Tagging SNPs in non-homologous end-joining pathway genes and risk of glioma

Yanhong Liu, Haishi Zhang, Keke Zhou, Lina Chen, Zhonghui Xu, Yu Zhong, Hongliang Liu, Rui Li, Yin Yao Shugart, Qingyi Wei, Li Jin, Fengping Huang, Daru Lu, Liangfu Zhou

Research output: Contribution to journalArticle

Abstract

Ionizing radiation is known to cause DNA damage, including single-strand and double-strand DNA breaks (DSBs), and the unrepair of DNA damage, particularly DSBs, may cause chromosome aberrations. Although the etiology of gliomas remains unclear, exposure to ionizing radiation has been identified as the only established risk factor. We hypothesized that polymorphisms of candidate genes involved in the DSBs repair pathway may contribute to susceptibility to glioma. We used a haplotype-based approach to investigate the role of 22 tagging single-nucleotide polymorphisms (tSNPs) of XRCC5, XRCC6 and XRCC7 in 771 glioma patients and 752 healthy controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by the unconditional logistic regression, haplotypes were inferred by the HAPLO.STAT program and gene-gene interactions were evaluated by the multifactor dimensionality reduction method. We found that, in the single-locus analysis, glioma risk was statistically significantly associated with three XRCC5 tSNPs (SNP1 rs828704, SNP6 rs3770502 and SNP7 rs9288516, P = 0.005, 0.042 and 0.003, respectively), one XRCC6 tSNP (SNP4 rs6519265, P = 0.044) but none of XPCC7 tSNPs. Haplotype-based association analysis revealed that gliomas risk was statistically significantly associated with one protective XRCC5 haplotype "CAGTT," accounting for a 40% reduction (OR= 0.60, 95% CI = 0.43-0.85) in glioma risk, and some positive gene-gene interactions were also evident. In conclusion, genetic variants of the genes involved in the DSB repair pathway may play a role in the etiology of glioma.

Original languageEnglish (US)
Pages (from-to)1906-1913
Number of pages8
JournalCarcinogenesis
Volume28
Issue number9
DOIs
StatePublished - Sep 2007

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Glioma
Single Nucleotide Polymorphism
Double-Stranded DNA Breaks
Haplotypes
Genes
Ionizing Radiation
DNA Repair
DNA Damage
Multifactor Dimensionality Reduction
Odds Ratio
Confidence Intervals
Chromosome Aberrations
Logistic Models

ASJC Scopus subject areas

  • Cancer Research

Cite this

Liu, Y., Zhang, H., Zhou, K., Chen, L., Xu, Z., Zhong, Y., ... Zhou, L. (2007). Tagging SNPs in non-homologous end-joining pathway genes and risk of glioma. Carcinogenesis, 28(9), 1906-1913. https://doi.org/10.1093/carcin/bgm073

Tagging SNPs in non-homologous end-joining pathway genes and risk of glioma. / Liu, Yanhong; Zhang, Haishi; Zhou, Keke; Chen, Lina; Xu, Zhonghui; Zhong, Yu; Liu, Hongliang; Li, Rui; Shugart, Yin Yao; Wei, Qingyi; Jin, Li; Huang, Fengping; Lu, Daru; Zhou, Liangfu.

In: Carcinogenesis, Vol. 28, No. 9, 09.2007, p. 1906-1913.

Research output: Contribution to journalArticle

Liu, Y, Zhang, H, Zhou, K, Chen, L, Xu, Z, Zhong, Y, Liu, H, Li, R, Shugart, YY, Wei, Q, Jin, L, Huang, F, Lu, D & Zhou, L 2007, 'Tagging SNPs in non-homologous end-joining pathway genes and risk of glioma', Carcinogenesis, vol. 28, no. 9, pp. 1906-1913. https://doi.org/10.1093/carcin/bgm073
Liu, Yanhong ; Zhang, Haishi ; Zhou, Keke ; Chen, Lina ; Xu, Zhonghui ; Zhong, Yu ; Liu, Hongliang ; Li, Rui ; Shugart, Yin Yao ; Wei, Qingyi ; Jin, Li ; Huang, Fengping ; Lu, Daru ; Zhou, Liangfu. / Tagging SNPs in non-homologous end-joining pathway genes and risk of glioma. In: Carcinogenesis. 2007 ; Vol. 28, No. 9. pp. 1906-1913.
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AU - Zhong, Yu

AU - Liu, Hongliang

AU - Li, Rui

AU - Shugart, Yin Yao

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AU - Huang, Fengping

AU - Lu, Daru

AU - Zhou, Liangfu

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AB - Ionizing radiation is known to cause DNA damage, including single-strand and double-strand DNA breaks (DSBs), and the unrepair of DNA damage, particularly DSBs, may cause chromosome aberrations. Although the etiology of gliomas remains unclear, exposure to ionizing radiation has been identified as the only established risk factor. We hypothesized that polymorphisms of candidate genes involved in the DSBs repair pathway may contribute to susceptibility to glioma. We used a haplotype-based approach to investigate the role of 22 tagging single-nucleotide polymorphisms (tSNPs) of XRCC5, XRCC6 and XRCC7 in 771 glioma patients and 752 healthy controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by the unconditional logistic regression, haplotypes were inferred by the HAPLO.STAT program and gene-gene interactions were evaluated by the multifactor dimensionality reduction method. We found that, in the single-locus analysis, glioma risk was statistically significantly associated with three XRCC5 tSNPs (SNP1 rs828704, SNP6 rs3770502 and SNP7 rs9288516, P = 0.005, 0.042 and 0.003, respectively), one XRCC6 tSNP (SNP4 rs6519265, P = 0.044) but none of XPCC7 tSNPs. Haplotype-based association analysis revealed that gliomas risk was statistically significantly associated with one protective XRCC5 haplotype "CAGTT," accounting for a 40% reduction (OR= 0.60, 95% CI = 0.43-0.85) in glioma risk, and some positive gene-gene interactions were also evident. In conclusion, genetic variants of the genes involved in the DSB repair pathway may play a role in the etiology of glioma.

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