Evidence map›Paper›PMID 32978169›Full record

ReviewCancer research2020

EZH2-Targeted Therapies in Cancer: Hype or a Reality.

Marie-Lisa Eich, Mohammad Athar, James E Ferguson, Sooryanarayana Varambally

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed
11.8field-weighted citation impact, top 1% 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

150 citing papers in PubMed, 239 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Reprogramming resistance in advanced lung cancer: epigenetic modulation to restore therapeutic vulnerability.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  5. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Epigenetic regulation of EZH2 by ncRNAs: mechanisms and oncogenic implications.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

90 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Marie-Lisa Eich *Institute of Pathology, University Hospital Cologne, Cologne, Germany.ORCID 0000-0002-8601-4598
Mohammad AtharDepartment of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama.
James E Ferguson *Department of Urology, The University of Alabama at Birmingham, Birmingham, Alabama.
Sooryanarayana Varambally *Department of Pathology, The University of Alabama at Birmingham, Birmingham, Alabama. svarambally@uabmc.edu.
University of Alabama at Birmingham · USUniversity Hospital Cologne · DE

Funding

TRAINING AND CAREER DEVELOPMENTU54CA118948 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI UPENDER MANNE · 2005 to 2026
$26.6M
Chemoprevention of environmental UVB-induced skin cancer in immunosuppressed miceR01ES026219 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ATHAR, MOHAMMAD · 2016 to 2020
$1.7M
NCI NIH HHS U54 CA118948NIEHS NIH HHS R01 ES026219
6 · The paper itself

Abstract

Next-generation genomic sequencing has identified multiple novel molecular alterations in cancer. Since the identification of DNA methylation and histone modification, it has become evident that genes encoding epigenetic modifiers that locally and globally regulate gene expression play a crucial role in normal development and cancer progression. The histone methyltransferase enhancer of zeste homolog 2 (EZH2) is the enzymatic catalytic subunit of the polycomb-repressive complex 2 (PRC2) that can alter gene expression by trimethylating lysine 27 on histone 3 (H3K27). EZH2 is involved in global transcriptional repression, mainly targeting tumor-suppressor genes. EZH2 is commonly overexpressed in cancer and shows activating mutations in subtypes of lymphoma. Extensive studies have uncovered an important role for EZH2 in cancer progression and have suggested that it may be a useful therapeutic target. In addition, tumors harboring mutations in other epigenetic genes such as

Indexed as

AnimalsDisease ProgressionEnhancer of Zeste Homolog 2 ProteinGene Expression Regulation, NeoplasticHistonesHumansImmunotherapyMolecular Targeted TherapyNeoplasmsSynthetic Lethal MutationsTumor Suppressor ProteinsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistonesTumor Suppressor Proteins

Identifiers

PMID32978169
PMCPMC8323716
OpenAlexW3088976686

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.