ReviewActa neuropathologica2022
Necrotic reshaping of the glioma microenvironment drives disease progression.
Review in Acta neuropathologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 77 citations in OpenAlex.
- The perinecrotic niche of glioblastoma drives tumor-associated macrophage polarization and immunosuppression via podoplanin-mediated CLEC5A activation.The Journal of clinical investigation · 2026Article
- From bioinformatics to bedside: PPBP drives glioblastoma progression under hypoxia via CXCR2/PI3K/Akt signaling and is targetable by Oenothein B.Cancer cell international · 2026Article
- Uncovering a feedback loop in glioblastoma that reinforces stemness and immunosuppression.The Journal of clinical investigation · 2026Article
- Review
- Consensus statement on microglial and macrophage functions in gliomas.Acta neuropathologica · 2026Review
- Precision Immunotherapeutics for Glioblastoma: Current Approaches and Emerging Strategies in 2026.Cells · 2026Review
- Targeting mesenchymal monocyte-derived macrophages to enhance the sensitivity of glioblastoma to temozolomide by inhibiting TNF/CELSR2/p65/Kla-HDAC1/EPAS1 axis.Journal of advanced research · 2026Article
- Perioperative coagulation profiling and postoperative lower-extremity venous thrombosis risk prediction in glioma patients.Journal of Cancer · 2026Article
- Histogram analysis of IVIM MRI for differentiating glioma IDH-1 status, grade, and Ki-67 expression: a comparison of bi-exponential models at multiple B-value.BMC medical imaging · 2025Article
- Identification of SAMD9 as an adaptive response gene to environmental changes and its association with overall survival and immunotherapeutic response in glioblastoma.Cancer cell international · 2025Article
- MRI-based prediction of DNA methylation grade in IDH-mutant astrocytomas using qualitative imaging features and tumor volumetrics.Neuroradiology · 2025Article
- Tumor necrosis facilitates perihilar cholangiocarcinoma metastasis by ANGPTL6-augmented vessel permeability and tumor dissemination.JHEP reports : innovation in hepatology · 2025Article
- Enhanced glioma semantic segmentation using U-net and pre-trained backbone U-net architectures.Scientific reports · 2025Article
- Glioblastoma: A Multidisciplinary Approach to Its Pathophysiology, Treatment, and Innovative Therapeutic Strategies.Biomedicines · 2025Review
- Glioblastoma at the crossroads: current understanding and future therapeutic horizons.Signal transduction and targeted therapy · 2025Review
- Transglutaminase 2 function in glioblastoma tumor efferocytosis.Cell death & disease · 2025Article
- Insights of immune cell heterogeneity, tumor-initiated subtype transformation, drug resistance, treatment and detecting technologies in glioma microenvironment.Journal of advanced research · 2025Review
- Phosphorescence-basediScience · 2025Article
- A clinically relevant model and method to study necrosis as a driving force in glioma restructuring and progression.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Comparative Clinical-Imaging and Histogenetic Analysis Between Astrocytoma IDH-Mutant Grade 4 and Glioblastoma IDH-Wildtype-Is There Really a Worse One?Diagnostics (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Glioblastoma is the most common primary brain tumor and has a dismal prognosis. The development of central necrosis represents a tipping point in the evolution of these tumors that foreshadows aggressive expansion, swiftly leading to mortality. The onset of necrosis, severe hypoxia and associated radial glioma expansion correlates with dramatic tumor microenvironment (TME) alterations that accelerate tumor growth. In the past, most have concluded that hypoxia and necrosis must arise due to "cancer outgrowing its blood supply" when rapid tumor growth outpaces metabolic supply, leading to diffusion-limited hypoxia. However, growing evidence suggests that microscopic intravascular thrombosis driven by the neoplastic overexpression of pro-coagulants attenuates glioma blood supply (perfusion-limited hypoxia), leading to TME restructuring that includes breakdown of the blood-brain barrier, immunosuppressive immune cell accumulation, microvascular hyperproliferation, glioma stem cell enrichment and tumor cell migration outward. Cumulatively, these adaptations result in rapid tumor expansion, resistance to therapeutic interventions and clinical progression. To inform future translational investigations, the complex interplay among environmental cues and myriad cell types that contribute to this aggressive phenotype requires better understanding. This review focuses on contributions from intratumoral thrombosis, the effects of hypoxia and necrosis, the adaptive and innate immune responses, and the current state of targeted therapeutic interventions.
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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.