Evidence map›Paper›PMID 29432558›Full record

ArticleNeuro-oncology2018

Models of epigenetic age capture patterns of DNA methylation in glioma associated with molecular subtype, survival, and recurrence.

Peter Liao, Quinn T Ostrom, Lindsay Stetson, Jill S Barnholtz-Sloan

Abstract read
In one paragraph

Article in Neuro-oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
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

36 citing papers in PubMed.

  1. Trial
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  6. Review
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  10. Cancer biology & therapy · 2024
    Article
  11. Article
  12. Article
  13. Practical immunomodulatory landscape of glioblastoma multiforme (GBM) therapy.Journal of the Egyptian National Cancer Institute · 2024
    Review
  14. Article
  15. Review
  16. Identification ofBiomedicines · 2024
    Article
  17. Article
  18. Article
  19. Spatial heterogeneity in DNA methylation and chromosomal alterations in diffuse gliomas and meningiomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Article
  20. Article
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.

Peter LiaoCase Comprehensive Cancer Center, Case Western Reserve University School of Medicine.
Quinn T OstromCase Comprehensive Cancer Center, Case Western Reserve University School of Medicine.
Lindsay StetsonCase Comprehensive Cancer Center, Case Western Reserve University School of Medicine.
Jill S Barnholtz-SloanCase Comprehensive Cancer Center, Case Western Reserve University School of Medicine.

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MARK R CHANCE · 1987 to 2026
$142.3M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
Case Western Reserve University/Cleveland Clinic CTSA (TL1)TL1RR024991 · NCRR · CASE WESTERN RESERVE UNIVERSITY · PI DAVIS, PAMELA B · 2007 to 2011
$2.1M
NCI NIH HHS P30 CA043703NIGMS NIH HHS T32 GM007250
6 · The paper itself

Abstract

Background: Models of epigenetic aging (epigenetic clocks) have been implicated as potentially useful markers for cancer risk and prognosis. Using 2 previously published methods for modeling epigenetic age, Horvath's clock and epiTOC, we investigated epigenetic aging patterns related to World Health Organization grade and molecular subtype as well as associations of epigenetic aging with glioma survival and recurrence. Methods: Epigenetic ages were calculated using Horvath's clock and epiTOC on 516 lower-grade glioma and 141 glioblastoma cases along with 136 nontumor (normal) brain samples. Associations of tumor epigenetic age with patient chronological age at diagnosis were assessed with correlation and linear regression, and associations were validated in an independent cohort of 203 gliomas. Contribution of epigenetic age to survival prediction was assessed using Cox proportional hazards modeling. Sixty-three samples from 18 patients with primary-recurrent glioma pairs were also analyzed and epigenetic age difference and rate of epigenetic aging of primary-recurrent tumors were correlated to time to recurrence. Results: Epigenetic ages of gliomas were near-universally accelerated using both Horvath's clock and epiTOC compared with normal tissue. The 2 independent models of epigenetic aging were highly associated with each other and exhibited distinct aging patterns reflective of molecular subtype. EpiTOC was found to be a significant independent predictor of survival. Epigenetic aging of gliomas between primary and recurrent tumors was found to be highly variable and not significantly associated with time to recurrence. Conclusions: We demonstrate that epigenetic aging reflects coherent modifications of the epigenome and can potentially provide additional prognostic power for gliomas.

Indexed as

DNA MethylationEpigenesis, GeneticAdultAgedAge FactorsAgingBiomarkers, TumorBrainBrain NeoplasmsCase-Control StudiesFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticGliomaHumansMaleBiomarkers, Tumor

Identifiers

PMID29432558
PMCPMC6007761

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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.