ArticleMolecular therapy. Oncology2025
An oncolytic herpes simplex virus armed with IL-12 for treatment of preclinical glioblastoma.
Article in Molecular therapy. Oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is a devastating brain cancer with a 5-year survival rate of ∼5% despite current treatment regimens. Multiple oncolytic herpes simplex viruses (oHSV) have been designed for GBM therapy, but clinical trials have thus far met with limited success. A potential reason for this lack of efficacy is the immunosuppressive tumor microenvironment (TME) of GBM. Here we used an oHSV (KOS strain) armed with interleukin (IL)-12 (oHSV:IL-12) in an attempt to overcome this immunosuppression and analyzed the immunological and therapeutic impact in murine CT2A and GL261N4 orthotopic syngeneic glioma models. Unarmed oHSV failed to enhance survival in animals bearing syngeneic GBM tumors. However, oHSV:IL-12 induced significant and durable therapeutic benefits. TME interrogation following oHSV:IL-12 therapy revealed a significant accumulation of macrophages and cytotoxic T cells. Further investigation using single cell RNA-sequencing of GL261N4 tumors treated with either oHSV or oHSV:IL-12, indicated that oHSV:IL-12 induced robust macrophage accumulation within the TME and encouraged T cell receptor clonotype expansion compared to controls. These data point to the propensity of the IL-12 transgene to manipulate the myeloid compartment within the glioma TME, promote T cell expansion, and improve survival.
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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 Socratic graph.