Evidence map›Paper›PMID 37940068›Full record

ArticleCancer letters2023

Androgen receptor inhibition suppresses anti-tumor neutrophil response against bone metastatic prostate cancer via regulation of TβRI expression.

Massar Alsamraae, Diane Costanzo-Garvey, Benjamin A Teply, Shawna Boyle, Gary Sommerville, Zachary T Herbert, Colm Morrissey, Alicia J Dafferner, Maher Y Abdalla, Rachel W Fallet and 10 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 18 citations in OpenAlex.

  1. Molecular Mechanisms and Immune Regulation in Prostate Cancer: A Review.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Article
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  5. Androgens are a Key Factor Affecting Immune Related Diseases.The world journal of men's health · 2026
    Review
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  7. Article
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  11. Article
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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

20 authors at 5 institutions in 1 country.

Massar AlsamraaeDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA.
Diane Costanzo-GarveyDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA.
Benjamin A TeplyFred & Pamela Buffett Cancer Center, Omaha, NE, USA; Division of Oncology & Hematology/Oncology, Department of Internal Medicine, University of Nebraska Medical Center Omaha, NE, USA.
Shawna BoyleFred & Pamela Buffett Cancer Center, Omaha, NE, USA.
Gary SommervilleDana Farber Cancer Institute, Boston, MA, USA.
Zachary T HerbertDana Farber Cancer Institute, Boston, MA, USA.
Colm MorrisseyUniversity of Washington, Seattle, WA, USA.
Alicia J DaffernerDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA.
Maher Y AbdallaDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA.
Rachel W FalletDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA.
Tammy KielianDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA.
Heather Jensen-SmithFred & Pamela Buffett Cancer Center, Omaha, NE, USA; Eppley Institute for Research in Cancer and Allied Diseases, Omaha, NE, USA.
Edson I deOliveiraDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA.
Keqiang ChenLaboratory of Cancer Innovation, National Cancer Institute, Frederick, MD, USA.
Ian A BettencourtLaboratory of Cancer Innovation, National Cancer Institute, Frederick, MD, USA.
Ji Ming WangLaboratory of Cancer Innovation, National Cancer Institute, Frederick, MD, USA.
Daniel W McVicarLaboratory of Cancer Innovation, National Cancer Institute, Frederick, MD, USA.
Tyler KeeleyDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA.
Fang YuDepartment of Biostatistics, University of Nebraska Medical Center, Omaha, NE, USA.
Leah M CookDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA; Fred & Pamela Buffett Cancer Center, Omaha, NE, USA. Electronic address: leah.cook@unmc.edu.
University of Nebraska Medical Center · USNational Cancer Institute · USSusan Thompson Buffett Foundation · USDana-Farber Cancer Institute · USUniversity of Washington · US

Funding

TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PETER S NELSON · 2002 to 2026
$58.1M
UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Joann B. Sweasy · 1985 to 2026
$55.0M
Translational Imaging and Behavioral Assessment (TIBA) CoreP20GM130447 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Anna Dunaevsky · 2020 to 2026
$20.7M
Nebraska Center for Nanomedicine- Pilot ProjectsP30GM127200 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI OUPICKY, DAVID · 2018 to 2022
$5.7M
Light-Sheet Fluorescence MicroscopeS10OD030486 · OD · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JENSEN-SMITH, HEATHER COLLEEN · 2021 to 2021
$477k
NCI NIH HHS P30 CA036727NCI NIH HHS P50 CA097186NIGMS NIH HHS P20 GM130447NIGMS NIH HHS P30 GM127200NIH HHS S10 OD030486
6 · The paper itself

Abstract

Bone metastatic disease of prostate cancer (PCa) is incurable and progression in bone is largely dictated by tumor-stromal interactions in the bone microenvironment. We showed previously that bone neutrophils initially inhibit bone metastatic PCa growth yet metastatic PCa becomes resistant to neutrophil response. Further, neutrophils isolated from tumor-bone lost their ability to suppress tumor growth through unknown mechanisms. With this study, our goal was to define the impact of metastatic PCa on neutrophil function throughout tumor progression and to determine the potential of neutrophils as predictive biomarkers of metastatic disease. Using patient peripheral blood polymorphonuclear neutrophils (PMNs), we identified that PCa progression dictates PMN cell surface markers and gene expression, but not cytotoxicity against PCa. Importantly, we also identified a novel phenomenon in which second generation androgen deprivation therapy (ADT) suppresses PMN cytotoxicity via increased transforming growth factor beta receptor I (TβRI). High dose testosterone and genetic or pharmacologic TβRI inhibition rescued androgen receptor-mediated neutrophil suppression and restored neutrophil anti-tumor immune response. These studies highlight the ability to leverage standard-care ADT to generate neutrophil anti-tumor responses against bone metastatic PCa.

Indexed as

Bone NeoplasmsProstatic NeoplasmsAndrogen AntagonistsAndrogensCell Line, TumorHumansMaleNeutrophilsReceptors, AndrogenTumor MicroenvironmentAndrogen AntagonistsAndrogensReceptors, Androgen

Identifiers

PMID37940068
PMCPMC10710875
OpenAlexW4388449310

What OpenQuestion holds

Textmetadata
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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.