Evidence map›Paper›PMID 34052326›Full record

ReviewCancer letters2021

Aging of the progenitor cells that initiate prostate cancer.

Jack Freeland, Preston D Crowell, Jenna M Giafaglione, Paul C Boutros, Andrew S Goldstein

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.4field-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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Age-Associated Proteomic Changes in Human Spermatozoa.International journal of molecular sciences · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Natural Compounds for Preventing Age-Related Diseases and Cancers.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

5 authors at 1 institution in 1 country.

Jack FreelandMolecular Biology Interdepartmental Program, University of California, Los Angeles, USA.
Preston D CrowellMolecular Biology Interdepartmental Program, University of California, Los Angeles, USA.
Jenna M GiafaglioneMolecular Biology Interdepartmental Program, University of California, Los Angeles, USA.
Paul C BoutrosDepartments of Human Genetics & Urology, Jonsson Comprehensive Cancer Center and Institute for Precision Health, University of California, Los Angeles, USA.
Andrew S GoldsteinDepartments of Molecular, Cell and Developmental Biology & Urology, Broad Stem Cell Research Center and Jonsson Comprehensive Cancer Center, University of California, Los Angeles, USA. Electronic address: agoldstein@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
UCLA SPORE IN PROSTATE CANCERP50CA092131 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REITER, ROBERT E · 2002 to 2023
$42.6M
UCLA NIGMS T32 Program AssessmentT32GM007185 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TORRES, JORGE · 1985 to 2020
$21.7M
Development of Protein Biomarkers in Post-DRE Urine for use in Liquid Biopsy of Prostate CancerU01CA214194 · NCI · EASTERN VIRGINIA MEDICAL SCHOOL · PI BOUTROS, PAUL CHRISTOPHER, KISLINGER, THOMAS · 2016 to 2021
$2.5M
The Origins of Metabolic Reprogramming in Prostate CancerR01CA237191 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GOLDSTEIN, ANDREW S · 2019 to 2023
$2.0M
NCI NIH HHS P30 CA016042NCI NIH HHS P50 CA092131NCI NIH HHS R01 CA237191NCI NIH HHS U01 CA214194NIGMS NIH HHS T32 GM007185
6 · The paper itself

Abstract

Many organs experience a loss of tissue mass and a decline in regenerative capacity during aging. In contrast, the prostate continues to grow in volume. In fact, age is the most important risk factor for prostate cancer. However, the age-related factors that influence the composition, morphology and molecular features of prostate epithelial progenitor cells, the cells-of-origin for prostate cancer, are poorly understood. Here, we review the evidence that prostate luminal progenitor cells are expanded with age. We explore the age-related changes to the microenvironment that may influence prostate epithelial cells and risk of transformation. Finally, we raise a series of questions about models of aging and regulators of prostate aging which need to be addressed. A fundamental understanding of aging in the prostate will yield critical insights into mechanisms that promote the development of age-related prostatic disease.

Indexed as

AgingAnimalsEpithelial CellsHumansMaleProstatic NeoplasmsStem CellsTumor MicroenvironmentEpitheliumMicroenvironmentMutationsOldOrganoid

Identifiers

PMID34052326
PMCPMC8494000
OpenAlexW3163960128

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.