Evidence map›Paper›PMID 25348195›Full record

ArticleThe Journal of pathology2015

A human prostatic bacterial isolate alters the prostatic microenvironment and accelerates prostate cancer progression.

Brian W Simons, Nicholas M Durham, Tullia C Bruno, Joseph F Grosso, Anthony J Schaeffer, Ashley E Ross, Paula J Hurley, David M Berman, Charles G Drake, Praveen Thumbikat and 1 more

Abstract read
In one paragraph

Article in The Journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
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  9. A Bird's-Eye View of the Pathophysiologic Role of the Human Urobiota in Health and Disease: Can We Modulate It?Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Review
  10. Article
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  14. Article
  15. Article
  16. Review
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  19. Why Do Epidemiologic Studies Find an Inverse Association Between Intraprostatic Inflammation and Prostate Cancer: A Possible Role for Colliding Bias?Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2021
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Brian W SimonsThe Brady Urological Institute, Department of Urology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Nicholas M Durham
Tullia C Bruno
Joseph F Grosso
Anthony J Schaeffer
Ashley E Ross
Paula J Hurley
David M Berman
Charles G Drake
Praveen Thumbikat
Edward M Schaeffer
Johns Hopkins University · USNorthwestern University · USQueen's University · CA

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
CELLULAR &MOLECULAR MECH OF INFLAMMATORY REACTIONST32AI007247 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Joel L Pomerantz · 1985 to 2026
$10.2M
T cells in Chronic Pelvic PainR01DK094898 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI THUMBIKAT, PRAVEEN · 2013 to 2016
$1.5M
NCI NIH HHS P30 CA006973NIDDK NIH HHS R01 DK094898
6 · The paper itself

Abstract

Inflammation is associated with several diseases of the prostate including benign enlargement and cancer, but a causal relationship has not been established. Our objective was to characterize the prostate inflammatory microenvironment after infection with a human prostate-derived bacterial strain and to determine the effect of inflammation on prostate cancer progression. To this end, we mimicked typical human prostate infection with retrograde urethral instillation of CP1, a human prostatic isolate of Escherichia coli. CP1 bacteria were tropic for the accessory sex glands and induced acute inflammation in the prostate and seminal vesicles, with chronic inflammation lasting at least 1 year. Compared to controls, infection induced both acute and chronic inflammation with epithelial hyperplasia, stromal hyperplasia, and inflammatory cell infiltrates. In areas of inflammation, epithelial proliferation and hyperplasia often persist, despite decreased expression of androgen receptor (AR). Inflammatory cells in the prostates of CP1-infected mice were characterized at 8 weeks post-infection by flow cytometry, which showed an increase in macrophages and lymphocytes, particularly Th17 cells. Inflammation was additionally assessed in the context of carcinogenesis. Multiplex cytokine profiles of inflamed prostates showed that distinct inflammatory cytokines were expressed during prostate inflammation and cancer, with a subset of cytokines synergistically increased during concurrent inflammation and cancer. Furthermore, CP1 infection in the Hi-Myc mouse model of prostate cancer accelerated the development of invasive prostate adenocarcinoma, with 70% more mice developing cancer by 4.5 months of age. This study provides direct evidence that prostate inflammation accelerates prostate cancer progression and gives insight into the microenvironment changes induced by inflammation that may accelerate tumour initiation or progression.

Indexed as

Disease ProgressionAdenocarcinomaAnimalsCell ProliferationCytokinesDisease Models, AnimalEscherichia coliHumansHyperplasiaMaleMiceMice, Inbred C57BLProstateProstatic NeoplasmsProstatitisReceptors, AndrogenCytokinesReceptors, AndrogenEscherichia coliinflammationmouseprostateprostatitis

Identifiers

PMID25348195
PMCPMC4352321
OpenAlexW2056530323

What OpenQuestion holds

Textmetadata
LicenceTDM
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.