The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer
Open accessPublished version of a preprint
Abstract
With the combination of KRASG12C and EGFR inhibitors, KRAS is becoming a druggable target in colorectal cancer. However, secondary resistance limits its efficacy. Using cell lines, patient-derived xenografts, and patient samples, we detected a heterogeneous pattern of putative resistance alterations expected primarily to prevent inhibition of ERK signaling by drugs at progression. Serial analysis of patient blood samples on treatment demonstrates that most of these alterations are detected at a low frequency except for KRASG12C amplification, a recurrent resistance mechanism that rises in step with clinical progression. Upon drug withdrawal, resistant cells with KRASG12C amplification undergo oncogene-induced senescence, and progressing patients experience a rapid fall in levels of this alteration in circulating DNA. In this new state, drug resumption is ineffective as mTOR signaling is elevated. However, our work exposes a potential therapeutic vulnerability, whereby therapies that target the senescence response may overcome acquired resistance. Significance: Clinical resistance to KRASG12C–EGFR inhibition primarily prevents suppression of ERK signaling. Most resistance mechanisms are subclonal, whereas KRASG12C amplification rises over time to drive a higher portion of resistance. This recurrent resistance mechanism leads to oncogene-induced senescence upon drug withdrawal and creates a potential vulnerability to senolytic approaches. Watch the interview with Sandra Misale, PhD, recipient of the 2025 Cancer Discovery Early Career Award: https://vimeo.com/1100471486 This article is highlighted in the In This Issue feature, p. 1
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
“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 [53]
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
“KRAS G12C amplification was a consistent resistance mechanism that increased in frequency over the duration of the treatment of CRC patients and cell lines treated with combinations of KRAS and EGFR inhibitors [101].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [101]
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
“Post-treatment analysis of NSCLC and CRC samples from patients treated with either sotorasib or adagrasib identified de novo oncogenic mutations secondary to treatment, including multiple amplifications and point mutations in KRAS G12C itself [101].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [101]
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
“Of note, cells that become resistant to the combination of KRASi and EGFRi are sensitive to mTOR inhibition [101].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [101]
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
“Furthermore, emerging genetic alterations have been shown to mediate resistance to KRAS G12C inhibitors combined with EGFR inhibitors in CRC patients.”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [53]
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
“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 [53]
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
“Analysis of cell-free DNA (cfDNA) in 12 CRC patients treated with sotorasib/panitumumab or adagrasib/cetuximab combinations identified secondary RAS mutations, KRAS amplifications, or both in 58.3% of sampled patients [53].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [53]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“In CRC patients co-treated with KRASi and EGFRi, low-frequency non-G12C KRAS mutations were detected in circulating tumor DNA, but were not well maintained over time [101].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [101]
The cited source says what the claim attributes to it.
In the citing paper
“Co-inhibiting KRAS and EGFR can shut down feedback loops activated by KRAS monotherapy [96,101,124].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [101]
The cited source says what the claim attributes to it.
In the citing paper
“Recent studies have identified several mechanisms of resistance to this combination, including secondary KRAS mutations, alterations in genes upstream or downstream of KRAS, and alterations in other RAS homologs.7,17,18”
From Paneth-like transition drives resistance to dual targeting of KRAS and EGFR in colorectal cancer (2026) · cites this paper as [17]
The cited source says what the claim attributes to it.
In the citing paper
“Notably, multiple resistance mutations often emerge in relapsed tumors within the same patient,7,17,18 which poses challenges to targeting heterogenous resistance mechanisms at the time of progressing disease.”
From Paneth-like transition drives resistance to dual targeting of KRAS and EGFR in colorectal cancer (2026) · cites this paper as [17]
The cited source says what the claim attributes to it.
In the citing paper
“Upon disease progression with divarasib plus cetuximab, the majority (92.9%) of patients profiled had at least one genomic alteration that may be associated with treatment resistance similarly to two previous reports26,27, which is higher than that of patients treated with divarasib (30.2%) or other KRAS G12C inhibitors as single agent11,28,29.”
From Divarasib plus cetuximab in KRAS G12C-positive colorectal cancer: a phase 1b trial (2024) · cites this paper as [26]
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 [35]
Experimental — accuracy not yet measuredIn the citing paper
“This is in line with previous reports of acquired KRAS mutations and acquired RTK/RAS/MAPK/PI3K pathway alterations following concurrent KRASG12C and EGFR inhibition in colorectal cancer (31, 32).”
From Efficacy and Safety of Adagrasib plus Cetuximab in Patients with KRAS G12C-Mutated Metastatic Colorectal Cancer (2024) · cites this paper as [31]
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
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
Fast and accurate short read alignment with Burrows-Wheeler transform
Li, H., & Durbin, R. (2009) · Bioinformatics · doi:10.1093/bioinformatics/btp324 · Cited by 58,607
Cutadapt removes adapter sequences from high-throughput sequencing reads
Martin, M. (2011) · EMBnet.journal · doi:10.14806/ej.17.1.200 · Cited by 33,889
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
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 1×
“…pattern of putative resistance alterations expected primarily to prevent inhibition of ERK signaling by drugs at alterations are detected at a low frequency except for KRAS amplification, a recurrent resistance In this new state, drug resumption is ineffective as mTOR signaling is elevated.”
Self-citationZehir, 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 · cited 3×
“It acts as a signaling switch that, when bound to GTP, KRAS is the most mutated oncogene in human cancer (1).”
InfluentialSelf-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
Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
Xue, W., Zender, L., Miething, C., Dickins, R. A., Hernando, E., Krizhanovsky, V., Cordon-Cardo, C., & Lowe, S. W. (2007) · Nature · doi:10.1038/nature05529 · Cited by 2,473
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-citationAbsolute quantification of somatic DNA alterations in human cancer
Carter, S. L., Cibulskis, K., Helman, E., McKenna, A., Shen, H., Zack, T. I., Laird, P. W., Onofrio, R. C., Winckler, W., Weir, B. A., et al. (2012) · Nature Biotechnology · doi:10.1038/nbt.2203 · Cited by 2,031
Cited by
Sorted by citations
Items 101–145 of 145
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
Co-targeting KRASG12D and the HER family is efficacious in colorectal cancer
Kilroy, M. K., Wischmeier, C., Park, B. S., Choi, D., Feroz, W., Mishra, R., & Garrett, J. T. (2025) · Carcinogenesis · doi:10.1093/carcin/bgaf036 · 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
Ojala, V. K., Ahonen, S., Peltola, S., Tuohisto-Kokko, A., Esparta, O., Suominen, P., Jokilammi, A., Farahani, I. K., Chakroborty, D., Dibus, N., et al. (2025) · Molecular Oncology · doi:10.1002/1878-0261.70189 · Cited by 2
Exploiting intracellular oncogenic proteins to release cytotoxins
Schild, M., & Gillingham, D. G. (2026) · RSC Medicinal Chemistry · doi:10.1039/d5md00764j · Cited by 1
Siegfried, G., Liu, Y., He, Z., Évrard, S., Badiola, I., Pernot, S., Creemers, J. W. M., & Khatib, A. (2026) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2026.189620 · Cited by 1
Guo, Y., Zhong, Y., Hu, P., Chen, Y., Guo, W., Chen, J., Guan, P., Zhou, Z., Zhu, F., Zeng, X., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-73805-7 · Cited by 1
Self-citationMartis, G. J., Souza, E. J. D., Mugali, P. S., & Gaonkar, S. L. (2026) · RSC Advances · doi:10.1039/d6ra05942b · 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
Zhou, Y., Chen, X., Chapman, J. S., & Barrett, M. T. (2024) · BMC Genomics · doi:10.1186/s12864-024-10850-w · Cited by 1
Miyahira, A. K., Sharifi, M. N., Chesner, L. N., El-Kenawi, A., Haas, R., Sena, L. A., Tewari, A. K., Pienta, K. J., & Soule, H. R. (2024) · The Prostate · doi:10.1002/pros.24826 · Cited by 1
Targeting AXL Overcomes Adaptive Resistance to KRAS Inhibition in KRAS-Driven CancerPreprint
Thege, F. I., Kramer, A., Kreisz, N., Salim, I., Girma, E. G., Welte, L., Adams, E., Pluchinsky, A., Kirschstein, E., Harder, O. E., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.08.02.742234 · Cited by 1
KRAS G12C mutation in metastatic colorectal cancer: a new target
Ibrahim, R., Saleh, K., Chahine, C., Khoury, R., Khalife, N., & Cesne, A. L. (2023) · Future Oncology · doi:10.2217/fon-2023-0223 · Cited by 1
Prahallad, A., Weiss, A., Voshol, H., Kerr, G., Sprouffske, K., Yuan, T. L., Ruddy, D. A., Meistertzheim, M., Kazic-Legueux, M., Kottarathil, T., et al. (2023) · doi:10.1158/0008-5472.c.6982749
Prahallad, A., Weiss, A., Voshol, H., Kerr, G., Sprouffske, K., Yuan, T. L., Ruddy, D. A., Meistertzheim, M., Kazic-Legueux, M., Kottarathil, T., et al. (2023) · doi:10.1158/0008-5472.c.6982749.v1
Recent updates of clinical trials for colorectal cancer
Prajapati, V. D., Roy, S. D., Shinde, S., & Prajapati, B. G. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-13870-6.00012-x
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
PHALCON: phylogeny-aware variant calling from large-scale single-cell panel sequencing datasetsPreprint
Priya, Chowdary, S. B. V., Gautam, A., & Zafar, H. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.12.26.630385
Wu, J., Lai, Y., Li, J., Zhai, L., Asthana, P., Chen, L., Chen, M., Chen, B., Gurung, S., Lyu, J., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.05.02.651972
Mohammadi, M., Bhat, M. A., Li, T., Wei, N., Patil, P., Mo, C., Thielen, N., Huang, Z., Du, J., Goldstein, D. Y., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.08.13.669992
Alpaddli, R., Hardiany, N. S., & Wanandi, S. I. (2025) · Current Aging Science · doi:10.2174/0118746098365760250903112703
Oligo-CALL: A next-generation barcoding platform for studying resistance to targeted therapy
Liu, Y., Ban, Y., & Gao, D. (2025) · Science Advances · doi:10.1126/sciadv.adw9990
Kong, Y., Jiang, R., Zhou, H., Ge, M., Lin, H., Wang, Y., Yao, R., Wang, Q., Liang, X., Li, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26401882
Kong, Y., Jiang, R., Zhou, H., Ge, M., Lin, H., Wang, Y., Yao, R., Wang, Q., Liang, X., Li, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26755408
Zhu, X., Li, C., Gao, Y., Zhang, Q., Wang, T., Zhou, H., Bu, F., Chen, J., Mao, X., He, Y., et al. (2024) · Figshare · doi:10.6084/m9.figshare.24923721
Self-citationKong, Y., Jiang, R., Zhou, H., Ge, M., Lin, H., Wang, Y., Yao, R., Wang, Q., Liang, X., Li, J., et al. (2024) · Figshare · doi:10.6084/m9.figshare.26402034
Wang, J., & Mo, Y. (2025) · Acta Mathematica Scientia · doi:10.1007/s10473-026-0124-3
Gentile, C., Feng, W. W., Lenahan, S. M., Ying, A. W., Card, D. C., Wu, F. T. H., Pham, N., Radulovich, N., Cao, P. M., Hueniken, K., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.02.27.708377
From undruggable to actionable: advances in KRAS targeting in colorectal cancer
Chan, M., Shelke, M., Townsend, A. R., Roy, A. C., Broadbridge, V. T., Karapetis, C. S., & Price, T. J. (2026) · Academia oncology. · doi:10.20935/acadonco8216
Thielen, N., Wei, N., Nagai, E., Houston, M. A., Augenlicht, L. H., Shin, A. E., Gabre, J. T., Rustgi, A. K., Ha, G., LaFave, L. M., et al. (2026) · npj Precision Oncology · doi:10.1038/s41698-026-01384-3 · Cited by 1
Lin, Y., Cai, R., Huang, L., Lin, T., Lin, A., Lin, Z., Jiang, S., Zhu, Y., Yuan, Y., & Su, S. (2026) · Foods · doi:10.3390/foods15091608
Self-citationMutant KRAS dosage contributes to heterogeneity in lung cancer therapeutic responsePreprint
Browne, A. T., McCann, C., McDaid, W. J., Lewis, N., Sridhar, S., Doherty, G. J., Moss, D. Y., Downs, M., Marry, S., Phillips, A. R., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.06.723208
Reprogramming paneth-like plasticity: FGFR3 as a key to overcoming KRAS-EGFR resistance in CRC
Yin, Z., Guo, X., Liu, X., & DeNardo, D. G. (2026) · Targetome · doi:10.48130/targetome-0026-0020
WEE1 kinase inhibition to overcome acquired resistance to targeted therapies in colorectal cancer
Buzo, K., Bizzozero, L., Lentini, M., Opattová, A., Suárez, B. H., Torres, M., Chiabotto, G., Nisticò, C., Lazzari, G. D., Zanella, E. R., et al. (2026) · EMBO Molecular Medicine · doi:10.1038/s44321-026-00434-4
Choi, P. H., Meredith, J., Sharma, M., Chen, X., Qiu, J., Markov, V., de Stanchina, E., Singh, M., & Rosen, N. X. (2026) · Cell Reports · doi:10.1016/j.celrep.2026.117559
Self-citationTherapeutic inhibition of RAS in non-small cell lung cancer
Nichols, K. B., & Herzberg, B. O. (2026) · Frontiers in Oncology · doi:10.3389/fonc.2026.1817943
Jiang, L., Luo, Y., Liang, H., Feng, X., Huang, Y., Li, Y., Wang, Z., Xu, T., Zou, H., Li, Z., et al. (2026) · Human Cell · doi:10.1007/s13577-026-01405-0
Genomic landscape and clinical characteristics of ERBB2/HER2 -mutated colorectal cancers
Aksu, M., Peniche, P. Z., Baytar, D. K., Jambunathan, B., Jan, Y. J., Hsieh, R. W., Rahman, S., Krauss, J., Veenstra, C. M., & Şahin, İ. H. (2026) · The Oncologist · doi:10.1093/oncolo/oyag302
Mariano, M. P., Sgarilli, E., Mijnlieff, D., Visuvasam, B., Blesio, A., Digiacomo, G., Cavazzoni, A., Ferracin, M., & Giovannetti, E. (2026) · Cancer Drug Resistance · doi:10.20517/cdr.2026.52
Tojjari, A., Pourbahrighesmat, S., Alkhazna, S., & Saeed, A. (2026) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2026.105597
Orive-Ramos, A., Gaire, B., Adamopoulos, C., Baars, B., Desaunay, M., Kou, Z., Matenoglou, E., Coma, S., Gutiérrez, N., Mohammed, K., et al. (2026) · Cancer Discovery · doi:10.1158/2159-8290.cd-25-1596 · Cited by 1
Binding kinetics enable tumor-selective MAPK and growth suppression by a Type 1 RAF InhibitorPreprint
Desaunay, M., Peters, T., Matenoglou, E., Baars, B., Gaire, B., Orive-Ramos, A., Ren, L., Lyssikatos, J. P., Burkard, M., Dacus, D., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.10.05.756774
Wen, Y., Sun, H., Xiong, N., Xu, X., Ye, Y., Shen, Z., & Wang, C. (2026) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2026.189735
Hamidi, A. A., Moaven, O., Mahmoudian, R. A., & Abbaszadegan, M. R. (2026) · Experimental Hematology and Oncology · doi:10.1186/s40164-026-00849-2
Wang, X., Ding, L., Meng, W., Byrnes, E., Loo, S. K., Sun, S., Chen, L., Li, T., Wang, M.-T., Pennathur, A., et al. (2026) · Science Advances · doi:10.1126/sciadv.aeb9836
Metadata
- Authors
- Yaeger, R., Mezzadra, R., Sinopoli, J., Bian, Y., Marasco, M., Kaplun, E., Gao, Y., Zhao, H., Paula, A. D. C., Zhu, Y., Perez, A. C., Chadalavada, K., Tse, E., Chowdhry, S., Bowker, S., Chang, Q., Qeriqi, B., Weigelt, B., Nanjangud, G. J., Berger, M. F., Der-Torossian, H., Anderes, K., Socci, N. D., Shia, J., Riely, G. J., Murciano-Goroff, Y. R., Li, B. T., Christensen, J. G., Reis-Filho, J. S., Solit, D. B., de Stanchina, E., Lowe, S. W., Rosen, N., & Misale, S.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Boundless Bio (United States) (US)
- 9Mirati Therapeutics, Inc., San Diego, California.
- Mirati Therapeutics (United States) (US)
- 1Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York.
- 4Antitumour Assessment Core Facility, Memorial Sloan Kettering Cancer Center, New York, New York.
- Corresponding author
- Yaeger, Rona
- Misale, Sandra
- ORCID
- Yaeger, Rona
- Mezzadra, Riccardo
- Sinopoli, Jenna
- Bian, Yu
- Marasco, Michelangelo
- Kaplun, Esther
- Gao, Yijun
- Zhao, HuiYong
- Paula, Arnaud Da Cruz
- Zhu, Yingjie
- Perez, Almudena Chaves
- Chadalavada, Kalyani
- Tse, Edison
- Chowdhry, Sudhir
- Bowker, Sydney
- Chang, Qing
- Qeriqi, Besnik
- Weigelt, Britta
- Nanjangud, Gouri J.
- Berger, Michael F.
- Der-Torossian, Hirak
- Anderes, Kenna
- Socci, Nicholas D.
- Shia, Jinru
- Riely, Gregory J.
- Murciano-Goroff, Yonina R.
- Li, Bob T.
- Christensen, James G.
- Reis-Filho, Jorge S.
- Solit, David B.
- de Stanchina, Elisa
- Lowe, Scott W.
- Rosen, Neal
- Misale, Sandra
- Venue
- Cancer Discovery
- Published
- 2022-11-10
- Volume
- 13
- Issue
- 1
- Pages
- 41-55
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC9827113
- OpenAlex
- W4308683759
- Cited by
- 144
- References
- 51
- Citations by year
- 2026: 37 · 2025: 49 · 2024: 36 · 2023: 22
- FWCI
- 11.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cancer Discovery (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Funders
- National Institutes of Health (R01 CA233736, U54 OD020355, P30 CA008748, K30 UL1TR00457)
- Cancer Research Institute (CRI 3441)
- Conquer Cancer Foundation (YIA)
- Topics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- 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
- Keywords
- KRAS G12C, EGFR inhibition, acquired drug resistance, colorectal cancer, KRAS amplification, ERK signaling, oncogene-induced senescence, mTOR signaling, circulating tumor DNA, senolytic therapy, patient-derived xenografts
- MeSH terms
- Animals, Disease Models, Animal, Humans, Mutation, Colorectal Neoplasms, Signal Transduction, Proto-Oncogene Proteins p21(ras), Drug Resistance, Neoplasm, ErbB Receptors
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
