Evidence map›Paper›PMID 34477880›Full record

ArticleNeuro-oncology2022

Relationship between genetically determined telomere length and glioma risk.

Charlie N Saunders, Ben Kinnersley, Richard Culliford, Alex J Cornish, Philip J Law, Richard S Houlston

Open access · hybridAbstract read
In one paragraph

Article in Neuro-oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  16. GermlineGenes · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Charlie N SaundersDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.ORCID 0000-0001-7221-1358
Ben KinnersleyDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.ORCID 0000-0003-1783-6296
Richard CullifordDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
Alex J CornishDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
Philip J LawDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
Richard S HoulstonDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
Institute of Cancer Research · GB

Funding

Cancer Research UK C1298/A8362
6 · The paper itself

Abstract

backgroundTelomere maintenance is increasingly recognized as being fundamental to glioma oncogenesis with longer leukocyte telomere length (LTL) reported to increase risk of glioma. To gain further insight into the relationship between telomere genetics and risk of glioma, we conducted several complementary analyses, using genome-wide association studies data on LTL (78 592 individuals) and glioma (12 488 cases and 18 169 controls).

methodsWe performed both classical and summary Mendelian randomization (SMR), coupled with heterogeneity in dependent instruments tests, at genome-wide significant LTL loci to examine if an association was mediated by the same causal variant in glioma. To prioritize genes underscoring glioma-LTL associations, we analyzed gene expression and DNA methylation data.

resultsGenetically increased LTL was significantly associated with increased glioma risk, random-effects inverse variance weighted ORs per 1 SD unit increase in the putative risk factor (odds ratio [OR]SD) 4.79 (95% confidence interval: 2.11-10.85; P = 1.76 × 10-4). SMR confirmed the previously reported LTL associations at 3q26.2 (TERC; PSMR = 1.33 × 10-5), 5p15.33 (TERT; PSMR = 9.80 × 10-27), 10q24.33 (STN1 alias OBFC1; PSMR = 4.31 × 10-5), and 20q13.3 (STMN3/RTEL1; PSMR = 2.47 × 10-4) glioma risk loci. Our analysis implicates variation at 1q42.12 (PSMR = 1.55 × 10-2), 6p21.3 (PSMR = 9.76 × 10-3), 6p22.2 (PSMR = 5.45 × 10-3), 7q31.33 (PSMR = 6.52 × 10-3), and 11q22.3 (PSMR = 8.89 × 10-4) as risk factors for glioma risk. While complicated by patterns of linkage disequilibrium, genetic variation involving PARP1, PRRC2A, CARMIL1, POT1, and ATM-NPAT1 was implicated in the etiology of glioma.

conclusionsThese observations extend the role of telomere-related genes in the development of glioma.

Indexed as

Genome-Wide Association StudyGliomaHumansLeukocytesPolymorphism, Single NucleotideRisk FactorsTelomereTelomere HomeostasisgliomaMendelian randomizationrisk factorstelomere length

Identifiers

PMID34477880
PMCPMC8804896
OpenAlexW3197161339

What OpenQuestion holds

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LicenceCC BY-NC
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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.