DNA repair activity of 8-oxoguanine DNA glycosylase 1 (OGG1) in human lymphocytes is not dependent on genetic polymorphism Ser326/Cys326

Janssen, Kai; Schlink, Kirsten; Götte, Walter; Hippler, Birgit; Kaina, Bernd; Oesch, Franz

doi:10.1016/s0921-8777(01)00096-9

Cited by 104 publications

(79 citation statements)

References 36 publications

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“…This result is consistent with in vitro studies demonstrating no influence of the codon 326 polymorphism on enzyme activity. 38,39 Alternatively, these results are also consistent with a dominant role for bulky adducts (PAHs) in the G:C-to-T:A transversions seen in tobacco-related cancer. 16 These adducts are repaired by nucleotide excision repair and could mask any influence of the codon 326 polymorphism on the repair of 8-OH-dG.…”

Section: Discussionsupporting

confidence: 70%

“…Kohno et al 37 showed that the hOGG1 326Ser protein had substantially higher DNA repair activity than the 326Cys variant in an in vitro bacterial complementation activity assay. However, another detailed biochemical study showed that both the purified hOGG1 326Ser and hOGG1 326Cys proteins did not differ appreciably in their enzymatic activities or in their capacity to reduce the frequency of induced mutations in an E. coli strain defective in the repair of 8-OH-G. 38 Similarly, Janssen et al 39 also evaluated OGG1 activity in an 8-oxoG oligonucleotide assay and showed no difference in enzyme activity due to the codon 326 polymorphism.…”

Section: Discussionmentioning

confidence: 99%

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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

Ying

Ahrendt

2004

Intl Journal of Cancer

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Human 8-oxoguanine DNA glycosylase 1 (hOGG1) plays a major role in the repair of 8-hydroxyguanine, one of the major forms of DNA damage generated by reactive oxygen species in tobacco smoke. If left unrepaired by hOGG1, 8-hydroxyguanine can produce G:C-to-T:A transversions. Recent studies have suggested that the hOGG1 Ser326Cys polymorphism is associated with both a decrease in enzyme activity and an increased risk of lung cancer. To define the interaction between tobacco carcinogens, hOGG1-mediated DNA repair and DNA damage, we examined the role of the hOGG1 Ser326Cys polymorphism in mutation of the p53 gene in non small cell lung cancer (NSCLC). Tumor and nonneoplastic DNA were collected from 141 cigarette smokers with NSCLC. Key words: lung cancer; hOGG1 polymorphism; p53 mutation; oxidative damage; epidemiology Tobacco use is the leading cause of preventable death in the United States. 1 One in 5 deaths and over 30% of cancer-related mortality are associated with tobacco use in this country. 1 Lung cancer is the leading cause of death among smokers and the most common cause of cancer-related death among both males and females in the United States and other developed countries. 2 In 2003, an estimated 171,900 new cases of primary lung cancer were diagnosed and an estimated 157,200 people died of this malignancy in the United States. 3 Epidemiologic studies have demonstrated that most cases of lung cancer are directly attributable to cigarette smoking. 2 Only 5-10% of all of the lung cancers occur in patients without a prior history of cigarette smoking. 2,4 Compared with nonsmokers, smokers have a 10-fold greater risk of dying from lung cancer, and in heavy smokers this risk increases to 15-to 25-fold. 5 Despite the strong association between cigarette smoking and lung cancer, only 11% of lifelong smokers will develop lung cancer. 6 Obviously, other factors must play a role in determining individual susceptibility to tobacco carcinogens.Individual susceptibility to exogenous exposures such as tobacco smoke varies with the presence of single nucleotide polymorphisms in a variety of critical genes. 7 Low penetrance susceptibility genes have common variants and often interact with environmental factors leading to sporadic cancer and contributing substantially to the population incidence of cancer. 8 -10 Polymorphisms in some of the genes involved in the metabolic activation [cytochrome P4501A1 (CYP1A1)] and detoxification [glutathione S-transferase M1 (GSTM1)] of tobacco carcinogens as well as in the repair of DNA damage (XRCC1, XPD, p53) have been associated with an increased risk of lung cancer. [11][12][13][14] Tobacco smoke is a complex mixture of over 55 carcinogens. 15 Cigarette smoking and specific tobacco carcinogens are associated with an increase in gene mutations in the lung, including those induced from oxidative damage. 4,16 -19 Repair of these DNA lesions is a complex process with specific types of DNA damage undergoing repair by specific multienzyme pathways. 9 Base excision repair (BER) is impo...

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Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 99%

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

Ying

Ahrendt

2004

Intl Journal of Cancer

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“…The most studied is the single nucleotide polymorphism at codon 326 (Ser326Cys). Homozygous carriers of the variant form of the OGG1 Ser326Cys gene appear to have reduced repair capacity for oxidised DNA lesions (31,32), but this association has not been found in all investigations (33).…”

Section: Discussionmentioning

confidence: 90%

The Association of OGG1 Ser326Cys Polymorphism and Urinary 8-OHdG Levels With Lung Cancer Susceptibility: A Hospital-Based Case-Control Study in Turkey

Karahalıl

Emerce

Koçer

et al. 2008

Archives of Industrial Hygiene and Toxicology

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High incidence and poor prognosis of lung cancer make it a major health problem worldwide. Although smoking is a major cause of lung cancer, only some smokers develop lung cancer, which suggests that there is a genetic predisposition in some individuals. 8-OHG is an important oxidative base lesion and may elevate due to cancer and smoking. It is repaired by 8-hydroxyguanine DNA glycosylase 1 (OGG1), which has several polymorphisms. Although the Ser326Cys polymorphism is consistently associated with a range of cancers, findings about this polymorphism and lung cancer risk are contradictory. To date, no study has examined this association in the Turkish population. We conducted a case-control study to investigate the association between OGG1 Ser326Cys polymorphism and the risk of lung cancer using PCR-RFLP. We also evaluated gene-smoking interaction and excretion of urinary 8-OHdG. Our results suggest that the OGG1 Ser326Cys polymorphism is not a genetic risk factor for lung cancer, and that the heterozygous genotype is associated with a significantly reduced risk for lung cancer. The levels of 8-OHdG did not correlate with the polymorphism and smoking. Larger association studies are needed to validate our findings, and mechanistic studies are needed to elucidate the underlying molecular mechanisms of this association.

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“…56 The catalytic efficiency of excision of 8-oxoG by lymphocyte extracts and purified fractions of wild-type OGG1 and the S326 variant have also been measured. In the lymphocyte assay, the efficiency of removal of 8-oxoG by the S326 variant was similar to that of the wild-type enzyme, 57 but the catalytic efficiency of the S326C variant was nearly 2-fold less than that of the wild-type protein when purified proteins were assayed. 56 Interestingly, the R46Q renal tumor-associated OGG1 variant has significantly less 8-oxoG excision activity when compared to WT.…”

mentioning

confidence: 86%

Is Base Excision Repair a Tumor Suppressor Mechanism?

Sweasy¹,

Lang²,

DiMaio³

2006

Cell Cycle

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The base excision repair pathway is critical for the removal of oxidized and methylated bases from the DNA. Much of this DNA damage arises endogenously, as a result of oxygen metabolism. Several proteins including DNA glycosylases, the APE1 endonuclease, DNA polymerase β and DNA ligase, act in a highly regulated and coordinated manner during base excision repair to excise the base adducts from the DNA and restore the normal DNA sequence. Both germline and tumor-associated variants of genes encoding these proteins have been identified in humans. In many cases, the protein variant has been shown to have properties that could contribute to the development of cancer, suggesting that base excision repair acts as a tumor suppressor mechanism in humans. Limited epidemiological studies are consistent with this view. Our review of the literature indicates that additional laboratory and epidemiological studies of the role of base excision repair in cancer etiology is warranted.

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DNA repair activity of 8-oxoguanine DNA glycosylase 1 (OGG1) in human lymphocytes is not dependent on genetic polymorphism Ser326/Cys326

Cited by 104 publications

References 36 publications

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

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

The Association of OGG1 Ser326Cys Polymorphism and Urinary 8-OHdG Levels With Lung Cancer Susceptibility: A Hospital-Based Case-Control Study in Turkey

Is Base Excision Repair a Tumor Suppressor Mechanism?

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