<i>hOGG1</i> Ser326Cys polymorphism and G:C‐to‐T:A mutations: No evidence for a role in tobacco‐related non small cell lung cancer

Ying, Haoqiang; Ahrendt, Steven A.

doi:10.1002/ijc.20730

Cited by 19 publications

(11 citation statements)

References 36 publications

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“…No difference in catalytic activities was observed between the hOGG1 326C and hOGG1 326S alleles in several studies [40–46]. However, the hOGG1 encoded by the wild-type 326S allele exhibited higher DNA repair activity than the hOGG1 326C variant in other studies [38, 47–50]. …”

Section: Resultsmentioning

confidence: 94%

Single Nucleotide Polymorphisms in DNA Repair Genes and Prostate Cancer Risk

Park

Huang

Sellers

2009

Methods in Molecular Biology

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The specific causes of prostate cancer are not known. However, multiple etiological factors, including genetic profile, metabolism of steroid hormones, nutrition, chronic inflammation, family history of prostate cancer, and environmental exposures are thought to play significant roles. Variations in exposure to these risk factors may explain inter-individual differences in prostate cancer risk. However, regardless of the precise mechanism(s), a robust DNA repair capacity may mitigate any risks conferred by mutations from these risk factors. Numerous single nucleotide polymorphisms (SNPs) in DNA repair genes have been found, and studies of these SNPs and prostate cancer risk are critical to understanding the response of prostate cells to DNA damage. A few SNPs in DNA repair genes cause significantly increased risk of prostate cancer, however, in most cases, the effects are moderate and often depend upon interactions among the risk alleles of several genes in a pathway or with other environmental risk factors. This report reviews the published epidemiologic literature on the association of SNPs in genes involved in DNA repair pathways and prostate cancer risk.

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Section: Resultsmentioning

confidence: 94%

Single Nucleotide Polymorphisms in DNA Repair Genes and Prostate Cancer Risk

Park

Huang

Sellers

2009

Methods in Molecular Biology

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“…However, a biological function of hOGG1 Ser326Cys polymorphism was not supported, as the hOGG1-Cys variant was not associated with p53 mutation in patients with lung cancer. 30 This discrepancy may have been due to the predominant influence of APE1 on the DNA glycosylase activity of hOGG1. In the present study, we consistently found that the hOGG1 Ser326Cys polymorphism was not associated with p53 mutation in the present population; however, p53 mutation was significantly more frequent in participants who had hOGG1-Cys alleles plus the APE1 Asp/Asp genotype.…”

Section: Discussionmentioning

confidence: 99%

The APE1 Asp/Asp Genotype and the Combination of APE1 Asp/Asp and hOGG1-Cys Variants Are Associated With Increased p53 Mutation in Non^|^ndash;Small Cell Lung Cancer

Lin

Chen

Cheng

et al. 2012

Journal of Epidemiology

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BackgroundThe hOGG1 Ser326Cys polymorphism is associated with lung cancer risk, but there are limited data regarding an association between the APE1 Asp148Glu polymorphism and lung cancer. Biological evidence shows that the hOGG1-Cys allele results in less DNA repair activity; however, this is not associated with p53 mutation in lung cancer. Therefore, we investigated whether an interaction between hOGG1 and APE1 is associated with the frequency of p53 mutation in lung cancer.MethodsWe studied 217 Taiwanese adults with primary lung cancer. DNA polymorphisms of hOGG1 and APE1 were determined by polymerase chain reaction (PCR)-based restriction fragment length polymorphism. Mutations in p53 exons 5–8 were detected by direct sequencing. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% CIs for the risk of p53 mutation associated with polymorphisms of hOGG1 and APE1 in lung cancer.ResultsAs expected, no association between hOGG1 polymorphism and p53 mutation was observed in this population. However, a higher risk of p53 mutation was found in participants with the APE1 Asp/Asp genotype than in those with the APE1-Glu allele (OR, 2.15; 95% CI, 1.19–3.87; P = 0.011). The risk of p53 mutation was also higher in participants with APE1 Asp/Asp plus hOGG1-Cys than in those with APE1-Glu plus hOGG1 Ser/Ser (OR, 3.72; 95% CI, 1.33–10.40; P = 0.012).ConclusionsThese results suggest that the APE1 Asp/Asp genotype and the combination of the APE1 Asp/Asp and hOGG1-Cys variants are associated with increased risk of p53 mutation in non–small cell lung cancer.

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“…Specifically, hOGG1 Ser326Cys polymorphism, commonly observed in lung cancer, has been shown to reduce hOgg1 enzyme activity, suggesting that this polymorphism plays an important role in the risk for lung cancer (Kohno et al, 1998;Wikman et al, 2000). However, the contribution of the Ser326Cys polymorphism to lung cancer remains controversial as other studies suggested that there may be no association of this polymorphism with the risk of lung cancer development, and further that the contribution of Ser326Cys to lung cancer risk may be different among different geographic populations (Wikman et al, 2000;Vogel et al, 2004;Hu and Ahrendt, 2005). Further studies are needed to assess the importance of the interpopulation variation to cancer susceptibility.…”

Section: Discussionmentioning

confidence: 99%

Oxidized guanine lesions and hOgg1 activity in lung cancer

et al. 2005

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In humans, the oxidatively induced DNA lesion 8-hydroxyguanine (8-oxoG) is removed from DNA by hOgg1, a DNA glycosylase/AP lyase that specifically incises 8-oxoG opposite cytosine. We analysed the expression of hOGG1 mRNA in 18 lung cancer and three normal cell lines. Although hOGG1 was overexpressed in most cell lines, 2/18 (11.1%) showed a lower hOGG1 mRNA and protein expression (B80% decrease) relative to normal cell lines. Liquid chromatography/mass spectrometry analysis showed increased levels of 8-oxoG in the two cell lines with the lowest hOGG1 mRNA expression. We examined the ability of nuclear and mitochondrial extracts to incise 8-oxoG lesion in cell lines H1650 and H226 expressing lower hOGG1 mRNA and H1915 and H1975 with higher than normal hOGG1 mRNA expression. Both nuclear and mitochondrial extracts from H1915 and H1975 cells were proficient in 8-oxoG removal. However, both cell lines with the lowest hOGG1 mRNA expression exhibited a severe reduction in 8-oxoG incision in both nuclear and mitochondrial extracts. Under-expression of hOGG1 mRNA and hOgg1 protein was associated with a decrease in mitochondrial DNA repair in response to oxidative damaging agents. These results provide evidence for defective incision of 8-oxoG in both nuclear and mitochondria of H1650 and H226 lung cancer cell lines. These results may implicate 8-oxoG repair defects in certain lung cancers.

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hOGG1 Ser326Cys polymorphism and G:C‐to‐T:A mutations: No evidence for a role in tobacco‐related non small cell lung cancer

Cited by 19 publications

References 36 publications

Single Nucleotide Polymorphisms in DNA Repair Genes and Prostate Cancer Risk

Single Nucleotide Polymorphisms in DNA Repair Genes and Prostate Cancer Risk

The APE1 Asp/Asp Genotype and the Combination of APE1 Asp/Asp and hOGG1-Cys Variants Are Associated With Increased p53 Mutation in Non^|^ndash;Small Cell Lung Cancer

Oxidized guanine lesions and hOgg1 activity in lung cancer

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