Advertisement
Browse Subject Areas
?

Click through the PLOS taxonomy to find articles in your field.

For more information about PLOS Subject Areas, click here.

  • Loading metrics

Open Access

Peer-reviewed

Research Article

The Effect of hOGG1 Ser326Cys Polymorphism on Cancer Risk: Evidence from a Meta-Analysis

  • Bingbing Wei,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • You Zhou,

    Affiliation Minerva Foundation Institute for Medical Research, Biomedicum 2U, Helsinki, Finland

    ⨯
  • Zhuoqun Xu ,

    xuzq@wuxiph.com

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Bo Xi,

    Affiliation Department of Maternal and Child Health Care, School of Public Health, Shandong University, Jinan, China

    ⨯
  • Huan Cheng,

    Affiliation Department of Urology, First Affiliated Hospital of Nanjing Medical University, Nanjing, China

    ⨯
  • Jun Ruan,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Ming Zhu,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Qiang Hu,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Qiang Wang,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Zhirong Wang,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Zhiqiang Yan,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Ke Jin,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Deqi Zhou,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Feng Xuan,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Xing Huang,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • Jianfeng Shao,

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  •  [ ... ],
  • Peng Lu

    Affiliation Department of Urology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi, China

    ⨯
  • [ view all ]
  • [ view less ]

Abstract

Background

Human oxoguanine glycosylase 1 (hOGG1) in base excision repair (BER) pathway plays a vital role in DNA repair. Numerous epidemiological studies have evaluated the association between hOGG1 Ser326Cys polymorphism and the risk of cancer. However, the results of these studies on the association remain conflicting. To derive a more precise estimation of the association, we conducted a meta-analysis.

Methodology/Principal Findings

A comprehensive search was conducted to identify the eligible studies of hOGG1 Ser326Cys polymorphism and cancer risk. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association. We found that the hOGG1 Ser326Cys polymorphism was significantly associated with overall cancer risk (Cys/Cys vs. Ser/Ser: OR = 1.19, 95%CI = 1.09–1.30, P<0.001; Cys/Cys vs. Cys/Ser+Ser/Ser: OR = 1.16, 95%CI = 1.08–1.26, P<0.001). Moreover, in subgroup analyses by cancer types, the stronger significant association between hOGG1 Ser326Cys polymorphism and lung cancer risk was found (Cys/Cys vs. Ser/Ser: OR = 1.29, 95%CI = 1.16–1.44, P<0.001; Cys/Cys vs. Cys/Ser+Ser/Ser: OR = 1.22, 95%CI = 1.12–1.33, P<0.001). The significant effects of hOGG1 Ser326Cys polymorphism on colorectal, breast, bladder, prostate, esophageal, and gastric cancer were not detected. In addition, in subgroup analyses by ethnicities, we found that the hOGG1 Ser326Cys polymorphism was associated with overall cancer risk in Asians (Cys/Cys vs. Ser/Ser: OR = 1.21, 95%CI = 1.10–1.33, P<0.001).

Conclusions

This meta-analysis showed that hOGG1 326Cys allele might be a low-penetrant risk factor for lung cancer.

Citation: Wei B, Zhou Y, Xu Z, Xi B, Cheng H, Ruan J, et al. (2011) The Effect of hOGG1 Ser326Cys Polymorphism on Cancer Risk: Evidence from a Meta-Analysis. PLoS ONE 6(11): e27545. https://doi.org/10.1371/journal.pone.0027545

Editor: Deodutta Roy, Florida International University, United States of America

Received: June 1, 2011; Accepted: October 18, 2011; Published: November 17, 2011

Copyright: © 2011 Wei et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The authors have no support or funding to report.

Competing interests: The authors have declared that no competing interests exist.

Introduction

DNA damage plays a vital role in carcinogenesis [1], which generally occurs through different mechanisms such as by-product of normal cellular metabolism or the result of exposure to biological and environmental mutagens. DNA damage, if it is not repaired, could lead to apoptosis or mutation, which may cause induction of carcinogenesis [1]. It is suggested that reactive oxygen species (ROS) could induce both base lesions and single strand breaks in DNA [1]. The 8-hydroxy-2-deoxyguanine (8-OH-dG) is a major form of DNA damage, which is produced by reactive free radicals.

The presence of 8-OH-dG in DNA is thought to be a major cause of G:C to T:A transversion, because 8-OH-dG could direct the incorporation of adenine as well as cytosine opposite the lesion [2]. Thus, 8-OH-dG is a highly mutagenic DNA lesion in vivo [3], [4] unless it is repaired prior to DNA replication. The DNA repair enzyme human oxoguanine glycosylase 1 (hOGG1) is a DNA glycosylase/AP lyase that has been indicated to play an important role in preventing carcinogenesis by repairing oxidative damage to DNA [5]. Specifically, glycosylase/AP lyase could efficiently catalyze the excision and removal of 8-OH-dG adducts. HOGG1 may play a vital role in maintaining genome integrity and preventing the development of cancer.

Genetic variations in hOGG1 gene are increasingly studied for an elevated cancer risk because of the critical roles in stabilizing genome integrity. The hOGG1 gene has codon 326 polymorphism (Ser326Cys, rs1052133), and Cys326 has lower ability to prevent mutagenesis by 8-OH-dG than Ser326 in human cells in vivo [5]. So far, there were so many reports about the association of hOGG1 Ser326Cys polymorphism with risk of different cancers, including breast [6]–[18], prostate [19]–[25], pancreatic [26], [27], bladder [28]–[34], gallbladder [35]–[38], gastric [39]–[49], colorectal [50]–[63], esophageal [64]–[68], lung [69]–[85], cervical cancers [86], [87], and so on [88]–[101].

One study showed that the hOGG1 Ser326Cys polymorphism was associated with an increased risk of colorectal cancer (odds ratio: 2.3; 95% confidence interval: 1.1–5.0), the risk being higher in younger individuals [60]. Canbay et al [63] found that hOGG1 Ser326Cys polymorphism might be associated with increased risk of colorectal cancer in a Turkish population. However, other studies [53], [54], [59] did not show the significant association between the Ser326Cys polymorphism and colorectal cancer. Numerous studies and systematic approaches examined the role of the Ser326Cys polymorphism in lung cancer susceptibility. One meta-analysis showed that the overall odds ratio of homozygote for the hOGG1 326Cys allele against those for the hOGG1 326Ser allele was 1.24 (95% confidence interval: 1.01–1.53), suggesting that the locus was involved in susceptibility to lung cancer [83]. In contrast, another meta-analysis reported no significant association [102]. Some studies [15], [16] indicated that the Ser326Cys polymorphism was not associated with breast cancer. However, Sangrajrang et al [11] found that Thai women with variant allele of hOGG1 were likely to have an increased susceptibility to breast cancer. In addition, Chen et al [24] found that hOGG1 Ser326Cys polymorphism was associated with prostate cancer risk whereas Nock et al [22] did not find the significant association in the total study population.

On the whole, the results about the association between hOGG1 Ser326Cys polymorphism and cancer risk were conflicting and inconclusive. To derive a more precise estimation of the association, we performed a meta-analysis.

Materials and Methods

Identification and eligibility of relevant studies

PubMed (1956 to 30 July 2011) and Embase (1947 to 30 July 2011) database search was performed using following search terms: “oxoguanine glycosylase 1, hOGG1 or OGG1”, “polymorphism or variant”, and “cancer, neoplasm or tumor”. Additional studies were identified by a hand search of the references of original studies. In case of the studies with the same or overlapping data, we selected the most recent ones with the largest number of subjects. Studies included in this meta-analysis should meet the following criteria: (a) evaluation the association of hOGG1 Ser326Cys polymorphism and cancer risk published in English language, (b) use a case-control design, (c) contain available genotype frequency, and (d) the distribution of genotypes in the controls was consistent with Hardy-Weinberg equilibrium (HWE).

Data extraction

Two investigators independently extracted the data and reached a consensus on all the items. For each study, the following characteristics were collected: last name of first author, year of publication, country of origin, ethnicity, numbers of genotyped cases and controls. Different ethnic descents were categorized as Caucasians (at least 80% of Caucasians included), Asians, and Africans. If a study did not state the ethnic descendent or if it was not possible to separate participants according to such phenotype, the group reported was termed “mixed ethnicity”. In addition, if only one cancer type was included in a study in the meta-analysis, it was combined into the “mixed cancer” group. For study [49] including subjects of different ethnic groups, data were extracted separately for each ethnic group whenever possible. Because the studies [19], [31], [56], [87], [103] only provided the information of genotypes as “Cys/Cys+Cys/Ser” and Ser/Ser without data for other genotypes, we could only calculate the OR for the dominant genetic model.

Statistical analysis

The strength of the association between hOGG1 Ser326Cys polymorphism and cancer risk was measured by odds ratios (ORs) with 95% confidence intervals (CIs). We first estimated the risks of the Cys/Cys and Ser/Cys genotypes on risk of cancer, compared with the wild-type Ser/Ser homozygote, then evaluated the risks of “Cys/Cys+Ser/Cys vs. Ser/Ser” and “Cys/Cys vs. Ser/Cys+Ser/Ser” on risk of cancer, assuming dominant and recessive effects of the variant Cys allele, respectively. Subgroup analysis was also performed based on different ethnicities, cancer types, age, and sex.

Heterogeneity was evaluated with a chi-square-based Q test among the studies (P<0.10 was considered significant) [104], [105]. When the heterogeneity was present, the random effects model was used to calculate the pooled OR [106], whereas the fixed effects model was used in its absence [107]. Sensitivity analysis was performed to assess the stability of the results.

For control group of each study, the allelic frequency was calculated, and the observed genotype frequencies of the hOGG1 Ser326Cys polymorphism were assessed for Hardy-Weinberg equilibrium (HWE) by using the Pearson chi-square test; P<0.05 was considered significant. Funnel plots and Egger's linear regression test were used to provide diagnosis of the potential publication bias [108].

All statistical tests for this meta-analysis were performed with STATA (version 10.0; Stata Corporation, College Station, TX) and SPSS for Windows (version 11.0; SPSS, Inc., Chicago, IL).

Results

Study characteristics

For cancer susceptibility related to hOGG1 Ser326Cys polymorphism, articles were retrieved based on the search criteria. Study selection process was shown in Figure 1. Among them, the distribution of genotypes in the controls was not consistent with HWE in 13 studies, which were excluded in the meta-analysis. 5 additional studies were excluded because of overlapping data. Finally, a total of 91 case-control studies involving 31,297 cancer cases and 39,033 controls were included in the meta-analysis. The characteristics of included studies were summarized in Table S1. There were 42 studies of Caucasian descendants and 35 studies of Asian descendants. Cancers were confirmed histologically or pathologically in most studies. There were 14 studies of colorectal cancer, 19 studies of lung cancer, 12 studies of breast cancer, 6 studies of bladder cancer, 4 studies of prostate cancer, 11 studies of gastric cancer, 5 studies of esophageal cancer, 6 studies of head and neck cancer, 2 studies of gallbladder cancer, and 2 studies of ALL. There were 57 studies, in which the data on age of cancer cases and controls were shown in detail. Among them, the age-matched control subjects were used in 42 studies, which were included in subgroup analyses by age. 19 studies, which specifically reported data according to gender, were eligible for subgroup analyses by sex. In addition, the distribution of genotypes in the controls was consistent with HWE in all studies (P>0.05).

thumbnail
Download:
Figure 1. Flow chart of study selection based on the inclusion and exclusion criteria.

https://doi.org/10.1371/journal.pone.0027545.g001

Quantitative synthesis

The 326Cys allele frequencies in controls of different ethnicities were calculated. The frequency of the 326Cys allele was 47.07% (95%CI = 43.39–50.75%) among Asian controls, which was significantly higher than that of Caucasian controls (23.62%; 95%CI = 20.43–26.81%, P<0.001; Figure S1).

We carried out a meta-analysis of the hOGG1 Ser326Cys polymorphism overall, and in subgroups according to cancer types and ethnic groups under various genetic models (Table S2). Overall, we found that the hOGG1 Ser326Cys polymorphism was significantly associated with the risk of cancer (Cys/Cys vs. Ser/Ser: OR = 1.19, 95%CI = 1.09–1.30, P<0.001; Cys/Cys vs. Cys/Ser+Ser/Ser: OR = 1.16, 95%CI = 1.08–1.26, P<0.001; Table S2, Figure S2). In subgroup analyses by cancer types, we found that the hOGG1 Ser326Cys polymorphism was significantly associated with lung cancer (Cys/Cys vs. Ser/Ser: OR = 1.29, 95%CI = 1.16–1.44, P<0.001; Cys/Cys vs. Cys/ Ser+Ser/Ser: OR = 1.22, 95%CI = 1.12–1.33, P<0.001; Table S2, Figure 2), but not with colorectal, breast, bladder, prostate, and gastric cancer. In addition, we found that the hOGG1 Ser326Cys polymorphism was significantly associated with the risk of head and neck cancer (Cys/Cys vs. Ser/Ser: OR = 1.71, 95%CI = 1.05–2.78, P = 0.03).

thumbnail
Download:
Figure 2. Forest plot of lung cancer risk associated with hOGG1 Ser326Cys polymorphism (for Cys/Cys vs. Ser/Ser).

The squares and horizontal lines correspond to the study-specific OR and 95% CI. The area of the squares reflects the weight (inverse of the variance). The diamond represents the summary OR and 95% CI.

https://doi.org/10.1371/journal.pone.0027545.g002

In subgroup analyses by ethnicities, we found that the hOGG1 Ser326Cys polymorphism was associated with overall cancer risk in Asian population (Cys/Cys vs. Ser/Ser: OR = 1.21, 95%CI = 1.10–1.33, P<0.001; Cys/Cys vs. Cys/Ser+Ser/Ser: OR = 1.14, 95%CI = 1.03–1.26, P = 0.004; Cys/Cys+Cys/Ser vs. Ser/Ser: OR = 1.12, 95%CI = 1.05–1.19, P<0.001; Table S2). In subgroup analyses by age, we found that the hOGG1 Ser326Cys polymorphism was associated with overall cancer risk among cancer cases (<60 years) and cancer cases (≥60 years), respectively (Table S3). In addition, in subgroup analyses by sex, we found that the Ser326Cys polymorphism was not associated with overall cancer risk among women and men, respectively (Table S3).

Ethnicity-specific effect of hOGG1 Ser326Cys polymorphism on cancer risk

When the data were analyzed in subgroups of subjects stratified by ethnicities, we found that the hOGG1 Ser326Cys polymorphism was significantly associated with overall cancer risk among Asians (Cys/Cys vs. Ser/Ser: OR = 1.21, 95%CI = 1.10–1.33, P<0.001; Table S2). The results of logistic regression analyses showed joint effects between Asians and hOGG1 Ser326Cys polymorphism (P<0.01).

Test of heterogeneity

The heterogeneity was reckoned between each of the studies using the Q-test. Overall, the significant heterogeneity was found (Cys/Cys vs. Ser/Ser: Pheterogeneity<0.001; Cys/ Ser vs. Ser/Ser: Pheterogeneity<0.001; Cys/Cys vs. Cys/Ser+Ser/Ser: Pheterogeneity<0.001; Cys/Cys+Cys/Ser vs. Ser/Ser: Pheterogeneity<0.001). In stratified analyses by cancer types, we did not find the significant heterogeneity for lung cancer under two genetic models (Cys/Cys vs. Ser/Ser: Pheterogeneity = 0.40; Cys/Cys vs. Cys/ Ser+Ser/Ser: Pheterogeneity = 0.40).

Sensitivity analysis

In the sensitivity analysis, the influence of each study on the pooled OR was examined by repeating the meta-analysis while omitting each study, one at a time. This procedure confirmed the stability of the overall result (data not shown). However, in the subgroup by ethnicities, sensitivity analyses show that P value of Z-test for statistical significance of the summary OR (Cys/Cys vs. Cys/Ser+Ser/Ser) among Caucasians is 0.06 when excluding one study by Obtulowicz et al.

Publication bias

Begg's funnel plot and Egger's test were conducted to assess the publication bias of the literatures. The shape of funnel plots did not reveal any evidence of funnel plot asymmetry. Egger's test further provided statistical evidence of funnel plot symmetry (Cys/Cys vs. Ser/Ser: P = 0.28; Cys/Ser vs. Ser/Ser: P = 0.57; Cys/Cys vs. Cys/Ser+Ser/Ser: P = 0.20; Cys/Cys+Cys/Ser vs. Ser/Ser: P = 0.21). The results did not show any evidence of publication bias.

Discussion

The hOGG1, which is generally involved in DNA repair, has been studied extensively on its relationship with different types of cancer, such as breast [6]–[18], prostate [19]–[25], pancreatic [26], [27], bladder [28]–[34], gallbladder [35]–[38], gastric [39]–[49], colorectal [50]–[63], esophageal [64]–[68], lung [69]–[85], cervical cancers [86], [87], and so on [88]–[101]. Previous conclusions of numerous studies on the association between the hOGG1 Ser326Cys polymorphism and cancer risk remain conflicting and contradictory. The conflicting results are possibly because of a small effect of the Ser326Cys polymorphism on cancer risk or the relatively low statistical power of published studies. Hence, this meta-analysis was needed to provide a quantitative approach for combining the different results.

The present meta-analysis, including 31,297 cancer cases and 39,033 controls, explored the relationship between the Ser326Cys polymorphism and overall cancer risk. In the meta-analysis, we found that the hOGG1 Ser326Cys polymorphism was significantly associated with overall cancer risk. In subgroup analyses by cancer types, the significant association between the hOGG1 Ser326Cys polymorphism and lung cancer risk was further detected. This result was consistent with previous study [109]. In addition, in subgroup analyses by ethnicities, we found that the hOGG1 Ser326Cys polymorphism was significantly associated with overall cancer risk in Asian population. However, sensitivity analyses suggested that the significant association between the Ser326Cys polymorphism and overall cancer risk among Caucasians lacked convincing evidence.

The hOGG1 encodes a DNA glycosylase that is thought to be involved in base excision repair of oxidatively damaged DNA [110]. The hOGG1 could catalyze the cleavage of the glycosylic bond between the modified base and the sugar moiety, leaving an abasic apurinic/apyrimidinic site in DNA; the resulting apurinic/apyrimidinic site is then incised, and the repair is completed by successive actions of a phosphodiesterase, a DNA polymerase, and a DNA liagse [111]–[113]. With respect to the important roles of hOGG1 in DNA repair, it is biologically plausible that hOGG1 Ser326Cys polymorphism may modulate the risk of cancer. This hypothesis was confirmed by our data. In addition, because of the relatively small sample size on head and neck cancer, the result about head and neck cancer needed further confirmation.

We did not find that hOGG1 Ser326Cys polymorphism was significantly associated with cancer risk in Caucasian population and other cancer types including breast, prostate, pancreatic, bladder, gallbladder, gastric, colorectal, and esophageal cancer, suggesting the influence of the genetic variant may be masked by the presence of other as-yet unidentified causal genes involved in carcinogenesis. In addition, we found that the frequency of the 326Cys allele was 47.07% among Asian controls, which was significantly higher than that of Caucasian controls (23.62%, P<0.001), which may also affect the roles of hOGG1 Ser326Cys polymorphism on cancer risk in Asians and Caucasians.

Several limitations of the meta-analysis should be addressed. First, limited data restricted our evaluation on potential gene-gene interaction. Second, there was not enough data on African population in this meta-analysis. Third, our results were based on unadjusted evaluation. In order to provide a more precise estimation on the basis of adjustment for confounders, well-designed studies are warranted by taking potential confounders such as alcohol and smoking into account.

In summary, this meta-analysis provided evidence of the association between hOGG1 Ser326Cys polymorphism and cancer risk, supporting the hypothesis that hOGG1 Ser326Cys polymorphism might be a low-penetrant susceptibility marker of lung cancer. Moreover, sophisticated gene-gene interaction should be considered in future analysis, which would lead a better, comprehensive understanding of the association between hOGG1 Ser326Cys polymorphism and cancer risk.

Supporting Information

Figure S1.

Frequencies of the variant alleles among controls stratified by ethnicities. The“○” and “*” represent outlier.

https://doi.org/10.1371/journal.pone.0027545.s001

(TIF)

Figure S2.

Forest plot of overall cancer risk associated with hOGG1 Ser326Cys polymorphism (for Cys/Cys vs. Ser/Ser). The squares and horizontal lines correspond to the study-specific OR and 95% CI. The area of the squares reflects the weight (inverse of the variance). The diamond represents the summary OR and 95% CI.

https://doi.org/10.1371/journal.pone.0027545.s002

(TIF)

Table S1.

Characteristics of studies included in the meta-analysis.

https://doi.org/10.1371/journal.pone.0027545.s003

(DOC)

Table S2.

Stratified analyses of the hOGG1 Ser326Cys polymorphism on cancer risk.

https://doi.org/10.1371/journal.pone.0027545.s004

(DOC)

Table S3.

Stratified analyses of the hOGG1 Ser326Cys polymorphism on cancer risk by age and sex.

https://doi.org/10.1371/journal.pone.0027545.s005

(DOC)

Author Contributions

Conceived and designed the experiments: ZX BW. Performed the experiments: BW HC JR MZ YZ BX. Analyzed the data: ZX BW YZ. Contributed reagents/materials/analysis tools: BW YZ HC. Wrote the paper: BW YZ ZX BX HC JR MZ QH QW ZW ZY KJ DZ FX XH JS PL.

References

  1. 1. Weiss JM, Goode EL, Ladiges WC, Ulrich CM (2005) Polymorphic variation in hOGG1 and risk of cancer: a review of the functional and epidemiologic literature. Mol Carcinog 42: 127–41.
  2. 2. Shibutani S, Takeshita M, Grollman AP (1991) Insertion of specific bases during DNA synthesis past the oxidation-damaged base 8-oxodG. Nature 349: 431–4.
  3. 3. Cheng KC, Cahill DS, Kasai H, Nishimura S, Loeb LA (1992) 8-Hydroxyguanine, an abundant form of oxidative DNA damage, causes G----T and A----C substitutions. J Biol Chem 267: 166–72.
  4. 4. Moriya M, Ou C, Bodepudi V, Johnson F, Takeshita M, et al. (1991) Site-specific mutagenesis using a gapped duplex vector: a study of translesion synthesis past 8-oxodeoxyguanosine in E. coli. Mutat Res 254: 281–8.
  5. 5. Yamane A, Kohno T, Ito K, Sunaga N, Aoki K, et al. (2004) Differential ability of polymorphic OGG1 proteins to suppress mutagenesis induced by 8-hydroxyguanine in human cell in vivo. Carcinogenesis 25: 1689–94.
  6. 6. Hsu MS, Yu JC, Wang HW, Chen ST, Hsiung CN, et al. (2009) Synergistic Effects of Polymorphisms in DNA Repair Genes and Endogenous Estrogen Exposure on Female Breast Cancer Risk. Ann Surg Oncol.
  7. 7. Sterpone S, Mastellone V, Padua L, Novelli F, Patrono C, et al. (2010) Single-nucleotide polymorphisms in BER and HRR genes, XRCC1 haplotypes and breast cancer risk in Caucasian women. J Cancer Res Clin Oncol 136: 631–6.
  8. 8. Sterpone S, Cornetta T, Padua L, Mastellone V, Giammarino D, et al. (2010) DNA repair capacity and acute radiotherapy adverse effects in Italian breast cancer patients. Mutat Res 684: 43–8.
  9. 9. Synowiec E, Stefanska J, Morawiec Z, Blasiak J, Wozniak K (2008) Association between DNA damage, DNA repair genes variability and clinical characteristics in breast cancer patients. Mutat Res 648: 65–72.
  10. 10. Romanowicz-Makowska H, Smolarz B, Makowski M, Polac I, Pertynski T (2008) Ser326Cys polymorphism in DNA repair genes hOGG1 in breast cancer women. Pol J Pathol 59: 201–4.
  11. 11. Sangrajrang S, Schmezer P, Burkholder I, Waas P, Boffetta P, et al. (2008) Polymorphisms in three base excision repair genes and breast cancer risk in Thai women. Breast Cancer Res Treat 111: 279–88.
  12. 12. Rossner P Jr, Terry MB, Gammon MD, Zhang FF, Teitelbaum SL, et al. (2006) OGG1 polymorphisms and breast cancer risk. Cancer Epidemiol Biomarkers Prev 15: 811–5.
  13. 13. Cai Q, Shu XO, Wen W, Courtney R, Dai Q, et al. (2006) Functional Ser326Cys polymorphism in the hOGG1 gene is not associated with breast cancer risk. Cancer Epidemiol Biomarkers Prev 15: 403–4.
  14. 14. Zhang Y, Newcomb PA, Egan KM, Titus-Ernstoff L, Chanock S, et al. (2006) Genetic polymorphisms in base-excision repair pathway genes and risk of breast cancer. Cancer Epidemiol Biomarkers Prev 15: 353–8.
  15. 15. Choi JY, Hamajima N, Tajima K, Yoo KY, Yoon KS, et al. (2003) hOGG1 Ser326Cys polymorphism and breast cancer risk among Asian women. Breast Cancer Res Treat 79: 59–62.
  16. 16. Vogel U, Nexo BA, Olsen A, Thomsen B, Jacobsen NR, et al. (2003) No association between OGG1 Ser326Cys polymorphism and breast cancer risk. Cancer Epidemiol Biomarkers Prev 12: 170–1.
  17. 17. Loizidou MA, Michael T, Neuhausen SL, Newbold RF, Marcou Y, et al. (2009) DNA-repair genetic polymorphisms and risk of breast cancer in Cyprus. Breast Cancer Res Treat 115: 623–7.
  18. 18. Roberts MR, Shields PG, Ambrosone CB, Nie J, Marian C, et al. (2011) Single-nucleotide polymorphisms in DNA repair genes and association with breast cancer risk in the web study. Carcinogenesis 32: 1223–30.
  19. 19. Zhang J, Dhakal IB, Greene G, Lang NP, Kadlubar FF (2010) Polymorphisms in hOGG1 and XRCC1 and risk of prostate cancer: effects modified by plasma antioxidants. Urology 75: 779–85.
  20. 20. Dhillon VS, Yeoh E, Fenech M (2009) DNA repair gene polymorphisms and prostate cancer risk in South Australia-results of a pilot study. Urol Oncol.
  21. 21. Agalliu I, Kwon EM, Salinas CA, Koopmeiners JS, Ostrander EA, et al. (2010) Genetic variation in DNA repair genes and prostate cancer risk: results from a population-based study. Cancer Causes Control 21: 289–300.
  22. 22. Nock NL, Cicek MS, Li L, Liu X, Rybicki BA, et al. (2006) Polymorphisms in estrogen bioactivation, detoxification and oxidative DNA base excision repair genes and prostate cancer risk. Carcinogenesis 27: 1842–8.
  23. 23. Nam RK, Zhang WW, Jewett MA, Trachtenberg J, Klotz LH, et al. (2005) The use of genetic markers to determine risk for prostate cancer at prostate biopsy. Clin Cancer Res 11: 8391–7.
  24. 24. Chen L, Elahi A, Pow-Sang J, Lazarus P, Park J (2003) Association between polymorphism of human oxoguanine glycosylase 1 and risk of prostate cancer. J Urol 170: 2471–4.
  25. 25. Xu J, Zheng SL, Turner A, Isaacs SD, Wiley KE, et al. (2002) Associations between hOGG1 sequence variants and prostate cancer susceptibility. Cancer Res 62: 2253–7.
  26. 26. Li D, Suzuki H, Liu B, Morris J, Liu J, et al. (2009) DNA repair gene polymorphisms and risk of pancreatic cancer. Clin Cancer Res 15: 740–6.
  27. 27. McWilliams RR, Bamlet WR, Cunningham JM, Goode EL, de Andrade M, et al. (2008) Polymorphisms in DNA repair genes, smoking, and pancreatic adenocarcinoma risk. Cancer Res 68: 4928–35.
  28. 28. Gangwar R, Ahirwar D, Mandhani A, Mittal RD (2009) Do DNA repair genes OGG1, XRCC3 and XRCC7 have an impact on susceptibility to bladder cancer in the North Indian population? Mutat Res 680: 56–63.
  29. 29. Narter KF, Ergen A, Agachan B, Gormus U, Timirci O, et al. (2009) Bladder cancer and polymorphisms of DNA repair genes (XRCC1, XRCC3, XPD, XPG, APE1, hOGG1). Anticancer Res 29: 1389–93.
  30. 30. Arizono K, Osada Y, Kuroda Y (2008) DNA repair gene hOGG1 codon 326 and XRCC1 codon 399 polymorphisms and bladder cancer risk in a Japanese population. Jpn J Clin Oncol 38: 186–91.
  31. 31. Huang M, Dinney CP, Lin X, Lin J, Grossman HB, et al. (2007) High-order interactions among genetic variants in DNA base excision repair pathway genes and smoking in bladder cancer susceptibility. Cancer Epidemiol Biomarkers Prev 16: 84–91.
  32. 32. Karahalil B, Kocabas NA, Ozcelik T (2006) DNA repair gene polymorphisms and bladder cancer susceptibility in a Turkish population. Anticancer Res 26: 4955–8.
  33. 33. Figueroa JD, Malats N, Real FX, Silverman D, Kogevinas M, et al. (2007) Genetic variation in the base excision repair pathway and bladder cancer risk. Hum Genet 121: 233–42.
  34. 34. Kim EJ, Jeong P, Quan C, Kim J, Bae SC, et al. (2005) Genotypes of TNF-alpha, VEGF, hOGG1, GSTM1, and GSTT1: useful determinants for clinical outcome of bladder cancer. Urology 65: 70–5.
  35. 35. Srivastava K, Srivastava A, Mittal B (2011) Polymorphisms in ERCC2, MSH2, and OGG1 DNA repair genes and gallbladder cancer risk in a population of Northern India. Cancer 116: 3160–9.
  36. 36. Srivastava A, Srivastava K, Pandey SN, Choudhuri G, Mittal B (2009) Single-nucleotide polymorphisms of DNA repair genes OGG1 and XRCC1: association with gallbladder cancer in North Indian population. Ann Surg Oncol 16: 1695–703.
  37. 37. Huang WY, Gao YT, Rashid A, Sakoda LC, Deng J, et al. (2008) Selected base excision repair gene polymorphisms and susceptibility to biliary tract cancer and biliary stones: a population-based case-control study in China. Carcinogenesis 29: 100–5.
  38. 38. Jiao X, Huang J, Wu S, Lv M, Hu Y, et al. (2007) hOGG1 Ser326Cys polymorphism and susceptibility to gallbladder cancer in a Chinese population. Int J Cancer 121: 501–5.
  39. 39. Engin AB, Karahalil B, Engin A, Karakaya AE (2011) DNA repair enzyme polymorphisms and oxidative stress in a Turkish population with gastric carcinoma. Mol Biol Rep 38: 5379–86.
  40. 40. Sun LM, Shang Y, Zeng YM, Deng YY, Cheng JF (2010) HOGG1 polymorphism in atrophic gastritis and gastric cancer after Helicobacter pylori eradication. World J Gastroenterol 16: 4476–82.
  41. 41. Palli D, Polidoro S, D'Errico M, Saieva C, Guarrera S, et al. (2010) Polymorphic DNA repair and metabolic genes: a multigenic study on gastric cancer. Mutagenesis 25: 569–75.
  42. 42. Malik MA, Zargar SA, Mittal B (2010) Lack of influence of DNA repair gene OGG1 codon 326 polymorphisms of gastric cancer risk in the Kashmir valley. Asian Pac J Cancer Prev 11: 165–8.
  43. 43. Canbay E, Agachan B, Gulluoglu M, Isbir T, Balik E, et al. (2010) Possible associations of APE1 polymorphism with susceptibility and HOGG1 polymorphism with prognosis in gastric cancer. Anticancer Res 30: 1359–64.
  44. 44. Capella G, Pera G, Sala N, Agudo A, Rico F, et al. (2008) DNA repair polymorphisms and the risk of stomach adenocarcinoma and severe chronic gastritis in the EPIC-EURGAST study. Int J Epidemiol 37: 1316–25.
  45. 45. Farinati F, Cardin R, Bortolami M, Nitti D, Basso D, et al. (2008) Oxidative DNA damage in gastric cancer: CagA status and OGG1 gene polymorphism. Int J Cancer 123: 51–5.
  46. 46. Poplawski T, Arabski M, Kozirowska D, Blasinska-Morawiec M, Morawiec Z, et al. (2006) DNA damage and repair in gastric cancer–a correlation with the hOGG1 and RAD51 genes polymorphisms. Mutat Res 601: 83–91.
  47. 47. Tsukino H, Hanaoka T, Otani T, Iwasaki M, Kobayashi M, et al. (2004) hOGG1 Ser326Cys polymorphism, interaction with environmental exposures, and gastric cancer risk in Japanese populations. Cancer Sci 95: 977–83.
  48. 48. Takezaki T, Gao CM, Wu JZ, Li ZY, Wang JD, et al. (2002) hOGG1 Ser(326)Cys polymorphism and modification by environmental factors of stomach cancer risk in Chinese. Int J Cancer 99: 624–7.
  49. 49. Hanaoka T, Sugimura H, Nagura K, Ihara M, Li XJ, et al. (2001) hOGG1 exon7 polymorphism and gastric cancer in case-control studies of Japanese Brazilians and non-Japanese Brazilians. Cancer Lett 170: 53–61.
  50. 50. Brevik A, Joshi AD, Corral R, Onland-Moret NC, Siegmund KD, et al. (2010) Polymorphisms in base excision repair genes as colorectal cancer risk factors and modifiers of the effect of diets high in red meat. Cancer Epidemiol Biomarkers Prev 19: 3167–73.
  51. 51. Engin AB, Karahalil B, Engin A, Karakaya AE (2010) Oxidative stress, Helicobacter pylori, and OGG1 Ser326Cys, XPC Lys939Gln, and XPD Lys751Gln polymorphisms in a Turkish population with colorectal carcinoma. Genet Test Mol Biomarkers 14: 559–64.
  52. 52. Obtulowicz T, Swoboda M, Speina E, Gackowski D, Rozalski R, et al. (2010) Oxidative stress and 8-oxoguanine repair are enhanced in colon adenoma and carcinoma patients. Mutagenesis 25: 463–71.
  53. 53. Curtin K, Samowitz WS, Wolff RK, Ulrich CM, Caan BJ, et al. (2009) Assessing tumor mutations to gain insight into base excision repair sequence polymorphisms and smoking in colon cancer. Cancer Epidemiol Biomarkers Prev 18: 3384–8.
  54. 54. Sliwinski T, Krupa R, Wisniewska-Jarosinska M, Pawlowska E, Lech J, et al. (2009) Common polymorphisms in the XPD and hOGG1 genes are not associated with the risk of colorectal cancer in a Polish population. Tohoku J Exp Med 218: 185–91.
  55. 55. Hansen RD, Krath BN, Frederiksen K, Tjonneland A, Overvad K, et al. (2009) GPX1 Pro(198)Leu polymorphism, erythrocyte GPX activity, interaction with alcohol consumption and smoking, and risk of colorectal cancer. Mutat Res 664: 13–9.
  56. 56. Kasahara M, Osawa K, Yoshida K, Miyaishi A, Osawa Y, et al. (2008) Association of MUTYH Gln324His and APEX1 Asp148Glu with colorectal cancer and smoking in a Japanese population. J Exp Clin Cancer Res 27: 49.
  57. 57. Stern MC, Conti DV, Siegmund KD, Corral R, Yuan JM, et al. (2007) DNA repair single-nucleotide polymorphisms in colorectal cancer and their role as modifiers of the effect of cigarette smoking and alcohol in the Singapore Chinese Health Study. Cancer Epidemiol Biomarkers Prev 16: 2363–72.
  58. 58. Pardini B, Naccarati A, Novotny J, Smerhovsky Z, Vodickova L, et al. (2008) DNA repair genetic polymorphisms and risk of colorectal cancer in the Czech Republic. Mutat Res 638: 146–53.
  59. 59. Park HW, Kim IJ, Kang HC, Jang SG, Ahn SA, et al. (2007) The hOGG1 Ser326Cys polymorphism is not associated with colorectal cancer risk. J Epidemiol 17: 156–60.
  60. 60. Moreno V, Gemignani F, Landi S, Gioia-Patricola L, Chabrier A, et al. (2006) Polymorphisms in genes of nucleotide and base excision repair: risk and prognosis of colorectal cancer. Clin Cancer Res 12: 2101–8.
  61. 61. Hansen R, Saebo M, Skjelbred CF, Nexo BA, Hagen PC, et al. (2005) GPX Pro198Leu and OGG1 Ser326Cys polymorphisms and risk of development of colorectal adenomas and colorectal cancer. Cancer Lett 229: 85–91.
  62. 62. Kim JI, Park YJ, Kim KH, Song BJ, Lee MS, et al. (2003) hOGG1 Ser326Cys polymorphism modifies the significance of the environmental risk factor for colon cancer. World J Gastroenterol 9: 956–60.
  63. 63. Canbay E, Cakmakoglu B, Zeybek U, Sozen S, Cacina C, et al. (2011) Association of APE1 and hOGG1 polymorphisms with colorectal cancer risk in a Turkish population. Curr Med Res Opin 27: 1295–302.
  64. 64. Lagadu S, Lechevrel M, Sichel F, Breton J, Pottier D, et al. (2010) 8-oxo-7,8-dihydro-2′-deoxyguanosine as a biomarker of oxidative damage in oesophageal cancer patients: lack of association with antioxidant vitamins and polymorphism of hOGG1 and GST. J Exp Clin Cancer Res 29: 157.
  65. 65. Upadhyay R, Malik MA, Zargar SA, Mittal B (2010) OGG1 Ser326Cys polymorphism and susceptibility to esophageal cancer in low and high at-risk populations of northern India. J Gastrointest Cancer 41: 110–5.
  66. 66. Ferguson HR, Wild CP, Anderson LA, Murphy SJ, Johnston BT, et al. (2008) No association between hOGG1, XRCC1, and XPD polymorphisms and risk of reflux esophagitis, Barrett's esophagus, or esophageal adenocarcinoma: results from the factors influencing the Barrett's adenocarcinoma relationship case-control study. Cancer Epidemiol Biomarkers Prev 17: 736–9.
  67. 67. Xing DY, Tan W, Song N, Lin DX (2001) Ser326Cys polymorphism in hOGG1 gene and risk of esophageal cancer in a Chinese population. Int J Cancer 95: 140–3.
  68. 68. Hao B, Wang H, Zhou K, Li Y, Chen X, et al. (2004) Identification of genetic variants in base excision repair pathway and their associations with risk of esophageal squamous cell carcinoma. Cancer Res 64: 4378–84.
  69. 69. Lan Q, Mumford JL, Shen M, Demarini DM, Bonner MR, et al. (2004) Oxidative damage-related genes AKR1C3 and OGG1 modulate risks for lung cancer due to exposure to PAH-rich coal combustion emissions. Carcinogenesis 25: 2177–81.
  70. 70. Chang JS, Wrensch MR, Hansen HM, Sison JD, Aldrich MC, et al. (2009) Base excision repair genes and risk of lung cancer among San Francisco Bay Area Latinos and African-Americans. Carcinogenesis 30: 78–87.
  71. 71. Kohno T, Kunitoh H, Mimaki S, Shiraishi K, Kuchiba A, et al. (2011) Contribution of the TP53, OGG1, CHRNA3, and HLA-DQA1 genes to the risk for lung squamous cell carcinoma. J Thorac Oncol 6: 813–7.
  72. 72. Qian B, Zhang H, Zhang L, Zhou X, Yu H, et al. (2011) Association of genetic polymorphisms in DNA repair pathway genes with non-small cell lung cancer risk. Lung Cancer 73: 138–46.
  73. 73. Okasaka T, Matsuo K, Suzuki T, Ito H, Hosono S, et al. (2009) hOGG1 Ser326Cys polymorphism and risk of lung cancer by histological type. J Hum Genet 54: 739–45.
  74. 74. Chang CH, Hsiao CF, Chang GC, Tsai YH, Chen YM, et al. (2009) Interactive effect of cigarette smoking with human 8-oxoguanine DNA N-glycosylase 1 (hOGG1) polymorphisms on the risk of lung cancer: a case-control study in Taiwan. Am J Epidemiol 170: 695–702.
  75. 75. Miyaishi A, Osawa K, Osawa Y, Inoue N, Yoshida K, et al. (2009) MUTYH Gln324His gene polymorphism and genetic susceptibility for lung cancer in a Japanese population. J Exp Clin Cancer Res 28: 10.
  76. 76. Karahalil B, Emerce E, Kocer B, Han S, Alkis N, et al. (2008) The association of OGG1 Ser326Cys polymorphism and urinary 8-OHdG levels with lung cancer susceptibility: a hospital-based case-control study in Turkey. Arh Hig Rada Toksikol 59: 241–50.
  77. 77. De Ruyck K, Szaumkessel M, De Rudder I, Dehoorne A, Vral A, et al. (2007) Polymorphisms in base-excision repair and nucleotide-excision repair genes in relation to lung cancer risk. Mutat Res 631: 101–10.
  78. 78. Sorensen M, Raaschou-Nielsen O, Hansen RD, Tjonneland A, Overvad K, et al. (2006) Interactions between the OGG1 Ser326Cys polymorphism and intake of fruit and vegetables in relation to lung cancer. Free Radic Res 40: 885–91.
  79. 79. Kohno T, Kunitoh H, Toyama K, Yamamoto S, Kuchiba A, et al. (2006) Association of the OGG1-Ser326Cys polymorphism with lung adenocarcinoma risk. Cancer Sci 97: 724–8.
  80. 80. Park J, Chen L, Tockman MS, Elahi A, Lazarus P (2004) The human 8-oxoguanine DNA N-glycosylase 1 (hOGG1) DNA repair enzyme and its association with lung cancer risk. Pharmacogenetics 14: 103–9.
  81. 81. Le Marchand L, Donlon T, Lum-Jones A, Seifried A, Wilkens LR (2002) Association of the hOGG1 Ser326Cys polymorphism with lung cancer risk. Cancer Epidemiol Biomarkers Prev 11: 409–12.
  82. 82. Sugimura H, Kohno T, Wakai K, Nagura K, Genka K, et al. (1999) hOGG1 Ser326Cys polymorphism and lung cancer susceptibility. Cancer Epidemiol Biomarkers Prev 8: 669–74.
  83. 83. Hung RJ, Brennan P, Canzian F, Szeszenia-Dabrowska N, Zaridze D, et al. (2005) Large-scale investigation of base excision repair genetic polymorphisms and lung cancer risk in a multicenter study. J Natl Cancer Inst 97: 567–76.
  84. 84. Ito H, Hamajima N, Takezaki T, Matsuo K, Tajima K, et al. (2002) A limited association of OGG1 Ser326Cys polymorphism for adenocarcinoma of the lung. J Epidemiol 12: 258–65.
  85. 85. Wikman H, Risch A, Klimek F, Schmezer P, Spiegelhalder B, et al. (2000) hOGG1 polymorphism and loss of heterozygosity (LOH): significance for lung cancer susceptibility in a caucasian population. Int J Cancer 88: 932–7.
  86. 86. Niwa Y, Matsuo K, Ito H, Hirose K, Tajima K, et al. (2005) Association of XRCC1 Arg399Gln and OGG1 Ser326Cys polymorphisms with the risk of cervical cancer in Japanese subjects. Gynecol Oncol 99: 43–9.
  87. 87. Farkasova T, Gurska S, Witkovsky V, Gabelova A (2008) Significance of amino acid substitution variants of DNA repair genes in radiosusceptibility of cervical cancer patients; a pilot study. Neoplasma 55: 330–7.
  88. 88. Gorgens H, Muller A, Kruger S, Kuhlisch E, Konig IR, et al. (2007) Analysis of the base excision repair genes MTH1, OGG1 and MUTYH in patients with squamous oral carcinomas. Oral Oncol 43: 791–5.
  89. 89. Laantri N, Jalbout M, Khyatti M, Ayoub WB, Dahmoul S, et al. (2011) XRCC1 and hOGG1 genes and risk of nasopharyngeal carcinoma in North African countries. Mol Carcinog 50: 732–7.
  90. 90. Cho EY, Hildesheim A, Chen CJ, Hsu MM, Chen IH, et al. (2003) Nasopharyngeal carcinoma and genetic polymorphisms of DNA repair enzymes XRCC1 and hOGG1. Cancer Epidemiol Biomarkers Prev 12: 1100–4.
  91. 91. Sliwinski T, Przybylowska K, Markiewicz L, Rusin P, Pietruszewska W, et al. (2011) MUTYH Tyr165Cys, OGG1 Ser326Cys and XPD Lys751Gln polymorphisms and head neck cancer susceptibility: a case control study. Mol Biol Rep 38: 1251–61.
  92. 92. Zhang Z, Shi Q, Wang LE, Sturgis EM, Spitz MR, et al. (2004) No Association between hOGG1 Ser326Cys polymorphism and risk of squamous cell carcinoma of the head and neck. Cancer Epidemiol Biomarkers Prev 13: 1081–3.
  93. 93. Elahi A, Zheng Z, Park J, Eyring K, McCaffrey T, et al. (2002) The human OGG1 DNA repair enzyme and its association with orolaryngeal cancer risk. Carcinogenesis 23: 1229–34.
  94. 94. Krupa R, Sobczuk A, Poplawski T, Wozniak K, Blasiak J (2011) DNA damage and repair in endometrial cancer in correlation with the hOGG1 and RAD51 genes polymorphism. Mol Biol Rep 38: 1163–70.
  95. 95. De Ruyck K, Van Eijkeren M, Claes K, Morthier R, De Paepe A, et al. (2005) Radiation-induced damage to normal tissues after radiotherapy in patients treated for gynecologic tumors: association with single nucleotide polymorphisms in XRCC1, XRCC3, and OGG1 genes and in vitro chromosomal radiosensitivity in lymphocytes. Int J Radiat Oncol Biol Phys 62: 1140–9.
  96. 96. Zhao H, Qin C, Yan F, Wu B, Cao Q, et al. (2011) hOGG1 Ser326Cys Polymorphism and Renal Cell Carcinoma Risk in a Chinese Population. DNA Cell Biol 30: 317–21.
  97. 97. Li Q, Huang L, Rong L, Xue Y, Lu Q, et al. (2011) hOGG1 Ser326Cys polymorphism and risk of childhood acute lymphoblastic leukemia in a Chinese population. Cancer Sci 102: 1123–7.
  98. 98. Stanczyk M, Sliwinski T, Cuchra M, Zubowska M, Bielecka-Kowalska A, et al. (2011) The association of polymorphisms in DNA base excision repair genes XRCC1, OGG1 and MUTYH with the risk of childhood acute lymphoblastic leukemia. Mol Biol Rep 38: 445–51.
  99. 99. Sakamoto T, Higaki Y, Hara M, Ichiba M, Horita M, et al. (2006) hOGG1 Ser326Cys polymorphism and risk of hepatocellular carcinoma among Japanese. J Epidemiol 16: 233–9.
  100. 100. Dianzani I, Gibello L, Biava A, Giordano M, Bertolotti M, et al. (2006) Polymorphisms in DNA repair genes as risk factors for asbestos-related malignant mesothelioma in a general population study. Mutat Res 599: 124–34.
  101. 101. Vogel U, Olsen A, Wallin H, Overvad K, Tjonneland A, et al. (2004) No association between OGG1 Ser326Cys and risk of basal cell carcinoma. Cancer Epidemiol Biomarkers Prev 13: 1680–1.
  102. 102. Li H, Hao X, Zhang W, Wei Q, Chen K (2008) The hOGG1 Ser326Cys polymorphism and lung cancer risk: a meta-analysis. Cancer Epidemiol Biomarkers Prev 17: 1739–45.
  103. 103. Klinchid J, Chewaskulyoung B, Saeteng S, Lertprasertsuke N, Kasinrerk W, et al. (2009) Effect of combined genetic polymorphisms on lung cancer risk in northern Thai women. Cancer Genet Cytogenet 195: 143–9.
  104. 104. Lau J, Ioannidis JP, Schmid CH (1997) Quantitative synthesis in systematic reviews. Ann Intern Med 127: 820–6.
  105. 105. Berman NG, Parker RA (2002) Meta-analysis: neither quick nor easy. BMC Med Res Methodol 2: 10.
  106. 106. Mantel N, Haenszel W (1959) Statistical aspects of the analysis of data from retrospective studies of disease. J Natl Cancer Inst 22: 719–48.
  107. 107. DerSimonian R, Laird N (1986) Meta-analysis in clinical trials. Control Clin Trials 7: 177–88.
  108. 108. Egger M, Davey Smith G, Schneider M, Minder C (1997) Bias in meta-analysis detected by a simple, graphical test. BMJ 315: 629–34.
  109. 109. Kiyohara C, Takayama K, Nakanishi Y (2010) Lung cancer risk and genetic polymorphisms in DNA repair pathways: a meta-analysis. J Nucleic Acids 701760.
  110. 110. Boiteux S, Radicella JP (2000) The human OGG1 gene: structure, functions, and its implication in the process of carcinogenesis. Arch Biochem Biophys 377: 1–8.
  111. 111. Dianov GL, Souza-Pinto N, Nyaga SG, Thybo T, Stevnsner T, et al. (2001) Base excision repair in nuclear and mitochondrial DNA. Prog Nucleic Acid Res Mol Biol 68: 285–97.
  112. 112. Karahalil B, Hogue BA, de Souza-Pinto NC, Bohr VA (2002) Base excision repair capacity in mitochondria and nuclei: tissue-specific variations. FASEB J 16: 1895–902.
  113. 113. Gu D, Wang M, Zhang Z, Chen J (2010) Lack of association between the hOGG1 Ser326Cys polymorphism and breast cancer risk: evidence from 11 case-control studies. Breast Cancer Res Treat 122: 527–31.