Association between the OGG1 Ser326Cys and APEX1 Asp148Glu polymorphisms and lung cancer risk: a meta-analysis

Wu, Wei; He, Xiaofeng; Qin, Jiangbo; Su, Jie; Li, Shaoxia; Liu, Yi; Zhang, Ying; Wang, Wei

doi:10.1007/s11033-012-2035-8

Cited by 23 publications

(12 citation statements)

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“…Extending this observation, we, in a large Han Chinese population, examined three common polymorphisms in RAGE gene and found that carriers of mutant genotypes of promoter polymorphism rs1800625 and coding polymorphism rs2070600 in 3rd exon exhibited strikingly increased risk for lung cancer, which was further potentiated by our following haplotype analyses. More recently, a systematic review of 3491 lung cancer patients and 4708 controls detected significant association of Asp148Glu (rs1130409) polymorphism with lung cancer, especially in Asian populations [16], in agreement with the results of our single-locus analyses. In this context, it is reasonable to hypothesize that genetic defects of RAGE and APE1 genes might increase the risk of developing lung cancer.…”

Section: Discussionsupporting

confidence: 90%

Contributory Role of Five Common Polymorphisms of RAGE and APE1 Genes in Lung Cancer among Han Chinese

et al. 2013

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BackgroundLung cancer is the leading cause of cancer mortality in China. Given the ubiquitous nature of gene-to-gene interaction in lung carcinogenesis, we sought to evaluate five common polymorphisms from advanced glycosylation end product-specific receptor (RAGE) and apurinic/apyrimidinic endonuclease 1 (APE1) genes in association with lung cancer among Han Chinese.Methods and Results819 patients with lung cancer and 803 cancer-free controls were recruited from Qiqihar city. Genotypes of five examined polymorphisms (RAGE gene: rs1800625, rs1800624, rs2070600; APE1 gene: rs1760944, rs1130409) were determined by ligase detection reaction method. Data were analyzed by R software and multifactor dimensionality reduction (MDR). Hardy-Weinberg equilibrium was satisfied for all five polymorphisms. Overall differences in the genotype and allele distributions were significant for rs1800625 (Pgenotype<0.0005; Pallele<0.0005), rs2070600 (Pgenotype = 0.005; Pallele = 0.004) and rs1130409 (Pgenotype = 0.009; Pallele = 0.004) polymorphisms. Haplotype C-A-A (alleles in order of rs1800625, rs1800624 and rs2070600) of RAGE gene was overrepresented in patients, and conferred a 2.1-fold increased risk of lung cancer (95% confidence interval: 1.52–2.91), independent of confounding factors. Further application of MDR method to five examined polymorphisms identified the overall best interaction model including rs2070600 and rs1130409 polymorphisms. This model had a maximal testing accuracy of 64.63% and a maximal cross-validation consistency of 9 out of 10 at the significant level of 0.006.ConclusionsOur findings demonstrated a potential interactive contribution of RAGE and APE1 genes to the pathogenesis of lung cancer among Han Chinese. Further studies are warranted to confirm or refute these findings.

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Section: Discussionsupporting

confidence: 90%

Contributory Role of Five Common Polymorphisms of RAGE and APE1 Genes in Lung Cancer among Han Chinese

et al. 2013

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“…Two analyses focusing on a single locus suggested that the 1349 T>G polymorphism was not associated with lung cancer risk among Asians or Caucasians [21,23]. This result contrasts with another analysis, in which the number of studies was obviously smaller than a former and the current meta-analyses, suggesting an increased lung cancer risk in Asians [22]. The divergency highlights that it is worthwhile to carry out an extremely large-scale study to establish the association with high confidence.…”

Section: Discussioncontrasting

confidence: 72%

“…The majority of published studies have evaluated the impact of polymorphisms in relatively small populations. Most importantly, meta-analyses of lung cancer risk in relation to the aforementioned polymorphisms either using a single locus or including limited data also generated substantially inconsistent results [20][21][22][23]. We therefore conducted a more comprehensive evaluation of the hypothesis that HAP1 polymorphisms predispose to lung cancer.…”

Section: Introductionmentioning

confidence: 99%

Evaluating the association of polymorphisms in the HAP1 gene with lung cancer risk: a meta-analysis

et al. 2014

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Studies on the relationship of HAP1 polymorphisms (-141 T > G; 1349 T > G) and lung cancer risk to date indicated controversial results. This study was devised to clarify whether the polymorphisms predispose to lung cancer. We searched Embase and PubMed up to March 2014 to identify relevant studies. Data from the eligible studies were independently extracted by two investigators. Pooled odds ratio (OR) was calculated to assess the associations between lung cancer risk and the abovementioned polymorphisms. A total of 15 case-control studies were included in this meta-analysis. Both overall analysis and stratified analysis by ethnicity and smoking status indicated no association between lung cancer risk and the 1349 T > G polymorphism. However, a significantly reduced risk of lung cancer was found among carriers of the GG genotype of the -141 T > G polymorphism, as compared with those of the TT genotype (homozygote model: OR = 0.82, 95% confidence interval (CI) 0.73 to 0.93, P(OR) = 0.002). Likewise, the GG genotype was also found to decrease lung cancer risk compared to the GT + TT genotypes (recessive model: OR = 0.82, 95 % CI 0.73 to 0.92, P(OR) = 0.001). Our meta-analysis suggests that the -141 T > G polymorphism, but not the 1349 T > G polymorphism, may have protective effects for lung cancer.

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“…Increased risk among smokers [94,95] Increased resistance to cisplatin OR: 1.342 [96] 83.3% (20 out of 24) of cisplatin-resistant tumors show high APE1 expression levels [97] …”

Section: Thr 656 Gly Increased Expressionmentioning

confidence: 99%

“…Required for the repair of DSBs [16,17,103,104] Mutated Lower expression providing a better outcome in lung cancer patients [105] Increase in resistance to a wide range of DNA-damaging agents and radiation therapy [106][107][108][109] Low expression of BRCA1pS1423 was associated with a worse survival [110] atM ATM acts as a central mediator of the radioprotective machinery, participating in cellular stress responses, control of cell cycle checkpoints, repair of DSBs, and initiation of apoptosis Ser 62160 Gly>Ala Higher risk of lung cancer than those with the G allele OR: 1.6 [111] Ser 227060 T Increased risk of lung cancer OR: 1.55 [112] Ser 170548 C Increased risk of lung cancer OR: 1.51 [112] p53 Plays a role in apoptosis, genomic stability, and inhibition of angiogenesis [94][95]113] Frequently mutated or inactivated, including homozygous deletions and abnormally sized messenger RNAs, as well as a variety of point or small mutations Mutations lead to poorer patient prognosis and decreased survival [114] Ku70/80 Involved in numerous cellular processes including apoptosis, regulation of specific gene transcription, regulation of heat shock-induced responses and telomere maintenance [115][116][117][118] Ku70 (rs2267437) Increased risk of lung cancer OR: 1.32 [119] …”

Section: Brca1mentioning

confidence: 99%

DNA Repair Pathways and their Therapeutic Potential in Lung Cancer

Burgess

Croft

Wallace

et al. 2014

Lung Cancer Manage.

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practice points• A normal cycling cell can encounter up to 30,000 DNA damage events in 1 day, which are repaired by distinct pathways that target and repair specific lesions.• Platinum-based chemotherapeutics exert toxicity through the formation of irreparable base adducts and DNA crosslinks, which direct the cancerous cells towards apoptotic death.• The selective pressure exerted on the tumor eventuates genetic drift and may provide the cancerous cells resistance to many anticancer therapies.• Several distinct while overlapping pathways exist within the cell to detect and repair the various DNA damage lesions that may occur.• The inaccurate repair of DNA lesions may lead to mutations within the cell and drive tumorigenesis.• Many cancers contain mutations in DNA repair genes, for example, more than 90% of small cell lung cancers and 50% of all non-small-cell lung cancers carry mutations in tP53, encoding the important tumor suppressor, p53.• Many anticancer therapies, including platinum-based chemotherapeutics and replication inhibitors, induce apoptosis within the cell through the formation of irreparable DNA damage.• The deregulation of DNA repair proteins within cells may provide an attractive therapeutic window. Such an approach is exemplified by the PARP inhibitors, which show potential use in the treatment of cancers deficient of functional BRCA1 or BRCA2. In addition, these drugs may show increased efficacy in combination with DNA-damaging agents.• Resistance to platinum-based agents may be acquired through multiple mechanisms, including mutation or deregulation of DNA repair proteins, alteration of membrane transport protein activity and chromatin remodeling.

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Association between the OGG1 Ser326Cys and APEX1 Asp148Glu polymorphisms and lung cancer risk: a meta-analysis

Cited by 23 publications

References 50 publications

Contributory Role of Five Common Polymorphisms of RAGE and APE1 Genes in Lung Cancer among Han Chinese

Contributory Role of Five Common Polymorphisms of RAGE and APE1 Genes in Lung Cancer among Han Chinese

Evaluating the association of polymorphisms in the HAP1 gene with lung cancer risk: a meta-analysis

DNA Repair Pathways and their Therapeutic Potential in Lung Cancer

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