ReviewCerebellum (London, England)2018
Epigenetic Drivers in Pediatric Medulloblastoma.
Review in Cerebellum (London, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
55 citing papers in PubMed, 78 citations in OpenAlex.
- Genomic alterations in pediatric tumors: clinical relevance and translational insights.Pediatric research · 2026Article
- Neurosurgical Application of Artificial Intelligence in Pediatric Neuro-Oncology.Journal of Korean Neurosurgical Society · 2026Article
- Identification of Raptor and GLI1 as USP37 substrates highlight its context-specific function in medulloblastoma cells.Oncogene · 2026Article
- Human stem cell models for group 3 medulloblastoma uncover JARID1B as a regulator of the chromatin landscape.bioRxiv : the preprint server for biology · 2025Article
- The MYC-dependent lncRNA MB3 inhibits apoptosis in Group 3 Medulloblastoma by regulating the TGF-β pathway via HMGN5.Cell death & disease · 2025Article
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- Clinicopathological insights of supratentorial embryonal tumor with medulloblastoma-like histopathology in adulthood: A case report.Biomedical reports · 2025Article
- Development and Clinical Validation of Molecular Subgrouping in Medulloblastoma by Targeted Methylation Sequencing.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- AZIN1 level is increased in medulloblastoma and correlates with c-Myc activity and tumor phenotype.Journal of experimental & clinical cancer research : CR · 2025Article
- The Role of Chronic Inflammation in Pediatric Cancer.Cancers · 2025Review
- Group 3 medulloblastoma transcriptional networks collapse under domain specific EP300/CBP inhibition.Nature communications · 2024Article
- Long-read sequencing for brain tumors.Frontiers in oncology · 2024Review
- Review
- Article
- Review
- Exploring the Molecular Complexity of Medulloblastoma: Implications for Diagnosis and Treatment.Diagnostics (Basel, Switzerland) · 2023Review
- A neurodevelopmental epigenetic programme mediated by SMARCD3-DAB1-Reelin signalling is hijacked to promote medulloblastoma metastasis.Nature cell biology · 2023Article
- Advances on Epigenetic Drugs for Pediatric Brain Tumors.Current neuropharmacology · 2023Review
- Linked-read based analysis of the medulloblastoma genome.Frontiers in oncology · 2023Article
- Epigenetics and immune cells in medulloblastoma.Frontiers in genetics · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Epigenetics is the process by which gene expression is regulated by events other than alterations of the genome. This includes DNA methylation, histone modifications, chromatin remodeling, microRNAs, and long non-coding RNAs. Methylation of DNA, chromatin remodeling, and histone modifications regulate the chromatin and access of transcription factors to DNA and in turn gene transcription. Alteration of chromatin is now recognized to be deregulated in many cancers. Medulloblastoma is an embryonal tumor of the cerebellum and the most common malignant brain tumor in children, that occurs only rarely in adults. Medulloblastoma is characterized by four major molecularly and histopathologically distinct groups, wingless (WNT), sonic hedgehog (SHH), group 3 (G3), and group 4 (G4), that, except for WNT, are each now subdivided in several subgroups. Gene expression array, next-generation sequencing, and methylation profiling of several hundred primary tumors by several consortia and independent groups revealed that medulloblastomas harbor a paucity of mutations most of which occur in epigenetic regulators, genetic alterations in oncogenes and tumor suppressors, in addition to copy number alterations and chromosome gains and losses. Remarkably, some tumors have no reported mutations, suggesting that some genes required for oncogenesis might be regulated by epigenetic mechanisms which are still to be uncovered and validated. This review will highlight several epigenetic regulators focusing mainly on histone modifiers identified in medulloblastoma.
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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.