Ser326Cys polymorphism inhOGG1 gene and risk of esophageal cancer in a Chinese population

Xing, De; Tan, Wen; Song, Nan; Lin, Dong

doi:10.1002/1097-0215(20010520)95:3<140::aid-ijc1024>3.0.co;2-2

Cited by 138 publications

(81 citation statements)

References 34 publications

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“…There have been studies showing an increased risk of esophageal squamous cell carcinoma in the presence of certain BER SNPs [12,29,31,32]. However, in our population of patients, we found no significant increase in risk for several individual BER SNPs or in a joint analysis under any model of inheritance.…”

Section: Discussioncontrasting

confidence: 86%

“…The SNPs were XPD Lys751Gln, XPD Asp312Asn, ERCC1 8092C/A, and ERCC1 118C/T in the NER pathway, and XRCC1 Arg399Gln, APE1 Asp148Glu and hOGG1 Ser326Cys in the BER pathway. Although a number of studies have examined a selection of these polymorphisms in relation to other cancers, including esophageal squamous cell carcinoma [28][29][30][31][32], an evaluation of these two pathways has not been reported comprehensively for esophageal adenocarcinoma.…”

Section: Introductionmentioning

confidence: 99%

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Polymorphisms of the NER pathway genes, ERCC1 and XPD are associated with esophageal adenocarcinoma risk

Tse

Zhai

Zhou

et al. 2008

Cancer Causes Control

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Purpose-Functional variation in DNA repair capacity through single nucleotide polymorphisms (SNPs) of key repair genes is associated with a higher risk of developing various types of cancer. Studies have focused on the nucleotide excision repair (NER) and base excision repair (BER) pathways. We investigated whether variant alleles in seven SNPs within these pathways increased the risk of esophageal adenocarcinoma. NIH Public Access Author ManuscriptCancer Causes Control. Author manuscript; available in PMC 2011 June 1. Results-Variant alleles in NER SNPs XPD Lys751Gln (AOR = 1.50, 95% CI 1.1-2.0), ERCC1 8092 C/A (AOR = 1.44, 95% CI 1.1-1.9), and ERCC1 118C/T (AOR = 1.42, 95% CI 1.0-1.9) were individually associated with esophageal adenocarcinoma risk. An increasing number of variant alleles in NER SNPs showed a significant trend with esophageal adenocarcinoma risk (p = 0.007).Conclusions-The presence of variant alleles in NER genes increases risk of esophageal adenocarcinoma. There is evidence of an additive role for SNPs along a common DNA repair pathway. Future larger studies of esophageal adenocarcinoma etiology should evaluate entire biological pathways.

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Section: Discussioncontrasting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Polymorphisms of the NER pathway genes, ERCC1 and XPD are associated with esophageal adenocarcinoma risk

Tse

Zhai

Zhou

et al. 2008

Cancer Causes Control

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“…DOI 10.1002/em well as metabolic homeostasis. In this regard, the Ser326Cys mutation has been associated with human lung squamous cell carcinomas [Lu et al, 1997;Chevillard et al, 1998;Sugimura et al, 1999;Wikman et al, 2000;Le Marchand et al, 2002;Paz-Elizur et al, 2003;Okasaka et al, 2009], orolaryngeal [Elahi et al, 2002], esophageal [Xing et al, 2001], kidney [Chevillard et al, 1998;Audebert et al, 2000Audebert et al, , 2002, and gastric cancers [Farinati et al, 2008]. Recently, two studies have also reported an association between the Ser326Cys mutation and increased body mass index and susceptibility to Type II diabetes [Daimon et al, 2009;Thameem et al, 2010].…”

Section: Nth1mentioning

confidence: 99%

Oxidative DNA damage in disease—Insights gained from base excision repair glycosylase‐deficient mouse models

Sampath

2014

Environ and Mol Mutagen

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Cellular components, including nucleic acids, are subject to oxidative damage. If left unrepaired, this damage can lead to multiple adverse cellular outcomes, including increased mutagenesis and cell death. The major pathway for repair of oxidative base lesions is the base excision repair pathway, catalyzed by DNA glycosylases with overlapping but distinct substrate specificities. To understand the role of these glycosylases in the initiation and progression of disease, several transgenic mouse models have been generated to carry a targeted deletion or overexpression of one or more glycosylases. This review summarizes some of the major findings from transgenic animal models of altered DNA glycosylase expression, especially as they relate to pathologies ranging from metabolic disease and cancer to inflammation and neuronal health. Environ. Mol. Mutagen. 55:689-703, 2014. V C 2014 Wiley Periodicals, Inc.

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“…[24][25][26][27] In order not to interfere with our analysis of hOGG1 polymorphism on the susceptibility to the pterygium, the subjects suffering from benign or malignant tumours were excluded. On the other hand, owing to the fact that the veterans accounted for approximately 50% of our patients, there were higher proportions of male sex and outdoor occupation type in our patients and controls.…”

Section: Discussionmentioning

confidence: 99%

“…It has been proved in an Escherichia coli complementation assay 23 that the DNA repair activity of hOGG1-Cys 326 protein is lower than that of hOGG1-Ser 326 . The hOGG1 Cys/Cys homozygosity has been reported to increase the risks of lung cancer, 24 oesophageal cancer, 25 orolaryngeal cancer, 26 and stomach cancer. 27 Additionally, some studies revealed the impact of this genetic polymorphism on patients suffering from chronic oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Genetic polymorphism of hOGG1 and risk of pterygium in Chinese

Hc¹,

Cc²,

Wm³

et al. 2004

Eye

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Purpose Ultraviolet irradiation is known to cause oxidative DNA damage and is thought to be a major factor implicated in the pathogenesis of pterygium. The highly mutagenic 8-hydroxy-2 0 -deoxyguanosine, a marker for the evaluation of photo-oxidative DNA damage, can be repaired by human 8-oxoguanine glycosylase I (hOGG1). A transition of C to G at nucleotide position 1245 in exon 7 of the hOGG1 gene is associated with the substitution of cysteine for serine at codon 326. In this study, we investigated the association of the hOGG1 Ser326Cys polymorphism with pterygium in a Chinese population. Methods In all, 70 patients and 86 controls were enrolled in this study. The Ser326Cys polymorphism was determined by the polymerase chain reaction-restriction fragment-length polymorphism analysis. The association between this genetic polymorphism and risk of pterygium was examined by w 2 -test and logistic regression. Results The allelic frequencies for the Ser and Cys variants of hOGG1 gene were not significantly different between the two groups. However, when compared with Ser/ Ser and Ser/Cys genotypes combined, we found that the homozygous Cys/Cys genotype was more prevalent in pterygium patients than controls (P ¼ 0.024) with the odds ratio being 2.2 (95% CI: 1.1-4.5). In the pterygium group, the mean age of patients with the Cys/Cys genotype was younger than those with the other two genotypes (P ¼ 0.025). Conclusions Our findings suggest that the 1245C-G transition in exon 7 of the hOGG1 gene, which results in Ser326Cys substitution of the enzyme, might play a role in the susceptibility of humans to pterygium.

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Ser326Cys polymorphism inhOGG1 gene and risk of esophageal cancer in a Chinese population

Cited by 138 publications

References 34 publications

Polymorphisms of the NER pathway genes, ERCC1 and XPD are associated with esophageal adenocarcinoma risk

Polymorphisms of the NER pathway genes, ERCC1 and XPD are associated with esophageal adenocarcinoma risk

Oxidative DNA damage in disease—Insights gained from base excision repair glycosylase‐deficient mouse models

Genetic polymorphism of hOGG1 and risk of pterygium in Chinese

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