ArticleNature communications2025
Local therapeutic platform prevents postsurgical GBM recurrence by diminishing GICs and reshaping immunosuppressive microenvironment.
Article in Nature communications, 2025. 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
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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
3 citing papers in PubMed.
- The Invasive Margin of Glioblastoma as a Molecular Ecosystem: Spatial Heterogeneity, Tumor-Host Interactions, and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Glioblastoma as a neuro-immune network disorder: rethinking the tumor microenvironment, neural circuit integration, and therapeutic resistance.Oncology reviews · 2026Review
- Engineered nanomedicine remodels the postoperative cavity microenvironment to suppress glioblastoma recurrence.Theranostics · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Glioblastoma multiforme (GBM) is characterized by aggressive invasiveness and poor prognosis, and presents a significant clinical challenge due to incomplete surgical resection, poor blood‒brain barrier penetration of therapeutic agents, and inevitable recurrence mainly driven by residual glioma-initiating cells (GICs) and an immunosuppressive microenvironment. Therefore, there is an urgent need to kill remaining GICs and reverse the immunosuppressive tumor microenvironment to prevent postoperative recurrence of GBM. Here, we design an injectable therapeutic platform that targets and kills remaining GICs and reverses the immunosuppressive microenvironment after postoperative resection to prevent the recurrence of GBM. This platform comprises GIC-targeting exosomes that carry siRNA for Notch1 and mitoxantrone to reduce the stemness of GICs and kill residual GICs and glioma cells, respectively, and an immune activator (interleukin-12), which can remodel the immunosuppressive tumor microenvironment, ultimately suppressing postoperative GBM relapse. Our work provides a perspective into the effective inhibition of postresection recurrence of 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 Socratic graph.