Evidence map›Paper›PMID 25088980›Full record

ReviewThe American journal of pathology2014

Stromal androgen receptor in prostate development and cancer.

Mandeep Singh, Ruchi Jha, Jonathan Melamed, Ellen Shapiro, Simon W Hayward, Peng Lee

Open access · hybridAbstract readReview
In one paragraph

Review in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 82 citations in OpenAlex.

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  15. Patterns of indolence in prostate cancer (Review).Experimental and therapeutic medicine · 2022
    Review
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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

6 authors at 2 institutions in 1 country.

Mandeep SinghDepartment of Pathology, New York University School of Medicine, New York, New York.
Ruchi JhaDepartment of Pathology, New York University School of Medicine, New York, New York.
Jonathan MelamedDepartment of Pathology, New York University School of Medicine, New York, New York.
Ellen ShapiroDepartment of Urology, New York University School of Medicine, New York, New York.
Simon W HaywardDepartments of Urologic Surgery and Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address: simon.hayward@vanderbilt.edu.
Peng LeeDepartment of Pathology, New York University School of Medicine, New York, New York; Department of Urology, New York University School of Medicine, New York, New York; New York Harbor Healthcare System, New York University School of Medicine, New York, New York. Electronic address: peng.lee@nyumc.org.
New York University · USVanderbilt University Medical Center · US

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ADRIANA HEGUY · 1985 to 2026
$83.1M
Predicting Prostate Cancer AggressivenessU01CA151924 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI ANDERSON, ALEXANDER ROBERTSON ALLAN, AYALA, GUSTAVO ENRIQUE · 2011 to 2015
$2.8M
Signaling Pathway Alterations in the Racial Disparity of Prostate CancerU01CA149556 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LEE, PENG, ZHANG, DAVID Y · 2011 to 2016
$1.9M
A signal pathway-based signature for metastatic prostate cancerI01BX001505 · VA · VA MEDICAL CENTER · PI LEE, PENG · 2014 to 2014
–
BLRD VA I01 BX001505NCI NIH HHS 1U01CA149556-01A1NCI NIH HHS 3U01CA149556-01S1NCI NIH HHS P30 CA016087NCI NIH HHS U01 CA149556NCI NIH HHS U01 CA151924
6 · The paper itself

Abstract

The androgen receptor (AR) in stromal cells contributes significantly to the development and growth of prostate during fetal stages as well as during prostate carcinogenesis and cancer progression. During prostate development, stromal AR induces and promotes epithelial cell growth, as observed from tissue recombinant and mouse knockout studies. During prostate carcinogenesis and progression, the stromal cells begin to lose AR expression as early as at the stage of high-grade prostatic intraepithelial neoplasia. The extent of loss of stromal AR is directly proportional to the degree of differentiation (Gleason grade) and progression of prostate cancer (PCa). Co-culture studies suggested that stromal AR inhibits the growth of malignant epithelial cells, possibly through expression of certain paracrine factors in the presence of androgens. This functional reversal of stromal AR, from growth promotion during fetal prostate development to mediating certain growth-inhibiting effects in cancer, explains to some extent the reason that loss of AR expression in stromal cells may be crucial for development of resistance to androgen ablation therapy for PCa. From a translational perspective, it generates the need to re-examine the current therapeutic options and opens a fundamental new direction for therapeutic interventions, especially in advanced PCa.

Indexed as

Gene Expression Regulation, NeoplasticAndrogensDisease ProgressionEpithelial CellsHumansMaleProstateProstatic NeoplasmsReceptors, AndrogenStromal CellsAndrogensAR protein, humanReceptors, Androgen

Identifiers

PMID25088980
PMCPMC4188859
OpenAlexW2066669998

What OpenQuestion holds

Textmetadata
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.