Evidence map›Paper›PMID 30462709›Full record

ArticlePloS one2018

Association analysis of RTEL1 variants with risk of adult gliomas in a Korean population.

Suhg Namgoong, Hyun Sub Cheong, Jeong-Hyun Kim, Lyoung Hyo Kim, Jung Yeon Seo, Seok-Gu Kang, Seon-Jin Yoon, Se Hoon Kim, Jong Hee Chang, Hyoung Doo Shin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 33% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

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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

10 authors at 4 institutions in 1 country.

Suhg NamgoongDepartment of Life Science, Sogang University, Seoul, Republic of Korea.
Hyun Sub CheongDepartment of Genetic Epidemiology, SNP Genetics Inc., Seoul, Republic of Korea.
Jeong-Hyun KimAsan Institute for Life Sciences, University of Ulsan Collage of Medicine, Seoul, Republic of Korea.
Lyoung Hyo KimDepartment of Genetic Epidemiology, SNP Genetics Inc., Seoul, Republic of Korea.
Jung Yeon SeoDepartment of Life Science, Sogang University, Seoul, Republic of Korea.
Seok-Gu KangDepartment of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea.
Seon-Jin YoonDepartment of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea.
Se Hoon KimDepartment of Pathology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Jong Hee ChangDepartment of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea.
Hyoung Doo ShinDepartment of Life Science, Sogang University, Seoul, Republic of Korea.ORCID 0000-0003-1732-7838
Yonsei University · KRSogang University · KRSNP Genetics (South Korea) · KRUniversity of Ulsan · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have identified multiple loci for inherited susceptibility to glioma development, including the regulator of telomere elongation helicase 1 (RTEL1). However, the association between RTEL1 variants and risk of glioma has not been well understood. Therefore, we sought to comprehensively examine the genetic interaction between RTEL1 variants and risk of glioma with respect to defined histological and molecular subtypes. We employed a case-control study involving 250 adult glioma patients with previous molecular alterations and 375 population-based controls within Korean populations. Statistical analyses on the association between RTEL1 single nucleotide polymorphisms (SNPs) and glioma risk were conducted using unconditional logistic regression. Additional conditional and stepwise analyses were performed on significant RTEL1 SNPs. We detected significant associations (Bonferroni P < .05) between six SNPs (rs6089953, rs3848669, rs6010620, rs3787089, rs6062302, and rs115303435) and risk of glioma in the Korean subjects. The two coding variants, rs6062302 (D664D) and rs115303435 (A1059T), were plausibly causal variants and were independent among the significantly associated RTEL1 variants. The glioma subgroup analyses showed that the causal variants (rs6062302 and rs115303435) may be associated with increased risk of glioma regardless of histological grades and molecular alterations. This study provides a deeper understanding of relationships between RTEL1 variants and risk of glioma. Further studies are required to ascertain the impact of those variants on glioma susceptibility.

Indexed as

Polymorphism, Single NucleotideAdultAgedAstrocytomaBrain NeoplasmsCase-Control StudiesDNA HelicasesFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHumansLogistic ModelsMaleMiddle AgedMutation, MissenseOligodendrogliomaDNA HelicasesRTEL1 protein, human

Identifiers

PMID30462709
PMCPMC6248978
OpenAlexW2900923368

What OpenQuestion holds

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LicenceCC BY
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.