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http://purl.uniprot.org/citations/28320150http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28320150http://www.w3.org/2000/01/rdf-schema#comment"

Background

VTI1A and ETFA were identified recently as susceptibility genes for non-glioblastoma (GBM) of glioma risk in European populations, but the genetic etiology and pathogenesis of glioma have not been fully elucidated. Here, we aimed to investigate whether common genetic variants in VTI1A and ETFA predispose Han Chinese individuals to glioma.

Methods

The association of thirteen common tagging single nucleotide polymorphisms (SNPs) in VTI1A and ETFA genes with glioma were assessed in a hospital-based case-control study including 473 non-GBM of glioma patients and 1046 cancer-free controls.

Results

Two SNPs (rs11196067 in VTI1A and rs1801591 in ETFA) were found to be significantly associated with non-GBM of glioma risk (rs11196067, adjusted P=0.00018, adjusted odds ratio (OR)=1.37, 95% confidence interval (CI)=1.16-1.61; rs1801591, adjusted P=0.000022, adjusted OR=1.72, 95% CI=1.34-2.20). In further stratified analysis, they were both more pronounced in the adult subgroup. In haplotype-based analysis, two haplotypes were identified to be significant association with glioma. The haplotype "TGA" (P=0.002) in VTI1A and the haplotype "ACA" (P<0.001) in ETFA had a 1.5-fold and 3-fold increased glioma risk respectively, compared with corresponding non-carriers.

Conclusions

In summary, our results indicate that genetic variants in VTI1A and ETFA may modify individual susceptibility to non-GBM of glioma in the Han Chinese population and support the role of the VTI1A and ETFA genes in the occurrence of glioma."xsd:string
http://purl.uniprot.org/citations/28320150http://purl.org/dc/terms/identifier"doi:10.1016/j.jns.2017.02.013"xsd:string
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/author"Deng Z."xsd:string
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/author"Li R."xsd:string
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/author"Wang M."xsd:string
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/author"Xu G."xsd:string
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/author"Wang N."xsd:string
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/author"Bao G."xsd:string
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/name"J Neurol Sci"xsd:string
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/pages"282-288"xsd:string
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/title"Additional evidence supports association of common genetic variants in VTI1A and ETFA with increased risk of glioma susceptibility."xsd:string
http://purl.uniprot.org/citations/28320150http://purl.uniprot.org/core/volume"375"xsd:string
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