Lung cancer in smoking patients inversely alters the activity of hOGG1 and hNTH1

Radák, Zsolt; Goto, Sataro; Nakamoto, Hideko; Udud, Katalin; Papai, Z.; Horváth, Ildikó

doi:10.1016/j.canlet.2004.07.008

Cited by 18 publications

(7 citation statements)

References 20 publications

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“…Although 16p13.3 has been reported to be amplified rarely, it contains TSC2 gene, which has been described to be affected by LOH in 29% of lung adenocarcinomas (Takamochi et al, 2004). Also NTHL1 gene on 16p13.3, which is involved in 8oxoG repair, has been shown to have a lower expression in lung cancer compared than normal lung tissue (Radak et al, 2005) In the present study, one of the possibly asbestosrelated chromosomal regions according to gene expression and CGH array results, 19p13, was further verified by microsatellite analysis on a larger number of tumors. LOH of 19p is common in lung cancer (SanchezCespedes et al, 2001), but its relation with asbestos exposure has not been studied previously.…”

Section: Discussionmentioning

confidence: 99%

Gene expression and copy number profiling suggests the importance of allelic imbalance in 19p in asbestos-associated lung cancer

et al. 2007

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Asbestos is a pulmonary carcinogen known to give rise to DNA and chromosomal damage, but the exact carcinogenic mechanisms are still largely unknown. In this study, gene expression arrays were performed on lung tumor samples from 14 heavily asbestos-exposed and 14 nonexposed patients matched for other characteristics. Using a two-step statistical analysis, 47 genes were revealed that could differentiate the tumors of asbestos-exposed from those of non-exposed patients. To identify asbestosassociated regions with DNA copy number and expressional changes, the gene expression data were combined with comparative genomic hybridization microarray data. As a result, a combinatory profile of DNA copy number aberrations and expressional changes significantly associated with asbestos exposure was obtained. Asbestosrelated areas were detected in 2p21-p16. 3, 3p21.31, 5q35.2-q35.3, 16p13.3, 19p13.3-p13.1 and 22q12.3-q13.1. The most prominent of these, 19p13, was further characterized by microsatellite analysis in 62 patients for the differences in allelic imbalance (AI) between the two groups of lung tumors. 79% of the exposed and 45% of the non-exposed patients (P ¼ 0.008) were found to be carriers of AI in their lung tumors. In the exposed group, AI in 19p was prevalent regardless of the histological tumor type. In adenocarcinomas, AI in 19p appeared to occur independently of the asbestos exposure.

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Section: Discussionmentioning

confidence: 99%

Gene expression and copy number profiling suggests the importance of allelic imbalance in 19p in asbestos-associated lung cancer

et al. 2007

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“…In patients with adenocarcinoma of the lung, but not with squamous cell carcinoma, there was reduced capacity of normal lung tissue and blood leukocytes to repair εAde and εCyt 132. However, in smokers with non‐small cell lung carcinoma, activity of hOGG1, a DNA glycosylase was increased in tumor biopsies relative to normal lung tissue, while the activity of hNTH1, an AP endonuclease, was decreased 133…”

Section: Repair Of Dna Adductsmentioning

confidence: 97%

“…132 However, in smokers with non-small cell lung carcinoma, activity of hOGG1, a DNA glycosylase was increased in tumor biopsies relative to normal lung tissue, while the activity of hNTH1, an AP endonuclease, was decreased. 133 Using another approach, DNA damage and repair capacity in lymphocytes from non-small cell lung cancer cases and controls was assessed by the comet assay. 134 In this study, it was found that constitutive DNA damage, BPDEinduced damage and repair following BPDE-induced damage were all significantly higher in cases than in controls.…”

Section: Repair Of Dna Adductsmentioning

confidence: 99%

DNA and protein adducts in human tissues resulting from exposure to tobacco smoke

Phillips

Venitt

2012

Intl Journal of Cancer

124

122

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Tobacco smoke contains a variety of genotoxic carcinogens that form adducts with DNA and protein in the tissues of smokers. Not only are these biochemical events relevant to the carcinogenic process, but the detection of adducts provides a means of monitoring exposure to tobacco smoke. Characterization of smoking‐related adducts has shed light on the mechanisms of smoking‐related diseases and many different types of smoking‐derived DNA and protein adducts have been identified. Such approaches also reveal the potential harm of environmental tobacco smoke (ETS) to nonsmokers, infants and children. Because the majority of tobacco‐smoke carcinogens are not exclusive to this source of exposure, studies comparing smokers and nonsmokers may be confounded by other environmental sources. Nevertheless, certain DNA and protein adducts have been validated as biomarkers of exposure to tobacco smoke, with continuing applications in the study of ETS exposures, cancer prevention and tobacco product legislation. Our article is a review of the literature on smoking‐related adducts in human tissues published since 2002.

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“…Evidence has suggested that decreased BER function is associated with an increased risk of lung cancer. 10,11 For example, Paz-Elizur et al 10 found that low hOGG activities were associated with an elevated risk of lung cancer. Loss of OGG activity in yeast is associated with a mutator phenotype that accumulates GC to TA transversions.…”

Section: Discussionmentioning

confidence: 99%

8‐Hydroxy‐2′‐deoxyguanosine (8‐OH‐dG) as a potential survival biomarker in patients with nonsmall‐cell lung cancer

Shen

Deininger

Hunt

et al. 2006

Cancer

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BACKGROUND.8‐Hydroxy‐2′‐deoxyguanosine (8‐OH‐dG) is 1 of the most abundant oxidative products of cellular DNA. Accumulation of impaired 8‐OH‐dG could lead to increased genomic instability that in turn could lead to a more malignant phenotypic behavior of tumors. Therefore, the effects of 8‐OH‐dG on survival in 99 resected nonsmall‐cell lung cancer (NSCLC) patients was evaluated.METHODS.The enzyme‐linked immunosorbent assay was applied to measure the levels of 8‐OH‐dG in tumor DNA. The median levels of 8‐OH‐dG were 6.5 pmol/μg for all study subjects.RESULTS.Patients with low levels of 8‐OH‐dG had significantly longer survival times compared with those with high levels of 8‐OH‐dG (log‐rank test: P < .001). In Cox regression analysis, patients with high levels of 8‐OH‐dG had an over 3‐fold increased hazard of death. In addition, a statistically significant correlation between levels of 8‐OH‐dG and age was noted (rho = 0.206, P = .048). Furthermore, we observed a genotype‐phenotype modification between hOGG1 gene polymorphism (Ser326Cys) and levels of 8‐OH‐dG.CONCLUSIONS.The results demonstrated that levels of 8‐OH‐dG could predict survival in resected NSCLC patients. It is postulated that an intact base excision repair mechanism may reduce the accumulation of oxidative DNA damage that is thought to contribute to the tumor's malignant potential and therefore the risk of death. Cancer 2007 © 2006 American Cancer Society.

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Lung cancer in smoking patients inversely alters the activity of hOGG1 and hNTH1

Cited by 18 publications

References 20 publications

Gene expression and copy number profiling suggests the importance of allelic imbalance in 19p in asbestos-associated lung cancer

Gene expression and copy number profiling suggests the importance of allelic imbalance in 19p in asbestos-associated lung cancer

DNA and protein adducts in human tissues resulting from exposure to tobacco smoke

8‐Hydroxy‐2′‐deoxyguanosine (8‐OH‐dG) as a potential survival biomarker in patients with nonsmall‐cell lung cancer

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