Evidence map›Paper›PMID 33949714›Full record

ArticleThe Prostate2021

Characterization of tumor-associated macrophages in prostate cancer transgenic mouse models.

Amber E de Groot, Kayla V Myers, Timothy E G Krueger, Ashley L Kiemen, Natalia H Nagy, Alexandria Brame, Vicente E Torres, Zhongyuan Zhang, Levent Trabzonlu, W Nathaniel Brennen and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Prostate, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 20 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

14 authors at 2 institutions in 1 country.

Amber E de GrootDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-4506-1910
Kayla V MyersDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-0748-1092
Timothy E G KruegerDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-7477-4012
Ashley L KiemenDepartment of Chemical and Biomolecular Engineering, Johns Hopkins Whiting School of Engineering, Baltimore, Maryland, USA.
Natalia H NagyDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Alexandria BrameDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Vicente E TorresDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Zhongyuan ZhangDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Levent TrabzonluDepartment of Pathology and Laboratory Medicine, Loyola University Medical Center, Maywood, Illinois, USA.
W Nathaniel BrennenDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0001-9807-7433
Denis WirtzDepartment of Chemical and Biomolecular Engineering, Johns Hopkins Whiting School of Engineering, Baltimore, Maryland, USA.
Angelo M De MarzoDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Sarah R AmendDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-5606-1262
Kenneth J PientaDepartment of Urology, James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-4138-2186
Johns Hopkins University · USLoyola University Medical Center · US

Funding

TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI DENMEADE, SAMUEL R · 1992 to 2020
$43.9M
Tumor microvesicle-mediated modulation of the bone microenvironmentP01CA093900 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KELLER, EVAN T · 2004 to 2024
$29.6M
TRANS_NETWORK PROJECTSU54CA143803 · NCI · PRINCETON UNIVERSITY · PI GETZENBERG, ROBERT H. · 2009 to 2013
$14.2M
The Role of Physical Cues in Collective Cell InvasionU54CA210173 · NCI · JOHNS HOPKINS UNIVERSITY · PI PIENTA, KENNETH J., WIRTZ, DENIS · 2016 to 2020
$9.9M
Multidiciplinary Integrative Genomic Approach to Distinguish Lethal from Indolent Prostate Cancer in Men of Europena and African AncestryU01CA196390 · NCI · JOHNS HOPKINS UNIVERSITY · PI DE MARZO, ANGELO MICHAEL, PIENTA, KENNETH J. · 2015 to 2020
$5.8M
Mechanisms That Regulate Dormancy of Disseminated Tumor Cells in the Bone MarrowU54CA163124 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHIOZAWA, YUSUKE · 2011 to 2015
$3.0M
Reactive Stroma and Tumor Associated Macrophages in Prostate Cancer ProgressionU01CA143055 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PIENTA, KENNETH J., ROWLEY, DAVID R · 2010 to 2014
$2.7M
NCI NIH HHS P01 CA093900NCI NIH HHS P50 CA058236NCI NIH HHS U01 CA143055NCI NIH HHS U01 CA196390NCI NIH HHS U54 CA143803NCI NIH HHS U54 CA163124NCI NIH HHS U54 CA210173
6 · The paper itself

Abstract

backgroundTumor-associated macrophages (TAMs) are critical components of the tumor microenvironment (TME) in prostate cancer. Commonly used orthotopic models do not accurately reflect the complete TME of a human patient or the natural initiation and progression of a tumor. Therefore, genetically engineered mouse models are essential for studying the TME as well as advancing TAM-targeted therapies. Two common transgenic (TG) models of prostate cancer are Hi-Myc and transgenic adenocarcinoma of the mouse prostate (TRAMP), but the TME and TAM characteristics of these models have not been well characterized.

methodsTo advance the Hi-Myc and TRAMP models as tools for TAM studies, macrophage infiltration and characteristics were assessed using histopathologic, flow cytometric, and expression analyses in these models at various timepoints during tumor development and progression.

resultsIn both Hi-Myc and TRAMP models, macrophages adopt a more pro-tumor phenotype in higher histological grade tumors and in older prostate tissue. However, the Hi-Myc and TRAMP prostates differ in their macrophage density, with Hi-Myc tumors exhibiting increased macrophage density and TRAMP tumors exhibiting decreased macrophage density compared to age-matched wild type mice.

conclusionsThe macrophage density and the adenocarcinoma cancer subtype of Hi-Myc appear to better mirror patient tumors, suggesting that the Hi-Myc model is the more appropriate in vivo TG model for studying TAMs and TME-targeted therapies.

Indexed as

AnimalsGene Expression Regulation, NeoplasticMaleMiceMice, TransgenicProstatic NeoplasmsTumor-Associated MacrophagesTumor MicroenvironmentHi-Mycpro-tumorTAMTRAMPtumor microenvironment

Identifiers

PMID33949714
PMCPMC8720375
OpenAlexW3158376733

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.