ArticleNeuro-oncology2026
Laser interstitial thermal therapy enhances bidirectional blood-brain barrier permeability in glioblastoma.
Article in Neuro-oncology, 2026. 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.
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Who cites it
3 citing papers in PubMed.
- MFSD2A in health and disease: lysolipid transport, barrier physiology, and translational boundaries.Molecular biomedicine · 2026Review
- Review
- Integrating Endovascular Drug Delivery into the Therapeutic Landscape of Glioblastoma.Cancers · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
backgroundLaser interstitial thermal therapy (LITT) is a minimally invasive treatment for glioblastoma that increases blood-brain barrier (BBB) permeability. However, the mechanisms and spatiotemporal features of this effect remain unclear. It is also unknown whether LITT promotes release of circulating tumor DNA (ctDNA).
methodsUsing our previously developed LITT mouse model, we employed single-cell RNA-sequencing (scRNA-seq) to investigate gene expression changes in endothelial cells following LITT in the naive mouse brain. Brains were also harvested at multiple time points to assess LITT effects on tight junction (TJ) integrity and transcytosis via immunofluorescence and transmission electron microscopy. Human glioblastoma tissues were analyzed to monitor ambient caveolae-mediated transcytosis in tumor regions. Finally, ctDNA levels in mouse plasma were quantified using digital-droplet PCR following LITT.
resultsLITT triggered downregulation of pathways related to cell-cell junctions and upregulation of transcytosis. LITT transiently disrupted TJ integrity for 7 days up to 100 µm away from the ablation zone. Further, LITT increased caveolae-mediated transcytosis in endothelial cells for 21 days, peaking at 14 days, in part due to suppression of the transcytosis inhibitor Mfsd2a. LITT facilitated ctDNA detection in mouse plasma at 1 h, 3 days, 7 days, and 14 days post-procedure.
conclusionsOur study demonstrates that LITT transiently disrupts the BBB in the periphery of the ablation with endothelial TJ disruption and transcytosis upregulation following distinct time courses. LITT effects on the BBB are bidirectional and enhance ctDNA release in addition to enabling brain entry of agents.
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Registered trials
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