Evidence map›Paper›PMID 32917647›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2020

Evidence that EZH2 Deregulation is an Actionable Therapeutic Target for Prevention of Prostate Cancer.

Deborah L Burkhart, Katherine L Morel, Kristine M Wadosky, David P Labbé, Phillip M Galbo, Zafardjan Dalimov, Bo Xu, Massimo Loda, Leigh Ellis

Open access · greenAbstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. 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

9 authors at 7 institutions in 2 countries.

Deborah L BurkhartDepartment of Oncologic Pathology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Katherine L MorelDepartment of Oncologic Pathology, Dana-Farber Cancer Institute, Boston, Massachusetts.ORCID 0000-0002-7968-4032
Kristine M WadoskyDepartment of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, New York.
David P LabbéDivision of Urology, Department of Surgery, McGill University and Research Institute of the McGill University Health Centre, Montréal, Québec, Canada.ORCID 0000-0001-8864-8765
Phillip M GalboDepartment of Cell Biology, Albert Einstein College of Medicine, New York, New York.ORCID 0000-0002-5391-598X
Zafardjan DalimovState University of New York at Buffalo, Buffalo, New York.
Bo XuDepartment of Pathology, Roswell Park Cancer Institute, Buffalo, New York.
Massimo LodaDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, New York.
Leigh EllisDepartment of Oncologic Pathology, Dana-Farber Cancer Institute, Boston, Massachusetts. Leigh_Ellis@dfci.harvard.edu.
Dana-Farber Cancer Institute · USRoswell Park Comprehensive Cancer Center · USAlbert Einstein College of Medicine · USBroad Institute · USCornell University · USMcGill University Health Centre · CAUniversity at Buffalo, State University of New York · US

Funding

YAP1 and RB1 cooperate to regulate lung cancer lineage plasticity and therapeutic resistanceU24CA274159 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI DAVID W. GOODRICH, Alan David Hutson · 2022 to 2026
$8.5M
Exploiting RB1 deficiency for the treatment of lethal neuroendocrine prostate cancerR01CA207757 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI ELLIS, LEIGH, GOODRICH, DAVID W. · 2016 to 2020
$2.8M
ATR Dependency as a Novel Therapeutic Target in Lethal RB Deficient ProstateCancerR01CA252468 · NCI · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI Leigh Ellis · 2020 to 2026
$1.5M
Novel Mouse Models to define Genetic Drivers of Aggressive Prostate CancerR21CA205627 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI ELLIS, LEIGH · 2016 to 2017
$395k
CIHR PJT-162246NCI NIH HHS R01 CA207757NCI NIH HHS R01 CA252468NCI NIH HHS R21 CA205627NCI NIH HHS U24 CA274159
6 · The paper itself

Abstract

Chemoprevention trials for prostate cancer by androgen receptor or androgen synthesis inhibition have proven ineffective. Recently, it has been demonstrated that the histone methlytransferase, EZH2 is deregulated in mouse and human high-grade prostatic intraepithelial neoplasia (HG-PIN). Using preclinical mouse and human models of prostate cancer, we demonstrate that genetic and chemical disruption of EZH2 expression and catalytic activity reversed the HG-PIN phenotype. Furthermore, inhibition of EZH2 function was associated with loss of cellular proliferation and induction of Tp53-dependent senescence. Together, these data provide provocative evidence for EZH2 as an actionable therapeutic target toward prevention of prostate cancer.

Indexed as

Cell ProliferationCellular SenescenceCRISPR-Cas SystemsAnimalsEnhancer of Zeste Homolog 2 ProteinHumansMaleMiceMice, Inbred C57BLMice, KnockoutProstatic Intraepithelial NeoplasiaProstatic NeoplasmsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, human

Identifiers

PMID32917647
PMCPMC7718322
OpenAlexW3086558880

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.