ArticleOncoimmunology2026
Oncolytic virus OVV-03 enhances CAR-T cell therapy against glioblastoma via immune modulation and specific HER2 upregulation.
Article in Oncoimmunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Enhancing persistence while managing cytokine release syndrome to embrace next-generation CAR-T cell therapy.Journal of translational medicine · 2026Review
- The tumor microenvironment: a dynamic ecosystem and therapeutic nexus in modern oncology.Frontiers in pharmacology · 2026Review
- Clinical significance and oncogenic role of ECHDC2 in glioblastoma: a comprehensive analysis based on bioinformatics andFrontiers in genetics · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) remains therapeutically challenging due to treatment resistance and immunosuppression. Oncolytic virotherapy offers a promising strategy. This study engineered OVV-03, a novel HER2-armed oncolytic vesicular stomatitis virus (VSV), and evaluated its efficacy against GBM. OVV-03 demonstrated potent infectivity and cytotoxicity in GBM cell lines and patient-derived cells, inducing caspase-dependent apoptosis and suppressing proliferation/clonogenicity. In murine GBM models, OVV-03 significantly suppressed tumor growth, improved survival, and enhanced CD8⁺ T cell infiltration. Single-cell RNA sequencing revealed OVV-03 remodels the tumor immune microenvironment by boosting cytotoxic T cell activity and inhibiting immunosuppressive pathways, notably PD-L1/PD-1 signaling. Mechanistically, OVV-03 downregulated PD-L1 by inhibiting the JNK-c-Fos/c-Jun axis, reversible by TNF-
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.