Evidence map›Paper›PMID 26206478›Full record

ArticleBrain pathology (Zurich, Switzerland)2016

Molecular Analysis of Pediatric Oligodendrogliomas Highlights Genetic Differences with Adult Counterparts and Other Pediatric Gliomas.

David Nauen, Lisa Haley, Ming-Tseh Lin, Arie Perry, Caterina Giannini, Peter C Burger, Fausto J Rodriguez

Abstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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  4. Analysis of the PJournal of molecular neuroscience : MN · 2021
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  5. Rare occurrence of IDH2 mutation in adolescent oligodendroglioma with 1p/19q co-deletion: a case report.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2020
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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

7 authors at 4 institutions in 1 country.

David NauenDepartment of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Lisa HaleyDepartment of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Ming-Tseh LinDepartment of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Arie PerryDepartment of Pathology, Division of Neuropathology, University of California San Francisco School of Medicine, San Francisco, CA.
Caterina GianniniLaboratory of Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, MN.
Peter C BurgerDepartment of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Fausto J RodriguezDepartment of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, MD.
Johns Hopkins University · USJohns Hopkins Medicine · USMayo Clinic · USUniversity of California, San Francisco · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
NCI NIH HHS P30 CA006973
6 · The paper itself

Abstract

Oligodendroglioma represents a distinctive neoplasm in adults but similar neoplasms occur rarely in children. We studied 20 cases of pediatric oligodendroglioma by SNP array (median age 9 years, range 1-19; 15 grade II and 5 grade III). Cytogenetic abnormalities were present in 8 (53%) grade II and all five anaplastic oligodendrogliomas. Most changes were in the form of deletion and copy neutral loss of heterozygosity (LOH). The most common abnormality was 1p deletion (n = 5). Whole arm 1p19q co-deletion was present in three cases from adolescent patients and 9p loss in 3, including one low-grade oligodendroglioma with CDKN2A homozygous deletion. Common losses were largely limited to the anaplastic subset (n = 5) and included 3q29 (n = 3), 11p (n = 3), 17q (n = 3), 4q (n = 2), 6p (n = 2), 13q (n = 2), 14q (n = 2), 17p (n = 2) and whole Ch 18 loss (n = 2). Gains were non-recurrent except for whole Ch 7 (n = 2) and gain on 12q (n = 2) including the MDM2 locus. Possible germ line LOH (or uniparental disomy) was present in seven cases (35%), with one focal abnormality (22q13.1-13.2) in two. BRAF-KIAA1549 fusions and BRAF p.V600E mutations were absent (n = 13 and 8). In summary, cytogenetic alterations in pediatric oligodendrogliomas are characterized mostly by genomic losses, particularly in anaplastic tumors.

Indexed as

AdolescentBrainBrain NeoplasmsChildChild, PreschoolDNA Mutational AnalysisFemaleHumansImmunohistochemistryInfantIn Situ Hybridization, FluorescenceLoss of HeterozygosityMaleNeoplasm GradingOligodendrogliomaPolymorphism, Single NucleotideBRAF protein, humanProto-Oncogene Proteins B-rafBRAFcytogeneticsFISHoligodendrogliomapediatric gliomaSNP array

Identifiers

PMID26206478
PMCPMC4724334
OpenAlexW1585437692

What OpenQuestion holds

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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.