ArticleNature communications2017
Hotspots of aberrant enhancer activity punctuate the colorectal cancer epigenome.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.
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
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.
- Genetic Variant Associated With Survival of Patients With Stage II-III Colon Cancer.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2020Pooled it
- IL-26-driven epigenetic remodeling promotes immune evasion in colorectal cancer.Nature communications · 2026Article
- AP1 Transcription Factor in the Regulation of the Urokinase Plasminogen Activation System.Biomolecules · 2026Review
- Genetic risk factors modulate the association between physical activity and colorectal cancer.BMC medicine · 2026Article
- Characterization of cis-regulatory elements and functional variants in colorectal cancer using epigenomics and CRISPRi screenings.Nature cancer · 2025Article
- Advances in Epigenomic Sequencing and Their Applications in Cancer Diagnostics.Precision chemistry · 2025Review
- Coordinated gene expression within sustained STAT3-associated chromatin conformations contributes to hepatocellular carcinoma progression.Cancer communications (London, England) · 2025Article
- Genetic risk factors modulate the association between physical activity and colorectal cancer.Research square · 2025Article
- Comprehensive multimodal and multiomic profiling reveals epigenetic and transcriptional reprogramming in lung tumors.Communications biology · 2025Article
- DKK1-SE recruits AP1 to activate the target gene DKK1 thereby promoting pancreatic cancer progression.Cell death & disease · 2024Article
- Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer.Science advances · 2024Article
- The epigenetic landscape in intestinal stem cells and its deregulation in colorectal cancer.Stem cells (Dayton, Ohio) · 2024Review
- Two genome-wide interaction loci modify the association of nonsteroidal anti-inflammatory drugs with colorectal cancer.Science advances · 2024Article
- Fusobacterium nucleatum infection modulates the transcriptome and epigenome of HCT116 colorectal cancer cells in an oxygen-dependent manner.Communications biology · 2024Article
- Super enhancer lncRNAs: a novel hallmark in cancer.Cell communication and signaling : CCS · 2024Review
- Predicting mechanism of immune response in microsatellite instability colorectal cancer.Heliyon · 2024Article
- TSCRE: a comprehensive database for tumor-specificNAR cancer · 2024Article
- Targeting super-enhancer activity for colorectal cancer therapy.American journal of translational research · 2024Review
- Enhancer Recognition: A Transformer Encoder-Based Method with WGAN-GP for Data Augmentation.International journal of molecular sciences · 2023Article
- Cooperation of MLL1 and Jun in controlling H3K4me3 on enhancers in colorectal cancer.Genome biology · 2023Article
16 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
19 authors at 5 institutions in 1 country.
Funding
Abstract
In addition to mutations in genes, aberrant enhancer element activity at non-coding regions of the genome is a key driver of tumorigenesis. Here, we perform epigenomic enhancer profiling of a cohort of more than forty genetically diverse human colorectal cancer (CRC) specimens. Using normal colonic crypt epithelium as a comparator, we identify enhancers with recurrently gained or lost activity across CRC specimens. Of the enhancers highly recurrently activated in CRC, most are constituents of super enhancers, are occupied by AP-1 and cohesin complex members, and originate from primed chromatin. Many activate known oncogenes, and CRC growth can be mitigated through pharmacologic inhibition or genome editing of these loci. Nearly half of all GWAS CRC risk loci co-localize to recurrently activated enhancers. These findings indicate that the CRC epigenome is defined by highly recurrent epigenetic alterations at enhancers which activate a common, aberrant transcriptional programme critical for CRC growth and survival.
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.