<i>XRCC3</i> genetic polymorphism, smoking, and lung carcinoma risk in minority populations

Wang, M.P.H. Yunfei; Liang, Dong; Spitz, Margaret; Zhang, Kerang; Dong, Qiong; Amos, Christopher I.; Wu, Xifeng

doi:10.1002/cncr.11692

Cited by 27 publications

(20 citation statements)

References 48 publications

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“…In another lung cancer study carried out by Wang et al, no significant association between the XRCC3 variant allele polymorphism and lung cancer risk was noted. However, a significantly increased risk for lung cancer (OR ¼ 5.20; 95% CI: 1.59-17.03) was evident in heavy smokers with the variant T allele genotypes (Wang et al, 2003d). Furthermore, a joint effect of the T allele and heavy smoking was observed (OR ¼ 37.31; 95% CI: 11.43-121.72).…”

Section: Dna Damage and Repairmentioning

confidence: 96%

Genetic susceptibility to tobacco-related cancer

et al. 2004

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Although cigarette smoking is the dominant risk factor for several epithelial cancers, only a small fraction of individuals with tobacco exposure develop cancer. The underlying hypothesis is that genetic factors may render certain smokers more susceptible to cancer than others. Genetic alterations in critical regulatory pathways may predispose cells to carcinogenesis. These pathways include regulation of xenobiotic metabolism; control of genomic stability, including DNA repair mechanisms, cell-cycle checkpoints, apoptosis and telomere length; and control of microenvironmental factors, such as matrix metalloproteinases, inflammation and growth factors. In addition, epigenetic events, such as promoter hypermethylation and loss of imprinting, are also involved in carcinogenesis. In this review, we will summarize recent advances in genetic susceptibility to tobacco-related cancer. Emphasizing on risk assessment, we will describe how genetic variations in the above-mentioned genetic pathways modify the tobacco-related cancer risk. In addition, we will discuss how genetic variations may assist in predicting clinical outcome, such as the natural history of cancer and treatment response. The measurements of genetic susceptibility by both genotypic and phenotypic assays are covered in the text. Finally, we present a number of current concerns that need to be addressed as the exciting field of molecular cancer epidemiology advances rapidly.

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Section: Dna Damage and Repairmentioning

confidence: 96%

Genetic susceptibility to tobacco-related cancer

et al. 2004

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“…Such DNA damage may lead to tumorigenesis if left unrepaired. Smokers usually are exposed to a larger biologically available dose of reactive intermediates from tobacco carcinogens compared with non smokers and, hence, may suffer greater DNA damage that cannot be repaired efficiently (Wang et al, 2003). Tobacco smoke contains procarcinogenic compounds that are metabolized into reactive intermediates and cause DNA damage.…”

Section: Discussionmentioning

confidence: 99%

Association of RAD 51 135 G/C, 172 G/T and XRCC3 Thr241Met Gene Polymorphisms with Increased Risk of Head and Neck Cancer

Kayani

Khan²,

Baig³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Homologous recombination repair (HRR) plays an important role in protection against carcinogenic factors. Genes regulating the HRR mechanisms may impair their functions and consequently result in increased cancer susceptibility. RAD 51 and XRCC3 are key regulators of the HRR pathway and genetic variability in these may contribute to the appearance and progression of various cancers including head and neck cancer (HNC). The aim of the present study was to compare the distribution of genotypes of RAD51 (135G/C, 172 G/T) and XRCC3 (Thr241Met) polymorphisms between HNC patients and controls. Each polymorphism was genotyped using the polymerase chain reaction-restriction fragment length polymerase (PCR-RFLP) technique in 200 pathologically confirmed HNC patients along with 150 blood samples from normal, disease free healthy individuals. We observed that homozygous variant CC genotype of RAD51 135G/C was associated with a 2.5 fold increased HNC risk (OR=2.5; 95%CI=0.69-9.53; p<0.02), while second polymorphism of RAD 51 172 G/T, heterozygous variant GT genotype was associated with a 1.68 fold (OR=1.68; 95%CI=1.08-2.61; p<0.02) elevation when compared with controls. In the case of the Thr241Met polymorphism of XRCC3, we observed a 16 fold (OR=16; 95% CI= 3.78-69.67; p<0.0002) increased HNC risk in patients compared to controls. These results further suggested that RAD51 (135G/C, 172 G/T) and XRCC3 (Thr241Met) polymorphisms may be effective biomarkers for genetic susceptibility to HNC. Larger studies are needed to confirm our findings and identify the underlying mechanisms.

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“…A previous study demonstrated that polymorphisms in both genes (XRCC1 Arg399Gln and XRCC3 T241M) had a synergistic effect, increasing the lung cancer risk (Guo et al, 2013). In addition, tobacco smoke contains procarcinogenic compounds that are metabolized into reactive intermediates and cause DNA damage, which may interact with the T241M polymorphism to result in lung cancer (Wang et al, 2003). Further studies involving larger sample sizes should be conducted to investigate the potential relationships between the effect of environmental factors on the T241M polymorphism and lung cancer risk.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have found several risk factors for lung cancer, including smoking tobacco and being around others' smoke, environmental exposure at home or work (such as radon gas or asbestos), and personal history (such as having radiation therapy or a family history of lung cancer). In addition, genetic factors play an impor tant role in the development of the disease (Wang et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

XRCC3 T241M polymorphism and lung cancer risk in the Han Chinese population: a meta-analysis

Zhang¹,

Wen²,

Yang³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Numerous studies have evaluated the association between the X-ray repair cross-complementing group 3 (XRCC3) T241M polymorphism and lung cancer risk; however, the actual association is controversial. We examined whether the T241M polymorphism confers a lung cancer risk in China. We searched the PubMed, Google Scholar, and China National Knowledge Infrastructure databases to identify studies that examined the association between the XRCC3 T241M polymorphism and the risk of lung cancer. We estimated the pooled odds ratio with its 95% confidence interval to assess this association. A total of 3977 patients with lung cancer and 3761 controls from 8 comparative studies were included in this meta-analysis. The meta-analysis results revealed no significant association between the XRCC3 T241M polymorphism and lung cancer risk. In the subgroup analysis, 6 studies with sample sizes over 500 found that the T241M polymorphism had no association with lung cancer. The XRCC3 T241M polymorphism may not be a risk factor for lung cancer. However, larger studies involving a stratified case-control population and biological characterization are needed to validate this finding.

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XRCC3 genetic polymorphism, smoking, and lung carcinoma risk in minority populations

Cited by 27 publications

References 48 publications

Genetic susceptibility to tobacco-related cancer

Genetic susceptibility to tobacco-related cancer

Association of RAD 51 135 G/C, 172 G/T and XRCC3 Thr241Met Gene Polymorphisms with Increased Risk of Head and Neck Cancer

XRCC3 T241M polymorphism and lung cancer risk in the Han Chinese population: a meta-analysis

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