Evidence map›Paper›PMID 23190500›Full record

ArticleNeuro-oncology2013

Inhibition of EZH2 suppresses self-renewal and induces radiation sensitivity in atypical rhabdoid teratoid tumor cells.

Irina Alimova, Diane K Birks, Peter S Harris, Jeffrey A Knipstein, Sujatha Venkataraman, Victor E Marquez, Nicholas K Foreman, Rajeev Vibhakar

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Neuro-oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
4.3field-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

86 citing papers in PubMed, 137 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Bioavailability, Metabolism, and Excretion of [Clinical pharmacology in drug development · 2025
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

26 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

8 authors at 1 institution in 1 country.

Irina AlimovaDepartment of Pediatrics and Section of Pediatric Hematology/Oncology/BMT, Children’s Hospital Colorado, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado 80045, USA.
Diane K Birks
Peter S Harris
Jeffrey A Knipstein
Sujatha Venkataraman
Victor E Marquez
Nicholas K Foreman
Rajeev Vibhakar
Children's Hospital Colorado · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Brain Enriched MicroRNA 128a and 9/9+: Impact on medulloblastoma pathogenesisK08NS059790 · NINDS · UNIVERSITY OF IOWA · PI VIBHAKAR, RAJEEV · 2008 to 2013
$844k
NCI NIH HHS P30 CA046934NINDS NIH HHS K08 NS059790
6 · The paper itself

Abstract

introductionOverexpression of the Polycomb repressive complex 2 (PRC2) subunit Enhancer of Zeste 2 (EZH2) occurs in several malignancies, including prostate cancer, breast cancer, medulloblastoma, and glioblastoma multiforme. Recent evidence suggests that EZH2 may also have a role in rhabdoid tumors. Atypical teratoid/rhabdoid tumor (ATRT) is a rare, high-grade embryonal brain tumor that occurs most commonly in young children and carries a very poor prognosis. ATRTs are characterized by absence of the chromatin remodeling protein SMARCB1. Given the role of EZH2 in regulating epigenetic changes, we investigated the role of EZH2 in ATRT.

methodsMicroarray analysis was used to evaluate expression of EZH2 in ATRT tumor samples. We used shRNA and a chemical inhibitor of EZH2 to examine the impact of EZH2 inhibition on cell growth, proliferation, and tumor cell self-renewal.

resultsHere, we show that targeted disruption of EZH2 by RNAi or pharmacologic inhibition strongly impairs ATRT cell growth, suppresses tumor cell self-renewal, induces apoptosis, and potently sensitizes these cells to radiation. Using functional analysis of transcription factor activity, we found the cyclin D1-E2F axis to be repressed after EZH2 depletion in ATRT cells.

conclusionsOur observations provide evidence that EZH2 disruption alters cell cycle progression and may be an important new therapeutic target, particularly in combination with radiation, in ATRT.

Indexed as

Cell ProliferationCellular SenescenceRadiation ToleranceAdolescentApoptosisBiomarkers, TumorBlotting, WesternCell CycleCerebellumChildEnhancer of Zeste Homolog 2 ProteinGene Expression ProfilingHumansImmunoenzyme TechniquesOligonucleotide Array Sequence AnalysisPolycomb Repressive Complex 2Biomarkers, TumorEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanPolycomb Repressive Complex 2RNA, MessengerRNA, Small Interfering

Identifiers

PMID23190500
PMCPMC3548579
OpenAlexW2143302156

What OpenQuestion holds

Textmetadata
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.