ReviewCancer metastasis reviews2026
Metabolic dependencies and neural progenitor dysregulation: driving forces in paediatric high-grade glioma development.
Review in Cancer metastasis reviews, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paediatric high-grade gliomas (pHGGs) are the most lethal brain tumours in children, characterised by profound epigenetic dysregulation and limited treatment options. The 2021 WHO Classification has established a molecular framework that distinguishes pHGGs as biologically distinct from adult glioblastoma, recognising four major subtypes: H3K27-altered diffuse midline glioma, H3G34-mutant diffuse hemispheric glioma, infant-type hemispheric glioma, and the rare IDH-mutant gliomas. Each subtype exhibits unique epigenetic landscapes, metabolic dependencies, and therapeutic vulnerabilities, necessitating subtype-specific treatment strategies. This review explores the molecular classification of pHGGs and examines the critical role of the tumour microenvironment in disease progression. We focus on glioma stem cells as central drivers of tumour initiation, maintenance, and therapeutic resistance, highlighting their remarkable cellular plasticity and ability to dynamically transition between different states. Particular attention is given to metabolic reprogramming in pHGGs, including alterations in glucose and lipid metabolism, and the exceptional metabolic flexibility of glioma stem cells that enables adaptation to microenvironmental pressures. Importantly, we discuss the intimate crosstalk between metabolism and epigenetic regulation, whereby metabolites serve as essential cofactors for chromatin-modifying enzymes-exemplified by α-ketoglutarate maintaining low H3K27me3 in H3K27M tumours and 2-hydroxyglutarate driving hypermethylation in IDH-mutant gliomas. We review preclinical models that have advanced pHGG research and discuss emerging immunotherapeutic approaches, including CAR T-cell therapies and oncolytic viruses. By synthesising current understanding of pHGG biology, this review aims to identify promising therapeutic avenues that exploit the unique metabolic and epigenetic vulnerabilities of each molecular subtype.
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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 Socratic graph.