Evidence map›Paper›PMID 41668119›Full record

ArticleActa neuropathologica communications2026

Relationship between genetically determined telomere length and childhood glioma risk.

Naying Zhou, Shaobo Li, Jon Foss-Skiftesvik, Anna M Dahlin, Jonas Bybjerg-Grauholm, Beatrice Melin, Adam J de Smith, Kyle M Walsh, Joseph L Wiemels

Abstract read
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In one paragraph

Article in Acta neuropathologica communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Naying ZhouDepartment of Population and Public Health Science, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Shaobo LiDepartment of Population and Public Health Science, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Jon Foss-SkiftesvikDepartment of Neurosurgery, Rigshospitalet Copenhagen University Hospital, Copenhagen, Denmark.
Anna M DahlinDepartment of Diagnostics and Intervention, Oncology, Umeå University, Umeå, Sweden.
Jonas Bybjerg-GrauholmDepartment of Congenital Disorders, Statens Serum Institute, Copenhagen, Denmark.
Beatrice MelinDepartment of Diagnostics and Intervention, Oncology, Umeå University, Umeå, Sweden.
Adam J de SmithDepartment of Population and Public Health Science, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Kyle M WalshDepartment of Neurosurgery and Duke Cancer Institute, Duke University School of Medicine, DUMC, Durham, NC, USA.
Joseph L WiemelsDepartment of Population and Public Health Science, Center for Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. wiemels@usc.edu.

Funding

Genetic Susceptibility to Pediatric Glioma inIndividuals and Diverse populationsR01CA194189 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI WALSH, KYLE M, WIEMELS, JOSEPH LEO · 2015 to 2020
$5.0M
NCI NIH HHS R01 CA194189NCI NIH HHS R01CA194189Tobacco-Related Disease Research Program T33IR6502
6 · The paper itself

Abstract

While longer genetically predicted leukocyte telomere length (LTL) has been linked to increased glioma risk in adults, this association has not been investigated in pediatric populations. In this study, we applied Mendelian randomization (MR) and polygenic risk score (PRS) analyses to investigate the relationship between LTL and pediatric glioma risk, using 4,069 cases and 8,778 controls from the largest available childhood glioma meta-GWAS. Results suggested longer genetically predicted LTL was significantly associated with increased childhood glioma risk, with OR per 1 standard deviation increase in LTL of 2.12 (95% CI 1.32–3.39, P = .002) in the multi-ancestry group and 2.16 (95% CI 1.16–4.03; P = .015) in the European group. Key SNPs contributing to risk of childhood glioma included rs59294613 (POT1), rs8105767 (ZNF208), and rs7705526 (TERT), which differed from the top variants previously identified in adult glioma using the same genetic instruments. Age-stratified MR revealed a stronger association in children diagnosed after the age of 6 (OR = 1.89; P < .001) vs. ≤ 6 years (OR = 1.04; P = .732; Phet = .006). PRS analysis further supported this age-stratified findings by demonstrating a positive association between LTL PRS and age at glioma diagnosis, particularly within age 0–10. This trend suggests a progressively greater influence of LTL on glioma risk in older children compared to younger children. In conclusion, this study provides the first genetic evidence linking longer genetically predicted LTL to increased pediatric glioma risk. While overall consistent with adult findings, distinct single-SNP associations, and age-dependent effects highlight unique biological mechanisms in children with glioma, warranting further direct investigation into telomere dynamics in early-life gliomagenesis.

Indexed as

Brain NeoplasmsGenetic Predisposition to DiseaseGliomaTelomereTelomere HomeostasisAdolescentChildChild, PreschoolFemaleGenetic Risk ScoreGenome-Wide Association StudyHumansInfantLeukocytesMaleMendelian Randomization AnalysisPOT1 protein, humanShelterin ComplexTelomere-Binding ProteinsAge–gene interactionChildhood cancerLeukocyte telomere lengthMendelian randomizationPediatric gliomaPolygenic risk score

Identifiers

PMID41668119
PMCPMC13085377

What Socratic holds

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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 Socratic graph.