Evidence map›Paper›PMID 26580594›Full record

ReviewInternational journal of molecular sciences2015

EZH2 in Bladder Cancer, a Promising Therapeutic Target.

Mónica Martínez-Fernández, Carolina Rubio, Cristina Segovia, Fernando F López-Calderón, Marta Dueñas, Jesús M Paramio

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. HMGA1 induces EZH2 overexpression in human B-cell lymphomas.American journal of cancer research · 2021
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Emerging biomarkers in urothelial carcinoma: Challenges and opportunities.Cancer treatment and research communications · 2020
    Article
  18. Article
  19. Article
  20. Article
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

6 authors at 1 institution in 1 country.

Mónica Martínez-FernándezMolecular Oncology Unit, CIEMAT (Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas), Avenida Complutense nº40. 28040 Madrid, Spain. monica.martinez@ciemat.es.
Carolina RubioMolecular Oncology Unit, CIEMAT (Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas), Avenida Complutense nº40. 28040 Madrid, Spain. carolina.rubio@externos.ciemat.es.
Cristina SegoviaMolecular Oncology Unit, CIEMAT (Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas), Avenida Complutense nº40. 28040 Madrid, Spain. Cristina.Segovia@ciemat.es.
Fernando F López-CalderónMolecular Oncology Unit, CIEMAT (Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas), Avenida Complutense nº40. 28040 Madrid, Spain. FernandoFeliciano.Lopez@externos.ciemat.es.
Marta DueñasMolecular Oncology Unit, CIEMAT (Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas), Avenida Complutense nº40. 28040 Madrid, Spain. marta.duenas@ciemat.es.
Jesús M ParamioMolecular Oncology Unit, CIEMAT (Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas), Avenida Complutense nº40. 28040 Madrid, Spain. jesusm.paramio@ciemat.es.
Research Institute Hospital 12 de Octubre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bladder Cancer (BC) represents a current clinical and social challenge. The recent studies aimed to describe the genomic landscape of BC have underscored the relevance of epigenetic alterations in the pathogenesis of these tumors. Among the epigenetic alterations, histone modifications occupied a central role not only in cancer, but also in normal organism homeostasis and development. EZH2 (Enhancer of Zeste Homolog 2) belongs to the Polycomb repressive complex 2 as its catalytic subunit, which through the trimethylation of H3 (Histone 3) on K27 (Lysine 27), produces gene silencing. EZH2 is frequently overexpressed in multiple tumor types, including BC, and plays multiple roles besides the well-recognized histone mark generation. In this review, we summarize the present knowledge on the oncogenic roles of EZH2 and its potential use as a therapeutic target, with special emphasis on BC pathogenesis and management.

Indexed as

AnimalsAntineoplastic AgentsDNA MethylationEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticGene Expression Regulation, NeoplasticGene SilencingHistonesHumansMicroRNAsMolecular Targeted TherapyPolycomb Repressive Complex 2Protein BindingRNA, Long NoncodingUrinary Bladder NeoplasmsAntineoplastic AgentsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistonesMicroRNAsPolycomb Repressive Complex 2RNA, Long Noncodingbladder cancerEZH2lncRNAmiRNAPolycomb

Identifiers

PMID26580594
PMCPMC4661858
OpenAlexW2116090152

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.