ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
GLUL Confers Perivascular Cancer-Associated Fibroblasts With Pro-Angiogenic Capacity to Promote Glioma Progression.
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. 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.
- Radiation-activated astrocytes promote tumor progression through CXCL12 secretion and induce resistance to anti-PD-1 immunotherapy.Translational cancer research · 2026Article
- GLUL Confers Perivascular Cancer-Associated Fibroblasts With Pro-Angiogenic Capacity to Promote Glioma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Integrated network toxicology, bioinformatics, and molecular docking reveal the potential molecular mechanisms linking bisphenol A to glioma progression.Frontiers in bioinformatics · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Glioblastoma (GBM) is a malignant brain tumor characterized by profound angiogenic activity and immunosuppressive features. A burgeoning body of research has focused on elucidating the functional effects of stromal cells within the tumor microenvironment (TME) and developing stroma-targeted therapeutic strategies. Notably, cancer-associated fibroblasts (CAFs), essential stromal components of the TME, have garnered significant attention for their functional orchestration in glioma progression. The proteomic landscape of human primary CAFs from GBM samples has revealed the dynamic remodeling of differential protein expression in the TME, but the functional role of glutamate-ammonia ligase (GLUL) as a novel CAF target remains elusive. This study confirms that GLUL knockdown profoundly abrogated the architectural intricacy inherent to CAF-supported vasculature in vitro and in vivo. Additionally, CAF-specific GLUL knockdown attenuates tumor growth and extends median survival in a humanized orthotopic glioma model. Furthermore, GLUL-driven activation of PI3K/AKT signaling as the central regulator of CAF-mediated vascular niche formation is delineated in glioma progression. This study highlights that targeting GLUL in CAFs is a novel stroma-focused therapeutic paradigm for GBM by disrupting pro-angiogenic signaling. Collectively, these findings elucidate key aspects of CAF biology and their regulatory functions in tumor progression, underscoring the therapeutic potential of targeting CAFs in 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 OpenQuestion graph.