ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Redirecting Monocyte Differentiation With Engineered Extracellular Vesicles for Glioma Immunotherapy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
During glioma progression, monocytes abundantly infiltrate but primarily differentiate into immunosuppressive macrophages to promote tumor growth. Redirecting monocyte differentiation offers a compelling yet underexplored therapeutic opportunity. In this work, we found M1-polarized macrophage-derived extracellular vesicles (M1-EVs) efficiently induced monocytes to differentiate into anti-tumor macrophages via tumor necrosis factor alpha (TNF-α)-mediated signaling. Despite promising, the therapeutic efficacy of M1-EVs was constrained by insufficient glioma accumulation and CD47-mediated phagocytic inhibition. To address this challenge, we further engineered M1-EVs with dual-targeting specificity by genetically incorporating a tumor-directed chimeric antigen receptor (CAR) against IL13Rα2 or EGFRvIII together with CD47-blocking SIRPα variants. The resulting dual-targeting EVs (M1-CS-EVs) exhibited enhanced blood-brain barrier (BBB) penetration and glioma accumulation while locally disrupting CD47-SIRPα interactions. In three orthotopic glioma models, M1-CS-EVs elicited a potent anti-tumor immune response and enhanced tumor phagocytosis, significantly suppressing tumor growth while prolonging animal survival. Our findings establish a platform technology for directing monocyte differentiation toward anti-tumor phenotypes, offering a broadly applicable strategy for glioma treatment.
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.