Evidence map›Paper›PMID 34035460›Full record

ArticleProstate cancer and prostatic diseases2022

Inflammatory bowel disease induces inflammatory and pre-neoplastic changes in the prostate.

Anuj S Desai, Vinay Sagar, Barbara Lysy, Adam B Weiner, Oliver S Ko, Conor Driscoll, Yara Rodriguez, Rajita Vatapalli, Kenji Unno, Huiying Han and 12 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Prostate cancer and prostatic diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. In Vivo Microendoscopy in the Near-Infrared II Window.Small (Weinheim an der Bergstrasse, Germany) · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 2 institutions in 2 countries.

Anuj S Desai *Department of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Vinay Sagar *Department of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Barbara LysyDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Adam B WeinerDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.ORCID 0000-0002-1912-042X
Oliver S KoDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Conor DriscollDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Yara RodriguezDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Rajita VatapalliDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Kenji UnnoDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Huiying HanDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Jason E CohenDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Amanda X VoDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Minh PhamDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Michael ShinDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Ketan Jain-PosterDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Jennifer RossDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Elizabeth G MorencyDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Travis J MeyersDepartment of Epidemiology and Biostatistics, University of California, San Francisco (UCSF), San Francisco, CA, USA.
John S WitteDepartment of Epidemiology and Biostatistics, University of California, San Francisco (UCSF), San Francisco, CA, USA.
Jennifer WuDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Sarki A AbdulkadirDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.ORCID 0000-0003-2963-2899
Shilajit D KunduDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. s-kundu@northwestern.edu.ORCID 0000-0001-5532-1408
Northwestern University · USUniversity of California, San Francisco · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEONIDAS C. PLATANIAS · 1993 to 2026
$153.9M
Targeting FOXA1-downstream pathways: a novel therapeutic strategy for castration-resistant prostate cancerP50CA180995 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ABDULKADIR, SARKI A., HUSSAIN, MAHA H · 2015 to 2025
$19.9M
Modeling Prostate TumorigenesisR01CA094858 · NCI · VANDERBILT UNIVERSITY · PI ABDULKADIR, SARKI A. · 2002 to 2012
$2.5M
NCI NIH HHS P30 CA060553NCI NIH HHS P50 CA180995NCI NIH HHS R01 CA094858
6 · The paper itself

Abstract

backgroundInflammatory bowel disease (IBD) has been implicated as a risk factor for prostate cancer, however, the mechanism of how IBD leads to prostate tumorigenesis is not known. Here, we investigated whether chronic intestinal inflammation leads to pro-inflammatory changes associated with tumorigenesis in the prostate.

methodsUsing clinical samples of men with IBD who underwent prostatectomy, we analyzed whether prostate tumors had differences in lymphocyte infiltrate compared to non-IBD controls. In a mouse model of chemically-induced intestinal inflammation, we investigated whether chronic intestinal inflammation could be transferred to the wild-type mouse prostate. In addition, mouse prostates were evaluated for activation of pro-oncogenic signaling and genomic instability.

resultsA higher proportion of men with IBD had T and B lymphocyte infiltration within prostate tumors. Mice with chronic colitis showed significant increases in prostatic CD45 + leukocyte infiltration and elevation of three pro-inflammatory cytokines-TIMP-1, CCL5, and CXCL1 and activation of AKT and NF-kB signaling pathways. Lastly, mice with chronic colitis had greater prostatic oxidative stress/DNA damage, and prostate epithelial cells had undergone cell cycle arrest.

conclusionsThese data suggest chronic intestinal inflammation is associated with an inflammatory-rich, pro-tumorigenic prostatic phenotype which may explain how gut inflammation fosters prostate cancer development in men with IBD.

Indexed as

ColitisInflammatory Bowel DiseasesProstatic NeoplasmsAnimalsCarcinogenesisDextran SulfateDisease Models, AnimalHumansInflammationMaleMiceMice, Inbred C57BLProstateDextran Sulfate

Identifiers

PMID34035460
PMCPMC8647933
OpenAlexW3164080717

What OpenQuestion holds

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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.