ArticleOncotarget2016
Cell line with endogenous EGFRvIII expression is a suitable model for research and drug development purposes.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- The Prognostic Significance of Epidermal Growth Factor Receptor Amplification and Epidermal Growth Factor Receptor Variant III Mutation in Glioblastoma: A Systematic Review and Meta-Analysis with Implications for Targeted Therapy.International journal of molecular sciences · 2025Pooled it
- Co-expression of non-signaling CARs enhances EGFRvIII-specific CAR T-cell cytotoxicity against head and neck squamous cell carcinoma.BMC cancer · 2026Article
- EGFRvIII Reduces Neural Stem/Progenitor Marker Expression in GFAP-Negative iNSCs: Evidence for a Context-Dependent Cellular Response.International journal of molecular sciences · 2026Article
- Novel EGFR tyrosine kinase inhibitors exhibiting intrinsic fluorescence.Investigational new drugs · 2026Article
- First molecules to reactivate RASBMC cancer · 2025Article
- PD1CD28 chimeric molecule enhances EGFRvⅢ specific CAR-T cells in xenograft experiments in mouse models.PloS one · 2024Article
- Visualization of Cellular Membranes in 2D and 3D Conditions Using a New Fluorescent DithienothiopheneInternational journal of molecular sciences · 2023Article
- Inhibitory potency of the nettle lectin on neovascularization: a biomolecule for carbohydrate-mediated targeting of angiogenesis.Molecular biology reports · 2023Article
- Increased EGFRvIII Epitope Accessibility after Tyrosine Kinase Inhibitor Treatment of Glioblastoma Cells Creates More Opportunities for Immunotherapy.International journal of molecular sciences · 2023Article
- Phenotypical Flexibility of the EGFRvIII-Positive Glioblastoma Cell Line and the Multidirectional Influence of TGFβ and EGF on These Cells-EGFRvIII Appears as a Weak Oncogene.International journal of molecular sciences · 2022Article
- Novel Cyclic Peptides for Targeting EGFR and EGRvIII Mutation for Drug Delivery.Pharmaceutics · 2022Article
- Extrachromosomal circular DNA in cancer drug resistance and its potential clinical implications.Frontiers in oncology · 2022Review
- Review
- Gaps and Doubts in Search to Recognize Glioblastoma Cellular Origin and Tumor Initiating Cells.Journal of oncology · 2020Review
- A way to understand idiopathic senescence and apoptosis in primary glioblastoma cells - possible approaches to circumvent these phenomena.BMC cancer · 2019Article
- Advancing towards Effective Glioma Therapy: MicroRNA Derived from Umbilical Cord Mesenchymal Stem Cells' Extracellular Vesicles.The Malaysian journal of medical sciences : MJMS · 2019Review
- EGFRJournal of oncology · 2019Review
- CyclicOncotarget · 2018Article
- Low Incidence along with Low mRNA Levels ofJournal of Cancer · 2017Article
- Efficient and simple approach to in vitro culture of primary epithelial cancer cells.Bioscience reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is the most common and malignant brain tumor, characterized by high cellular heterogeneity. About 50% of glioblastomas are positive for EGFR amplification, half of which express accompanying EGFR mutation, encoding truncated and constitutively active receptor termed EGFRvIII. Currently, no cell models suitable for development of EGFRvIII-targeting drugs exist, while the available ones lack the intratumoral heterogeneity or extrachromosomal nature of EGFRvIII.The reports regarding the biology of EGFRvIII expressed in the stable cell lines are often contradictory in observations and conclusions. In the present study, we use DK-MG cell line carrying endogenous non-modified EGFRvIII amplicons and derive a sub-line that is near depleted of amplicons, whilst remaining identical on the chromosomal level. By direct comparison of the two lines, we demonstrate positive effects of EGFRvIII on cell invasiveness and populational growth as a result of elevated cell survival but not proliferation rate. Investigation of the PI3K/Akt indicated no differences between the lines, whilst NFκB pathway was over-active in the line strongly expressing EGFRvIII, finding further supported by the effects of NFκB pathway specific inhibitors. Taken together, these results confirm the important role of EGFRvIII in intrinsic and extrinsic regulation of tumor behavior. Moreover, the proposed models are stable, making them suitable for research purposes as well as drug development process utilizing high throughput approach.
Indexed as
Identifiers
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.