Evidence map›Paper›PMID 23280628›Full record

ArticleGenetic epidemiology2013

Analysis of 60 reported glioma risk SNPs replicates published GWAS findings but fails to replicate associations from published candidate-gene studies.

Kyle M Walsh, Erik Anderson, Helen M Hansen, Paul A Decker, Matt L Kosel, Thomas Kollmeyer, Terri Rice, Shichun Zheng, Yuanyuan Xiao, Jeffrey S Chang and 11 more

Abstract read
In one paragraph

Article in Genetic epidemiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 4 pooled it
2.0field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 4 syntheses or guidelines pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Polymorphisms in IL-4/IL-13 pathway genes and glioma risk: an updated meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Pooled it
  4. Pooled it
  5. Article
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  8. Review
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  11. Genome-Wide Association Studies in Glioma.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
    Review
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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

21 authors at 4 institutions in 1 country.

Kyle M WalshDepartment of Neurological Surgery, University of California, San Francisco, San Francisco, CA 94143, USA. Kyle.Walsh@ucsf.edu
Erik Anderson
Helen M Hansen
Paul A Decker
Matt L Kosel
Thomas Kollmeyer
Terri Rice
Shichun Zheng
Yuanyuan Xiao
Jeffrey S Chang
Lucie S McCoy
Paige M Bracci
Joe L Wiemels
Alexander R Pico
Ivan Smirnov
Daniel H Lachance
Hugues Sicotte
Jeanette E Eckel-Passow
John K Wiencke
Robert B Jenkins
Margaret R Wrensch
University of California, San Francisco · USMayo Clinic · USNeurological Surgery · USGladstone Institutes · US

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
Tissue CoreP50CA097257 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joseph F Costello · 2002 to 2026
$57.4M
Targeted MV-CEA as a Potent Antitumor Agent against GBMP50CA108961 · NCI · MAYO CLINIC ROCHESTER · PI O'NEILL, BRIAN PATRICK · 2004 to 2015
$22.5M
CALIFORNIA'S PARTICIPATION IN THE NATIONAL CANCER PREVENTION AND CONTRO PROGRAMU58DP000807 · DP · PUBLIC HEALTH INSTITUTE · PI SNIPES, KURT P · 2007 to 2011
$22.5M
GENETIC EPIDEMIOLOGY OF MALIGNANT GLIOMAR01CA052689 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WIENCKE, JOHN K., WRENSCH, MARGARET R. · 1991 to 2015
$20.5M
Training in Molecular& Genetic Epidemiology of CancerR25CA112355 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WITTE, JOHN S. · 2005 to 2018
$6.5M
Identification of 9p and 20q Germline Alterations in Glioblastoma PathogenesisRC1NS068222 · NINDS · MAYO CLINIC ROCHESTER · PI JENKINS, ROBERT B. · 2009 to 2010
$984k
NCCDPHP CDC HHS 1U58 DP000807-01NCCDPHP CDC HHS U58 DP000807NCI NIH HHS HHSN261201000034CNCI NIH HHS HHSN261201000035CNCI NIH HHS HHSN261201000035INCI NIH HHS HHSN261201000036CNCI NIH HHS P30 CA015083NCI NIH HHS P30 CA15083NCI NIH HHS P50 CA097257NCI NIH HHS P50CA097257NCI NIH HHS P50 CA108961NCI NIH HHS P50CA108961NCI NIH HHS R01 CA052689NCI NIH HHS R01CA52689NCI NIH HHS R25 CA112355NCI NIH HHS R25CA112355NINDS NIH HHS RC1 NS068222NINDS NIH HHS RC1NS068222Z
6 · The paper itself

Abstract

Genomewide association studies (GWAS) and candidate-gene studies have implicated single-nucleotide polymorphisms (SNPs) in at least 45 different genes as putative glioma risk factors. Attempts to validate these associations have yielded variable results and few genetic risk factors have been consistently replicated. We conducted a case-control study of Caucasian glioma cases and controls from the University of California San Francisco (810 cases, 512 controls) and the Mayo Clinic (852 cases, 789 controls) in an attempt to replicate previously reported genetic risk factors for glioma. Sixty SNPs selected from the literature (eight from GWAS and 52 from candidate-gene studies) were successfully genotyped on an Illumina custom genotyping panel. Eight SNPs in/near seven different genes (TERT, EGFR, CCDC26, CDKN2A, PHLDB1, RTEL1, TP53) were significantly associated with glioma risk in the combined dataset (P < 0.05), with all associations in the same direction as in previous reports. Several SNP associations showed considerable differences across histologic subtype. All eight successfully replicated associations were first identified by GWAS, although none of the putative risk SNPs from candidate-gene studies was associated in the full case-control sample (all P values > 0.05). Although several confirmed associations are located near genes long known to be involved in gliomagenesis (e.g., EGFR, CDKN2A, TP53), these associations were first discovered by the GWAS approach and are in noncoding regions. These results highlight that the deficiencies of the candidate-gene approach lay in selecting both appropriate genes and relevant SNPs within these genes.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyPolymorphism, Single NucleotideAgedCaliforniaCase-Control StudiesCentral Nervous System NeoplasmsDNA HelicasesErbB ReceptorsFemaleGenes, p16Genes, p53GliomaHumansIntracellular Signaling Peptides and ProteinsMaleDNA HelicasesEGFR protein, humanErbB ReceptorsIntracellular Signaling Peptides and Proteinslong noncoding RNA CCDC26, humanNerve Tissue ProteinsPHLDB1 protein, humanRNA, Long NoncodingRTEL1 protein, humanTelomeraseTERT protein, human

Identifiers

PMID23280628
PMCPMC3670948
OpenAlexW2120594153

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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.