Evidence map›Paper›PMID 21292688›Full record

ArticleNeuro-oncology2011

Chromosome 17 alterations identify good-risk and poor-risk tumors independently of clinical factors in medulloblastoma.

Martin G McCabe, L Magnus Bäcklund, Hui Sun Leong, Koichi Ichimura, V Peter Collins

Open access · hybridAbstract read
In one paragraph

Article in Neuro-oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. The Prognostic Value of Amplification of theDiseases (Basel, Switzerland) · 2025
    Article
  2. Article
  3. Survival-Related Genes on Chromosomes 6 and 17 in Medulloblastoma.International journal of molecular sciences · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Observational
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Noninvasive detection of glutamate predicts survival in pediatric medulloblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    Article
  14. Cytogenetic prognostication within medulloblastoma subgroups.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014
    Article
  15. Article
  16. Article
  17. Signaling pathway and molecular subgroups of medulloblastoma.International journal of clinical and experimental pathology · 2013
    Review
  18. 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

5 authors at 4 institutions in 2 countries.

Martin G McCabeManchester Academic Health Science Centre, School of Cancer and Enabling Sciences, University of Manchester, The Christie NHS Foundation Trust, Withington, Manchester M20 4BX, UK. martin.mccabe@manchester.ac.uk
L Magnus Bäcklund
Hui Sun Leong
Koichi Ichimura
V Peter Collins
Addenbrooke's Hospital · GBCancer Research UK Manchester Institute · GBKarolinska Institutet · SEUniversity of Cambridge · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current risk stratification schemas for medulloblastoma, based on combinations of clinical variables and histotype, fail to accurately identify particularly good- and poor-risk tumors. Attempts have been made to improve discriminatory power by combining clinical variables with cytogenetic data. We report here a pooled analysis of all previous reports of chromosomal copy number related to survival data in medulloblastoma. We collated data from previous reports that explicitly quoted survival data and chromosomal copy number in medulloblastoma. We analyzed the relative prognostic significance of currently used clinical risk stratifiers and the chromosomal aberrations previously reported to correlate with survival. In the pooled dataset metastatic disease, incomplete tumor resection and severe anaplasia were associated with poor outcome, while young age at presentation was not prognostically significant. Of the chromosomal variables studied, isolated 17p loss and gain of 1q correlated with poor survival. Gain of 17q without associated loss of 17p showed a trend to improved outcome. The most commonly reported alteration, isodicentric chromosome 17, was not prognostically significant. Sequential multivariate models identified isolated 17p loss, isolated 17q gain, and 1q gain as independent prognostic factors. In a historical dataset, we have identified isolated 17p loss as a marker of poor outcome and 17q gain as a novel putative marker of good prognosis. Biological markers of poor-risk and good-risk tumors will be critical in stratifying treatment in future trials. Our findings should be prospectively validated independently in future clinical studies.

Indexed as

Chromosome AberrationsAdolescentAdultCerebellar NeoplasmsChildChild, PreschoolChromosomes, Human, Pair 17HumansInfantInfant, NewbornIn Situ Hybridization, FluorescenceMedulloblastomaPrognosisRisk FactorsSurvival RateYoung Adult

Identifiers

PMID21292688
PMCPMC3064691
OpenAlexW2112460795

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.