Polymorphisms of<i>LIG4</i>and<i>XRCC4</i>involved in the NHEJ pathway interact to modify risk of glioma

Liu, Yanhong; Zhou, Keke; Zhang, Haishi; Shugart, Yin Yao; Chen, Lina; Xu, Zhonghui; Zhong, Yixi; Liu, Hongliang; Li, Jin; Wei, Qingyi; Huang, Fei; Lu, Daru; Zhou, Lei

doi:10.1002/humu.20645

Cited by 60 publications

(45 citation statements)

References 46 publications

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“…We have listed about 20 epidemiological studies reporting positive associations between DNA repair polymorphisms and cancer risk (Table 1 [29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45] ). Only a small proportion of studies were large (five studies were more than 500 pair cases and controls) and population based; however, some consistencies in results are apparent.…”

Section: Pbts Molecular Epidemiologic Studies With Focus On Dna Repairmentioning

confidence: 99%

Molecular Epidemiology of Primary Brain Tumors

Liu

Kyritsis

et al. 2009

Neurotherapeutics

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Summary:Although primary brain tumors (PBTs) are generally considered to be a multifactorial disorder, understanding the genetic basis and etiology of the disease is essential for PBT risk assessment. Understanding of the genetic susceptibility for PBT has come from studies of rare genetic syndromes, linkage analysis, family aggregation, early-onset pediatric cases, and mutagen sensitivity. There are currently no effective markers to assess biological dose of exposures and genetic heterogeneity. The priorities recently recommended by the Brain Tumor Epidemiology Consortium emphasized the need for expanding research in genetics and molecular epidemiology. In this article, we review the literature to identify molecular epidemiologic case-control studies of PBTs that were hypothesis-driven and focused on four hypothesized candidate pathways: DNA repair, cell cycle, metabolism, and inflammation. We summarize the results in terms of genetic associations of single nucleotide polymorphisms of these pathways. We also discuss future research directions based on available evidence and technologies, and conclude that high resolution whole genome approach with significantly large sample size could rapidly advance our understanding of the genetic etiology of PBTs. Literature searches were done on PubMed in March 2009 with the terms glioma, glioblastoma, brain tumor, association, and polymorphism, and we only reviewed English language publications.

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Section: Pbts Molecular Epidemiologic Studies With Focus On Dna Repairmentioning

confidence: 99%

Molecular Epidemiology of Primary Brain Tumors

Liu

Kyritsis

et al. 2009

Neurotherapeutics

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“…In our previously published studies, we have demonstrated that some representative tSNPs of genes involved in the NHEJ pathway may modulate risk of gliomas. 23,24 Also, these results suggest that the genetic interaction between DNA repair genes may play an important role in the etiology of gliomas.…”

Section: Discussionmentioning

confidence: 80%

“…23,24 Briefly, all subjects, including case and control groups, were unrelated Han Chinese people from Shanghai City and its surrounding regions in east China. Patients newly diagnosed with pathologically confirmed gliomas were recruited into study group between October 2004 and May 2006 at the Department of Neurosurgery of Huashan Hospital of Fudan University, Shanghai, China.…”

Section: Study Populationmentioning

confidence: 99%

XRCC3 haplotypes and risk of gliomas in a Chinese population: A hospital‐based case‐control study

Zhou

Liu

Zhang

et al. 2009

Intl Journal of Cancer

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In mammalian cells, X-ray repair cross-complementing group3 (XRCC3) plays an important role in the DNA double-strand breaks (DSBs) repair by homologous recombination. Genetic polymorphisms in the XRCC3 gene may potentially affect the repair of DSBs and thus confer susceptibility to gliomas. In this study, we used a haplotype-based approach to investigate whether 4 tagging single nucleotide polymorphisms of the XRCC3 gene are associated with risk of gliomas in 771 glioma patients and 752 cancerfree controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by the unconditional logistic regression, and haplotype associations were estimated using Haplo.Stat. After adjustment for age and sex, the variant G allele of rs861530 and T allele of rs3212092 were significantly associated with an increased risk of gliomas (AG/GG versus AA: adjusted OR 5 1.44, 95% CI 5 1.15-1.80, p 5 0.001 and CT/TT versus CC: adjusted OR 5 1.66, 95% CI 5 1.12-2.46, p 5 0.013, respectively). Consistent with these results, XRCC3 haplotype ''GGCC'' containing rs861530 G allele and haplotype ''AGTC'' containing rs3212092 T allele were also significantly associated with an elevated risk of gliomas compared with the common haplotype ''AGCC'' (adjusted OR 5 1.35, 95% CI 5 1.14-1.58, p 5 0.000 and adjusted OR 5 1.67, 95% CI 5 1.11-2.52, p 5 0.015, respectively). Our results suggest that common genetic variants in the XRCC3 gene may modulate glioma risk. ' 2009 UICC

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“…Breast Cancer Caucasian The polymorphism was significantly associated with a decrease in breast cancer risk (P = 0.04) Liu et al [100] rs3093739 Glioma Asian The polymorphism was significantly associated with glioma risk (P = 0.009) Liu et al [101] rs7325927 Glioblastoma Caucasian The polymorphism was significantly associated with glioblastoma survival (P = 0.008) SNP: Single nucleotide polymorphism.…”

Section: Caucasianmentioning

confidence: 99%

Ovarian cancer and DNA repair: DNA ligase IV as a potential key

Assis

Pereira²,

Medeiros³

2013

WJCO

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Ovarian cancer (OC) is the sixth most common cancer and the seventh cause of death from cancer in women. The etiology and the ovarian carcinogenesis still need clarification although ovulation may be determinant due to its carcinogenic role in ovarian surface epithelium. The link between ovarian carcinogenesis and DNA repair is well established and it became clear that alterations in DNA damage response may affect the risk to develop OC. Polymorphisms are variations in the DNA sequence that exist in normal individuals of a population and are capable to change, among other mechanisms, the balance between DNA damage and cellular response. Consequently, genetic variability of the host has a great role in the development, progression and consequent prognosis of the oncologic patient as well as in treatment response. Standard treatment for OC patients is based on cytoreductive surgery, followed by chemotherapy with a platinum agent and a taxane. Although 80% of the patients respond to the first-line therapy, the development of resistance is common although the mechanisms underlying therapy failure remain mostly unknown. Because of their role in oncology, enzymes involved in the DNA repair pathways, like DNA Ligase IV (LIG4), became attractive study targets. It has been reported that variations in LIG4 activity can lead to a hyper-sensitivity to DNA damage, deregulation of repair and apoptosis mechanisms, affecting the susceptibility to cancer development and therapy response. To overcome resistance mechanisms, several investigations have been made and the strategy to target crucial molecular pathways, such as DNA repair, became one of the important areas in clinical oncology. This review aims to elucidate the link between DNA repair and OC, namely which concerns the role of LIG4 enzyme, and how genetic polymorphisms in LIG4 gene can modulate the activity of the enzyme and affect the ovarian carcinogenesis and treatment response. Moreover, we try to understand how LIG4 inhibition can be a potential contributor for the development of new cancer treatment strategies.

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Polymorphisms ofLIG4andXRCC4involved in the NHEJ pathway interact to modify risk of glioma

Cited by 60 publications

References 46 publications

Molecular Epidemiology of Primary Brain Tumors

Molecular Epidemiology of Primary Brain Tumors

XRCC3 haplotypes and risk of gliomas in a Chinese population: A hospital‐based case‐control study

Ovarian cancer and DNA repair: DNA ligase IV as a potential key

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