Evidence map›Paper›PMID 27081636›Full record

ArticleWorld journal of clinical oncology2016

Targeting Enhancer of Zeste Homolog 2 as a promising strategy for cancer treatment.

Irene Marchesi, Luigi Bagella

Open access · hybridAbstract read
In one paragraph

Article in World journal of clinical oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  9. Updates in Management of Malignant Pleural Mesothelioma.Current treatment options in oncology · 2023
    Review
  10. Review
  11. Emerging Roles of LncRNAs in the EZH2-regulated Oncogenic Network.International journal of biological sciences · 2021
    Review
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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

2 authors at 2 institutions in 2 countries.

Irene MarchesiIrene Marchesi, Luigi Bagella, Department of Biomedical Sciences, Division of Biochemistry, University of Sassari, 07100 Sassari, Italy.
Luigi BagellaIrene Marchesi, Luigi Bagella, Department of Biomedical Sciences, Division of Biochemistry, University of Sassari, 07100 Sassari, Italy.
Temple University · USUniversity of Sassari · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycomb group proteins represent a global silencing system involved in development regulation. In specific, they regulate the transition from proliferation to differentiation, contributing to stem-cell maintenance and inhibiting an inappropriate activation of differentiation programs. Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb repressive complex 2, which induces transcriptional inhibition through the tri-methylation of histone H3, an epigenetic change associated with gene silencing. EZH2 expression is high in precursor cells while its level decreases in differentiated cells. EZH2 is upregulated in various cancers with high levels associated with metastatic cancer and poor prognosis. Indeed, aberrant expression of EZH2 causes the inhibition of several tumor suppressors and differentiation genes, resulting in an uncontrolled proliferation and tumor formation. This editorial explores the role of Polycomb repressive complex 2 in cancer, focusing in particular on EZH2. The canonical function of EZH2 in gene silencing, the non-canonical activities as the methylation of other proteins and the role in gene transcriptional activation, were summarized. Moreover, mutations of EZH2, responsible for an increased methyltransferase activity in cancer, were recapitulated. Finally, various drugs able to inhibit EZH2 with different mechanism were described, specifically underscoring the effects in several cancers, in order to clarify the role of EZH2 and understand if EZH2 blockade could be a new strategy for developing specific therapies or a way to increase sensitivity of cancer cells to standard therapies.

Indexed as

Anticancer drugsCancer therapyEnhancer of Zeste Homolog 2Enhancer of Zeste Homolog 2 inhibitorsEpigeneticsHistone methyltransferasePolycomb group proteins

Identifiers

PMID27081636
PMCPMC4826959
OpenAlexW2329196618

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.