ReviewMolecular cancer2018
BRD4 and Cancer: going beyond transcriptional regulation.
Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 417 papers.
What it found
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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
417 citing papers in PubMed, 702 citations in OpenAlex.
- PROTACs in cancer therapy: targeted degradation of GPX4, PARP and epigenetic regulators.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- Antitumor activity and structure-activity relationship of poly (ADP-ribose) polymerase (PARP)-based dual inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- BUB signaling in cancer and molecular insights into targeted therapies.Communications biology · 2026Review
- TNFα-driven epigenetic upregulation of TIGIT creates a targetable vulnerability in tumors.Oncogene · 2026Article
- Structural characteristics and SARs of EZH2 inhibitors.Molecular diversity · 2026Review
- MMP2Mol: a matched molecular pairs-based framework for ligand-based de novo drug design.Briefings in bioinformatics · 2026Article
- Multi-sampling allows intra-tumoral heterogeneity querying and vulnerability profiling in glioblastoma.Neuro-oncology · 2026Article
- Histone modifications: mechanisms, metabolic regulation, and therapeutic targeting in cancer.Precision clinical medicine · 2026Review
- Tumour-specific bioorthogonal synthesis of proteolysis-targeting chimeras and nanoparticles boosts T cell activity.Nature biomedical engineering · 2026Article
- BRD4 binds the nucleosome via both histone and DNA interactions.Molecular cell · 2026Article
- A BRD4/p300/SP1 epigenetic cascade drives microglial P2X4R transcription and promotes neuropathic pain.Journal of neuroinflammation · 2026Article
- Epigenetic Alterations in Hepatocellular Carcinoma: Mechanisms and Biomarkers for Precision Therapy.Cancers · 2026Review
- BET inhibition curbs macrophage inflammation, lipid accumulation, and atherogenesis by disrupting the YAP/TAZ-BRD4 axis.Journal of leukocyte biology · 2026Article
- Article
- Clinical Significance of Bromodomain-Containing Protein 9 in Colorectal Cancer.Annals of surgical oncology · 2026Article
- Targeting BRD2 and BRD4 inhibit the growth of KSHV-infected immortalized endothelial cells through suppression of LANA translation.PLoS pathogens · 2026Article
- Perturbation of BRD4 and p300 activity suppresses super enhancer‑drivenOncology reports · 2026Article
- Computational identification of putative mRNA-miRNA signatures in chemoresistant and metastatic triple-negative breast cancer.Biochemistry and biophysics reports · 2026Article
- 3D genome architecture and epigenetic regulation of lineage identity in advanced prostate cancer.Endocrinology · 2026Review
- Discovery of a KLHL41 Ligand for Muscle Specific Protein Degradation.Nature communications · 2026Article
357 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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRD4, member of the Bromodomain and Extraterminal (BET) protein family, is largely acknowledged in cancer for its role in super-enhancers (SEs) organization and oncogenes expression regulation. Inhibition of BRD4 shortcuts the communication between SEs and target promoters with a subsequent cell-specific repression of oncogenes to which cancer cells are addicted and cell death. To date, this is the most credited mechanism of action of BET inhibitors, a class of small molecules targeting BET proteins which are currently in clinical trials in several cancer settings.However, recent evidence indicates that BRD4 relevance in cancer goes beyond its role in transcription regulation and identifies this protein as a keeper of genome stability.Indeed, a non-transcriptional role of BRD4 in controlling DNA damage checkpoint activation and repair as well as telomere maintenance has been proposed, throwing new lights into the multiple functions of this protein and opening new perspectives on the use of BETi in cancer. Here we discuss the current available information on non-canonical, non-transcriptional functions of BRD4 and on their implications in cancer biology. Integrating this information with the already known BRD4 role in gene expression regulation, we propose a "common" model to explain BRD4 genomic function. Furthermore, in light of the transversal function of BRD4, we provide new interpretation for the cytotoxic activity of BETi and we discuss new possibilities for a wide and focused employment of these drugs in clinical settings.
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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.