ArticleNeuro-oncology advances
The influence of VEGFR-2 blockade and focused ultrasound blood-brain barrier opening on the glioma-immune landscape.
Article in Neuro-oncology advances. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Narrowing of glioma vascular caliber via chronic VEGFR2 blockade improves the uniformity of focused ultrasound-mediated small molecule drug delivery.Journal of controlled release : official journal of the Controlled Release Society · 2026Article
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Authors and funding
12 authors.
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Abstract
Background: Glioblastoma (GBM) is an aggressive brain cancer with limited treatment options and high recurrence rates. The blood-brain barrier (BBB) impedes therapeutic delivery for the brain, limiting systemic treatment efficacy. Focused ultrasound (FUS) combined with microbubbles (MBs) can transiently open the BBB (BBBO), enhancing drug delivery and modulating the tumor immune microenvironment (TME). However, the disorganized and leaky vasculature in GBM limits the effectiveness of FUS-mediated BBBO. Vascular normalization using antiangiogenic therapy may enhance both immune modulation and delivery. This study aimed to investigate whether vascular normalization via VEGFR-2 blockade with DC101, alone or in combination with FUS+MBs, improves TME remodeling in a murine GBM model. Methods: CT2A glioma-bearing mice were treated with DC101, a VEGFR2 inhibitor, either alone or in combination with FUS+MBs. Tumor growth, survival, vessel permeability, immune cell profiling, and adhesion molecule expression were evaluated using immunohistochemistry, flow cytometry, and confocal microscopy. Results: DC101 monotherapy significantly reduced tumor growth and prolonged survival. It reduced tumor vessel permeability and increased ICAM1 expression on CD31 Conclusion: DC101-mediated vascular normalization beneficially remodels the GBM TME and creates a quiescent platform for supporting future FUS-based therapeutic delivery. This combinatorial strategy offers a promising approach to overcoming BBB-related barriers in glioma treatment.
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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 OpenQuestion graph.