ArticleScience advances2026
STING stimulation via supramolecular prodrug hydrogel boosts innate-adaptive immune cross-talk to prevent glioblastoma recurrence.
Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Current Perspectives on STING Agonists for Anticancer Drug Development.Chemical biology & drug design · 2026Review
- Review
- Local Nanomedicine and Nano-Enabled Biomaterials After Glioblastoma Resection.International journal of nanomedicine · 2026Review
- Engineered nanomedicine remodels the postoperative cavity microenvironment to suppress glioblastoma recurrence.Theranostics · 2026Review
- Tectochrysin alleviates Ang II-induced pathological cardiac hypertrophy by binding to STING and inhibiting STING/NFκB-mediated inflammation.Frontiers in pharmacology · 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM), the most aggressive primary brain tumor, demonstrates persistent resistance to immunotherapy due to its profoundly immunosuppressive microenvironment and markedly limited T cell infiltration. In this context, we engineered a STING agonist-incorporated prodrug hydrogel that orchestrates dual activation of innate and adaptive immunity to prevent postoperative GBM recurrence. We found that this in situ-forming hydrogel integrates seamlessly with tumor resection procedures, serves as a drug depot for sustained tumoral releases of therapeutic agents, and thus reprograms the tumor microenvironment by promoting M1 macrophage polarization, suppressing regulatory T cell activity, and enhancing cytotoxic T lymphocyte infiltration, thereby establishing a robust antitumor immune response. As a postoperative adjuvant therapy, the hydrogel effectively inhibits orthotopic GBM recurrence and extends animal survival while establishing durable immune memory against tumor rechallenge. Our findings demonstrate the translational potential of immunologically engineered hydrogels for STING-activated immunotherapy in preventing postresection GBM recurrence.
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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.