ReviewCancer cell2020
Epigenomic Reprogramming as a Driver of Malignant Glioma.
Review in Cancer cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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
72 citing papers in PubMed, 103 citations in OpenAlex.
- Depletion of CARM1 slows in vivo tumorigenicity and rewires developmental programming in glioma stem-like cells.Cell reports · 2026Article
- Hp1bp3 loss links chromatin reorganization to metabolic vulnerability in glioma.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Histone mark remodeling in cancer: an enhancer-centered perspective.Genes & genomics · 2026Review
- The conserved N-terminal SANT1-binding domain (SBD) of EZH2 regulates PRC2 activity.Genes & development · 2026Article
- Article
- Unrevealing the dual role of paired box and sex determining region Y related high mobility group box in glioblastoma.Discover oncology · 2026Review
- Article
- FCGBP Promotes Glioma Growth by Regulating JAK2/STAT3/c-Myc Pathway.Cancer medicine · 2026Article
- DNA actively regulates the "safety-belt" dynamics of condensin during loop extrusion.Nature communications · 2026Article
- Integrated single-cell and transcriptome sequencing data reveal the value of AOC1 in gliomas tumor microenvironment and prognosis.BMC cancer · 2025Article
- Characterization of cis-regulatory elements and functional variants in colorectal cancer using epigenomics and CRISPRi screenings.Nature cancer · 2025Article
- UBE2T-Mediated HP1α Ubiquitination Enhances Nucleolar Function and Promotes the Progression of IDH1/TP53-Mutant Glioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Gene regulatory networks analysis for the discovery of prognostic genes in gliomas.Scientific reports · 2025Article
- Loss of CARM1 alters the developmental programming of Glioma stem-like cells and creates a druggable NGFR/NTRK dependency.bioRxiv : the preprint server for biology · 2025Article
- The Complexity of Malignant Glioma Treatment.Cancers · 2025Review
- The translatome of glioblastoma.Molecular oncology · 2025Article
- SETD2 loss-of-function uniquely sensitizes cells to epigenetic targeting of NSD1-directed H3K36 methylation.Genome biology · 2025Article
- Oncogenic IDH1Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Smad1 Promotes Tumorigenicity and Chemoresistance of Glioblastoma by Sequestering p300 From p53.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The up-regulation of SYNCRIP promotes the proliferation and tumorigenesis via DNMT3A/p16 in colorectal cancer.Scientific reports · 2024Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Malignant gliomas are central nervous system tumors and remain among the most treatment-resistant cancers. Exome sequencing has revealed significant heterogeneity and important insights into the molecular pathogenesis of gliomas. Mutations in chromatin modifiers-proteins that shape the epigenomic landscape through remodeling and regulation of post-translational modifications on chromatin-are very frequent and often define specific glioma subtypes. This suggests that epigenomic reprogramming may be a fundamental driver of glioma. Here, we describe the key chromatin regulatory pathways disrupted in gliomas, delineating their physiological function and our current understanding of how their dysregulation may contribute to gliomagenesis.
Indexed as
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.