ArticleNeuro-oncology2025
EVA1-antibody drug conjugate is a new therapeutic strategy for eliminating glioblastoma-initiating cells.
Article in Neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed.
- MAP17 Enhances Chemoresistance and Tumorigenicity of Glioblastoma-Initiating Cells via the Canonical NF-кB Pathway.Cancer science · 2026Article
- Astrocytes in neuroinflammation and brain cancer.Molecular biomedicine · 2026Review
- Article
- Antibody therapies in glioblastoma: Overcoming micro-environmental barriers.Iranian journal of basic medical sciences · 2026Review
- Engineering antibody-drug conjugates targeting an adhesion GPCR, CD97.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Development and optimization of Eva1 (Journal for immunotherapy of cancer · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
backgroundThe discovery of glioblastoma (GBM)-initiating cells (GICs) has impacted GBM research. These cells are not only tumorigenic but also exhibit resistance to radiotherapy and chemotherapy. Therefore, it is crucial to characterize GICs thoroughly and identify new therapeutic targets. In a previous study, we successfully identified epithelial-V-like antigen 1 (EVA1) as a novel functional factor specific to GICs.
methodsHybridoma cells were generated by immunizing BALB/c mice with EVA1-Fc fusion protein. The reactivity of the supernatant from these hybridoma cells was examined using EVA1-overexpressing cells and GICs. Candidate antibodies were further selected using Biacore surface plasmon resonance analysis and 2 cytotoxicity assays-antibody-dependent cell cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). Among the antibodies, the cytotoxicity of the B2E5-antibody drug conjugate (B2E5-ADC) was evaluated by both adding it to cultured GICs and injecting it into GIC tumor-bearing brains.
resultsB2E5 demonstrated a high affinity for human EVA1 and effectively killed both EVA1-expressing cell lines and GICs in culture through ADCC and CDC. B2E5-ADC also exhibited strong cytotoxicity to GICs in culture and prevented their tumorigenesis in the brain when administered intracranially to the tumor-bearing brain.
conclusionOur data indicate that B2E5-ADC is a new and promising therapeutic strategy for GBM.
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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.