ReviewActa neuropathologica2014
Epigenetic dysregulation: a novel pathway of oncogenesis in pediatric brain tumors.
Review in Acta neuropathologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 37 citations in OpenAlex.
- Genomic and mutational landscape of anaplastic ependymoma: Insights from the AACR Project GENIE Consortium.Biomolecules & biomedicine · 2026Article
- Low-Grade Gliomas: Histological Subtypes, Molecular Mechanisms, and Treatment Strategies.Brain sciences · 2023Review
- Clinical and Translational Advances in Glioma Immunotherapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Review
- Epigenomics and immunotherapeutic advances in pediatric brain tumors.NPJ precision oncology · 2021Review
- Article
- Pharmacokinetic Principles and Their Application to Central Nervous System Tumors.Pharmaceutics · 2020Review
- Molecular markers and targeted therapy in pediatric low-grade glioma.Journal of neuro-oncology · 2020Review
- Review
- Molecularly Targeted Agents in the Therapy of Pediatric Brain Tumors.Paediatric drugs · 2020Review
- Immunotherapy for Medulloblastoma: Current Perspectives.ImmunoTargets and therapy · 2020Review
- Stalled developmental programs at the root of pediatric brain tumors.Nature genetics · 2019Article
- H3K27M induces defective chromatin spread of PRC2-mediated repressive H3K27me2/me3 and is essential for glioma tumorigenesis.Nature communications · 2019Article
- Radiation for ETMR: Literature review and case series of patients treated with proton therapy.Clinical and translational radiation oncology · 2019Article
- EZH2 Phosphorylation Promotes Self-Renewal of Glioma Stem-Like Cells Through NF-κB Methylation.Frontiers in oncology · 2019Article
- Mutant ATRX: uncovering a new therapeutic target for glioma.Expert opinion on therapeutic targets · 2018Review
- Characterizing temporal genomic heterogeneity in pediatric high-grade gliomas.Acta neuropathologica communications · 2017Article
- Immunotherapy for Pediatric Brain Tumors.Brain sciences · 2017Review
- Molecular Basis of Pediatric Brain Tumors.Neuromolecular medicine · 2017Review
- Diffuse intrinsic pontine gliomas-current management and new biologic insights. Is there a glimmer of hope?Neuro-oncology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
A remarkably large number of "epigenetic regulators" have been recently identified to be altered in cancers and a rapidly expanding body of literature points to "epigenetic addiction" (an aberrant epigenetic state to which a tumor is addicted) as a new previously unsuspected mechanism of oncogenesis. Although mutations are also found in canonical signaling pathway genes, we and others identified chromatin-associated proteins to be more commonly altered by somatic alterations than any other class of oncoprotein in several subgroups of childhood high-grade brain tumors. Furthermore, as these childhood malignancies carry fewer non-synonymous somatic mutations per case in contrast to most adult cancers, these mutations are likely drivers in these tumors. Herein, we will use as examples of this novel hallmark of oncogenesis high-grade astrocytomas, including glioblastoma, and a subgroup of embryonal tumors, embryonal tumor with multilayered rosettes (ETMR) to describe the novel molecular defects uncovered in these deadly tumors. We will further discuss evidence for their profound effects on the epigenome. The relative genetic simplicity of these tumors promises general insights into how mutations in the chromatin machinery modify downstream epigenetic signatures to drive transformation, and how to target this plastic genetic/epigenetic interface.
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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.