N-乙酰基转移酶基因多态性与肝癌易感性的关系

目的探讨N-乙酰基转移酶(NAT2)基因多态性与肝癌易感性的关系。方法应用自动实时荧光Light-Cycler技术,分析78例肝癌患者和112例健康志愿者NAT24个位点的基因多态性,比较肝癌患者与对照组间频率差异。结果 肝癌吸烟组NAT2慢乙酰化基因型频率(37.5％)与对照吸烟组(17.9％)比较差异有显著性(X2=4.67,P<0.05),并使患肝癌的危险度提高了2.76倍;肝癌非吸烟组NAT2慢乙酰化基因型频率(26.3％)与对照非吸烟组(16.1％)比较差异无显著性(X2=1.47,P>0.05)。结论携带NAT2慢乙酰化基因型的吸烟者可能是肝癌的高危人群。     

细胞色素CYP2A6基因多态性与COPD易感性的关系

目的探讨细胞色素CYP2A6基因多态性与COPD易感性的关系。方法应用聚合酶链反应-限制性片段长度多态性法(PCR-RFLP)检测40例COPD患者及37例健康体检者静脉血细胞色素P450 2A6位点等位基因和基因型。结果 1.COPD患者CYP2A6-163C>A位点基因缺失型(del)和野生型(wt)基因型频率为17.5%、82.5%,健康对照组分别为40.5%、59.5%,两组基因分布频率差异有统计学意义(χ2=5.000,P=0.025),携带CYP2A6wt基因型者较携带CYP2A6del基因型者患COPD风险增加(OR=0.31,95%CI=0.109-0.886,P<0.05)。2.在吸烟者中,携带CYP2A6wt基因型者较携带CYP2A6del基因型者患COPD风险增加(OR=0.24,95%CI=0.064-0.920,P<0.05),在不吸烟者中,携带CYP2A6wt、CYP2A6del基因型者之间患COPD风险无明显差异。结论 1.CYP2A6-163C>A基因多态性可能是COPD发病的危险因素。2.野生型(wt)可能为吸烟者患COPD的一个易感因素。     

N-乙酰基转移酶2基因多态性与结肠腺癌易感性的关系

目的探讨N-乙酰基转移酶2(NAT2)基因多态性与结肠腺癌遗传易感性的相关性。方法采用聚合酶链反应-限制性片断长度多态性(PCR-RELP)方法,检测168例结肠腺癌患者及204例健康对照者NAT2基因型和等位基因频率,分析正常人与结肠腺癌患者NAT2各等位基因频率及基因型频率的差异。结果在正常人及结肠腺癌患者中,NAT2各等位基因频率分布差异无统计学意义(P＞0．05)。但与正常对照组相比,结肠腺癌患者中慢型乙酰化基因型频率增高(42．8%比33．7%,P= 0．033,OR=1．576,95%CI：1．037～2．396)。根据不同临床特征分析,慢型乙酰化基因型频率在不同年龄结肠癌患者中差异无统计学意义(P＞0．05),但在远侧结肠癌(P=0．022,OR=2．305,95%CI：1．116～4．763)、Dukes C期(P=0．025,OR=2．065,95%CI：1．089～3．912)、低分化(P=0．031,OR=2．128,95%CI：1．065～4．251)患者中明显增高。结论NAT2慢型乙酰化基因型与结肠腺癌及与肿瘤部位、Dukes分期及分化程度显著相关。     

代谢酶基因GSTM1和广西人群胃癌遗传易感性的关系

目的探讨代谢酶基因GSTM1多态性与广西地区人群胃癌遗传易感性之间的相关性。方法采用PCR技术检测广西地区121例胃癌患者和138例健康人的GSTM1基因多态性的分布频率,分析其与广西地区胃癌遗传易感性之间的相关性以及与吸烟、饮酒在胃癌易感性中的交互作用。结果胃癌组GSTM1（-）基因型频率（54．5％）显著高于对照组（39．1％）（X^2=6．140,P=0．013）。携带GSTM1（-）基因型的个体患胃癌的风险是携带GSTM1（＋）基因型个体的2．13倍（95％CI=1．079-1．831,P=0．013）。在吸烟者中,携带GSTM1（-）基因型的个体较携带GSTM1（＋）基因型的个体患胃癌的风险明显增加（OR=3．247,95％CI=1．067—2．328,P=0．015）。其增加程度远远高于总的胃癌风险（OR=2．129）。在饮酒者中,携带GSTM1（-）基因型的个体较携带GSTM1（＋）基因型的个体患胃癌的风险亦明显增加（OR=3．117,95％CI=1．020—2．863,P=0．033）。其增加程度远远高于总的胃癌风险（OR=2．129）。结论GSTM1（-）基因型显著增加广西地区人群患胃癌的风险,且显著增加吸烟、饮酒者患胃癌的风险。     

细胞色素P4501A1基因多态性和谷胱甘肽硫转移酶基因缺失及烹调油烟暴露与非吸烟女性肺癌易感性的关系

目的 探讨细胞色素P4501 A1(CYP1A1)MspI位点多态性、谷胱甘肽硫转移酶(GSTM1)基因缺失及烹调油烟暴露与非吸烟女性肺癌易感性的关系.方法 2009年3一12月选择中南大学湘雅医院女性非吸烟的原发性肺癌患者及对照各160例,应用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)及聚合酶链反应(PCR)技术分别检测CYP1A1 MspI多态性及GSTM1基因型,分析基因的多态性、分型及烹调油烟暴露与肺癌遗传易感性的关系.结果 肺癌组及对照组烹调油烟暴露的频率分别为51.9%(83例)及33.7%(54例),差异有统计学意义(x2=10.734,P＜0.01);肺癌组MspI位点突变的等位基因频率为44.4%(71例),高于对照组(36.9%,59例),差异无统计学意义(X2=3.731,P＞0.05);携带突变型或杂合型基因同时又有油烟暴露个体患肺癌的风险明显增高,OR(odds ratio)值分别为3.032(95%CI为1.291～7.124)和2.769(95%CI为1.341～5.552);肺癌组GSTM1缺失型的频率为58.1%(93例),与对照组(45.0%,72例)比较,差异有统计学意义(X2=0.518,P＜0.05),GSTM1缺失型的个体患肺癌的风险明显增高,OR值为1.697(95%CI为1.090～2.640);携带GSTM1缺失型且有烹调油烟暴露的个体肺癌的易感性明显增加,其OR值为3.617(95%CI为1.899～6.891);GSTM1缺失型与CYP1A1 MspI杂合型或突变型联合作用时,个体患肺癌的风险亦增高,OR值分别为1.966(95%CI为1.007～3.836)和2.402(95%CI为1.023～5.640),差异明显.结论 烹调油烟暴露是非吸烟女性肺癌的危险因素;CYP1A1 MspI基因多态性与烹调油烟联合作用可增加肺癌发病的风险;GSTM1基因缺失可能是非吸烟女性肺癌的遗传易感因素,其与烹调油烟暴露联合作用可明显增加肺癌发病的风险,且GSTM1基因缺失与CYP1A1基因多态性存在交互作用.     

DNA修复基因XRCC3多态性与肺癌易感性的关系

目的 研究DNA修复基因XRCC3多态性与肺癌易感性的关系。方法采用病例一对照研究，于2006年9月至2007年1月收集上海肺科医院原发性肺癌患者291例及同期住院的非肿瘤患者273例，应用Taqman探针结合实时荧光PCR方法分析病例组和对照组XRCC3基因Thr241Met的多态性分布，比较不同基因型与肺癌易感性的关系以及基因多态性与吸烟对肺癌的交互作用。对照组与病例组的比较用X。检验，以调整比值比及95％可信区间表示相对危险度，所有统计检验均为双侧概率检验，所有资料均用SPSS软件进行统计。结果与携带XRCC3密码子241野生纯合基因型（Thr／Thr）且不吸烟者相比，携带同样基因型且吸烟者患肺癌的风险会增加，其调整比值比（OR值）为2．47[95％可信区间（CI）为1．49-4，08，P〈0．01]；携带有杂合基因型（Thr／Met）且吸烟者患肺癌的风险也会增加，其调整OR值为2．28（95％CI为1．21-6．60，P=0，017）。野生纯合基因型（Thr／Thr）且吸烟量少于30包年可能对肺腺癌有较弱的保护作用（OR=0．49，95％CI为0．26-0．93，P=0，03）。携带有XRCC3密码子241Met等位基因且吸烟者患肺鳞癌的风险明显增加（调整OR=9．69，95％CI为3．27-28．72，P〈0．01）。携带241Met等位基因且吸烟剂量〈30包年和≥30包年的患者患肺鳞癌的风险也不同，OR值分别为8，00（95％CI为1．97-32．52，P〈0．01）和11．67（95％CI为2．98～45．73，P〈0．01）。结论DNA修复基因XRCC3多态性可能对肺癌易感性产生影响，并可能与吸烟有一定的协同作用。     

TSPAN8基因多态性与广西扶绥县肝癌家系遗传易感性关系研究

目的探讨广西扶绥县肝癌高发家系TSPAN8基因单核苷酸多态性(SNP)与肝癌遗传易感性的关系。方法收集广西扶绥县肝癌高发区20个肝癌高发家系(肝癌患者20例及直系亲属59例)及10个正常对照家系(共40例)作为研究对象,运用飞行时间质谱分析技术(MALDI-TOF)检测TSPAN8基因rs2270587位点基因型,分析该基因位点多态性与肝癌家系遗传易感性的关系。结果 (1)TSPAN8基因rs2270587位点存在C、T两种等位基因型及CC、CT和TT三种基因型。(2)正常家系组及肝癌家系非患者组CT基因型个体罹患HCC的风险分别是CC基因型个体的0.34倍(95%CI=0.07~1.59,P0.05)和0.42倍(95%CI=0.11~1.66,P0.05);正常家系组中T等位基因个体罹患HCC的风险是C等位基因个体的0.29倍(95%CI=0.09~0.92,P=0.028),肝癌家系非患者组中T等位基因个体罹患HCC的风险是C等位基因个体的0.46倍(95%CI=0.15~1.42,P0.05)。结论 TSPAN8基因rs2270587位点多态性与广西肝癌遗传易感性有相关性,T等位基因型可能是广西扶绥县HCC发生的保护因素。     

MDM2基因309位点多态性与胃癌易感性的Meta分析

目的用Meta分析的方法定量评估MDM2基因309位点多态性与胃癌的易感性。方法计算机检索Pub Med、EMBASE、中文科技期刊数据库、中国生物医学文献数据库、中国期刊全文数据库、万方数据库。全面检索MDM2基因309位点多态性与胃癌易感性的病例对照研究,采用STATA软件进行统计分析。结果本研究最终纳入8篇病例对照研究进行Meta分析,病例组共纳入胃癌患者2 591例,对照组共纳入健康人群3 555例。Meta分析结果显示携带GG等位基因者患胃癌的风险是携带TT等位基因者的2.06倍(95%CI=1.38~3.07);携带GG等位基因者患胃癌的风险是携带GT等位基因者的1.69倍(95%CI=1.38~2.08);携带G等位基因者患胃癌的风险是携带T等位基因者的1.75倍(95%CI=1.39~2.20)。结论 MDM2基因309位点多态性与胃癌的易感性相关,携带G等位基因者增加了胃癌的发病风险。     

hTERT rs2736098、rs2075786及rs2736100位点多态性与中国人群肝癌易感性的meta分析

目的研究端粒酶逆转录基因多态性与中国人群肝癌易感性的关系。方法计算机检索中国知网(CNKI)、万方、pubmed、Web of science、EMBASE等数据库有关端粒酶逆转录基因多态性与中国人群肝癌易感性相关性的研究,按照标准纳入文献,提取数据,采用RevMan5.3和stata15.1软件进行meta分析。结果共纳入7篇文献,累计病例数2 564例,对照组2 770例。meta结果显示,rs2736098位点上,携带至少一个等位基因A的个体肝癌发病风险是携带GG基因型个体的1.28倍[OR=1.28,95%CI(1.01,1.62)];携带GA或AA基因型的个体罹患肝癌的风险是携带GG基因型个体的1.25倍[OR=1.25,95%CI(1.01,1.54)]。rs2075786位点上,携带等位基因T罹患肝癌的风险是携带等位基因C个体的1.92倍[OR=1.92,95%CI(1.52,2.43)]。结论 hTERT rs2736098位点,rs2075786位点多态性与中国人群肝癌易感性有关,rs2736100位点多态性并不能增加罹患肝癌的风险。     

吸烟者内皮素-1基因Lys198Asn多态性与冠心病关系的研究

目的探讨吸烟者内皮素-1(ET-1)基因Lys198Asn(G198T)多态性与中国汉族人群冠心病(CHD)的关系。方法将213例吸烟者和192例非吸烟者分为CHD组(198例)和对照组(207例),应用聚合酶链反应-单链构象多态性方法(PCR-SSCP)检测ET-1基因G198T多态性。按吸烟与否分析G198T多态性与CHD的关系。结果当ET-1基因G198T基因型为GG时,吸烟者的调整OR=2.35(95%CI:2.15–6.83,P=0.00);基因型为GT+TT时,不吸烟者的OR=2.05(95%CI:0.98-6.97,P=0.00),吸烟者的OR=5.65(95%CI:2.87–7.65,P=0.03);吸烟者的GT+TT型更可能患冠心病,风险是GG基因型的5.65倍(OR=5.65,95%CI:2.87–7.65,P=0.03)。结论吸烟者ET-1基因G198T多态性与中国汉族人群CHD的发病具有相关性,T等位基因可能是CHD的易感性标志。     

A pilot study testing the genetic polymorphism of N-acetyltransferase 2 as a risk factor in lung cancer

NAT2 as phase II enzyme is involved in the detoxification/activation of various drugs, environmental substances and carcinogenic compounds. A genotyping approach has been used to investigate NAT2 genotype with putative relevance in lung cancer in population of 110 Slovak-Caucasians patients and 167 non-malignant individuals from the same region. Slow acetylation was not observed to be a significant risk factor of lung cancer development (OR=1.19; 95% CI: 0.71-1.99). However, one genotype responsible for slow acetylation (NAT2*5B/*6) was observed significantly more frequently in lung cancer patients with squamous cell carcinoma compared with control subjects (OR=2.24; 95% CI: 1.14-4.34). Stratified analysis showed an increasing impact of the specific allelic combination NAT2*5B/*6 in non-smokers (OR=6.5; 95% CI: 1.25-15.08). In the case of squamous lung carcinoma an analysis revealed a tendency to adversely affect cancer risk in the individuals with the mentioned genotype in younger than 60 years (OR=3.14; 95% CI: 0.98-9.72) non-smokers (OR=10.40; 95% CI: 1.35-118.89) and in females (OR=4.25; 1.08-16.25). Additional studies are needed to confirm the results we observed and to assess the impact of other effects (specific allelic combinations, sex differences and histological subtype of lung cancer) on NAT2 susceptibility in lung carcinogenesis.     

白细胞介素8基因多态性与卵巢癌发生的关系

目的研究白细胞介素8(IL-8)+781基因多态性与卵巢癌发生风险之间的关系。方法筛选卵巢癌患者为疖例组和年龄匹配的健康人为对照组,应用聚合酶链反应-限制性片段长度多态性分析检测IL-8+781基因多态性结果携带基因型TT发生卵巢癌的风险显著高于携带基因型CC(OR=3.385,95%CI:1.361~8.418;P=0.009),携带等位基因T发生卵巢癌风险显著高于等位基因C(OR=1.704,95%CI:1.122~2.590;P=0.013)。结论 IL-8+781基因多态性可能影响卵巢癌的发生。     

Relationship between N-acetyl transferase-2 gene polymorphism and risk of bronchial asthma

There are still uncertainties as to the mechanism of many pathological conditions, among them allergic diseases. It has been suggest that acetylation rate may be a factor that influences the development of allergic diseases. The aim of the present study was to investigate further whether the genetic polymorphism of the NAT2 plays a role in susceptibility to bronchial asthma disease. Ninety-seven patients with bronchial asthma (atopic n= 62; non-atopic n= 35) and 104 healthy individuals were participated in this study. DNA was extracted from the leucocyte by high pure template preparation kit. NAT2*5A, NAT2*6A, NAT2*7A/B and NAT2*14A polymorphisms of NAT2 were detected by using LightCycler-NAT2 mutation detection kit by real time PCR with LightCycler instrument. We found that mutant NAT2*5A (OR= 3.84, 95% CI= 1.08-13.6) and NAT2*6A (OR= 5.27, 95% CI= 1.06-26.05) genotype could be associated with a high risk for the development of bronchial asthma according to the genotype. After grouping phenotype, the risk for bronchial asthma was more than two times higher (OR= 2.7, 95% CI= 1.07-6.97) in individuals with the slow NAT2*5A acetylator phenotype compared to the fast phenotype. Our study suggests that the NAT2 slow acetylators may be a determinant in susceptibility to asthma disease. This finding may have implications for the theories for the pathogenesis of the disease as well as for therapeutic aspects.     

N-乙酰化转移酶2基因多态性与抗结核药物所致肝损伤的相关性

目的 探讨N-乙酰化转移酶2(NAT2)基因多态性与抗结核药致肝损伤(ADIH)的相关性.方法 以抗结核治疗3个月内出现肝损伤的106例结核患者为病例组,未出现肝损伤的106例结核患者为配对对照.采用1:1匹配的病例对照研究和聚合酶链反应-限制性片段长度多态性分析(PCR-RFLP)技术,检测106对结核患者的NAT2基因481C/T、590G/A、857G/A位点多态性情况,并对主要环境影响因素和基因型进行单因素和多因素条件Logistic回归分析.结果 病例组NAT2基因的481C/T、590G/A、857G/A位点的T、A、A等位基因频率分别为7.5%、28.8%、17.9%,对照组分别为6.6%、18.9%、17.5%.病例组NAT2慢速乙酰化型的频率明显高于对照组,粗OR值为2.250(95%CI为1.140～4.441).对文化程度、职业、体质指数(BMI)、吸烟、饮酒和结核类型6个可疑危险因素进行了单因素分析,仅低BMI和饮酒为ADIH发生的危险因素.在多因素分析中调整BMI、饮酒两个因素后,NAT2乙酰化程度仍与ADIH的发生显著相关,调整OR值为2.246(95%CI为1.086～4.644).结论 NAT2基因慢速乙酰化型町能与ADIH的发生有关.     

Genetic polymorphisms of N-acetyltransferase 2 and colorectal cancer risk

AIM: To identify the distribution of N-acetyltrasferase 2 (NAT2) polymorphism in Hebei Han Chinese and the effects of the polymorphism on the development of colorectal cancer. METHODS: We performed a hospital-based case-control study of 237 healthy individuals and 83 colorectal cancer patients of Hebei Han Chinese. DMA was extracted from peripheral blood and cancer tissues. The genotypes of the polymorphisms were assessed by PCR-restriction fragment length polymorphism(RFLP). RESULTS: There were four NAT2 alleles of WT, Ml, M2, and M3 both in the healthy subjects and in the patients, and 10 genotypes of WT/WT, WT/M1, WT/M2, WT/M3, Ml/Ml, M1/M2, M1/M3, M2/M2, M2/M3, M3/M3. M2 allele was present in 15.61% of healthy subjects and 29.52% of patients (X2 = 15.31, P<0.0001), and M3 allele was present in 30.59% of healthy subjects and 16.87% of patients (X2 = 25.33, P<0.0001). There were more WT/M2 (X2 = 34.42,P<0.0001, odd ratio = 4.99,95%CI = 2.27-9.38) and less WT/M3 (x2 = 3.80, P= 0.03) in the patients than in the healthy subjects. In 70.3% of the patients, there was a difference in NAT2 genotype between their tumors and blood cells. Patients had more WT/M2 (X2 = 5.11, P= 0.02) and less M2/M3 (X2= 4.27, P= 0.039) in their blood cells than in the tumors. Furthermore, 53.8% (7/13) of M2/M3 in tumors were from WT/M2 of blood cells. CONCLUSION: There is a possible relationship between the NAT2 polymorphisms and colorectal cancer in Hebei Han Chinese. The genotype WT/M2 may be a risk factor for colorectal cancer.     

<Emphasis Type="Italic">NAT2</Emphasis> Fast Acetylator Genotype is Associated with an Increased Risk of Colorectal Cancer in Taiwan

In Taiwan, colorectal cancer has one of the highest rates of increased incidence in the past two decades. Heterocyclic amines from dietary cooked meats are metabolically activated by NAT2 (N-acetyltransferase 2), which are associated with colorectal cancer incidence. Thus, the NAT2 fast acetylator genotype may be associated with colorectal cancer risk. However, the association between the NAT2 genotype and colorectal cancer risk is not clearly understood. We conducted a study with 244 primary colorectal cancer cases and 299 cancer-free healthy control subjects to verify the association of NAT2 polymorphisms with the risk of Taiwanese colorectal cancer. Our data showed that subjects with the NAT2 W/W homozygous genotype had a 1.63-fold increased risk of colorectal cancer compared with those with the Mx/Mx slow acetylator genotype (95 percent confidence interval, 1.03–2.58); however, no risk was found in the W/Mx heterozygous and Mx/W+W/W fast acetylator genotypes. Being stratified by gender factors, the colorectal cancer risk in females with homozygous W/W or Mx/W+W/W fast acetylators increased 2.47-fold and 2.13-fold compared with those with the Mx/Mx slow acetylator genotype (95 percent confidence interval, 1.27–4.82 for W/W genotype; 95 percent confidence interval, 1.17–3.89 for Mx/W+W/W genotype); however, the risk of the NAT2 genotype and colorectal cancer was not observed in males. Collectively, patients with the NAT2 fast acetylator genotype were more prone to colorectal cancer and reflected the possibility that exposure to heterocyclic amines may contribute to colorectal cancer development in Taiwan, especially in Taiwanese females. Supported by grants from the Department of Health (DOH 94-TD-G-111-017) and the National Science Council (NSC95-2314-B-040-041, NSC95-2314-b040-002), The Executive Yuan, Republic of China. Presented at the Conference of Biomedical Sciences, Taipei, Taiwan, March 17 to 18, 2007. Chi-Chou Huang and Wen-Pin Chien contributed equally to this work.     

CYP2E1和NAT2基因多态性与抗结核药物诱导的药物性肝损伤关系的荟萃分析

目的明确细胞色素氧化酶P450 2E1(cytochrome P450 2E1,CYP2E1)和N-乙酰基转移酶-2(N-acetyltransferase-2,NAT2)基因多态性与抗结核药诱导的药物性肝损伤(anti-tuberculosis drug-induced hepatotoxicity,ATDH)之间的关系。方法计算机检索Medline/Pubmed、EMBASE、Web of Science数据库和Cochrane图书馆中所有有关CYP2E1基因多态性与ATDH关系的研究文献。根据文献纳入及排除标准筛选文献,并对文献进行质量评价。采用OR及95%CI作为分析疗效的统计量。采用Revman 5.0软件统计分析。结果共计纳入研究文献9篇,入选2049例研究对象。CYP2E1基因Pst I/Rsa I多态性中,c1/c1型比c1/c2和c2/c2型有更高的ATDH发生率(OR=1.38,95%CI:1.08~1.77,P=0.01);在Dra I多态性中各型之间无差异(OR=0.78,95%CI:0.51~1.18,P=0.23)。与携带NAT2快速或中速乙酰化的c1/c1型人群比较,携带NAT2慢速乙酰化的c1/c1型人群具有更高的ATDH风险(OR=3.10,P0.0001)。结论 CYP2E1基因c1/c1型是ATDH发生的风险因素,且合并慢速乙酰化的NAT2基因型时可进一步增加ATDH发生率。     

Possible association of NAT2 polymorphism with laryngeal cancer risk: an evidence-based meta-analysis

Purpose

N-acetyltransferase 2 (NAT2) plays an important role in the metabolism of various potential carcinogens, which can be subdivided into rapid and slow acetylation phenotype according to the different genotypes. A number of studies have been devoted to the association of NAT2 polymorphism with susceptibility to laryngeal carcinoma; however, the results were inconsistent and inconclusive. The aim of the present study was to conduct a meta-analysis assessing the possible association of NAT2 polymorphism with laryngeal cancer risk.

Methods

The relevant studies were identified through a search of PubMed, Embase, ISI Web of Knowledge, and Chinese National Knowledge Infrastructure until February 2011 and selected on the basis of the established inclusion criteria for publications, and then a meta-analysis was performed to quantitatively summarize the association of NAT2 polymorphism with laryngeal cancer susceptibility.

Results

Seven studies were included in the present meta-analysis, which described a total of 980 laryngeal cancer cases and 1,487 controls. The overall odds ratio (OR) for NAT2 slow and rapid acetylators was 0.99 (95% CI?=?0.71?C1.38) and 1.01 (95% CI?=?0.72?C1.40), respectively. When stratifying for race, the pooled ORs for NAT2 slow acetylator were 1.99 (95% CI?=?1.10?C3.63) in Asians and 0.85 (95% CI?=?0.62?C1.15) in Caucasians, and the pooled ORs for NAT2 rapid acetylator were 0.50 (95% CI?=?0.28?C0.91) in Asians and 1.18 (95% CI?=?0.87?C1.60) in Caucasians.

Conclusions

This meta-analysis suggested that there was overall lack of association between NAT2 polymorphism and laryngeal cancer risk; however, NAT2 slow acetylation may contribute to a risk factor for laryngeal cancer in Asians but not in Caucasians.