ReviewFrontiers in molecular biosciences2025
Niche-specific epigenetic interventions in the spatially heterogeneous glioblastoma microenvironmental landscape: strategies for radiotherapy enhancement.
Review in Frontiers in molecular biosciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed.
- Radiotherapy resistance in glioblastoma: Mechanistic insights and novel therapeutic approaches (Review).International journal of oncology · 2026Review
- The Natural Triterpenoid Alisol B Overcomes Temozolomide Resistance in Glioblastoma Through Multi-Target Mechanisms: Coordinated Epigenetic, Metabolic, and Cell-Cycle Reprogramming.International journal of molecular sciences · 2026Article
- The research landscape and future of targeting super-enhancers for cancer therapy: a bibliometric analysis.Discover oncology · 2026Article
- The Glymphatic-Immune Axis in Glioblastoma: Mechanistic Insights and Translational Opportunities.International journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) remains incurable, largely due to inherent radiotherapy resistance driven by synergistic crosstalk between spatial heterogeneity and epigenetic dysregulation. Distinct tumor microenvironments-hypoxic cores, invasive edges, and perivascular regions-harbor glioblastoma-initiating cells (GICs) with unique epigenetic traits that promote radiation evasion: hypoxic cores activate the HIF-SIRT axis to maintain quiescence; invasive edges employ EZH2-mediated H3K27me3 to drive proneural-mesenchymal transition (PMT); and perivascular niches utilize HDAC-DNA repair and BRD4-super-enhancer mechanisms to sustain stemness. Concurrent epigenetic alterations-such as MGMT promoter methylation, aberrant histone modifications, and chromatin remodeling-further enhance adaptive plasticity. This review synthesizes recent preclinical and clinical evidence (2019-2024) to delineate how spatial and epigenetic mechanisms form a "resistance loop" that subverts radiotherapy. We argue that effective radiosensitization requires niche-specific strategies: HDAC inhibitors in hypoxic regions to impair DNA repair, EZH2 inhibitors at invasive margins to suppress PMT, and BET inhibitors in perivascular zones to target stemness programs. We propose a "spatial-epigenetic precision pipeline" involving: (1) mapping niche-specific epigenetic signatures
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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.