Evidence map›Paper›PMID 26290144›Full record

ArticleJournal of neuro-oncology2015

CCND2, CTNNB1, DDX3X, GLI2, SMARCA4, MYC, MYCN, PTCH1, TP53, and MLL2 gene variants and risk of childhood medulloblastoma.

Anna M Dahlin, Mads V Hollegaard, Carl Wibom, Ulrika Andersson, David M Hougaard, Isabelle Deltour, Ulf Hjalmars, Beatrice Melin

Open access · hybridAbstract read
In one paragraph

Article in Journal of neuro-oncology, 2015. 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
0.8field-weighted citation impact, top 28% 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, 24 citations in OpenAlex.

  1. Review
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  16. Polymorphisms inCancer management and research · 2018
    Article
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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

8 authors at 3 institutions in 3 countries.

Anna M DahlinDepartment of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden. anna.dahlin@umu.se.
Mads V HollegaardDepartment of Congenital Disorders, Danish Centre for Neonatal Screening, Statens Serum Institut, Copenhagen, Denmark.
Carl WibomDepartment of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
Ulrika AnderssonDepartment of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
David M HougaardDepartment of Congenital Disorders, Danish Centre for Neonatal Screening, Statens Serum Institut, Copenhagen, Denmark.
Isabelle DeltourSection of Environment and Radiation, International Agency for Research on Cancer, Lyon, France.
Ulf HjalmarsDepartment of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
Beatrice MelinDepartment of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
Umeå University · SEStatens Serum Institut · DKCentre International de Recherche sur le Cancer · FR

Funding

World Health Organization 001
6 · The paper itself

Abstract

Recent studies have described a number of genes that are frequently altered in medulloblastoma tumors and that have putative key roles in the development of the disease. We hypothesized that common germline genetic variations in these genes may be associated with medulloblastoma development. Based on recent publications, we selected 10 genes that were frequently altered in medulloblastoma: CCND2, CTNNB1, DDX3X, GLI2, SMARCA4, MYC, MYCN, PTCH1, TP53, and MLL2 (now renamed as KMT2D). Common genetic variants (single nucleotide polymorphisms) annotating these genes (n = 221) were genotyped in germline DNA (neonatal dried blood spot samples) from 243 childhood medulloblastoma cases and 247 control subjects from Sweden and Denmark. Eight genetic variants annotating three genes in the sonic hedgehog signaling pathway; CCND2, PTCH1, and GLI2, were found to be associated with the risk of medulloblastoma (P(combined) < 0.05). The findings were however not statistically significant following correction for multiple testing by the very stringent Bonferroni method. The results do not support our hypothesis that common germline genetic variants in the ten studied genes are associated with the risk of developing medulloblastoma.

Indexed as

AdolescentBrain NeoplasmsChildChild, PreschoolCyclin D2DenmarkFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHumansKruppel-Like Transcription FactorsMaleMedulloblastomaNuclear ProteinsPatched-1 ReceptorPatched ReceptorsCCND2 protein, humanCyclin D2GLI2 protein, humanKruppel-Like Transcription FactorsNuclear ProteinsPatched-1 ReceptorPatched ReceptorsPTCH1 protein, humanReceptors, Cell SurfaceZinc Finger Protein Gli2Genetic association studiesGenetic variationMedulloblastomaPNETPrimitive neuroectodermal tumors

Identifiers

PMID26290144
PMCPMC4592490
OpenAlexW2166341146

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.