ReviewBiomedicines2025
Deciphering Medulloblastoma: Epigenetic and Metabolic Changes Driving Tumorigenesis and Treatment Outcomes.
Review in Biomedicines, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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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
7 citing papers in PubMed.
- Age-Dependent Toxicity Patterns in Medulloblastoma: A Comparative Analysis of Treatment-Related Adverse Events Between Pediatric and Adult Populations.Journal of clinical medicine · 2026Article
- Genome-wide DNA methylation analysis of pediatric medulloblastomas from a Brazilian cohort: an exploratory study.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Surgical resection in medulloblastoma: a crossroads in the molecular era.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2026Review
- Biomarkers of Treatment Response in Paediatric Medulloblastoma.Diagnostics (Basel, Switzerland) · 2026Review
- Medulloblastoma response to mevalonate pathway inhibition is independent of p53 status.Biology direct · 2026Article
- Exploring the lactate-metabolism related characteristics during the development of medulloblastoma through single-cell and bulk RNA-seq.Translational cancer research · 2026Article
- Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectivesMedulloblastoma is the most common malignant brain tumor in children and comprises four molecular subtypes-WNT, SHH, Group 3, and Group 4-each with distinct genetic, epigenetic, and metabolic features. Increasing evidence highlights the critical role of metabolic reprogramming and epigenetic alterations in driving tumor progression, therapy resistance, and clinical outcomes. This review aims to explore the interplay between metabolic and epigenetic mechanisms in medulloblastoma, with a focus on their functional roles and therapeutic implications.
methodsA comprehensive literature review was conducted using PubMed and relevant databases, focusing on recent studies examining metabolic pathways and epigenetic regulation in medulloblastoma subtypes. Particular attention was given to experimental findings from in vitro and in vivo models, as well as emerging preclinical therapeutic strategies targeting these pathways.
resultsMedulloblastoma exhibits metabolic adaptations such as increased glycolysis, lipid biosynthesis, and altered amino acid metabolism. These changes support rapid cell proliferation and interact with the tumor microenvironment. Concurrently, epigenetic mechanisms-including DNA methylation, histone modification, chromatin remodeling, and non-coding RNA regulation-contribute to tumor aggressiveness and treatment resistance. Notably, metabolic intermediates often serve as cofactors for epigenetic enzymes, creating feedback loops that reinforce oncogenic states. Preclinical studies suggest that targeting metabolic vulnerabilities or epigenetic regulators-and particularly their combination-can suppress tumor growth and overcome resistance mechanisms.
conclusionsThe metabolic-epigenetic crosstalk in medulloblastoma represents a promising area for therapeutic innovation. Understanding subtype-specific dependencies and integrating biomarkers for patient stratification could facilitate the development of precision medicine approaches that improve outcomes and reduce long-term treatment-related toxicity in pediatric patients.
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