Evidence map›Paper›PMID 37971878›Full record

ArticleJCI insight2024

Spatial transcriptomics identifies candidate stromal drivers of benign prostatic hyperplasia.

Anna S Pollack, Christian A Kunder, Noah Brazer, Zhewei Shen, Sushama Varma, Robert B West, Gerald R Cunha, Laurence S Baskin, James D Brooks, Jonathan R Pollack

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 8 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Anna S PollackDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Christian A KunderDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Noah BrazerDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Zhewei ShenDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Sushama VarmaDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Robert B WestDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Gerald R CunhaDepartment of Urology, University of California, San Francisco (UCSF), San Francisco, California, USA.
Laurence S BaskinDepartment of Urology, University of California, San Francisco (UCSF), San Francisco, California, USA.
James D BrooksDepartment of Urology, Stanford University School of Medicine, Stanford, California, USA.
Jonathan R PollackDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Stanford University · USUniversity of California, San Francisco · US

Funding

Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI Vittorio Sebastiano · 2007 to 2026
$71.4M
Stanford O'Brien Urology Research CenterU54DK130065 · NIDDK · STANFORD UNIVERSITY · PI JAMES D. BROOKS · 2021 to 2026
$8.3M
BMP5 cells and signaling in BPH pathogenesisR01DK123232 · NIDDK · STANFORD UNIVERSITY · PI BROOKS, JAMES D., POLLACK, JONATHAN R · 2020 to 2022
$710k
NCI NIH HHS P30 CA124435NIDDK NIH HHS R01 DK123232NIDDK NIH HHS U54 DK130065
6 · The paper itself

Abstract

Benign prostatic hyperplasia (BPH) is the nodular proliferation of the prostate transition zone in older men, leading to urinary storage and voiding problems that can be recalcitrant to therapy. Decades ago, John McNeal proposed that BPH originates with the "reawakening" of embryonic inductive activity by adult prostate stroma, which spurs new ductal proliferation and branching morphogenesis. Here, by laser microdissection and transcriptional profiling of the BPH stroma adjacent to hyperplastic branching ducts, we identified secreted factors likely mediating stromal induction of prostate glandular epithelium and coinciding processes. The top stromal factors were insulin-like growth factor 1 (IGF1) and CXC chemokine ligand 13 (CXCL13), which we verified by RNA in situ hybridization to be coexpressed in BPH fibroblasts, along with their cognate receptors (IGF1R and CXCR5) on adjacent epithelium. In contrast, IGF1 but not CXCL13 was expressed in human embryonic prostate stroma. Finally, we demonstrated that IGF1 is necessary for the generation of BPH-1 cell spheroids and patient-derived BPH cell organoids in 3D culture. Our findings partially support historic speculations on the etiology of BPH and provide what we believe to be new molecular targets for rational therapies directed against the underlying processes driving BPH.

Indexed as

Prostatic HyperplasiaAdultAgedEpitheliumFibroblastsGene Expression ProfilingHumansMaleProstateCell BiologyExpression profilingMolecular pathologyReproductive BiologyUrology

Identifiers

PMID37971878
PMCPMC10906230
OpenAlexW4388728990

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.