hOGG1基因多态性与川北地区肺癌易感性关系的研究

目的探讨四川北部地区汉族人群8-羟基鸟嘌呤糖苷酶(hOGG1)基因Ser326Cys位点多态性状况及其与该地区肺癌易感性的关系,并与其他地区人群进行比较。方法采用病例对照研究方法和聚合酶链式反应-限制性片段长度多态性(polymerise chain reaction-restriction fragment length polymorphism,PCR-RFLP)方法检测四川北部地区肺癌患者125例和非肿瘤患者125例(对照组)hOGG1基因第326位点Ser/Cys基因型分布,并比较不同基因型与肺癌发病危险的关系。结果病例组的Ser/Ser、Ser/Cys、Cys/Cys基因型频率分别为15.2%、27.2%、57.6%,而对照组分别为32.0%、42.4%、25.6%。χ2检验显示两组基因型分布差异有统计学意义(P<0.05)。与携带Ser/Ser基因型相比,携带Ser/Cys基因型者患肺癌风险增加(OR=1.351,95%CI=0.674～2.707,P=0.397),而携带Cys/Cys基因型者肺癌风险增加3倍(OR=4.737,95%CI=2.384～9.413,P=0.000)。结论 hOGG1基因Ser326Cys多态性可能与四川北部肺癌易感性有关,携带Cys/Cys基因型肺癌风险明显增加。     

hOGG1基因多态性与胃癌遗传易感性的关系

目的探讨人类8-羟基鸟嘌呤DNA糖苷酶1（hOGG1）基因多态性与胃癌遗传易感性的关系。方法收集河南郑州和开封地区98例胃癌患者和80例非肿瘤对照组志愿者外周血样,应用聚合酶链反应一限制性片段长度多态性（PCR—RFLP）检测法检测胃癌人群的外周血中DNA损伤修复酶基因多态性,分析其与肿瘤遗传易感性的关系。结果hOGGISer326Cys基因的各基因型频率在胃癌组和对照组间的分布差异有统计学意义（P〈0．05）。携带Cys326Cys基因型者胃癌的发病风险增加1．7倍（OR=I．706,95％CI=0．341～2．462,P=0．002）。hOGGlSer326Cys基因多态性与酒的交互作用增加胃癌的发病风险（S〉1,API=0．38）。结论Cys326Cys基因型是胃癌发病的危险基因型,携带Cys易感基因与饮酒交互作用时可能增加患胃癌的易感性。     

p21WAF1基因遗传多态性与乳腺癌发病关系的风险

目的 探讨p21WAF1基因多态性与乳腺癌遗传易感性之间的关系.方法 应用聚合酶链反应-限制性片断长度多态性(PCR-RFLP)方法检测117例乳腺癌患者和123例健康对照组外周血DNA p21WAF1基因第2外显子密码子31多态性的分布情况.结果 乳腺癌与健康对照组间p21WAF1基因第2外显子密码子31的A(arginine)、C(serine)等位基因频率分别54.27%、45.73%及50.00%、50.00%(P＞0.05).携带Ser/Arg和Arg/Arg基因型的个体与携带Ser/Ser基因型的个体比较,乳腺癌患病风险无明显增加(OR,1.108;95%CI,0.579-2.122).结论 p21WAF1基因第2外显子密码子31多态性可能与贵州地区汉族妇女乳腺癌的发病风险无相关性.     

TGF-β1基因多态性与高级别宫颈上皮内瘤变易感性的关系

目的研究转化生长因子β1(TGF-β1)基因多态性与高级别宫颈上皮内瘤变(CINⅡ-Ⅲ)遗传易感性的关系。方法选择191例CINⅡ-Ⅲ患者为病例组,207例年龄相匹配的正常者为对照组,采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)技术检测TGF-β1基因C509T和T869C多态性在两组中的频率和分布,比较不同基因型携带者患CINⅡ-Ⅲ的危险性。结果与携带T869CTT基因型相比,携带T869CTC/CC基因型者罹患CINⅡ-Ⅲ的风险升高1.582倍(OR=1.582,95%CI=1.026-2.438,P<0.05)。产次0-1次和不吸烟的女性携带T869CTC/CC基因型较携带TT基因型者罹患CINⅡ-Ⅲ的风险升高更为显著(P<0.05)。结论 TGF-β1T869C多态性可能与人群CINⅡ-Ⅲ的遗传易感性相关。     

XRCC1基因多态性与宫颈癌发病风险的关系

目的:探讨四川人群X线修复交叉互补基因1(XRCC1)Arg194Trp、Arg280His多态性与宫颈癌风险的关系.方法:采用病例-对照研究方法,PCR-RFLP检测123例宫颈癌病人及性别、年龄相匹配的175例正常人群XRCC1 Arg194Trp、Arg280His多态性分布及与宫颈癌风险的关系.结果:病例组和对照组Arg194Trp基因型频率分布差异有显著性(P＜0.05),Arg194Trp多态性可能与个体患宫颈癌风险相关,等位基因Trp可能增加个体患宫颈癌的风险(0R=1.617,95%CI=1.101～2.374,P＜0.05),Arg280His在两组中分布差异无显著性(P＞0.05).结论:Arg194Trp多态性可能与宫颈癌风险相关,Arg280His多态性与宫颈癌易感性无关.     

髓过氧化物酶基因-463 G>A多态性与早发冠心病的相关性

目的 探讨髓过氧化物酶(MPO)基因-463 G＞A多态性与早发冠心病(CHD)的相关性.方法 早发CHD 134例,对照145例,采用LDR-PCR测序分型技术分析两组患者MPO基因启动子区第-463位核苷酸多态基因型分布,及其与早发CHD的关系.结果 病例组A/A基因型及A等位基因频率低于对照组,病例组G/G基因型及G等位基因频率高于对照组.杂合子G/A在两组患者中差异无统计学意义.等位基因A对早发CHD易感性的保护作用有统计学意义(P＜0.01).携带至少一个等位基因A的患者早发CHD的发病风险降低达50%(OR=0.50,95%CI:0.27～0.93),A/A基因型的患者早发CHD的发病风险降低达89%(OR=0.11,95%CI:0.03～0.40).结论 MPO-463 G＞A基因多态性与早发冠心病的发病风险相关,MPO-463 A等位基因携带者患早发冠心病的风险明显降低.     

功能性BRCA1启动子c.-2265C/T多态性与卵巢癌易感性的相关性

目的 探讨BRCA1基因功能性启动子c.-2265C/T多态性与卵巢癌易感性的关联性.方法 应用MGB-TaqMan探针等位基因分型技术对123例上皮性卵巢癌患者(病例组)和123例与之年龄相匹配的健康汉族妇女(对照组)的外周血基因组DNA进行BRCA1功能性启动子c.-2265C/T单核苷酸多态性(SNP)基因型的检测,并进行相关性分析.结果 病例组中,CC基因型44例(35.8％),CT基因型62例(50.4％),TT基因型17例(13.8％);对照组中,CC基因型45例(36.6％),CT基因型60例(48.8％),TT基因型18例(14.6％);组间比较无统计学差异(P＞0.05).与CC基因型相比,TT基因型与降低卵巢癌中低分化腺癌、子宫内膜样癌及浆液性腺癌发病风险均无明显相关性(P＞0.05).结论 与C等位基因比较,T等位基因的纯合型未降低上皮性卵巢癌的发病风险.     

ELAC2基因变异与前列腺癌易感性

目的 研究elaC同系物2(ELAC2)基因变异与中国人群中前列腺癌易感性的关系.方法 采用PCR-限制性酶切片段长度多态性的方法,在210例前列腺癌患者和230例正常对照者中检测ELAC2基因Ser217Leu和Ala541Thr多态性,采用回归分析研究各基因型与前列腺癌发病风险的关系.结果 Ser217Leu多态性与前列腺癌发生并无明显相关,但是Ala541Thr多态位点对应的Ala/Thr基因型频率在前列腺癌组明显高于正常对照组该基因型出现的频率(10.5% vs.3.0%)(P＜0.01),该基因型显著增加了前列腺癌的易感性优势比(OR)=1.52,95%可信区间(CI)=1.78～8.62.而且Thr等位基因在前列腺癌患者中的频率明显大于正常对照组(5.2%vs.1.5%).结论 ELAC2基因Ala541Thr多态显著增加中国人群前列腺癌的发病风险.     

DNA修复基因XPD单核苷酸多态性与肺癌遗传易感性

目的探讨XPD基因单核苷酸多态性与肺癌遗传易感性的关系。方法以聚合酶链反应-限制性片段长度多态性方法分析肺癌患者(n=114)和按性别、年龄频数配比的对照者(n=114)XPD基因Asp312Asn和Lys751Gln位点的多态性,比较不同基因型与肺癌风险的关系,并探讨吸烟在其中的影响。结果与携带XPD312Asp/Asp基因型者比较,携带至少1个312Asn等位基因的个体罹患肺癌的风险增加1.55倍(95%CI1.02～2.39)。而与携带XPD751Lys/Lys基因型者比较,携带至少1个751Gln等位基因的个体罹患肺癌的风险并没有显著增加(校正OR=0.96;95%CI0.53～1.72)。交互作用分析显示,携带至少1个312Asn等位基因并吸烟者肺癌风险增加5.14倍(95%CI1.82～9.16),其中重度吸烟者肺癌风险增加高达7.32倍(95%CI2.17～21.18)。结论DNA修复基因XPD Asp312Asn多态性可能与山东地区汉族人群肺癌遗传易感性有关,并可显著增加吸烟对肺癌的危险性。     

蛋白激酶Cξ亚型基因多态性与2型糖尿病的相关性

目的 研究中国东南方汉族人群2型糖尿病家系的蛋白激酶Cξ亚型基因多态性,探讨其与2型糖尿病(T2DM)易感性的关系.方法 应用聚合酶链式反应-限制性片段长度多态性(PCR-RFLP)方法,对来自T2DM家系成员、无家族史的T2DM患者及正常对照的该基因rs381664位点进行基因分型.结果 rs381664位点基因型、等位基因频率在各组人群中分布差异无统计学意义.按年龄分层显示在家系大于50岁人群组中,突变型CC/CT型为保护性因素[OR 95% CI＝0.541 (0.323～0.905)].按BMI分层分析糖尿病相关生物学指标显示,在家系内对照组超重者和病例组肥胖者中,均发现携带TT基因型个体的胰岛素抵抗指数显著高于携带CC/CT型个体(P＜0.05).结论 蛋白激酶Cξ亚型基因rs381664位点多态性与胰岛素抵抗存在相关性,在50岁以上人群的T2DM发生中可能起到一定作用.     

The human 8-oxoguanine DNA N-glycosylase 1 (hOGG1) DNA repair enzyme and its association with lung cancer risk

OBJECTIVE: The human 8-oxoguanine DNA N-glycosylase 1 gene encodes a DNA glycosylase that is involved in the base excision repair of 8-hydroxy-2-deoxyguanine from oxidatively-damaged DNA and expressed in lung tissue. The codon 326 polymorphism in the hOGG1 gene has been suggested to reduce DNA repair enzyme activity based on in vitro functional analysis. The goal of the present study is to determine whether the codon 326 polymorphism was significantly associated with alterations in individual risk for lung cancer. METHODS: To determine whether hOGG1 plays a role in risk for lung cancer, we measured the prevalence of the Ser326Cys polymorphism in incident lung cancer patients and matched non-cancer controls. hOGG1 genotyping was performed by PCR-restriction fragment length polymorphism analysis of genomic DNA isolated from 179 Caucasian lung cancer cases and 358 controls individually matched in a 1:2 ratio by race-, sex- and age (+/- 5 years). RESULTS: Significantly increased risk for lung cancer was observed for both the hOGG1 326 (odds ratio [OR] = 1.9, 95% confidence interval [CI] = 1.2-2.9) and hOGG1 326 genotypes (OR = 3.8, 95% CI = 1.4-10.6). The increased risk for lung cancer was observed for subjects with both the hOGG1 326 (OR = 1.7, 95% CI = 1.1-2.8) and hOGG1 326 genotypes (OR = 4.9, 95% CI = 1.5-16.1) in ever-smokers. A significant association was found between hOGG1 genotypes and lung cancer risk with a dose-dependent effect with smoking. Significantly increased risk for variant hOGG1 genotypes was observed for all non-small cell lung cancer patients. CONCLUSION: These results suggest that the hOGG1 Ser326Cys polymorphism plays an important role in the risk for lung cancer and is linked to exposure to tobacco smoke.     

Genetic polymorphisms in hMTH1, hOGG1 and hMYH and risk of chronic benzene poisoning in a Chinese occupational population

Oxidative damage to DNA induced by benzene is an important mechanism of its genotoxicity, which leads to chronic benzene poisoning (CBP). Therefore, genetic variation in DNA repair genes may contribute to susceptibility to CBP in the exposed population. We hypothesized that single nucleotide polymorphisms (SNPs) in hMTH1, hOGG1 and hMYH genes are associated with risk of CBP. We genotyped SNPs at codon 83 of hMTH1, codon 326 of hOGG1, and codon 324 of hMYH in 152 CBP patients and 152 healthy workers occupationally exposed to benzene without poisoning manifestations. The genotypes were determined by polymerase chain reaction-restrained fragment length polymorphism (PCR-RFLP) technique. There were 2.51-fold [adjusted odds ratio (OR_adj), 2.51; 95% CI, 1.14-5.49; P = 0.02] and 2.49-fold (OR_adj, 2.49; 95% CI: 1.52-4.07; P < 0.01) increased risk of CBP for individuals carrying genotypes of hMTH1 83Val/Met + Met/Met and hOGG1 326Cys/Cys, respectively. Compared with individuals carrying genotypes of hOGG1 326Cys/Cys and hMYH 324His/His at the same time, there was a 0.33-fold (OR_adj, 0.33; 95% CI: 0.15-0.72; P < 0.05) decreased risk of CBP for those with genotypes of hOGG1 326Ser/Cys + Ser/Ser and hMYH 324His/Gln + Gln/Gln. In the smoking group, there was a 0.15-fold (OR_adj, 0.15; 95% CI, 0.03-0.68; P = 0.01) decreased risk of CBP for subjects carrying genotypes of hMYH 324His/Gln + Gln/Gln compared with those of genotype of hMYH 324His/His. Therefore, our results suggested that polymorphisms at codons 83 of hMTH1 and codon 326 of hOGG1 might contribute to CBP in a Chinese occupational population.     

Association of <Emphasis Type="Italic">hOGG1</Emphasis> genotype with life style and oxidative DNA damage among Chinese ethnic populations

To assess the natural variation of hOGG1 gene and the gene–environmental interactions, the hOGG1 codon 326 polymorphism and urinary 8-OHdG levels were investigated in large samples (n = 953) of healthy individuals from five Chinese ethnic populations by using PCR-RFLP and HPLC-ECD. Life-style parameters under study were obtained through a questionnaire. The allelic frequencies of the hOGG1 gene in the Chinese populations were found to be 0.16 (Ser/Ser), 0.49 (Ser/Cys) and 0.35 (Cys/Cys), respectively. The frequencies of Ser326Cys polymorphism were significantly different among the five Chinese ethnic populations (P = 0.002). No association was found between the hOGG1 gene polymorphism and other life-style parameters except for the association between Ser326Cys and smoking (P = 0.027). A significant increase of urinary 8-OHdG level was observed in Cys326Cys allelic healthy subjects (P = 0.033). These results suggest that there are natural variations of hOGG1 gene among Chinese ethnic populations. Smoking relates to Cys/Cys polymorphism frequencies, and oxidative DNA damage is repaired less in individuals with the hOGG1 Cys326Cys genotype.     

hOGG1 promoter methylation,hOGG1 genetic variants and their interactions for risk of coal-borne arsenicosis: A case-control study

To identify the effect of hOGG1 methylation, Ser326Cys polymorphism and their interactions on the risk of coal-borne arsenicosis, 113 coal-borne arsenicosis subjects and 55 reference subjects were recruited. Urinary arsenic contents were analyzed with ICP-MS. hOGG1 methylation and Ser326Cys polymorphism was measured by mehtylation-specific PCR and restriction fragment length polymorphism PCR in PBLCs, respectively. The results showed that the prevalence of methylated hOGG1 and variation genotype (326 ^Ser/Cys & 326 ^Cys/Cys) were increased with raised levels of urinary arsenic in arsenicosis subjects. Increased prevalence of methylated hOGG1 and variation genotype were associated with raised risk of arsenicosis. Moreover, the results revealed that variant genotype might increase the susceptibility to hOGG1 methylation. The interactions of methylated hOGG1 and variation genotype were also found to contribute to increased risk of arsenicosis. Taken together, hOGG1 hypermethylation, hOGG1 variants and their interactions might be potential biomarkers for evaluating risk of coal-borne arsenicosis.     

Polymorphic trial in oxidative damage of arsenic exposed Vietnamese

Arsenic causes DNA damage and changes the cellular capacity for DNA repair. Genes in the base excision repair (BER) pathway influence the generation and repair of oxidative lesions. Single nucleotide polymorphisms (SNPs) in human 8-oxoguanine DNA glycosylase (hOGG1) Ser326Cys; apurinic/apyrimidinic endonuclease (APE1) Asp148Glu; X-ray and repair and cross-complementing group 1 (XRCC1) Arg280His and Arg399Gln in the BER genes were analyzed, and the relationship between these 4 SNPs and the urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) concentrations of 100 Vietnamese population exposed to arsenic was investigated. Individuals with hOGG1 326Cys/Cys showed significantly higher urinary 8-OHdG concentrations than did those with 326 Ser/Cys and Ser/Ser. As for APE1 Asp148Glu, heterozygous subjects showed significantly higher urinary 8-OHdG concentrations than did those homozygous for Asp/Asp. Moreover, global ethnic comparison of the allelic frequencies of the 4SNPs was performed in 10 population and previous reported data. The mutant allele frequencies of hOGG1 Ser326Cys in the Asian populations were higher than those in the African and Caucasian populations. As for APE1 Asp148Glu, Caucasians showed higher mutant frequencies than those shown by African and Asian populations. Among Asian populations, the Bangladeshi population showed relatively higher mutant allele frequencies of the APE1 Asp148Glu polymorphism. This study is the first to demonstrate the existence of genetic heterogeneity in a worldwide distribution of SNPs (hOGG1 Ser326Cys, APE1 Asp148Glu, XRCC1 Arg280His, and XRCC1 Arg399Gln) in the BER genes.     

Rapid detection of the hOGG1 Ser326Cys polymorphism using LightCycler technology

Human 8-oxoguanine DNA glycosylase 1 (hOGG1) plays an important role in the repair of 8-oxo-7, 8-dihydro-2'-deoxyguanosine (8-oxodGuo), one of the major constituents in DNA damage. A recent in vitro study showed that the hOGG1 326Cys polymorphism (rs1052133) exhibits reduced 8-oxodGuo repair activity. This study aimed to develop a LightCycler (LC) assay to analyze the C>G polymorphism (Ser326Cys) in exon 7 of the hOGG1 gene followed by validation of the method using DNA samples from 260 polycyclic aromatic hydrocarbons(PAH)-exposed workers with known 8-oxodGuo DNA-adduct values measured by HPLC. Twenty DNA samples were analyzed by a PCR-RFLP analysis with Fnu4H I to generate control DNA. LC melting curve analyses of the hOGG1 exon 7 PCR product were characteristic of the probes hybridized to the non-mutated Ser-type (CC) at 65 degrees C, or to the Cys mutant (GG) at 59 degrees C. The distribution in the population of PAH-exposed workers (N=260) was 58% (CC), 38%(CG), and 4% (GG). The minor G allele displayed a frequency of 23 %. The distribution of 8-oxodGuo adducts for the Ser326Cys variants of hOGG1 revealed geometric means (GM) of 5.83 (CC), 5.27 (CG), and 6.53 (GG) 8-oxodGuo adducts/10(6)dGuo. Corresponding GM values of current smokers were 5.7 (CC), 5.6 (CG) and 7.0 (GG) 8-oxodGuo adducts/10(6) dGuo. The analysis of the Ser326Cys polymorphism in 260 DNA samples with this new LC assay revealed that this method is reliable for high throughput analysis of this key polymorphism in the hOGG1 gene.     

The hOGG1 Ser326Cys polymorphism and Huntington's disease

Increasing evidence supports a role for oxidative DNA damage and impaired DNA repair mechanisms in the pathogenesis of age related neurodegenerative diseases. Within this context there is a current interest in the understanding of the role played by polymorphisms of DNA repair genes in the inter-individual risk to develop neurodegenerative pathologies, as well as in the onset and the progression of disease symptoms. Particularly, somatic CAG repeat expansion of the gene encoding for huntingtin has been observed in tissues of patients affected by Huntington's disease (HD), including blood and brain. Recent evidence suggests that somatic CAG repeat expansion in HD cells might contribute to disease age at onset and is mediated by the DNA repair OGG1 enzyme, during the removal of 8-oxoguanine (8-oxoG) from the DNA. There is also evidence that the expression of hMTH1, which removes 8-oxoG from the nucleotide pool, protects mice from HD-like symptoms, and progenitor striatal cells from the toxic effects of the mutant huntingtin. The hOGG1 Ser326Cys polymorphism results in reduced OGG1 activity and increased 8-oxoG formation. In the present study, performed on blood DNA from 91 HD subjects, we observed that bearers of the mutant Cys326 allele (Ser326Cys + Cys326Cys) tend to have an increased number of CAG repeats of the expanded HD allele (P = 0.049); moreover bearers of at least one copy of the mutant Cys326 allele, mainly heterozygous subjects, showed a significant (P = 0.041) earlier disease onset than Ser326Ser wild-type individuals, suggesting a possible role of the hOGG1 Ser326Cys polymorphism in HD phenotype.     

Dose-dependent influence of genetic polymorphisms on DNA damage induced by styrene oxide, ethylene oxide and gamma-radiation

Styrene oxide (SO), ethylene oxide (EO) and gamma-radiation (G) are agents with a well-described metabolism and genotoxicity. EPHX1 and GSTs play an important role in the detoxification of electrophiles and oxidative stress. Enzymes involved in base excision repair (hOGG1, XRCC1), in rejoining single strand breaks (XRCC1) and in repair of cross-links and chromosomal double strand breaks (XRCC3) might have an impact on genotoxicity as well. In this study we assessed the dose-dependent effect of genetic polymorphisms in biotransforming (EPHX (Tyr113/His113 and His139/Arg139), GSTP1 (Ile105/Val105), GSTM1 and GSTT1) and DNA repair enzymes (hOGG1 (Ser326/Cys326), XRCC1 (Arg194/Trp194, Arg280/His280, Arg399/Gln399), XRCC3 (Thr241/Met241)) on the induced genotoxicity. Peripheral blood mononuclear cells from 20 individuals were exposed to 3 doses per agent (+control). Genotoxicity was evaluated by measuring comet tail length (TL) and micronucleus frequencies in binucleated cells (MNCB). Dose-dependent DNA damage was found for all agents and end-points, with the exception of MNCB induced by EO. Repeated measure ANOVA revealed a significant contribution of hOGG1 and XRCC3 genotypes to the inter-individual variability of TL and MNCB in cells exposed to EO and G. Homozygous hOGG1326 wild cells showed significantly lower EO-induced TL than the heterozygous cells. Significantly higher TL and MNCB were found in EO-exposed cells carrying the XRCC3(241)Met variant and the influence on TL was more pronounced at higher dose. In G-irradiated cells, TL was significantly higher in the hOGG1326 homozygous wild types compared with mutated genotypes. The influence of hOGG1326 on TL was borderline dose-dependent. We conclude that the influence of genetic polymorphisms of enzymes involved in DNA repair on induced genotoxicity depends on exposure dose.     

hOGG1 SER326CYS genetic polymorphism in a Turkish population

Oxidative DNA damage, caused by either endogenous or exogenous sources of reactive oxygen species (ROS), has been linked to aging, chronic degenerative diseases, inflammatory diseases and cancers. 8-Hydroxydeoxyguanine (8-OHdG) is a major lesion produced by ROS. Among various types of DNA base modifications, 8-OHdG has been the most widely studied and is considered a key biomarker of oxidative DNA damage. Human 8-oxoguanine DNA glycosylase 1 (hOGG1) is a key component of the base excision repair (BER) pathway and catalyzes the removal of 8-OHdG. Ethnic and inter-individual differences in hOGG1 activity and several kinds of polymorphisms at the hOOG1 gene locus have been observed in the different populations studied so far. Since no information is available on the inter-individual variability of the hOGG1 genotype in the Turkish population, we genotyped 206 healthy, unrelated Turkish individuals. The allelic frequencies of the hOGG1 gene in the Turkish population were found to be 0.50, 0.41 and 0.09 (Ser/Ser, Ser/Cys and Cys/Cys, respectively). Our results are similar to those for Caucasians studied previously but are different from Asian populations. It seems that there is a growing need for extensive genotype studies with respect to the hOGG1 gene due to its importance to various types of cancer and to smoking habits.