Evidence map›Paper›PMID 27613841›Full record

ArticleOncotarget2016

Common genetic variations in cell cycle and DNA repair pathways associated with pediatric brain tumor susceptibility.

Maral Adel Fahmideh, Catharina Lavebratt, Joachim Schüz, Martin Röösli, Tore Tynes, Michael A Grotzer, Christoffer Johansen, Claudia E Kuehni, Birgitta Lannering, Michaela Prochazka and 2 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. The Glu69Asp Polymorphism ofInternational journal of general medicine · 2022
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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

12 authors at 8 institutions in 5 countries.

Maral Adel FahmidehUnit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Catharina LavebrattNeurogenetics Unit, Department of Molecular Medicine and Surgery, Karolinska Institutet, and Center for Molecular Medicine, Karolinska University Hospital, L8:00, SE-171 76 Stockholm, Sweden.
Joachim SchüzSection of Environment and Radiation, International Agency for Research on Cancer (IARC), 69372 Lyon, France.
Martin RöösliDepartment of Epidemiology and Public Health, Swiss Tropical and Public Health Institute, 4002 Basel, Switzerland.
Tore TynesThe Cancer Registry of Norway, NO-0379 Oslo, Norway.
Michael A GrotzerDepartment of Oncology, University Children's Hospital of Zurich, 8032 Zurich, Switzerland.
Christoffer JohansenUnit of Survivorship, The Danish Cancer Society Research Centre, DK-2100 Copenhagen, Denmark.
Claudia E KuehniSwiss Childhood Cancer Registry, Institute of Social and Preventive Medicine, University of Bern, 3012 Bern, Switzerland.
Birgitta LanneringChildrens Cancer Center, Queen Silvia Childrens Hospital, SE-416 85 Gothenburg, Sweden.
Michaela ProchazkaUnit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Lisbeth S SchmidtDepartment of Clinical Genetics, University Hospital Rigshospitalet, DK-2100 Copenhagen, Denmark.
Maria FeychtingUnit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Karolinska Institutet · SERigshospitalet · DKCentre International de Recherche sur le Cancer · FRDrottning Silvias barn- och ungdomssjukhus · SENational Institute of Occupational Health · NOSwiss Tropical and Public Health Institute · CHUniversity Children's Hospital Zurich · CHUniversity of Bern · CH

Funding

World Health Organization 001
6 · The paper itself

Abstract

Knowledge on the role of genetic polymorphisms in the etiology of pediatric brain tumors (PBTs) is limited. Therefore, we investigated the association between single nucleotide polymorphisms (SNPs), identified by candidate gene-association studies on adult brain tumors, and PBT risk.The study is based on the largest series of PBT cases to date. Saliva DNA from 245 cases and 489 controls, aged 7-19 years at diagnosis/reference date, was genotyped for 68 SNPs. Data were analyzed using unconditional logistic regression.The results showed EGFRrs730437 and EGFRrs11506105 may decrease susceptibility to PBTs, whereas ERCC1rs3212986 may increase risk of these tumors. Moreover, stratified analyses indicated CHAF1Ars243341, CHAF1Ars2992, and XRCC1rs25487 were associated with a decreased risk of astrocytoma subtype. Furthermore, an increased risk of non-astrocytoma subtype associated with EGFRrs9642393, EME1rs12450550, ATMrs170548, and GLTSCRrs1035938 as well as a decreased risk of this subtype associated with XRCC4rs7721416 and XRCC4rs2662242 were detected.This study indicates SNPs in EGFR, ERCC1, CHAF1A, XRCC1, EME1, ATM, GLTSCR1, and XRCC4 may be associated with the risk of PBTs. Therefore, cell cycle and DNA repair pathways variations associated with susceptibility to adult brain tumors also seem to be associated with PBT risk, suggesting pediatric and adult brain tumors might share similar etiological pathways.

Indexed as

DNA RepairGenetic Predisposition to DiseasePolymorphism, Single NucleotideAdolescentBrain NeoplasmsCase-Control StudiesCell Cycle ProteinsChildDenmarkFemaleGene FrequencyGenotypeHumansMaleNorwayRegression AnalysisCell Cycle Proteinsbrain neoplasmgenetic association studypediatric brain tumorssingle nucleotide polymorphismsusceptibility

Identifiers

PMID27613841
PMCPMC5325391
OpenAlexW2512797738

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.