Evidence map›Paper›PMID 37907729›Full record

ReviewNature reviews. Urology2024

Prognostic and therapeutic potential of senescent stromal fibroblasts in prostate cancer.

Joakin O Mori, Isra Elhussin, W Nathaniel Brennen, Mindy K Graham, Tamara L Lotan, Clayton C Yates, Angelo M De Marzo, Samuel R Denmeade, Srinivasan Yegnasubramanian, William G Nelson and 4 more

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Urology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 23 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.

Joakin O MoriDepartment of Medicine, Boston University Chobanian & Avedisian School of Medicine and Boston Medical Center, Boston, MA, USA.ORCID 0000-0002-9033-8536
Isra ElhussinDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
W Nathaniel BrennenDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0001-9807-7433
Mindy K GrahamDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0003-2521-0373
Tamara L LotanDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-0494-9067
Clayton C YatesDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Angelo M De MarzoDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0003-4847-5307
Samuel R DenmeadeDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Srinivasan YegnasubramanianDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0003-0744-6606
William G NelsonDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-4379-0730
Gerald V DenisDepartment of Medicine, Boston University Chobanian & Avedisian School of Medicine and Boston Medical Center, Boston, MA, USA.ORCID 0000-0001-9886-0401
Elizabeth A PlatzDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.ORCID 0000-0003-3676-8954
Alan K MeekerDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Christopher M HeaphyDepartment of Medicine, Boston University Chobanian & Avedisian School of Medicine and Boston Medical Center, Boston, MA, USA. heaphyc@bu.edu.ORCID 0000-0003-4264-1810
Johns Hopkins University · USBoston University · US

Funding

TRANSGENIC MODELS FOR PROSTATE CANCER AND AUTOIMMUNITYP50CA058236 · NCI · JOHNS HOPKINS UNIVERSITY · PI NELSON, WILLIAM GEORGE · 1992 to 2020
$43.9M
Translational imaging biomarkers of the tumor microenvironment in early prostate cancerU54CA274370 · NCI · JOHNS HOPKINS UNIVERSITY · PI ANGELO Michael DE MARZO · 2022 to 2026
$9.1M
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 of BET bromodomain metabolic reprogramming in triple negative breast cancerR01CA222170 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI DENIS, GERALD V · 2018 to 2022
$3.1M
Multiscale analysis of metabolic inflammation as a driver of breast cancerU01CA243004 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI DENIS, GERALD V, EMILI, ANDREW · 2020 to 2024
$2.8M
A First-in-Class FAP-activated Protoxin to disrupt the Tumor-Stroma Parasitic Cycle fueling lethal Prostate Cancer ProgressionR01CA255259 · NCI · JOHNS HOPKINS UNIVERSITY · PI BRENNEN, WILLIAM NATHANIEL · 2021 to 2025
$2.1M
Stromal senescence in lethal prostate cancer: a novel target for prognosis and therapyR01CA255349 · NCI · JOHNS HOPKINS UNIVERSITY · PI MEEKER, ALAN KEITH, PLATZ, ELIZABETH A. · 2021 to 2025
$1.7M
NCI NIH HHS P50 CA058236NCI NIH HHS R01 CA222170NCI NIH HHS R01 CA255259NCI NIH HHS R01 CA255349NCI NIH HHS U01 CA196390NCI NIH HHS U01 CA243004NCI NIH HHS U54 CA274370
6 · The paper itself

Abstract

The stromal component of the tumour microenvironment in primary and metastatic prostate cancer can influence and promote disease progression. Within the prostatic stroma, fibroblasts are one of the most prevalent cell types associated with precancerous and cancerous lesions; they have a vital role in the structural composition, organization and integrity of the extracellular matrix. Fibroblasts within the tumour microenvironment can undergo cellular senescence, which is a stable arrest of cell growth and a phenomenon that is emerging as a recognized hallmark of cancer. Supporting the idea that cellular senescence has a pro-tumorigenic role, a subset of senescent cells exhibits a senescence-associated secretory phenotype (SASP), which, along with increased inflammation, can promote prostate cancer cell growth and survival. These cellular characteristics make targeting senescent cells and/or modulating SASP attractive as a potential preventive or therapeutic option for prostate cancer.

Indexed as

Cellular SenescenceFibroblastsProstatic NeoplasmsTumor MicroenvironmentHumansMalePrognosisStromal Cells

Identifiers

PMID37907729
PMCPMC11058122
OpenAlexW4388040184

What OpenQuestion holds

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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.