Evidence map›Paper›PMID 35571988›Full record

ArticleNeuro-oncology advances

Mitochondrial 1555 G>A variant as a potential risk factor for childhood glioblastoma.

Shaobo Li, Xiaowu Gai, Swe Swe Myint, Katti Arroyo, Libby Morimoto, Catherine Metayer, Adam J de Smith, Kyle M Walsh, Joseph L Wiemels

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuro-oncology advances. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 54% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

9 authors at 4 institutions in 1 country.

Shaobo LiCenter for Genetic Epidemiology, Department of Population and Public Health Sciences, University of Southern California, Los Angeles, California, USA.ORCID https://orcid.org/0000-0002-0544-5338
Xiaowu GaiCenter for Personalized Medicine, Children's Hospital of Los Angeles, Los Angeles, California, USA.
Swe Swe MyintCenter for Genetic Epidemiology, Department of Population and Public Health Sciences, University of Southern California, Los Angeles, California, USA.
Katti ArroyoCenter for Genetic Epidemiology, Department of Population and Public Health Sciences, University of Southern California, Los Angeles, California, USA.
Libby MorimotoSchool of Public Health, University of California Berkeley, Berkeley, California, USA.ORCID https://orcid.org/0000-0002-1509-739X
Catherine MetayerSchool of Public Health, University of California Berkeley, Berkeley, California, USA.
Adam J de SmithCenter for Genetic Epidemiology, Department of Population and Public Health Sciences, University of Southern California, Los Angeles, California, USA.
Kyle M WalshDivision of Neuro-epidemiology, Department of Neurosurgery, Duke University, Durham, North Carolina, USA.
Joseph L WiemelsCenter for Genetic Epidemiology, Department of Population and Public Health Sciences, University of Southern California, Los Angeles, California, USA.
University of Southern California · USBerkeley Public Health Division · USChildren's Hospital of Los Angeles · USDuke University · US

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
NCCDPHP CDC HHS U58 DP003862NCI NIH HHS HHSN261201000034CNCI NIH HHS HHSN261201000035CNCI NIH HHS HHSN261201000035INCI NIH HHS HHSN261201000140CNCI NIH HHS R01 CA194189
6 · The paper itself

Abstract

Background: Childhood glioblastoma multiforme (GBM) is a highly aggressive disease with low survival, and its etiology, especially concerning germline genetic risk, is poorly understood. Mitochondria play a key role in putative tumorigenic processes relating to cellular oxidative metabolism, and mitochondrial DNA variants were not previously assessed for association with pediatric brain tumor risk. Methods: We conducted an analysis of 675 mitochondrial DNA variants in 90 childhood GBM cases and 2789 controls to identify enrichment of mitochondrial variant associated with GBM risk. We also performed this analysis for other glioma subtypes including pilocytic astrocytoma. Nuclear-encoded mitochondrial gene variants were also analyzed. Results: We identified m1555 A>G was significantly associated with GBM risk (adjusted OR 29.30, 95% CI 5.25-163.4, Conclusion: We report for the first time a potential role played by a functional mitochondrial ribosomal RNA variant in childhood GBM risk, and a potential role for both mitochondrial and nuclear-mitochondrial DNA polymorphisms in GBM tumorigenesis. These data implicate cellular oxidative metabolic capacity as a contributor to the etiology of pediatric glioblastoma.

Indexed as

mitochondrial genomepediatric glioblastomarisk factorvariant

Identifiers

PMID35571988
PMCPMC9092641
OpenAlexW4223910383

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.