ArticleNature communications2022
MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02609269 (Prospective Expression Analysis Using The Decipher Genomics Resource for Intelligent Discovery), which is not on this map. Cited by 122 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.
Prospective Expression Analysis Using The Decipher Genomics Resource for Intelligent Discovery (GRID)® and Data Sharing Program
Who cites it
122 citing papers in PubMed, 142 citations in OpenAlex.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- Recurrent mechanisms of biallelic epigenetic inactivation reveal new putative tumour suppressor genes in prostate cancer.Nature communications · 2026Article
- Comprehensive Spatial Transcriptomic Profiling of Cribriform, Intraductal, Atypical Intraductal Proliferation, and Ductal Adenocarcinoma of the Prostate.Laboratory investigation; a journal of technical methods and pathology · 2026Article
- Spatial Mapping of the Precancer-to-Cancer Transition in Breast and Prostate.Cancer discovery · 2026Article
- DeepPathway: predicting pathway expression from histopathology images.Bioinformatics (Oxford, England) · 2026Article
- Photoproximity labeling of c-Myc reveals SLK as a cancer-specific co-regulator.Nature chemical biology · 2026Article
- Serum CCL2 and CCL7 in Prostate Cancer: Evaluation of Their Diagnostic Utility in Comparison with Benign Prostatic Hyperplasia and Healthy Controls.International journal of molecular sciences · 2026Article
- Development of Radioligand Therapy-Responsive Syngeneic Prostate Models through Murine Prostate-Specific Membrane Antigen Point Mutation.ACS pharmacology & translational science · 2026Article
- A MYC family switch: L-MYC drives and maintains neuroendocrine lineage programs in prostate cancer.Neoplasia (New York, N.Y.) · 2026Article
- Clinical and genomic predictors of sipuleucel-T outcomes in men with metastatic androgen pathway modulator resistant prostate cancer.Research square · 2026Article
- Mapping prostate cancer pathobiology: A review of genetically engineered mouse models (GEMMs).Gene · 2026Review
- Genomic Determinants of Lethality and Therapeutic Vulnerability in Castration-Resistant Prostate Cancer.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of Progression and Challenges for Intervention in the Natural History of Early Prostate Cancer: A Narrative Review.Current oncology (Toronto, Ont.) · 2026Review
- Review
- 3D genome architecture and epigenetic regulation of lineage identity in advanced prostate cancer.Endocrinology · 2026Review
- MIAAIM: Multi-omics image integration with dimensional reduction for tissue state mapping.PLoS computational biology · 2026Article
- Tumor-specific lncRNA IGF1R-AS1 trans-regulates chromatin interactions associated with oncogenic MYC signaling.Nature communications · 2026Article
- Genomic landscape and precision therapy in prostate cancer: current status and future directions.NPJ precision oncology · 2026Review
- A single cell transcriptional profile of benign prostatic hyperplasia.Scientific reports · 2026Article
- Androgen Receptor Drives Polyamine Synthesis, Creating a Vulnerability for Prostate Cancer.Cancer research · 2026Article
62 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
35 authors at 12 institutions in 3 countries.
Funding
Abstract
c-MYC (MYC) is a major driver of prostate cancer tumorigenesis and progression. Although MYC is overexpressed in both early and metastatic disease and associated with poor survival, its impact on prostate transcriptional reprogramming remains elusive. We demonstrate that MYC overexpression significantly diminishes the androgen receptor (AR) transcriptional program (the set of genes directly targeted by the AR protein) in luminal prostate cells without altering AR expression. Analyses of clinical specimens reveal that concurrent low AR and high MYC transcriptional programs accelerate prostate cancer progression toward a metastatic, castration-resistant disease. Data integration of single-cell transcriptomics together with ChIP-seq uncover an increase in RNA polymerase II (Pol II) promoter-proximal pausing at AR-dependent genes following MYC overexpression without an accompanying deactivation of AR-bound enhancers. Altogether, our findings suggest that MYC overexpression antagonizes the canonical AR transcriptional program and contributes to prostate tumor initiation and progression by disrupting transcriptional pause release at AR-regulated genes.
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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.