Evidence map›Paper›PMID 21138945›Full record

ArticleNeuro-oncology2011

Homozygous loss of ADAM3A revealed by genome-wide analysis of pediatric high-grade glioma and diffuse intrinsic pontine gliomas.

Jennifer Barrow, Martyna Adamowicz-Brice, Maria Cartmill, Donald MacArthur, James Lowe, Keith Robson, Marie-Anne Brundler, David A Walker, Beth Coyle, Richard Grundy

Abstract 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 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

66 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  14. Glioblastoma spheroids produce infiltrative gliomas in the rat brainstem.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2017
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6 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

10 authors.

Jennifer BarrowChildren's Brain Tumour Research Centre, School of Clinical Sciences, Queen's Medical Centre, University of Nottingham, Nottingham NG7 2UH.
Martyna Adamowicz-Brice
Maria Cartmill
Donald MacArthur
James Lowe
Keith Robson
Marie-Anne Brundler
David A Walker
Beth Coyle
Richard Grundy

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overall, pediatric high-grade glioma (pHGG) has a poor prognosis, in part due to the lack of understanding of the underlying biology. High-resolution 244 K oligo array comparative genomic hybridization (CGH) was used to analyze DNA from 38 formalin-fixed paraffin-embedded predominantly pretreatment pHGG samples, including 13 diffuse intrinsic pontine gliomas (DIPGs). The patterns of gains and losses were distinct from those seen in HGG arising in adults. In particular, we found 1q gain in up to 27% of our cohort compared with 9% reported in adults. A total of 13% had a balanced genetic profile with no large-scale copy number alterations. Homozygous loss at 8p12 was seen in 6 of 38 (16%) cases of pHGG. This novel deletion, which includes the ADAM3A gene, was confirmed by quantitative real-time PCR (qPCR). Loss of CDKN2A/CDKN2B in 4 of 38 (10%) samples by oligo array CGH was confirmed by fluorescent in situ hybridization on tissue microarrays and was restricted to supratentorial tumors. Only ∼50% of supratentorial tumors were positive for CDKN2B expression by immunohistochemistry (IHC), while ∼75% of infratentorial tumors were positive for CDKN2B expression (P = 0.03). Amplification of the 4q11-13 region was detected in 8% of cases and included PDGFRA and KIT, and subsequent qPCR analysis was consistent with the amplification of PDGFRA. MYCN amplification was seen in 5% of samples being significantly associated with anaplastic astrocytomas (P= 0.03). Overall, DIPG shared similar spectrum of changes to supratentorial HGG with some notable differences, including high-frequency loss of 17p and 14q and lack of CDKN2A/CDKN2B deletion. Informative genetic data providing insight into the underlying biology and potential therapeutic possibilities can be generated from archival tissue and typically small biopsies from DIPG. Our findings highlight the importance of obtaining pretreatment samples.

Indexed as

Loss of HeterozygosityADAM ProteinsAdolescentAdultBiomarkers, TumorBrain Stem NeoplasmsChildChild, PreschoolChromosome DeletionChromosome MappingChromosomes, Human, Pair 14Chromosomes, Human, Pair 17Comparative Genomic HybridizationCyclin-Dependent Kinase Inhibitor p16DNA, NeoplasmFemaleADAM3A protein, humanADAM ProteinsBiomarkers, TumorCyclin-Dependent Kinase Inhibitor p16DNA, NeoplasmMYCN protein, humanN-Myc Proto-Oncogene ProteinNuclear ProteinsOncogene ProteinsReceptor, Platelet-Derived Growth Factor alpha

Identifiers

PMID21138945
PMCPMC3064619

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.