Evidence map›Paper›PMID 24500421›Full record

SynthesisNeuro-oncology2014

Association between DNA repair gene polymorphisms and risk of glioma: a systematic review and meta-analysis.

Maral Adel Fahmideh, Judith Schwartzbaum, Paolo Frumento, Maria Feychting

Open access · bronzeAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Neuro-oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 11 pooled it
4.4field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 11 syntheses or guidelines pooled it, 59 citations in OpenAlex.

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  4. The potential role ofBioscience reports · 2018
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  15. Genetic variants inCancer innovation · 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

4 authors at 2 institutions in 2 countries.

Maral Adel FahmidehUnit of Epidemiology, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden (M.A.F., M.F.); Division of Epidemiology, College of Public Health, The Ohio State University, Columbus, Ohio (J.S.); Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden (P.F.).
Judith SchwartzbaumUnit of Epidemiology, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden (M.A.F., M.F.); Division of Epidemiology, College of Public Health, The Ohio State University, Columbus, Ohio (J.S.); Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden (P.F.).
Paolo FrumentoUnit of Epidemiology, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden (M.A.F., M.F.); Division of Epidemiology, College of Public Health, The Ohio State University, Columbus, Ohio (J.S.); Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden (P.F.).
Maria FeychtingUnit of Epidemiology, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden (M.A.F., M.F.); Division of Epidemiology, College of Public Health, The Ohio State University, Columbus, Ohio (J.S.); Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden (P.F.).
Karolinska Institutet · SEThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAssociation studies of germline DNA repair single nucleotide polymorphisms (SNPs) and glioma risk have yielded inconclusive results. We therefore performed a systematic review and meta-analysis of studies investigating this association.

methodsWe identified 27 eligible studies investigating 105 SNPs in 42 DNA repair genes. Of these, 10 SNPs in 7 genes were analyzed in at least 4 studies and were therefore included in our meta-analysis. The meta-analysis was performed for homozygote comparison, heterozygote comparison, and dominant and recessive models by applying a fixed- or random-effects model. The funnel and forest plots were created using RevMan software.

resultsWe found that SNPs rs3212986 (odds ratio [OR] = 1.35 (1.08-1.68), P = .008), rs13181 (OR = 1.18 (1.06-1.31), P = .002), and rs25487 (OR = 1.12 (1.03-1.22), P = .007) in DNA repair genes ERCC1, ERCC2 (XPD), and XRCC1 may increase the risk of glioma, while polymorphisms rs1136410 (OR = 0.78 (0.68-0.89), P = .0004) and rs12917 (OR = 0.84 (0.73-0.96), P = .01) in PARP1(ADPRT) and MGMT are associated with decreased susceptibility to glioma. No evidence of significant associations between ERCC2 rs1799793, OGG1 rs1052133, XRCC1 rs25489, XRCC1 rs1799782, or XRCC3 rs861539 and risk of glioma was observed.

conclusionThis study provides evidence that DNA repair genes ERCC1, ERCC2, and XRCC1 might be low-penetrance glioma-risk genes, while MGMT and PARP1 polymorphisms may confer protection against glioma.

Indexed as

DNA RepairPolymorphism, Single NucleotideBrain NeoplasmsGenetic Association StudiesGliomaHumansRisk Factorsbrain neoplasmDNA repairgliomameta-analysissingle nucleotide polymorphism

Identifiers

PMID24500421
PMCPMC4022225
OpenAlexW2109054687

What OpenQuestion holds

Textmetadata
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.