ArticleActa neuropathologica communications2024
Chronic hypoxia remodels the tumor microenvironment to support glioma stem cell growth.
Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Mapping the Cerebral Organoid Landscape: A Systematic Review of Preclinical 3D Models in Neuroscience.Advanced healthcare materials · 2026Pooled it
- Translational insights and clinical challenges of targeting cancer stem cells.Signal transduction and targeted therapy · 2026Review
- Organoids as brain tumour models: bridging the translational gap.Disease models & mechanisms · 2026Review
- Integrative Transcriptomic Analysis Identifies Hypoxia-responsive Cell Cycle Hub Genes as Prognostic Markers in Glioblastoma.Annals of neurosciences · 2026Article
- Modeling medulloblastoma pathogenesis and treatment in human cerebellar organoids.Genes & development · 2026Article
- Organoids to Model Tumor Microenvironment in Progression of Pathogenesis and Treatment Resistance in Glioblastoma Multiforme.Brain sciences · 2026Review
- Progress and challenges in the development of advanced pancreatic cancer organoids.Journal of experimental & clinical cancer research : CR · 2026Review
- Research progress on glioma drug resistance: mechanism analysis and therapeutic strategies.Frontiers in pharmacology · 2026Review
- Crosstalk in the brain tumor microenvironment: mechanisms, therapeutic strategies, and clinical advances.Military Medical Research · 2026Review
- Modeling gliomas with organoids: reconstructing the human neural microenvironment for translational neuro-oncology.Frontiers in oncology · 2026Review
- Multiple Primaries: Differences in Survival of Patients with Glioma with or Without Second Malignancies.Cancers · 2025Article
- Hypoxia and Multilineage Communication in 3D Organoids for Human Disease Modeling.Biomimetics (Basel, Switzerland) · 2025Review
- Engineering overexpressing SYNGR1 inhibited the progression of GBM cells by suppressing the intracellular FGF1-mediated LDs accumulation and cytoskeleton remodeling.Journal of neuro-oncology · 2025Article
- Deciphering the role of circular RNAs in cancer progression under hypoxic conditions.Medical oncology (Northwood, London, England) · 2025Review
- The Hypoxia-Associated High-Risk Cell Subpopulation Distinctly Enhances the Progression of Glioma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Preclinical and clinical advances to overcome hypoxia in glioblastoma multiforme.Cell death & disease · 2024Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Cerebral organoids co-cultured with patient derived glioma stem cells (GLICOs) are an experimentally tractable research tool useful for investigating the role of the human brain tumor microenvironment in glioblastoma. Here we describe long-term GLICOs, a novel model in which COs are grown from embryonic stem cell cultures containing low levels of GSCs and tumor development is monitored over extended durations (ltGLICOs). Single-cell profiling of ltGLICOs revealed an unexpectedly long latency period prior to GSC expansion, and that normal organoid development was unimpaired by the presence of low numbers of GSCs. However, as organoids age they experience chronic hypoxia and oxidative stress which remodels the tumor microenvironment to promote GSC expansion. Receptor-ligand modelling identified astrocytes, which secreted various pro-tumorigenic ligands including FGF1, as the primary cell type for GSC crosstalk and single-cell multi-omic analysis revealed these astrocytes were under the control of ischemic regulatory networks. Functional validation confirmed hypoxia as a driver of pro-tumorigenic astrocytic ligand secretion and that GSC expansion was accelerated by pharmacological induction of oxidative stress. When controlled for genotype, the close association between glioma aggressiveness and patient age has very few proposed biological explanations. Our findings indicate that age-associated increases in cerebral vascular insufficiency and associated regional chronic cerebral hypoxia may contribute to this phenomenon.
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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.