ReviewEpigenetics & chromatin2023
Etiology of super-enhancer reprogramming and activation in cancer.
Review in Epigenetics & chromatin, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 23 citations in OpenAlex.
- The DCBLD2 super-enhancer drives colorectal cancer progression through FOSL2/JUND-mediated activation of the CD146/AKT/TNFRSF6B pathway.Molecular biomedicine · 2026Article
- Article
- Perturbation of BRD4 and p300 activity suppresses super enhancer‑drivenOncology reports · 2026Article
- Integrative Mapping of SNHG1 RNA-Chromatin Contacts onto the Cancer-Specific Super-Enhancer Landscape in HCT116 Colorectal Cancer Cells.International journal of molecular sciences · 2026Article
- Superenhancers shape the landscape and repair dynamics of transcription-associated DNA breaks in cancer.Science advances · 2026Article
- Role of the Super-Enhancer Component Bromodomain Protein 4 in the Radiation Response of Human Head and Neck Squamous Cell Carcinoma Cells.Current issues in molecular biology · 2026Article
- Identification of a super enhancer associated gene signature for the prognosis prediction and regulatory mechanism exploration in breast cancer.Scientific reports · 2025Article
- DNA Circles as Vehicles for Genes to Evade Chromosomal Discipline.Genome biology and evolution · 2025Article
- Decoding cancer heterogeneity through super-enhancer landscapes: from subtype discovery to therapeutic opportunity.Briefings in bioinformatics · 2025Review
- MYC Binding Near Transcriptional End Sites Regulates Basal Gene Expression, Read-Through Transcription, and Intragenic Contacts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SEgene identifies links between super enhancers and gene expression across cell types.NPJ systems biology and applications · 2025Article
- DNA regulatory element cooperation and competition in transcription.BMB reports · 2024Review
- Epigenetic dysregulation in glioblastoma: potential pathways to precision medicine.Neurogenetics · 2024Review
- Mechanistic insights into super-enhancer-related genes as prognostic signatures in colon cancer.Aging · 2024Article
- Extrachromosomal DNA in cancer.Nature reviews. Cancer · 2024Review
- The Reign of Follistatin in Tumors and Their Microenvironment: Implications for Drug Resistance.Biology · 2024Review
- Targeting super-enhancer activity for colorectal cancer therapy.American journal of translational research · 2024Review
- Pathogenic role of super-enhancers as potential therapeutic targets in lung cancer.Frontiers in pharmacology · 2024Review
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 2 institutions in 1 country.
Funding
Abstract
Super-enhancers are large, densely concentrated swaths of enhancers that regulate genes critical for cell identity. Tumorigenesis is accompanied by changes in the super-enhancer landscape. These aberrant super-enhancers commonly form to activate proto-oncogenes, or other genes upon which cancer cells depend, that initiate tumorigenesis, promote tumor proliferation, and increase the fitness of cancer cells to survive in the tumor microenvironment. These include well-recognized master regulators of proliferation in the setting of cancer, such as the transcription factor MYC which is under the control of numerous super-enhancers gained in cancer compared to normal tissues. This Review will cover the expanding cell-intrinsic and cell-extrinsic etiology of these super-enhancer changes in cancer, including somatic mutations, copy number variation, fusion events, extrachromosomal DNA, and 3D chromatin architecture, as well as those activated by inflammation, extra-cellular signaling, and the tumor microenvironment.
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.