ArticleOncotarget2016
Simultaneous targeting of Eph receptors in glioblastoma.
Article in Oncotarget, 2016. 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, 56 citations in OpenAlex.
- An in silico approach to peptide-based dual-receptor targeting for IL13RA2 and VEGFR-2 extracellular domain.Journal of molecular modeling · 2026Article
- Multi-receptor targeted therapy of breast cancer and brain metastases with a novel QUAD-drug conjugate.Breast cancer research : BCR · 2025Article
- EphB2 receptor tyrosine kinase-mediated excitatory synaptic functions are negatively modulated by MDGA2.Progress in neurobiology · 2025Article
- Remote Control of Gold-Iron Nanowires Using Low-Frequency 1 Hz Magneto-Mechanical Therapy and Cesium 137 0.662 MeV Radiotherapy for Treatment of Glioblastoma Multiforme.ACS applied materials & interfaces · 2025Article
- Beyond cell-cell contact: therapeutic potential of Eph signaling in central nervous system tumors.Frontiers in molecular neuroscience · 2025Review
- Unveiling the therapeutic promise of EphA2 in glioblastoma: a comprehensive review.Discover oncology · 2024Review
- EphA3-targeted chimeric antigen receptor T cells are effective in glioma and generate curative memory T cell responses.Journal for immunotherapy of cancer · 2024Article
- EphA3 CAR T cells are effective against glioblastoma in preclinical models.Journal for immunotherapy of cancer · 2024Article
- Clinical Utility of Optical Genome Mapping for Improved Cytogenomic Analysis of Gliomas.Biomedicines · 2024Article
- Review
- Eph receptors and ephrins in cancer progression.Nature reviews. Cancer · 2024Review
- Molecular Determinants of EphA2 and EphB2 Antagonism Enable the Design of Ligands with Improved Selectivity.Journal of chemical information and modeling · 2023Article
- Clinical Prognostic Implications of Wnt Hub Genes Expression in Medulloblastoma.Cellular and molecular neurobiology · 2023Article
- Glioblastoma: Current Status, Emerging Targets, and Recent Advances.Journal of medicinal chemistry · 2022Review
- NEDD4 degrades TUSC2 to promote glioblastoma progression.Cancer letters · 2022Article
- Antibody-drug conjugates: beyond current approvals and potential future strategies.Exploration of targeted anti-tumor therapy · 2022Review
- Diversity in responses to oncolytic Lassa-vesicular stomatitis virus in patient-derived glioblastoma cells.Molecular therapy oncolytics · 2021Article
- Article
- Novel Receptor Tyrosine Kinase Pathway Inhibitors for Targeted Radionuclide Therapy of Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Review
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 1 country.
Funding
Abstract
Eph tyrosine kinase receptors are frequently overexpressed and functional in many cancers, and they are attractive candidates for targeted therapy. Here, we analyzed the expression of Eph receptor A3, one of the most up-regulated factors in glioblastoma cells cultured under tumorsphere-forming conditions, together with EphA2 and EphB2 receptors. EphA3 was overexpressed in up to 60% of glioblastoma tumors tested, but not in normal brain. EphA3 was localized in scattered areas of the tumor, the invasive ring, and niches near tumor vessels. EphA3 co-localized with macrophage/leukocyte markers, suggesting EphA3 expression on tumor-infiltrating cells of bone marrow origin. We took advantage of the fact that ephrinA5 (eA5) is a ligand that binds EphA3, EphA2 and EphB2 receptors, and used it to construct a novel targeted anti-glioblastoma cytotoxin. The eA5-based cytotoxin potently and specifically killed glioblastoma cells with an IC50 of at least 10-11 M. This and similar cytotoxins will simultaneously target different compartments of glioblastoma tumors while mitigating tumor heterogeneity.
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.