ArticleJCI insight2019
Genomic analysis of benign prostatic hyperplasia implicates cellular re-landscaping in disease pathogenesis.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04873427 (In Situ Clonal Heterogeneity in Prostatic Diagnostic Biopsies), which is not on this map. Cited by 31 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.
In Situ Clonal Heterogeneity in Prostatic Diagnostic Biopsies: Impact on Prostate Cancer Evolution and Clinical Outcome. A Retrospective, Proof of Concept Study
Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- Article
- Oxidative stress reprograms benign prostatic hyperplasia microenvironments: insights from integrative multi-omics and machine learning.Journal of translational medicine · 2026Article
- A single cell transcriptional profile of benign prostatic hyperplasia.Scientific reports · 2026Article
- A Case Series on the Efficacy and Safety of Transperineal Laser Ablation for Benign Prostatic Hyperplasia.Journal of clinical medicine · 2026Article
- SLC25A37 as a novel therapeutic target for benign prostatic hyperplasia: integrative analyses of single-cell RNA sequencing and genome-wide association studies.Open medicine (Warsaw, Poland) · 2026Article
- Extracellular vesicles as mediators of prostatic diseases: connecting function to diagnostic and therapeutic applications.Extracellular vesicles and circulating nucleic acids · 2026Review
- Identification of programmed cell death associated key genes in benign prostatic hyperplasia and prostate cancer development by integrated bioinformatics analysis and machine learning.Translational andrology and urology · 2025Article
- Single-Cell Sequencing Reveals That CD4Aging cell · 2025Article
- TIAM1 drives prostatic branching phenotype and is a potential therapeutic target for benign prostatic hyperplasia.JCI insight · 2025Article
- Immune repertoire profiling uncovers pervasive T cell clonal expansions in benign prostatic hyperplasia.The Journal of clinical investigation · 2025Article
- Establishing and Characterizing the Molecular Profiles, Cellular Features, and Clinical Utility of a Patient-Derived Xenograft Model Using Benign Prostatic Tissues.Laboratory investigation; a journal of technical methods and pathology · 2024Article
- Change in prostate tissue gene expression following finasteride or doxazosin administration in the medical therapy for prostatic symptoms (MTOPS) study.Scientific reports · 2024Article
- Bioinformatics in urology - molecular characterization of pathophysiology and response to treatment.Nature reviews. Urology · 2024Review
- Identification and functional activity of Nik related kinase (NRK) in benign hyperplastic prostate.Journal of translational medicine · 2024Article
- Spatial architectures of somatic mutations in normal prostate, benign prostatic hyperplasia and coexisting prostate cancer.Experimental & molecular medicine · 2024Article
- Spatial transcriptomics identifies candidate stromal drivers of benign prostatic hyperplasia.JCI insight · 2024Article
- Therapeutic potential of pomegranate juice-derived nanovesicles in nude mouse benign prostatic hyperplasia (BPH) xenograft model.Scientific reports · 2023Article
- Phenotype and Reactivity of Lymphocytes Expanded from Benign Prostate Hyperplasic Tissues and Prostate Cancer.Cancers · 2023Article
- Improving Whole Tomato Transformation for Prostate Health: Benign Prostate Hypertrophy as an Exploratory Model.International journal of molecular sciences · 2023Review
- Understanding human aging and the fundamental cell signaling link in age-related diseases: the middle-aging hypovascularity hypoxia hypothesis.Frontiers in aging · 2023Article
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
Abstract
Benign prostatic hyperplasia (BPH) is the most common cause of lower urinary tract symptoms in men. Current treatments target prostate physiology rather than BPH pathophysiology and are only partially effective. Here, we applied next-generation sequencing to gain new insight into BPH. By RNAseq, we uncovered transcriptional heterogeneity among BPH cases, where a 65-gene BPH stromal signature correlated with symptom severity. Stromal signaling molecules BMP5 and CXCL13 were enriched in BPH while estrogen regulated pathways were depleted. Notably, BMP5 addition to cultured prostatic myofibroblasts altered their expression profile towards a BPH profile that included the BPH stromal signature. RNAseq also suggested an altered cellular milieu in BPH, which we verified by immunohistochemistry and single-cell RNAseq. In particular, BPH tissues exhibited enrichment of myofibroblast subsets, whilst depletion of neuroendocrine cells and an estrogen receptor (ESR1)-positive fibroblast cell type residing near epithelium. By whole-exome sequencing, we uncovered somatic single-nucleotide variants (SNVs) in BPH, of uncertain pathogenic significance but indicative of clonal cell expansions. Thus, genomic characterization of BPH has identified a clinically-relevant stromal signature and new candidate disease pathways (including a likely role for BMP5 signaling), and reveals BPH to be not merely a hyperplasia, but rather a fundamental re-landscaping of cell types.
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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.