Evidence map›Paper›PMID 21046410›Full record

ArticleActa neuropathologica2010

MYB upregulation and genetic aberrations in a subset of pediatric low-grade gliomas.

Ruth G Tatevossian, Bo Tang, James Dalton, Tim Forshew, Andrew R Lawson, Jing Ma, Geoff Neale, Sheila A Shurtleff, Simon Bailey, Amar Gajjar and 3 more

Open access · greenAbstract read
In one paragraph

Article in Acta neuropathologica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 23% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Molecular Biomarker Testing for the Diagnosis of Diffuse Gliomas.Archives of pathology & laboratory medicine · 2022
    Guideline
  2. Review
  3. Article
  4. Clinical characteristics and detection of MYB-QKI fusions in patients with angiocentric glioma.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  5. Review
  6. Future perspective of targeted treatments in pediatric low-grade glioma (pLGG): the evolution of standard-of-care and challenges of a new era.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
    Review
  7. Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. MYB/MYBL1::QKI fusion-positive diffuse glioma.Journal of neuropathology and experimental neurology · 2023
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Pediatric low-grade glioma in the era of molecular diagnostics.Acta neuropathologica communications · 2020
    Review
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 3 institutions in 2 countries.

Ruth G TatevossianDepartment of Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Bo Tang
James Dalton
Tim Forshew
Andrew R Lawson
Jing Ma
Geoff Neale
Sheila A Shurtleff
Simon Bailey
Amar Gajjar
Suzanne J Baker
Denise Sheer
David W Ellison
St. Jude Children's Research Hospital · USQueen Mary University of London · GBRoyal Victoria Infirmary · GB

Funding

The DNA Damage Response and Tumorigenesis in the BrainP01CA096832 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI BAKER, SUZANNE J. · 2003 to 2025
$38.0M
Cancer Research UKNCI NIH HHS P01 CA096832
6 · The paper itself

Abstract

Recent studies of genetic abnormalities in pediatric low-grade gliomas (LGGs) have focused on activation of the ERK/MAPK pathway by KIAA1549-BRAF gene fusions in the majority of pilocytic astrocytomas (PAs) and by rare mutations in elements of the pathway across histopathologically diverse LGGs. This study reports that MYB, an oncogene not previously implicated in gliomagenesis, is activated in a diverse subset of pediatric LGGs. The study cohort comprised 57 pediatric LGGs and a comparative cohort of 59 pediatric high-grade gliomas (HGGs). The LGG cohort included 34 PAs and 23 diffuse gliomas; fibrillary astrocytomas (n = 14), oligodendroglial tumors (n = 7), and angiocentric gliomas (n = 2). MYB copy number abnormalities were disclosed using Affymetrix 6.0 SNP arrays and confirmed using interphase fluorescence in situ hybridization. Novel MYB amplifications that upregulate MYB RNA and protein expression were demonstrated in 2/14 diffuse astrocytomas. In addition, focal deletion of the terminal region of MYB was seen in 1 of 2 angiocentric gliomas (AGs). Increased expression of MYB was demonstrated by quantitative RT-PCR and immunohistochemistry. MYB upregulation at the protein level was demonstrated in a proportion of diffuse LGGs (60%), pilocytic astrocytomas (41%), and HGGs (19%), but abnormalities at the genomic level were only a feature of diffuse gliomas. Our data suggest that MYB may have a role in a subset of pediatric gliomas, through a variety of mechanisms in addition to MYB amplification and deletion.

Indexed as

Chromosome AberrationsAdolescentAge DistributionAge FactorsBrain NeoplasmsChildChild, PreschoolCohort StudiesFemaleGene AmplificationGene DeletionGenetic Predisposition to DiseaseGliomaHumansMaleMutationOncogene Proteins v-myb

Identifiers

PMID21046410
PMCPMC3066475
OpenAlexW2169225807

What OpenQuestion holds

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Registered trials

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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.