Evidence map›Paper›PMID 22109108›Full record

ArticleActa neuropathologica2012

Supratentorial and spinal pediatric ependymomas display a hypermethylated phenotype which includes the loss of tumor suppressor genes involved in the control of cell growth and death.

Hazel A Rogers, John-Paul Kilday, Cerys Mayne, Jennifer Ward, Martyna Adamowicz-Brice, Ed C Schwalbe, Steven C Clifford, Beth Coyle, Richard G Grundy

Open access · hybridAbstract read
In one paragraph

Article in Acta neuropathologica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  6. Limitations of currentOncotarget · 2018
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  15. Supratentorial ependymoma: disease control, complications, and functional outcomes after irradiation.International journal of radiation oncology, biology, physics · 2013
    Article
  16. Emerging insights into the ependymoma epigenome.Brain pathology (Zurich, Switzerland) · 2013
    Review
  17. Article
  18. Article
  19. 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

9 authors at 3 institutions in 1 country.

Hazel A RogersChildren's Brain Tumour Research Centre, Queen's Medical Centre, University of Nottingham, UK.
John-Paul Kilday
Cerys Mayne
Jennifer Ward
Martyna Adamowicz-Brice
Ed C Schwalbe
Steven C Clifford
Beth Coyle
Richard G Grundy
University of Nottingham · GBBrain Tumour Research · GBNewcastle University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic alterations, including methylation, have been shown to be an important mechanism of gene silencing in cancer. Ependymoma has been well characterized at the DNA copy number and mRNA expression levels. However little is known about DNA methylation changes. To gain a more global view of the methylation profile of ependymoma we conducted an array-based analysis. Our data demonstrated tumors to segregate according to their location in the CNS, which was associated with a difference in the global level of methylation. Supratentorial and spinal tumors displayed significantly more hypermethylated genes than posterior fossa tumors, similar to the 'CpG island methylator phenotype' (CIMP) identified in glioma and colon carcinoma. This hypermethylated profile was associated with an increase in expression of genes encoding for proteins involved in methylating DNA, suggesting an underlying mechanism. An integrated analysis of methylation and mRNA expression array data allowed us to identify methylation-induced expression changes. Most notably genes involved in the control of cell growth and death and the immune system were identified, including members of the JNK pathway and PPARG. In conclusion, we have generated a global view of the methylation profile of ependymoma. The data suggests epigenetic silencing of tumor suppressor genes is an important mechanism in the pathogenesis of supratentorial and spinal, but not posterior fossa ependymomas. Hypermethylation correlated with a decrease in expression of a number of tumor suppressor genes and pathways that could be playing an important role in tumor pathogenesis.

Indexed as

ApoptosisCell ProliferationChildCluster AnalysisCohort StudiesDNA MethylationEpendymomaFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansMaleOligonucleotide Array Sequence AnalysisPhenotypeSignal Transduction

Identifiers

PMID22109108
PMCPMC3316934
OpenAlexW1970073132

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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.