ArticleNature communications2019
MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAF
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Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 60 citations in OpenAlex.
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- Variable thresholds for phosphorylation targets of the ERK signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Therapy-induced mRNA, rRNA and tRNA methylation alterations confer tolerance phenotype in tumor cells: mechanism and implications.International journal of biological sciences · 2026Review
- EpCAM activates the ERK-EGR1 signaling axis and promotes TNF-α-induced the progression of anaplastic thyroid cancer.Journal of translational medicine · 2025Article
- RAF inhibitors activate the integrated stress response by direct activation of GCN2.Nature communications · 2025Article
- EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025Review
- TargetingBiotechnologia · 2025Article
- Role of Annexin 7 (ANXA7) as a Tumor Suppressor and a Regulator of Drug Resistance in Thyroid Cancer.International journal of molecular sciences · 2024Article
- Base editing screens define the genetic landscape of cancer drug resistance mechanisms.Nature genetics · 2024Article
- p57International journal of molecular sciences · 2024Article
- Reporter cell lines to screen for inhibitors or regulators of the KRAS-RAF-MEK1/2-ERK1/2 pathway.The Biochemical journal · 2024Article
- BRAF - a tumour-agnostic drug target with lineage-specific dependencies.Nature reviews. Clinical oncology · 2024Review
- Review
- BRAF Inhibitors in Metastatic Colorectal Cancer and Mechanisms of Resistance: A Review of the Literature.Cancers · 2023Review
- DNA replication stress and mitotic catastrophe mediate sotorasib addiction in KRASJournal of biomedical science · 2023Article
- Review
- ERK1/2 inhibitors act as monovalent degraders inducing ubiquitylation and proteasome-dependent turnover of ERK2, but not ERK1.The Biochemical journal · 2023Article
- Kras oncogene ablation prevents resistance in advanced lung adenocarcinomas.The Journal of clinical investigation · 2023Article
- ABL1/2 and DDR1 Drive MEKi Resistance in NRAS-Mutant Melanomas by Stabilizing RAF/MYC/ETS1 and Promoting RAF Homodimerization.Cancers · 2023Article
- Escape from G1 arrest during acute MEK inhibition drives the acquisition of drug resistance.NAR cancer · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 7 institutions in 2 countries.
Matthew J SaleSignalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK. matthew.sale@babraham.ac.uk.
Kathryn BalmannoSignalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
Jayeta SaxenaSignalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
Eiko OzonoSignalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
Katarzyna WojdylaProteomics Facility, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
Rebecca E McIntyreExperimental Cancer Genetics, Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, UK.
Rebecca GilleySignalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
Anna WoroniukSignalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
Karen D HowarthHutchison-MRC Research Centre, Department of Pathology, University of Cambridge, Hills Road, Cambridge, CB2 0XZ, UK.
Gareth HughesOncology Bioscience, Innovative Medicines and Early Development Biotech Unit, AstraZeneca, CRUK Cambridge Institute, Robinson Way, Cambridge, CB2 0RE, UK.
Jonathan R DryOncology Bioscience, Innovative Medicines and Early Development Biotech Unit, AstraZeneca, 35 Gatehouse Drive, Waltham, MA, 02451, USA.
Mark J ArendsDivision of Pathology, Centre for Comparative Pathology, Cancer Research UK Edinburgh Centre, MRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road South, Edinburgh, EH4 2XR, UK.ORCID http://orcid.org/0000-0002-6826-8770
Pilar CaroSignalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
David OxleyProteomics Facility, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK.
Susan AshtonOncology Bioscience, Innovative Medicines and Early Development Biotech Unit, AstraZeneca, Alderley Park, Macclesfield, SK10 4TG, UK.
David J AdamsExperimental Cancer Genetics, Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, UK.
Julio Saez-RodriguezEuropean Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Wellcome Genome Campus, Hinxton, Cambridgeshire, CB10 1SD, UK.ORCID http://orcid.org/0000-0002-8552-8976
Paul D SmithOncology Bioscience, Innovative Medicines and Early Development Biotech Unit, AstraZeneca, CRUK Cambridge Institute, Robinson Way, Cambridge, CB2 0RE, UK.ORCID http://orcid.org/0000-0002-2812-5978
Simon J CookSignalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK. simon.cook@babraham.ac.uk.
Babraham Institute · GBAstraZeneca (United Kingdom) · GBWellcome Sanger Institute · GBAstraZeneca (United States) · USEuropean Bioinformatics Institute · GBUniversity of Cambridge · GBWestern General Hospital · GB
Funding
Biotechnology and Biological Sciences Research Council BBS/E/B/000C0417Cancer Research UK 14867Wellcome Trust
Abstract
Acquired resistance to MEK1/2 inhibitors (MEKi) arises through amplification of BRAF
Indexed as
Antineoplastic AgentsApoptosisBenzimidazolesCell Line, TumorDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGene AmplificationGene Expression Regulation, NeoplasticHumansMaleMAP Kinase Kinase 1MAP Kinase Kinase 2MAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Antineoplastic AgentsAZD 6244BenzimidazolesBRAF protein, humanKRAS protein, humanMAP2K1 protein, humanMAP2K2 protein, humanMAPK1 protein, humanMAPK3 protein, humanMAP Kinase Kinase 1MAP Kinase Kinase 2Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Protein Kinase InhibitorsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)ZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1
Identifiers
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Textmetadata
LicenceCC BY
Read underepoch 390
Registered trials
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.