ArticleOncogene2010
EGFRvIV: a previously uncharacterized oncogenic mutant reveals a kinase autoinhibitory mechanism.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 4 citations in OpenAlex.
- EGFR: New Insights on Its Activation and Mutation in Tumor and Tumor Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- EGFR signaling and pharmacology in oncology revealed with innovative BRET-based biosensors.Communications biology · 2024Article
- Epidermal Growth Factor Receptor Inhibitors in Glioblastoma: Current Status and Future Possibilities.International journal of molecular sciences · 2024Review
- Distribution and favorable prognostic implication of genomic EGFR alterations in IDH-wildtype glioblastoma.Cancer medicine · 2023Article
- Allosteric activation of preformed EGF receptor dimers by a single ligand binding event.Frontiers in endocrinology · 2022Article
- Expanding the Disorder-Function Paradigm in the C-Terminal Tails of Erbbs.Biomolecules · 2021Review
- Review
- Exome sequencing identifies novel somatic variants in African American esophageal squamous cell carcinoma.Scientific reports · 2021Article
- Structural and dynamic characterization of the C-terminal tail of ErbB2: Disordered but not random.Biophysical journal · 2021Article
- EGFR forms ligand-independent oligomers that are distinct from the active state.The Journal of biological chemistry · 2020Article
- Rare epidermal growth factor receptor (EGFR) mutations in non-small cell lung cancer.Seminars in cancer biology · 2020Review
- The architecture of EGFR's basal complexes reveals autoinhibition mechanisms in dimers and oligomers.Nature communications · 2018Article
- Deep mutational analysis reveals functional trade-offs in the sequences of EGFR autophosphorylation sites.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Rigidity of the extracellular part of HER2: Evidence from engineering subdomain interfaces and shared-helix DARPin-DARPin fusions.Protein science : a publication of the Protein Society · 2017Article
- Activation of the EGF Receptor by Ligand Binding and Oncogenic Mutations: The "Rotation Model".Cells · 2017Review
- Splice Variants of the RTK Family: Their Role in Tumour Progression and Response to Targeted Therapy.International journal of molecular sciences · 2017Review
- Biophysical Evidence for Intrinsic Disorder in the C-terminal Tails of the Epidermal Growth Factor Receptor (EGFR) and HER3 Receptor Tyrosine Kinases.The Journal of biological chemistry · 2017Article
- Molecular mechanisms of the effect of TGF-β1 on U87 human glioblastoma cells.Oncology letters · 2016Article
- The EGFR-HER2 module: a stem cell approach to understanding a prime target and driver of solid tumors.Oncogene · 2016Review
- Aptamer targeting EGFRvIII mutant hampers its constitutive autophosphorylation and affects migration, invasion and proliferation of glioblastoma cells.Oncotarget · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Tumor cells often subvert normal regulatory mechanisms of signal transduction. This study shows this principle by studying yet uncharacterized mutants of the epidermal growth factor receptor (EGFR) previously identified in glioblastoma multiforme, which is the most aggressive brain tumor in adults. Unlike the well-characterized EGFRvIII mutant form, which lacks a portion of the ligand-binding cleft within the extracellular domain, EGFRvIVa and EGFRvIVb lack internal segments distal to the intracellular tyrosine kinase domain. By constructing the mutants and by ectopic expression in naive cells, we show that both mutants confer an oncogenic potential in vitro, as well as tumorigenic growth in animals. The underlying mechanisms entail constitutive receptor dimerization and basal activation of the kinase domain, likely through a mechanism that relieves a restraining molecular fold, along with stabilization due to association with HSP90. Phosphoproteomic analyses delineated the signaling pathways preferentially engaged by EGFRvIVb-identified unique substrates. This information, along with remarkable sensitivities to tyrosine kinase blockers and to a chaperone inhibitor, proposes strategies for pharmacological interception in brain tumors harboring EGFRvIV mutations.
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What OpenQuestion holds
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.