ArticleCell reports2014
Oncogene mimicry as a mechanism of primary resistance to BRAF inhibitors.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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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
55 citing papers in PubMed, 73 citations in OpenAlex.
- Anaplastic thyroid cancer: genomic landscape, molecular drivers and novel therapeutics.Nature reviews. Endocrinology · 2026Review
- Potent and selective LSD1 inhibitor DC551040 reveals a promising combination therapy for AML with insight into epigenetic dysregulation.Signal transduction and targeted therapy · 2026Article
- Pan-cancer inference and validation of hypermorphic, hypomorphic and neomorphic mutations.Nature genetics · 2026Article
- The Revolution of Targeted Therapies in Thyroid Cancer Treatment: Present and Future Promising Anti-Cancer Drugs.International journal of molecular sciences · 2025Review
- Genetic alterations in thyroid cancer mediating both resistance to BRAF inhibition and anaplastic transformation.Oncotarget · 2024Article
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- Oncogenic PKA signaling increases c-MYC protein expression through multiple targetable mechanisms.eLife · 2023Article
- Review
- Dual Inhibition of BRAF-MAPK and STAT3 Signaling Pathways in Resveratrol-Suppressed Anaplastic Thyroid Cancer Cells with BRAF Mutations.International journal of molecular sciences · 2022Article
- The effect of local non-thermal plasma therapy on the cancer-immunity cycle in a melanoma mouse model.Bioengineering & translational medicine · 2022Article
- The emerging role of mass spectrometry-based proteomics in drug discovery.Nature reviews. Drug discovery · 2022Review
- Genomic and Transcriptomic Correlates of Thyroid Carcinoma Evolution after BRAF Inhibitor Therapy.Molecular cancer research : MCR · 2022Article
- MAPK-pathway inhibition mediates inflammatory reprogramming and sensitizes tumors to targeted activation of innate immunity sensor RIG-I.Nature communications · 2021Article
- Fine-Tuning Lipid Metabolism by Targeting Mitochondria-Associated Acetyl-CoA-Carboxylase 2 inThyroid : official journal of the American Thyroid Association · 2021Article
- Article
- HER3-Receptor-Mediated STAT3 Activation Plays a Central Role in Adaptive Resistance toward Vemurafenib in Melanoma.Cancers · 2020Article
- Article
- Dual Inhibition of MAPK and JAK2/STAT3 Pathways Is Critical for the Treatment of BRAF Mutant Melanoma.Molecular therapy oncolytics · 2020Article
- The MAPK and AMPK signalings: interplay and implication in targeted cancer therapy.Journal of hematology & oncology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Despite the development of potent RAF/mitogen-activated protein kinase (MAPK) pathway inhibitors, only a fraction of BRAF-mutant patients benefit from treatment with these drugs. Using a combined chemogenomics and chemoproteomics approach, we identify drug-induced RAS-RAF-MEK complex formation in a subset of BRAF-mutant cancer cells characterized by primary resistance to vemurafenib. In these cells, autocrine interleukin-6 (IL-6) secretion may contribute to the primary resistance phenotype via induction of JAK/STAT3 and MAPK signaling. In a subset of cell lines, combined IL-6/MAPK inhibition is able to overcome primary resistance to BRAF-targeted therapy. Overall, we show that the signaling plasticity exerted by primary resistant BRAF-mutant cells is achieved by their ability to mimic signaling features of oncogenic RAS, a strategy that we term "oncogene mimicry." This model may guide future strategies for overcoming primary resistance observed in these tumors.
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Registered trials
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.