Evidence map›Paper›PMID 20570930›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2010

A distinct spectrum of copy number aberrations in pediatric high-grade gliomas.

Dorine A Bax, Alan Mackay, Suzanne E Little, Diana Carvalho, Marta Viana-Pereira, Narinder Tamber, Anita E Grigoriadis, Alan Ashworth, Rui M Reis, David W Ellison and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.

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  12. Cellular senescence in cancer: clinical detection and prognostic implications.Journal of experimental & clinical cancer research : CR · 2022
    Review
  13. Alternative RNA splicing defects in pediatric cancers: new insights in tumorigenesis and potential therapeutic vulnerabilities.Annals of oncology : official journal of the European Society for Medical Oncology · 2022
    Review
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30 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

13 authors at 5 institutions in 3 countries.

Dorine A BaxSection of Paediatric Oncology, The Institute of Cancer Research, Royal Marsden Hospital, Sutton, United Kingdom.
Alan Mackay
Suzanne E Little
Diana Carvalho
Marta Viana-Pereira
Narinder Tamber
Anita E Grigoriadis
Alan Ashworth
Rui M Reis
David W Ellison
Safa Al-Sarraj
Darren Hargrave
Chris Jones
University of Coimbra · PTUniversity of Minho · PTRoyal Marsden Hospital · GBInstitute of Cancer Research · GBSt. Jude Children's Research Hospital · US

Funding

Breast Cancer Now BREAST CANCER NOW RESEARCH CENTRECancer Research UK A6718
6 · The paper itself

Abstract

purposeAs genome-scale technologies begin to unravel the complexity of the equivalent tumors in adults, we can attempt detailed characterization of high-grade gliomas in children, that have until recently been lacking. Toward this end, we sought to validate and extend investigations of the differences between pediatric and adult tumors. EXPERIMENTAL

designWe carried out copy number profiling by array comparative genomic hybridization using a 32K bacterial artificial chromosome platform on 63 formalin-fixed paraffin-embedded cases of high-grade glioma arising in children and young people (<23 years).

resultsThe genomic profiles of these tumors could be subclassified into four categories: those with stable genomes, which were associated with a better prognosis; those with aneuploid and those with highly rearranged genomes; and those with an amplifier genotype, which had a significantly worse clinical outcome. Independent of this was a clear segregation of cases with 1q gain (more common in children) from those with concurrent 7 gain/10q loss (a defining feature of adults). Detailed mapping of all the amplification and deletion events revealed numerous low-frequency amplifications, including IGF1R, PDGFRB, PIK3CA, CDK6, CCND1, and CCNE1, and novel homozygous deletions encompassing unknown genes, including those at 5q35, 10q25, and 22q13. Despite this, aberrations targeting the "core signaling pathways" in adult glioblastomas are significantly underrepresented in the pediatric setting.

conclusionsThese data highlight that although there are overlaps in the genomic events driving gliomagenesis of all ages, the pediatric disease harbors a distinct spectrum of copy number aberrations compared with adults.

Indexed as

DNA Copy Number VariationsAdolescentAdultBrain NeoplasmsChildChild, PreschoolComparative Genomic HybridizationGene AmplificationGene DeletionGlioblastomaGliomaHumans

Identifiers

PMID20570930
PMCPMC2896553
OpenAlexW1999969244

What OpenQuestion holds

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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.