Evidence map›Paper›PMID 37059907›Full record

ReviewCancer metastasis reviews2023

Oncogenic super-enhancers in cancer: mechanisms and therapeutic targets.

Megan Bacabac, Wei Xu

Open access · greenAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.2field-weighted citation impact, top 4% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 34 citations in OpenAlex.

  1. PROTACs in cancer therapy: targeted degradation of GPX4, PARP and epigenetic regulators.Journal of enzyme inhibition and medicinal chemistry · 2026
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  19. Enhancer regulation in cancer: from epigenetics to mArchives of pharmacal research · 2025
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Megan BacabacMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, 1111 Highland Ave, Madison, WI, 53705, USA.
Wei XuMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, 1111 Highland Ave, Madison, WI, 53705, USA. wxu@oncology.wisc.edu.ORCID 0000-0003-3808-0045
University of Wisconsin–Madison · US

Funding

Training in Cancer Biology Training GrantT32CA009135 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SUGDEN, WILLIAM M. · 1985 to 2024
$10.4M
Protein Arginine Methylation in Breast CancerR01CA236356 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Wei Xu · 2019 to 2026
$2.9M
Ctr9 as a Predictive Biomarker for EZH2 Inhibitor SensitivityR01CA268183 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Wei Xu · 2022 to 2026
$2.0M
Functions of BRD8 in HR+/HER2+ breast cancerR01CA281024 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Wei Xu · 2023 to 2026
$1.6M
NCI NIH HHS R01 CA236356NCI NIH HHS R01 CA268183NCI NIH HHS R01 CA281024NCI NIH HHS T32 CA009135
6 · The paper itself

Abstract

Activation of oncogenes to sustain proliferative signaling and initiate metastasis are important hallmarks of cancer. Oncogenes are amplified or overexpressed in cancer cells and overexpression is often controlled at the level of transcription. Gene expression is tightly controlled by many cis-regulatory elements and trans-acting factors. Large clusters of enhancers known as "super-enhancers" drive robust expression of cell-fate determining transcription factors in cell identity. Cancer cells can take advantage of super-enhancers and become transcriptionally addicted to them leading to tumorigenesis and metastasis. Additionally, the cis-regulatory landscape of cancer includes aberrant super-enhancers that are not present in normal cells. The landscape of super-enhancers in cancer is characterized by high levels of histone H3K27 acetylation and bromodomain-containing protein 4 (BRD4), and Mediator complex. These chromatin features facilitate the identification of cancer type-specific and cell-type-specific super-enhancers that control the expression of important oncogenes to stimulate their growth. Disruption of super-enhancers via inhibiting BRD4 or other epigenetic proteins is a potential therapeutic option. Here, we will describe the discovery of super-enhancers and their unique characteristics compared to typical enhancers. Then, we will highlight how super-enhancer-associated genes contribute to cancer progression in different solid tumor types. Lastly, we will cover therapeutic targets and their epigenetic modulators.

Indexed as

NeoplasmsTranscription FactorsBromodomain Containing ProteinsCell Cycle ProteinsChromatinEnhancer Elements, GeneticHumansNuclear ProteinsBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsChromatinNuclear ProteinsTranscription FactorsBRD4Enhancer reprogrammingEpigenetic modulatorsMediatorMetastasisSuper-enhancers

Identifiers

PMID37059907
PMCPMC10527203
OpenAlexW4365503893

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.