ArticleCancers2013
Is glioblastoma an epigenetic malignancy?
Article in Cancers, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 63 citations in OpenAlex.
- LINE-1 hypomethylation in cell-free DNA of high-grade glioma patients correlates with tissue levels and is associated with reduced DNMT1 and H4K20me3 expression.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- What Epigenetics Teaches Us About Neuron-Glioma Interactions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- The role of lncRNAs in the interplay of signaling pathways and epigenetic mechanisms in glioma.Epigenomics · 2025Review
- Review
- Unravelling the mosaic: Epigenetic diversity in glioblastoma.Molecular oncology · 2024Review
- Genomic landscape of glioblastoma without IDH somatic mutation in 42 cases: a comprehensive analysis using RNA sequencing data.Journal of neuro-oncology · 2024Article
- DMRTA2 supports glioma stem-cell mediated neovascularization in glioblastoma.Cell death & disease · 2024Article
- MiR-128-3p - a gray eminence of the human central nervous system.Molecular therapy. Nucleic acids · 2024Review
- Rewiring of the promoter-enhancer interactome and regulatory landscape in glioblastoma orchestrates gene expression underlying neurogliomal synaptic communication.Nature communications · 2023Article
- Barriers to overcoming immunotherapy resistance in glioblastoma.Frontiers in medicine · 2023Review
- Article
- Glioblastoma: Current Status, Emerging Targets, and Recent Advances.Journal of medicinal chemistry · 2022Review
- Unique combinations of epigenetic modifiers synergistically impair the viability of the U87 glioblastoma cell line while exhibiting minor or moderate effects on normal stem cell growth.Medical oncology (Northwood, London, England) · 2022Article
- ADAR1-mediated RNA editing links ganglioside catabolism to glioblastoma stem cell maintenance.The Journal of clinical investigation · 2022Article
- Sox2 induces glioblastoma cell stemness and tumor propagation by repressing TET2 and deregulating 5hmC and 5mC DNA modifications.Signal transduction and targeted therapy · 2022Article
- Bioactive Compounds with Antiglioma Activity from Marine Species.Biomedicines · 2021Review
- Mapping chromatin accessibility and active regulatory elements reveals pathological mechanisms in human gliomas.Nature communications · 2021Article
- Metabolites in the Tumor Microenvironment Reprogram Functions of Immune Effector Cells Through Epigenetic Modifications.Frontiers in immunology · 2021Review
- BPTF regulates growth of adult and pediatric high-grade glioma through the MYC pathway.Oncogene · 2020Article
- The fungal metabolite chaetocin is a sensitizer for pro-apoptotic therapies in glioblastoma.Cell death & disease · 2019Article
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
No grant is acknowledged in the PubMed record.
Abstract
Epigenetic modifications control gene expression by regulating the access of nuclear proteins to their target DNA and have been implicated in both normal cell differentiation and oncogenic transformation. Epigenetic abnormalities can occur both as a cause and as a consequence of cancer. Oncogenic transformation can deeply alter the epigenetic information enclosed in the pattern of DNA methylation or histone modifications. In addition, in some cancers epigenetic dysfunctions can drive oncogenic transformation. Growing evidence emphasizes the interplay between metabolic disturbances, epigenomic changes and cancer, i.e., mutations in the metabolic enzymes SDH, FH, and IDH may contribute to cancer development. Epigenetic-based mechanisms are reversible and the possibility of "resetting" the abnormal cancer epigenome by applying pharmacological or genetic strategies is an attractive, novel approach. Gliomas are incurable with all current therapeutic approaches and new strategies are urgently needed. Increasing evidence suggests the role of epigenetic events in development and/or progression of gliomas. In this review, we summarize current data on the occurrence and significance of mutations in the epigenetic and metabolic enzymes in pathobiology of gliomas. We discuss emerging therapies targeting specific epigenetic modifications or chromatin modifying enzymes either alone or in combination with other treatment regimens.
Identifiers
What OpenQuestion holds
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.