ArticleNature genetics2022
Genetic determinants of chromatin reveal prostate cancer risk mediated by context-dependent gene regulation.
Article in Nature genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Association betweenFrontiers in oncology · 2025Pooled it
- Single-cell imaging analysis, therapeutic modeling and a Phase Ib trial validate BCL-2 as a target across heterogeneous castration-resistant prostate cancer.Signal transduction and targeted therapy · 2026Trial
- Identifying independent causal cell types for human diseases and risk variants.Cell genomics · 2026Article
- Article
- Origins and consequences of oncogenic 3D chromatin remodelling.Nature reviews. Cancer · 2026Review
- Decoding 3D chromatin architecture reveals distinct enhancer classes underlying hierarchical gene regulation in prostate cancer.Genome biology · 2026Article
- Developmental signaling reveals functionally enriched human-specific gene regulation in telencephalic progenitors.bioRxiv : the preprint server for biology · 2026Article
- NNMT Loss Drives Cancer Progression by enhancing SAM availability for mTORC1 Signaling and Chromatin Methylation.bioRxiv : the preprint server for biology · 2026Article
- Article
- Autoimmune non-coding variants perturb transcription factor-cofactor complex assembly linked to enhancer activity.bioRxiv : the preprint server for biology · 2026Article
- Generation of a comprehensive epigenomic atlas in clear cell renal cell carcinoma informs kidney cancer progression and heritability.Cell reports · 2026Article
- A gene-specific variance-control approach corrects polygenicity-driven inflation observed in transcriptome-wide association studies.American journal of human genetics · 2026Article
- SLPI in Prostate Cancer.Cancers · 2026Review
- Impact of disease-associated chromatin accessibility QTLs across immune cell types and contexts.Cell genomics · 2026Article
- GENEasso: a curated resource of credible disease-gene associations across complex diseases from GWAS summary statistics.Nucleic acids research · 2026Article
- SNAP: Streamlined Nextflow Analysis Pipeline for Immunoprecipitation-Based Epigenomic Profiling of Circulating Chromatin.bioRxiv : the preprint server for biology · 2025Article
- Investigating key genes and molecular mechanisms of prostate cancer and coronary heart disease through transcriptomics and experimental validation.Translational andrology and urology · 2025Article
- Non-coding genetic variants underlying higher prostate cancer risk in men of African ancestry.Nature communications · 2025Article
- Circulating chromatin reveals the effects of disease-associated variants on gene regulation.bioRxiv : the preprint server for biology · 2025Article
- Targeting histone H2B acetylated enhanceosomes via p300/CBP degradation in prostate cancer.Nature genetics · 2025Article
Corrections and comments
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Authors and funding
23 authors at 9 institutions in 4 countries.
Funding
Abstract
Many genetic variants affect disease risk by altering context-dependent gene regulation. Such variants are difficult to study mechanistically using current methods that link genetic variation to steady-state gene expression levels, such as expression quantitative trait loci (eQTLs). To address this challenge, we developed the cistrome-wide association study (CWAS), a framework for identifying genotypic and allele-specific effects on chromatin that are also associated with disease. In prostate cancer, CWAS identified regulatory elements and androgen receptor-binding sites that explained the association at 52 of 98 known prostate cancer risk loci and discovered 17 additional risk loci. CWAS implicated key developmental transcription factors in prostate cancer risk that are overlooked by eQTL-based approaches due to context-dependent gene regulation. We experimentally validated associations and demonstrated the extensibility of CWAS to additional epigenomic datasets and phenotypes, including response to prostate cancer treatment. CWAS is a powerful and biologically interpretable paradigm for studying variants that influence traits by affecting transcriptional regulation.
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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.