecular Biology · doi:10.3390/cimb48040341 · Cited by 1
KRAS and MYC synergistic inhibition: a powerful strategy targeting KRAS-mutant cancers
Yan, M., Liu, K., Xu, J., Liu, Y., Ji, L., & Zhang, S. (2026) · Molecular Cancer · doi:10.1186/s12943-026-02659-w · Cited by 1
Bao, Q., Chen, H., Wu, J., Wang, Y., Chen, X., Lin, Z., Xu, Y., & Chen, J. (2026) · APOPTOSIS · doi:10.1007/s10495-026-02347-6 · Cited by 1
Kapoor, A., Sansar, B., Gupta, A., Mishra, B. K., Rungta, A., Pal, A., Srivastava, S., Shah, M. J., Menon, N. S., Pai, T., et al. (2026) · Medical Oncology · doi:10.1007/s12032-026-03318-2 · Cited by 1
Chaperone directed heterobifunctional molecules circumvent KRASG12C inhibitor resistance
Pulido, I., Luan, Q., Pastor-Puente, S., Gunder, L. C., Wang, Y., Ying, C., Li, J., Sun, Y., Dai, Y., Ascoli, C., et al. (2025) · Cancer Letters · doi:10.1016/j.canlet.2025.217691 · Cited by 1
Scaglione, I. M., Bonato, A., Dodi, A., Sposito, M., Eccher, S., Avancini, A., Tregnago, D., Insolda, J., Milella, M., Pilotto, S., et al. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27062643 · Cited by 1
Vitale, A., Marafioti, M., Galassi, T., Madonia, G., Moro, M., & Dubois, M. (2026) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2026.105396 · Cited by 1
RAS Inhibitors: Changing the Paradigm from the Undruggable
Campana, F., Bellis, E. D., Porcaro, F., Guida, G. D., Gravara, L. D., Servetto, A., Morgillo, F., Papaccio, F., Filippelli, A., Corte, C. M. D., et al. (2026) · Pharmaceutics · doi:10.3390/pharmaceutics18070773 · Cited by 1
Lu, D., Osgood, T., Ma, S., Zhang, H., Kanke, M., Tan, J. A., Paudel, S. N., Zhou, H., Estrada, J., Yamawaki, T., et al. (2026) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-25-0794 · Cited by 1
Self-citationLi, X., Guo, Y., & Yang, S. (2026) · Pharmacological Research · doi:10.1016/j.phrs.2026.108367 · Cited by 1
A codon-defined translational program promotes RAS-driven cancer progression and drug resistance
Xing, S., Li, J., Ge, L., Shi, Z., Liang, Z., Ren, L., Huang, J., Zheng, Y., Chao, Y., Cheng, J., et al. (2026) · Vita · doi:10.15302/vita.2026.07.0049 · Cited by 1
Small-molecule RAS/RAF inhibitors target RAS-driven cancers via allosteric RAF disruption
Yoshikawa, Y., Kubota, H., Matsumoto, S., Makino, Y., Kawamura, T., Yuki, H., Sakai, N., Shibaike, A., Okamura, M., Fujimoto-Sakisaka, W., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-76337-2 · Cited by 1
Lee, Y., Hwang, S., Shin, H. Y., Choi, K., Seo, S., Kim, H., Yang, J. S., Kim, Y. J., Kim, Y.-M., & Song, E. J. (2026) · Experimental & Molecular Medicine · doi:10.1038/s12276-026-01837-6 · Cited by 1
Lineage identity governs oncogene dependence in mouse NSCLC models of KRAS inhibitor resistance
Mathey‐Andrews, N., Rodriguez, C. L., Shui, B., Patriotis, A. L., Rideout, W. M., Chen, V. Z., Murazzi, I., Ghazi, P., Cornwall-Brady, M. R., Liu, M., et al. (2026) · Nature Genetics · doi:10.1038/s41588-026-02768-8 · Cited by 1
SOS1 inhibitor combinations overcome KRAS inhibitor resistance
(2024) · Nature Cancer · doi:10.1038/s43018-024-00801-5 · Cited by 1
Zhou, Y., Chen, X., Chapman, J. S., & Barrett, M. T. (2024) · BMC Genomics · doi:10.1186/s12864-024-10850-w · Cited by 1
KRAS combination strategies: How well aligned is clinical and preclinical research?
Nadal, E., Ambrogio, C., Santamarı́a, D., & Lindsay, C. R. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21861-3.00018-8 · Cited by 2
Yang, P., & Li, Y. (2025) · Investigational New Drugs · doi:10.1007/s10637-025-01514-x · Cited by 1
Autres cibles addictives (KRAS, RET, HER2, NTRK…)
Simon, E., Abdayem, P., Planchard, D., & Greillier, L. (2022) · Revue des Maladies Respiratoires Actualités · doi:10.1016/s1877-1203(22)00120-3 · Cited by 1
State of the Art: onkogen alteriertes nichtkleinzelliges Lungenkarzinom im Stadium IV
Heinzen, S., Reis, H., Sebastian, M., Demes, M. C., & Stratmann, J. (2022) · Die Onkologie · doi:10.1007/s00761-022-01248-y · Cited by 1
Misale, S., Yaeger, R. D., Mezzadra, R., Sinopoli, J. C., Bian, Y., Marasco, M., Kaplun, E., Gao, Y., Zhao, H., Paula, A. D. C., et al. (2022) · Research Square · doi:10.21203/rs.3.rs-1236956/v1 · Cited by 1
Self-citationData from Facts and Hopes on RAS Inhibitors and Cancer Immunotherapy
Boumelha, J., Molina‐Arcas, M., & Downward, J. (2023) · doi:10.1158/1078-0432.c.6982714 · Cited by 1
Inhibition of ULK1/2 and KRASG12C controls tumor growth in preclinical models of lung cancerPreprint
Ghazi, P. C., O’Toole, K. T., Boggaram, S. S., Scherzer, M. T., Silvis, M. R., Zhang, Y., Jagannathan‐Bogdan, M., Smith, B. D., Lozano, G., Flynn, D. L., et al. (2024) · eLife · doi:10.7554/elife.96992.1 · Cited by 2
Challenges and opportunities of emerging mechanisms of resistance to KRASG12C inhibitors
Cecchini, M., & LoRusso, P. M. (2025) · Annals of Oncology · doi:10.1016/j.annonc.2025.03.009 · Cited by 1
Meraz, I. M., Wu, S., Xu, Y., Gao, L., Feng, M., Ren, C., Song, R., Zhang, R., Wang, Q., Xi, Y., et al. (2025) · eLife · doi:10.7554/elife.106875 · Cited by 1
Chang, W.-H., Vaughan, A. J., Stamey, A. G., Mancini, M., Hayashi, M., Yang, R. Y., Robb, R. N., Andrussier, D., Klomp, J. A., Waters, A. M., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.04.18.719329 · Cited by 1
Selective Pyroptosis in NF1-Deficient Cells through PKCδ AgonismPreprint
Hu, L., Tang, Y., Lin, Y., Pundavela, J., Scheffer, K. C., Schaeper, A., Rizvi, T. A., Wu, J., Zheng, Y., & Ratner, N. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.19.726276 · Cited by 1
Ching, Y. M., Narayanan, S., Klomp, J. A., Isermann, T., Loewe, S., Chang, W.-H., Waters, A. M., Peña, S. R. N., Baldelli, E., Martin, C. P., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.08.10.743026 · Cited by 1
Kano, Y. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27135796
Homan, T., Fortunato, F., Corso, G., Lopalco, P. L., Prato, R., & Martinelli, D. (2021) · Infectious Diseases and Therapy · doi:10.1007/s40121-021-00582-9
Droske, L. E., Ramirez-Mata, A. S., Cash, M. N., Estrada, J., Shank, S. D., Browning, A., Rafiei, F., Pond, S. L. K., Salemi, M., & Magalis, B. R. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.05.04.490630
PKC-alpha promotes phosphorylation of KRAS suppressing its oncogenic propertiesPreprint
Joglekar, T., Ku, A., Schollaert, E., Gong, Y., Stewart-Ornstein, J., Urisman, A., & Wang, M.-T. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.05.24.493257
High-Throughput Single-Cell Sequencing for Retroviral Reservoir CharacterizationPreprint
Droske, L. E., Shank, S. D., Cash, M. N., Pond, S. L. K., Salemi, M., & Magalis, B. R. (2022) · SSRN Electronic Journal · doi:10.2139/ssrn.4158004
Data from Genomic Landscapes and Hallmarks of Mutant RAS in Human Cancers
Scharpf, R. B., Balan, A., Ricciuti, B., Fiksel, J., Cherry, C., Wang, C., Lenoue-Newton, M. L., Rizvi, H. A., White, J. R., Baras, A. S., et al. (2023) · doi:10.1158/0008-5472.c.6514292.v1
Self-citationTargeting Rat Sarcoma Viral Oncogene Homolog for Treatment of Gastrointestinal Cancers
Robinson, H. R., Davis, S. L., & Lieu, C. H. (2023) · Advances in Oncology · doi:10.1016/j.yao.2023.01.011
Target Hyperactive ERK Signaling for Cancer Therapy
Yap, J., & Hu, J. (2023) · Springer eBooks · doi:10.1007/978-3-030-80962-1_257-1
Supplementary Figure S10 from Comutations and KRASG12C Inhibitor Efficacy in Advanced NSCLC
Negrao, M. V., Araújo, H. A., Lamberti, G., Cooper, A. J., Akhave, N. S., Zhou, T., Delasos, L., Hicks, J. K., Aldea, M. D., Minuti, G., et al. (2023) · doi:10.1158/2159-8290.23310275
Self-citationSupplementary Figure S10 from Comutations and KRASG12C Inhibitor Efficacy in Advanced NSCLC
Negrao, M. V., Araújo, H. A., Lamberti, G., Cooper, A. J., Akhave, N. S., Zhou, T., Delasos, L., Hicks, J. K., Aldea, M. D., Minuti, G., et al. (2023) · doi:10.1158/2159-8290.23310275.v1
Self-citationSupplementary Figure S10 from Comutations and KRASG12C Inhibitor Efficacy in Advanced NSCLC
Negrao, M. V., Araújo, H. A., Lamberti, G., Cooper, A. J., Akhave, N. S., Zhou, T., Delasos, L., Hicks, J. K., Aldea, M. D., Minuti, G., et al. (2023) · doi:10.1158/2159-8290.23641387
Self-citationTargeted Therapies for Pancreatic Cancer
Maitra, A. (2023) · Wiley eBooks · doi:10.1002/9781119876007.ch151
Autres cibles addictives (KRAS, RET, HER2, NTRK…)
Planchard, D., Simon, É., Abdayem, P., & Greillier, L. (2023) · Revue des Maladies Respiratoires Actualités · doi:10.1016/s1877-1203(23)00140-4
Adaptation to ARF6-depletion in KRAS-driven PDAC is abolished by targeting TLR2Preprint
Ghose, R., Das, S., Urgel-Solas, J., Pezzano, F., Datta, D., Ghose, U., Zapater, A. G., Lorente, N. P., Espinar, L., Garcia, L., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.11.30.569405
Making incurable pancreatic cancer curable
An, J., Xie, D., & Xie, K. (2023) · Malignancy Spectrum · doi:10.1002/msp2.19
Data from Facts and Hopes on RAS Inhibitors and Cancer Immunotherapy
Boumelha, J., Molina‐Arcas, M., & Downward, J. (2023) · doi:10.1158/1078-0432.c.6982714.v1
Peritoneal B1 and B2 cells respond differently to LPS and IL-21 stimulation
Li, D., Ma, Y., Miao, Y., Liu, S., Bi, Y., Ji, Y., Wu, Q., Zhou, C., & Ma, Y. (2024) · Molecular Immunology · doi:10.1016/j.molimm.2024.04.007
Oncogene inactivation-induced senescence facilitates tumor relapse
Schmitt, P., Hönig, K., Norcia, M. T., Nogueira, M. F., Flore, V., Vesperinas, I. S., Villoro-Agud, M., Peng, L., Safyürek, Z., Tariq, M., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-75021-9
Ghazi, P. C., O’Toole, K. T., Boggaram, S. S., Scherzer, M. T., Silvis, M. R., Zhang, Y., Jagannathan‐Bogdan, M., Smith, B. D., Lozano, G., Flynn, D. L., et al. (2024) · eLife · doi:10.7554/elife.96992.2.sa0
An Evolving Landscape: New Therapies for Metastatic Colorectal Cancer
Mo, C., Chadha, B., & Kuang, C. (2024) · Clinical Colorectal Cancer · doi:10.1016/j.clcc.2024.08.003
Mediating kinase activity in Ras-mutant cancer: potential for an individualised approach?
Healy, F. M., Turner, A. L., Marensi, V., & MacEwan, D. J. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1441938
Autres cibles addictives (KRAS, RET, HER2, NTRK...)
Cortot, A. B., Abdayem, P., & Planchard, D. (2024) · Revue des Maladies Respiratoires Actualités · doi:10.1016/s1877-1203(24)00090-9
Conclusions: the future of RAS drug discovery
Gill, A. L., & Shokat, K. M. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21861-3.00009-7
The emergence of pan-KRAS drugs
McConnell, D. B., & Kraut, N. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21861-3.00019-x
Immune-oncology potential of KRAS inhibitors
Molina‐Arcas, M., Boumelha, J., & Downward, J. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-21861-3.00013-9
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
