ArticleBMC genomics2017
Bromodomain protein 4 discriminates tissue-specific super-enhancers containing disease-specific susceptibility loci in prostate and breast cancer.
Article in BMC genomics, 2017. 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, 32 citations in OpenAlex.
- KLF7 regulates super-enhancer-driven IGF2BP2 overexpression to promote the progression of head and neck squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2024Article
- Bromodomain and Extra-Terminal Proteins in Brain Physiology and Pathology: BET-ing on Epigenetic Regulation.Biomedicines · 2023Review
- BET bromodomains as novel epigenetic targets for brain health and disease.Neuropharmacology · 2020Review
- Targeting DNA Damage Response in Prostate and Breast Cancer.International journal of molecular sciences · 2020Review
- Impact of Gene-Environment Interactions on Cancer Development.International journal of environmental research and public health · 2020Review
- Aberrant activation of super enhancer and choline metabolism drive antiandrogen therapy resistance in prostate cancer.Oncogene · 2020Article
- Targeting complexes of super-enhancers is a promising strategy for cancer therapy.Oncology letters · 2020Review
- Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation.Molecular oncology · 2020Article
- Co-inhibition of BET proteins and PI3Kα triggers mitochondrial apoptosis in rhabdomyosarcoma cells.Oncogene · 2020Article
- Dysregulated Transcriptional Control in Prostate Cancer.International journal of molecular sciences · 2019Review
- Dissecting Tissue-Specific Super-Enhancers by Integrating Genome-Wide Analyses and CRISPR/Cas9 Genome Editing.Journal of mammary gland biology and neoplasia · 2019Review
- Post-GWAS in prostate cancer: from genetic association to biological contribution.Nature reviews. Cancer · 2019Review
- Double-Edged Sword of Tumour Suppressor Genes in Schizophrenia.Frontiers in molecular neuroscience · 2019Review
- Recent Advances in Prostate Cancer Treatment and Drug Discovery.International journal of molecular sciences · 2018Review
- Epigenetic Regulation in Prostate Cancer Progression.Current molecular biology reports · 2018Review
- Review
- Super enhancers - new analyses and perspectives on the low hanging fruit.Transcription · 2018Article
- Exploiting Epigenetic Alterations in Prostate Cancer.International journal of molecular sciences · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundEpigenetic information can be used to identify clinically relevant genomic variants single nucleotide polymorphisms (SNPs) of functional importance in cancer development. Super-enhancers are cell-specific DNA elements, acting to determine tissue or cell identity and driving tumor progression. Although previous approaches have been tried to explain risk associated with SNPs in regulatory DNA elements, so far epigenetic readers such as bromodomain containing protein 4 (BRD4) and super-enhancers have not been used to annotate SNPs. In prostate cancer (PC), androgen receptor (AR) binding sites to chromatin have been used to inform functional annotations of SNPs.
resultsHere we establish criteria for enhancer mapping which are applicable to other diseases and traits to achieve the optimal tissue-specific enrichment of PC risk SNPs. We used stratified Q-Q plots and Fisher test to assess the differential enrichment of SNPs mapping to specific categories of enhancers. We find that BRD4 is the key discriminant of tissue-specific enhancers, showing that it is more powerful than AR binding information to capture PC specific risk loci, and can be used with similar effect in breast cancer (BC) and applied to other diseases such as schizophrenia.
conclusionsThis is the first study to evaluate the enrichment of epigenetic readers in genome-wide associations studies for SNPs within enhancers, and provides a powerful tool for enriching and prioritizing PC and BC genetic risk loci. Our study represents a proof of principle applicable to other diseases and traits that can be used to redefine molecular mechanisms of human phenotypic variation.
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.