Evidence map›Paper›PMID 26843108›Full record

SynthesisMolecular neurobiology2017

A Comprehensive Meta-analysis of Genetic Associations Between Key Polymorphic Loci in DNA Repair Genes and Glioma Risk.

Ling Qi, Hong-Quan Yu, Yu Zhang, Li-Juan Ding, Dong-Hai Zhao, Peng Lv, Wei-Yao Wang, Ye Xu

Abstract readMeta-Analysis
PubMed Publisher
In one paragraph

Synthesis in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 5 pooled it
1.6field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 5 syntheses or guidelines pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Article
  7. Review
  8. The Association ofJournal of Cancer · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
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

8 authors at 3 institutions in 1 country.

Ling QiDepartment of Pathology, Jilin Medical University, Jilin, 132013, China.
Hong-Quan YuDepartment of Neurosurgery, First Hospital of Jilin University, Changchun, 130021, China.
Yu ZhangDepartment of Neurosurgery, First Hospital of Jilin University, Changchun, 130021, China.
Li-Juan DingDepartment of Radiation Oncology, First Hospital of Jilin University, Changchun, 130021, China.
Dong-Hai ZhaoDepartment of Pathology, Jilin Medical University, Jilin, 132013, China.
Peng LvDepartment of Pathology, Jilin Medical University, Jilin, 132013, China.
Wei-Yao WangDepartment of Pathology, Jilin Medical University, Jilin, 132013, China.
Ye XuMedical Research Laboratory, Jilin Medical University, No.5 Jilin District, Jilin, 132013, China. xuye_mpc@outlook.com.
Jilin Medical University · CNFirst Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic variants found in DNA repair genes (ERCC1, rs3212986; ERCC2, rs13181; ERCC4, rs1800067; ERCC5, rs17655; XRCC1, rs1799782, rs25487, rs25489; XRCC3, rs861539) have been reported to have an ambivalent association with the development of glioma. In the present study, a meta-analysis was conducted to confirm the relationship, taking heterogeneity of population into consideration. We analyzed 21 articles of 6 genes along with 8 single nucleotide polymorphisms (SNPs) (24,078 cases and 30,926 healthy individuals), which assessed the relationship between nucleotide excision, base excision, double-strand break repair gene, and the development of glioma under five models. All statistical analysis was implemented by the software of R 3.2.1, and the relationships between key polymorphic loci in DNA repair genes and glioma were quantified by the pooled odds ratio (OR) and 95 % confidential intervals. Overall, the synthesized evidence demonstrated that the SNP of rs13181 and rs1799782 significantly increased the risk of glioma whereas SNP of rs1800067 were significantly associated with a decrease in the risk of glioma. Additionally, subgroup analyses of 8 SNPs by ethnicity indicated that the mutation of rs13181, rs1800067 were apparently protective factors of glioma among Asians, while the mutation of rs13181 was a risk factors of glioma in Caucasians. Furthermore, the mutation of rs1799782 significantly raises the risk of glioma for Asian. Our study suggested that rs13181*C and rs1799782*A are risk alleles for glioma; rs1800067*A are beneficial alleles for decreased susceptibility to glioma. Future studies with large sample size and other races are strongly recommended to confirm the results from this study.

Indexed as

Brain NeoplasmsDNA RepairGenetic Association StudiesGenetic LociGenetic Predisposition to DiseaseGenetic VariationGliomaHumansPolymorphism, Single NucleotideDNA repair genesERCCGenetic polymorphismsGliomaMeta-analysisXRCC

Identifiers

PMID26843108
OpenAlexW2268986409

What OpenQuestion holds

Textmetadata
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.