ArticleNature communications2024
VC-resist glioblastoma cell state: vessel co-option as a key driver of chemoradiation resistance.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
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Who cites it
32 citing papers in PubMed, 34 citations in OpenAlex.
- Brain barriers at the crossroads of glioma immune surveillance and immunotherapy response.Nature reviews. Cancer · 2026Review
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- Integrin inhibition differentially remodels vascular networks in lung metastases driven by vessel co-option or angiogenesis.Angiogenesis · 2026Article
- EDNRB-dependent endothelin signaling reduces proliferation and promotes proneural-to-mesenchymal transition in gliomas.Molecular oncology · 2026Article
- Multi-omics characterization of IDH-mutant astrocytoma-derived cell lines reveals NOTCH-regulated plastic quiescent astrocyte-like state and insights into progression.Acta neuropathologica communications · 2026Article
- Integrating Endovascular Drug Delivery into the Therapeutic Landscape of Glioblastoma.Cancers · 2026Review
- Role of NR2F2-mediated reprogramming of endothelial cells in glioblastoma progression.iScience · 2026Article
- Supervoxel-based multimodal MRI biomarkers reveal tumor heterogeneity in high-grade glioma for prognostic stratification and therapy response prediction.NPJ precision oncology · 2026Article
- Dissecting the aberrant vasculature of glioblastoma: mechanisms and therapeutic targets.Cancer metastasis reviews · 2026Review
- Tumor microenvironment shapes the spatial organization of glioblastoma cell states.Neuro-oncology · 2026Review
- Extracellular matrix stiffness conditions glioblastoma cells for long-term migration: Mechanical memory as a driver of invasion and recurrence in glioblastoma.Neuro-oncology · 2026Review
- FGFR1/YAP1 signaling in endothelial cells drives renal fibrosis and offers a therapeutic target.Frontiers in pharmacology · 2026Article
- Multi-Omics Integration for Advancing Glioma Precision Medicine.Annals of clinical and translational neurology · 2026Review
- Therapeutic Reprogramming of Glioblastoma Phenotypic States Using Multifunctional Heparin Nanoparticles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- NAT10-mediated N4-acetylcytidine (ac4C) modification of PIK3R2 mRNA promotes malignant progression of glioblastoma.Cell death & disease · 2025Article
- Pericytes orchestrate a tumor-restraining microenvironment in glioblastoma.Nature communications · 2025Article
- Invasive properties of patient-derived glioblastoma cells after reversible electroporationRadiology and oncology · 2025Article
- Proneural-mesenchymal hybrid glioblastoma cells are resistant to therapy and dependent on nuclear import.Neuro-oncology · 2025Article
- Heterogeneity phenotypes in recurrent glioblastoma: a multimodal MRI-based spatial mapping framework for precision treatment.BMC medical imaging · 2025Article
Corrections and comments
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Authors and funding
35 authors at 9 institutions in 4 countries.
Funding
Abstract
Glioblastoma (GBM) is a highly lethal type of cancer. GBM recurrence following chemoradiation is typically attributed to the regrowth of invasive and resistant cells. Therefore, there is a pressing need to gain a deeper understanding of the mechanisms underlying GBM resistance to chemoradiation and its ability to infiltrate. Using a combination of transcriptomic, proteomic, and phosphoproteomic analyses, longitudinal imaging, organotypic cultures, functional assays, animal studies, and clinical data analyses, we demonstrate that chemoradiation and brain vasculature induce cell transition to a functional state named VC-Resist (vessel co-opting and resistant cell state). This cell state is midway along the transcriptomic axis between proneural and mesenchymal GBM cells and is closer to the AC/MES1-like state. VC-Resist GBM cells are highly vessel co-opting, allowing significant infiltration into the surrounding brain tissue and homing to the perivascular niche, which in turn induces even more VC-Resist transition. The molecular and functional characteristics of this FGFR1-YAP1-dependent GBM cell state, including resistance to DNA damage, enrichment in the G2M phase, and induction of senescence/stemness pathways, contribute to its enhanced resistance to chemoradiation. These findings demonstrate how vessel co-option, perivascular niche, and GBM cell plasticity jointly drive resistance to therapy during 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 OpenQuestion graph.