ArticleCancer cell2013
EphA3 maintains tumorigenicity and is a therapeutic target in glioblastoma multiforme.
Article in Cancer cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 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
133 citing papers in PubMed, 214 citations in OpenAlex.
- Trial
- A metabolic shift favoring sphingosine 1-phosphate at the expense of ceramide controls glioblastoma angiogenesis.The Journal of biological chemistry · 2013Trial
- The YAP1 and EPHA3 receptor tyrosine kinase axis regulates cellular plasticity and treatment response.Cellular signalling · 2026Article
- Mapping kinase-dependent tumor immune adaptation with multiplexed single-cell CRISPR screens.bioRxiv : the preprint server for biology · 2026Article
- NF-κB and STAT3 signaling uniquely stratify survival in female glioblastoma patients.iScience · 2026Article
- Gene Expression Variations Induced by Sevoflurane in Glia and Glioma Cells and the Role of EPHA3 in Sevoflurane's Anti-Glioma Effect.Current medicinal chemistry · 2026Article
- Pathological neural and immune synapses in glioblastoma progression: mechanisms and therapeutic opportunities.Frontiers in neural circuits · 2026Review
- Multi-receptor targeted therapy of breast cancer and brain metastases with a novel QUAD-drug conjugate.Breast cancer research : BCR · 2025Article
- Development of a specific anti-human EphA3 monoclonal antibody, EaBiochemistry and biophysics reports · 2025Article
- Genetically Engineered Brain Organoids Recapitulate Spatial and Developmental States of Glioblastoma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Personalising glioblastoma medicine: explant organoid applications, challenges and future perspectives.Acta neuropathologica communications · 2025Review
- Beyond cell-cell contact: therapeutic potential of Eph signaling in central nervous system tumors.Frontiers in molecular neuroscience · 2025Review
- CAR-T in relapsed refractory high-grade glioma and glioblastoma - who, what, when and how?Ecancermedicalscience · 2025Review
- VIM-AS1, which is regulated by CpG methylation, cooperates with IGF2BP1 to inhibit tumor aggressiveness via EPHA3 degradation in hepatocellular carcinoma.Experimental & molecular medicine · 2024Article
- Master regulators of neurogenesis: the dynamic roles of Ephrin receptors across diverse cellular niches.Translational psychiatry · 2024Review
- EphA3 CAR T cells are effective against glioblastoma in preclinical models.Journal for immunotherapy of cancer · 2024Article
- EphA3-targeted chimeric antigen receptor T cells are effective in glioma and generate curative memory T cell responses.Journal for immunotherapy of cancer · 2024Article
- Ephs in cancer progression: complexity and context-dependent nature in signaling, angiogenesis and immunity.Cell communication and signaling : CCS · 2024Review
- Article
- Article
73 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
24 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Significant endeavor has been applied to identify functional therapeutic targets in glioblastoma (GBM) to halt the growth of this aggressive cancer. We show that the receptor tyrosine kinase EphA3 is frequently overexpressed in GBM and, in particular, in the most aggressive mesenchymal subtype. Importantly, EphA3 is highly expressed on the tumor-initiating cell population in glioma and appears critically involved in maintaining tumor cells in a less differentiated state by modulating mitogen-activated protein kinase signaling. EphA3 knockdown or depletion of EphA3-positive tumor cells reduced tumorigenic potential to a degree comparable to treatment with a therapeutic radiolabelled EphA3-specific monoclonal antibody. These results identify EphA3 as a functional, targetable receptor in GBM.
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.