ArticleNPJ precision oncology2025
ECM-based molecular subtypes define prognostic, EMT status, and therapeutic diversity in IDH-mutant gliomas.
Article in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed.
- Integrated Transcriptomic Analysis Reveals Coordinated Gliovascular Remodeling Across Diffuse Glioma Grades.Cancers · 2026Article
- Pharmacological Ascorbate Restrains Epithelial-Mesenchymal Transition and Invasion in Glioblastoma Cells via Extracellular HInternational journal of molecular sciences · 2026Article
- Extracellular Matrix-Related Gene Signature Implied Immunosuppressive Status and Adverse Survival in Diffuse Glioma Patients.Cancers · 2026Article
- Consensus statement on microglial and macrophage functions in gliomas.Acta neuropathologica · 2026Review
- Crosstalk in the brain tumor microenvironment: mechanisms, therapeutic strategies, and clinical advances.Military Medical Research · 2026Review
- Brain microenvironment orchestrates highly aggressive tumor variants: current trends and therapeutic approaches.Frontiers in aging neuroscience · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
IDH-mutant gliomas show prognostic heterogeneity despite favorable overall outcomes, necessitating refined molecular classification. While the extracellular matrix (ECM) critically regulates tumor progression, immunity, and EMT, its prognostic significance in IDH-mutant gliomas remains largely unexplored. Here, we employed unsupervised clustering of ECM-related genes across multiple glioma cohorts, identifying two distinct molecular subtypes: ECM1 and ECM2. ECM1 correlated with worse prognosis, characterized by heightened immune infiltration, elevated EMT activity, aggressive radiological features (peritumoral edema/necrosis), and enhanced proliferation, angiogenesis, stemness, and matrix remodeling capacities. A four-gene signature (CLCF1, COL11A1, CSPG5, and SULF1) robustly stratified patient risk in validation cohorts. Subtype-specific analyses revealed divergent metabolic pathways and predicted differential drug sensitivities, highlighting therapeutic opportunities. Our findings establish ECM-driven heterogeneity as a key determinant of IDH-mutant glioma behavior, offering a novel molecular taxonomy to guide precision oncology through targeted ECM-related biomarkers and therapies.
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Registered trials
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