谷胱甘肽硫转移酶M1与T1基因缺失增加鼻咽癌易感性(英文)

目的在中国西南的广西壮族自治区的鼻咽癌高发区内研究谷胱甘肽硫转移酶 M1与 T1遗传多态性与鼻咽癌易感的相关性。方法病例与对照研究这些酶的遗传多态性(GSTM1和 GSTT1零基因型),鼻咽癌总数为127例,对照207例。结果 GSTM1和 GSqT1零基因型的频数在 NPC 患者中较高,差异达统计学意义(P<0.001)。结论鼻咽癌是广西最常见癌症,GST 酶与多种环境致癌物的解毒相关,同合子缺失 GSTM1和 GSTT1与数种癌相关,生鼻咽癌危险性已知与环境因素如吸烟和 EB病毒感染相关联,我们的结果提示 GSTM1和 GSTF1缺失多态性与增加鼻咽癌易感性相关,若两种解毒酶基因同时缺失对鼻咽癌易感受性意义更重要。     

广西鼻咽癌患者解毒酶基因GSTM1和GSTT1缺失的研究

目的研究鼻咽癌高发区鼻咽癌患者对化学致癌物的遗传易感性。方法应用PCR技术,研究鼻咽癌患者与对照组健康者人体主要解毒酶谷胱甘肽硫转移酶(GST)M1(GSTM1)和GSTT1基因缺失多态性,估计其与鼻咽癌地区性高发的相关性。结果鼻咽癌高发区居民GSTM1或GSTT1缺失率偏高,分别为47.4%(64/135)和40.7%(55/135)。鼻咽癌患者GSTM1或GSTT1缺失率分别为61.5%(56/91)和59.3%(54/91),显著高于对照组(P<0.05,P<0.01)。特别是GSTM1和GSTT1两种基因双缺失者,在病例组与对照组间差异有极显著性(χ2=12.533,P=0.002)。结论鼻咽癌高发区人群及患者GSTM1和GSTT1高频联合缺失,可能为相应的环境致癌化学毒物遗传易感性和鼻咽癌患者的地区聚集原因。     

肝细胞癌、鼻咽癌患者谷胱甘肽硫转移酶M1和T1基因型分布

目的 探讨高危区肝细胞癌和鼻咽癌患者谷胱甘肽硫转移酶M1 (GSTM1) 及T1 (GSTT1)基因多态性的分布。方法 应用PCR技术检测181例肝细胞癌、126例鼻咽癌患者和641例对照组人体GSTM1和GSTT1基因型。结果 GSTM1空白基因型(null)在肝癌组、鼻咽癌组与对照组频率分别为65.2%、61.9%和47.6%,病例组与对照组比较,差异有统计学意义（P＜0.01)。GSTT1空白基因型(null)在肝癌组、鼻咽癌组与对照组频率分别为57.5%、62.7%和43.1%,病例组与对照组比较,差异有统计学意义（P＜0.001)。结论 在肝细胞癌、鼻咽癌高发区解毒酶基因GSTM1和GSTT1呈多态性分布,二者的null基因型均增加患肝细胞癌、鼻咽癌的风险。     

广西扶绥县肝癌高发家系谷胱甘肽转硫酶GSTM_1和GSTT_1基因多态性的研究

目的探讨广西扶绥县肝癌高发区壮族人群谷胱甘肽转硫酶GSTM1和GSTT1的基因多态性在肝癌家族聚集性中的作用,以及一级亲属与先证者之间HCC易感性的关系。方法采用病例-对照研究方法,收集21个广西扶绥县壮族肝癌家系76例,以及该地区21个对照家系68例,采用多重PCR技术和凝胶成像分析方法,对入选者GSTM1和GSTT1基因型进行检测,用ELISA法检测HBsAg,并将实验结果与临床资料相结合,进行统计学分析。结果①GSTM1基因空白型在肝癌家系组、对照家系组之间的频率分别为67.1%和36.8%(P=0.000);GSTT1基因空白型在肝癌家系组、对照家系组之间的频率分别为40.8%和19.1%(P=0.005);GSTM1和GSTT1基因同时缺失在肝癌家系组、对照家系组的频率分别为31.6%和2.9%(P=0.000)。②将GSTM1及GSTT1基因同时表达型为基准计算两基因联合作用的危险度,GSTM1基因缺失GSTT1基因表达型、GSTM1基因表达GSTT1基因缺失型、GSTM1基因及GSTT1基因联合缺失型的OR值分别为0.102、0.210和3.092。③GSTM1基因空白型在先证者与其直系亲属之间的频率分别为71.4%和65.5%(P=0.620),GSTT1基因空白型在先证者与其直系亲属之间的频率分别为47.6%和38.2%(P=0.454)。GSTM1和GSTT1基因同时缺失在先证者与其直系亲属之间的频率分别为33.3%和30.9%(P=0.839),差异均无统计学意义(P>0.05)。结论①GSTM1和GSTT1基因的多态性与肝癌家族聚集性相关;②GSTM1和GSTT1基因联合缺失与HCC的发生呈显著正相关,且两基因可能具有协同作用;③直系亲属与先证者HCC发生率无差别。     

肝细胞癌患者的谷胱甘肽硫转移酶基因缺失的研究

目的　研究广西黄曲霉毒素B1(AFB1)高污染区人群谷胱甘肽硫转移酶GSTM 1和GSTT1基因缺失多态性与肝细胞癌高发的相关性。方法　采用聚合酶链反应 (PCR)方法检测 110例高污染区肝细胞癌患者和 135例无癌健康对照者的GSTM1和GSTT1基因型分布。结果　正常对照组GSTM 1和GSTT1基因缺失率分别为 4 7.4 %和 4 0 .7% ,肝细胞癌组GSTM 1和GSTT1基因缺失率分别为 6 3.6 %和 6 0 .0 % ;GSTM 1基因缺失在肝细胞癌组和正常对照组之间 ,差异具有显著性意义 (P <0 .0 5 ) ;GSTT1基因缺失在肝细胞癌组和正常对照组之间差异具有非常显著性意义 (P <0 .0 1)。结论　肝细胞癌患者GSTM1和GSTT1基因缺失水平偏高可能是易感的原因之一。     

广西扶绥人群GSTM1和GSTT1基因多态性与肝癌易感性关系的研究

目的:探讨GSTM1和GSTT1基因多态性与肝癌易感性关系,以及基因与基因间的相互作用.方法: 应用病例-对照分析研究,采用多重PCR技术,对广西扶绥100例肝细胞癌患者、60例正常人群的GSTM1和GSTT1基因型进行检测.将实验结果与临床资料结合进行统计学分析.结果: GSTM1基因空白型在HCC组和正常对照组中的频率分别为59.0%、68.3%(P>0.05);HCC组GSTT1基因缺失频率(33.0%)显著高于正常对照组(18.3%);GSTM1和GSTT1基因同时缺失在肝癌组和对照组中的频率分别为22.0%和3.3%,两者差异有统计学意义.结论:1)GSTM1和GSTT1基因的缺失是通过遗传获得.2)GSTT1基因缺失是HCC的易感因素.3)GSTM1和GSTT1基因联合缺失与HCC的发生呈显著正相关,且两基因具有协同作用,可作为HCC高危人群筛选的有用指标.     

广西扶绥县肝癌高发家系谷胱甘肽转硫酶GSTM1和GSTT1基因多态性的研究

目的探讨广西扶绥县肝癌高发区壮族人群谷胱甘肽转硫酶GSTM1和GSTT1的基因多态性在肝癌家族聚集性中的作用,以及一级亲属与先证者之间HCC易感性的关系。方法采用病例一对照研究方法,收集21个广西扶绥县壮族肝癌家系76例,以及该地区21个对照家系68例,采用多重PCR技术和凝胶成像分析方法,对入选者GSTM1和GSTT1基因型进行检测,用ELISA法检测HBsAg,并将实验结果与临床资料相结合,进行统计学分析。结果（1）GSTM1基因空白型在肝癌家系组、对照家系组之间的频率分别为67．1％和36．8％（P=0．000）;GSTT1基因空白型在肝癌家系组、对照家系组之间的频率分别为40．8％和19．1％（P=-0．005）;GSTM1和GSTT1基因同时缺失在肝癌家系组、对照家系组的频率分别为31．6％和2．9％（P=0．000）。②将GSTM1及GSTT1基因同时表达型为基准计算两基因联合作用的危险度,GSTM1基因缺失GSTT1基因表达型、GSTM1基因表达GSTT1基因缺失型、GSTM1基因及GSTT1基因联合缺失型的OR值分别为0．102、0．210和3．092。（3）GSTM1基因空白型在先证者与其直系亲属之间的频率分别为71．4％和65．5％（P=0．620）,GSTT1基因空白型在先证者与其直系亲属之间的频率分别为47．6％和38．2％（P=0．454）。GSTM1和GSTT1基因同时缺失在先证者与其直系亲属之间的频率分别为33．3％和30．9％（P=-0．839）,差异均无统计学意义（P〉0．05）。结论（1）GSTM1和GSTT1基因的多态性与肝癌家族聚集性相关;（2）GSTM1和GSTT1基因联合缺失与HCC的发生呈显著正相关,且两基因可能具有协同作用;③直系亲属与先证者HCC发生率无差别。     

Ⅰ，Ⅱ相代谢酶基因多态性与胃癌遗传易感性的病例对照研究

目的　探讨Ⅰ、Ⅱ相代谢酶中CYP1A1 ,GSTM1和GSTT1基因多态性与胃癌遗传易感性的关系 ,以及基因 基因、基因 环境之间的交互作用。方法　采用社区为基础的病例对照研究 ,代谢酶基因多态性的检测用PCR和PCR RFLP方法 ,资料分析用SAS软件进行多因素Logistic回归分析。研究对象 :1 997年 1月～ 1 998年 1 2月经扬中市人民医院确诊 ,肠型胃癌病例1 1 2例 ;同期该地无上消化道肿瘤的“健康”人群为对照 ,共 675例。结果　在调整了混杂因素后 ,仅GSTM 1缺失基因型与胃癌易感性有显著性相关 ,OR =1 95(CI:1 2 2 3 1 4 ) ;当GSTM 1和GSTT1同时缺失时 ,对胃癌发生的交互作用有显著性意义 ,OR =1 98,CI :1 0 2 3 85 ;未见CYP1A1突变基因与GSTM1或GSTT1缺失基因型对胃癌的发生有交互作用。在多因素Lo gistic回归分析中 ,也以GSTM1缺失基因型为最重要的遗传危险因素 ,胃癌家族史也有显著意义 ,环境危险因素主要包括 :既往吸烟史和既往饮酒史。同时发现CYP1A1和GSTM 1基因与吸烟、饮酒因素存在交互作用。结论　具有GSTM 1缺失或CYP1A1突变基因型的个体属胃癌高危险人群 ,在肿瘤防治方案中应加以注意     

GSTM1、GSTT1基因多态性对宫颈癌患者新辅助化疗疗效及预后的影响

目的:研究谷胱苷肽硫转移酶M1（GSTM1）、谷胱苷肽硫转移酶T1（GSTT1）基因多态性对新辅助化疗（NACT）宫颈癌患者疗效的影响及与患者预后的关系。方法:选取2011年5月至2013年5月本院诊治的宫颈癌患者78例为研究对象,NACT采用铂类和紫杉醇类药物,GSTM1、GSTT1基因多态性检测采用多重PCR技术。结果:GSTM1和GSTT1基因在宫颈癌患者中呈多态性分布,GSTM1、GSTT1非缺失组患者总有效率显著高于GSTM1、GSTT1缺失组（P＜0.05）。GSTM1、GSTT1缺失组患者5年生存率显著低于GSTM1、GSTT1非缺失组患者（P＜0.05）。GSTM1、GSTT1基因缺失是影响NACT宫颈癌患者不良预后发生的独立危险因素（P＜0.05）。结论:不同GSTM1、GSTT1基因分型下,NACT对宫颈癌患者的疗效有显著差异,GSTM1、GSTT1基因缺失是影响NACT宫颈癌患者不良预后发生的独立危险因素。     

I、Ⅱ相代谢酶基因多态性与胃癌遗传易感性的病例对照研究

目的探讨I、Ⅱ相代谢酶中CYP1A1,GSTM1和GSTT1基因多态性与胃癌遗传易感性的关系,以及基因-基因、基因-环境之间的交互作用.方法采用社区为基础的病例对照研究,代谢酶基因多态性的检测用PCR和PCR-RFLP方法,资料分析用SAS软件进行多因素Logistic回归分析.研究对象:1997年1月～1998年12月经扬中市人民医院确诊,肠型胃癌病例112例;同期该地无上消化道肿瘤的"健康"人群为对照,共675例.结果在调整了混杂因素后,仅GSTM1缺失基因型与胃癌易感性有显著性相关,OR=1.95(CI:1.22-3.14);当GSTM1和GSTT1同时缺失时,对胃癌发生的交互作用有显著性意义,OR=1.98,CI:1.02-3.85;未见CYP1A1突变基因与GSTM1或GST1缺失基因型对胃癌的发生有交互作用.在多因素Lo gistic回归分析中,也以GSTM1缺失基因型为最重要的遗传危险因素,胃癌家族史也有显著意义,环境危险因素主要包括:既往吸烟史和既往饮酒史.同时发现CYP1A1和GSTM1基因与吸烟、饮酒因素存在交互作用.结论具有GSTM1缺失或CYPlAl突变基因型的个体属胃癌高危险人群,在肿瘤防治方案中应加以注意.     

Genetic Polymorphisms of Xenobiotic Metabolizing Genes (GSTM1, GSTT1, GSTP1), Gene-Gene Interaction with Association to Lung Cancer Risk in North India; A Case Control Study

Aim: In this case control study involving, 220 human subjects; polymorphisms in xenobiotic metabolizing genes (GST-M1, -T1 and -P1) and their association to lung cancer risk is being analysed among smokers and non-smokers. GSTM1 or GSTT1 gene polymorphism and amino acid changes in GSTP1 have been correlated and may be associated to lung cancer risk. Other factor includes exposure to environmental pollutants and life style choices. We have explored gene-gene and gene-environment interaction in the aetiology of lung cancer risk among north Indian population. Patients and Methods: For the study we have collected 120 lung cancer patient blood samples from Kamala Nehru Memorial Cancer Hospital, Allahabad, Uttar Pradesh and 100 matched controls. DNA was isolated and GST-M1 and - T1 genotyping were assessed by multiplex PCR whereas the GSTP1 polymorphism was analysed using restriction fragment length polymorphism. The risk of lung carcinogenesis was assessed using logistic regression analysis calculating the odd ratio (OR) with 95% confidence interval (CI). Results: The risk of lung carcinogenesis was three fold higher for null GSTT1 (OR=3.045, 95%CI=1.750-5.301, p-value <0.001) genotype; whereas other two types; GSTM1 (OR= 1.342, 95% CI=0.788-2.284, p-value=0.270) and GSTP1 (OR=0.806, 95% CI=0.526-1.236, p-value=0.323) showed no association to lung cancer susceptibility respectively. Smokers diagnosed with lung cancer had more null genotypes for GSTT1 (OR=4.773, 95%CI=1.939-11.751, p<0.001). The ‘at risk’ genotype combination GSTM1 (null) /GSTT1 (null) (OR=1.76, 95%CI; 0.920-3.370, p-value=0.03) showed increased susceptibility to lung cancer risk. The genotype combination of GSTT1 (null)/GSTP1 (Ile/Ile) (p=0.009) was associated with increased lung cancer risk. Conclusion: The results of this study suggest that; GSTT1 null genotype were more susceptible for lung cancer risk and smoking increases the susceptibility for lung cancer several folds among the North Indian population. Gene-gene interaction for null genotypes of GSTM1 and GSTT1 were correlated with higher risk of having lung cancer.     

Polymorphisms in the glutathione S-transferase class mu and theta genes interact and increase susceptibility to lung cancer in minority populations (Texas, United States)

The genes coding for separate isoforms of both the human glutathioneS-transferase class mu and class theta enzymes (GSTM1and GSTT1) arepolymorphic with a variable ethnic distribution. These enzymes detoxifyreactive epoxides, including carcinogens produced by tobacco smoke. Becauseof this, the null polymorphism in the GSTM1 gene (coding for the glutathioneS-transferase class mu enzyme) has been studied widely as a possible sourceof inherited susceptibility to smoking-related lung cancer. The more recentlydescribed null polymorphism in the GSTT1 gene also could contribute to anincreased risk of smoking-related lung cancer. As the incidence of lungcancer is known to differ by ethnicity, we have conducted a case-controlstudy in the United States of 108 African-Americans (Blacks) and 60Mexican-Americans (Hispanics) with lung cancer and 132 African-American(Black) and 146 Mexican-American (Hispanic) controls to investigate theassociation of the GSTT1 and GSTM1 polymorphi sms with lung cancer inminority populations. In the unadjusted data, there was a borderlinesignificant association of the GSTM1 null polymorphism with lung cancer inMexican-Americans (odds ratio [OR] = 1.8, 95 percent confidence interval [CI]= 1.0-3.3 ) that was not observed in African-Americans. The GSTT1 nullpolymorphism also had a higher prevalence in cases than controls in bothracial/ethnic groups, but this increase was not statistically significant.When the data were analyzed using logistic regression controlling for age,gender, race, and smoking, no significant association of either trait withlung cancer was observed, with ORs for both traits of approximately 1.3.However, when the prevalence of individuals who were null for bothpolymorphisms was compared by case status, a significant interaction wasobserved. Logistic regression models showed the OR for the association oflung cancer and the presence of both null polymorphisms compared with one(either GSTT1 or GSTM1) or no null genotype to be 2.9 (P < 0.04). Theseresults suggest that there may be carcinogenic intermediates in cigarettesmoke that are substrates for both the GSTT1 and GSTM1 enzymes, and that lungcancer risk is increased more than additively for individuals who have bothGSTT1 and GSTM1 null polymorphisms.     

Genetic Variation of GSTM1, GSTT1 and GSTP1 Genes in a South Indian Population

The glutathione S transferase (GST) family of enzymes play a vital role in the phase II biotransformation ofenvironmental carcinogens, pollutants, drugs and other xenobiotics. GSTs are polymorphic and the polymorphismsin GST genes have been associated with cancer susceptibility and prognosis. Moreover, distinct ethnic differenceshave been observed in the type and frequency of GST gene polymorphisms. Hence, the present study was aimed todetermine the frequencies of GSTM1, GSTT1 and GSTP1 polymorphisms in 255 healthy random volunteers fromSouth India. The GSTM1 and GSTT1 genotypes were determined by PCR and GSTP1 by PCR-RFLP using peripheralblood DNA.The GSTM1 and GSTT1 null genotype frequencies were found to be 22.4% and 17.6% respectively. TheGSTP1 allelic frequency was 0.78 for the Ile allele and 0.22 for the Val allele and the genotype frequency was 58.4%for Ile/Ile, 38.4% for Ile/Val, and 3.1% for Val/Val. Comparison of the frequencies of GST polymorphisms observedin the present study with other Indian and world populations revealed a distinctive nature of the South Indianpopulation with respect to polymorphims at the GST gene loci. A better understanding of carcinogen metabolizinggene distribution should contribute to risk assessment of humans exposed to environmental carcinogens.     

Frequency and Association Of GSTM1 and GSTT1 Gene Polymorphisms with Survival in Breast Cancer Patients

Objective: Glutathione S-transferase M1 and T1 (GSTM1 and GSTT1) are the key detoxification enzymes of xenobiotics, including chemotherapeutic drugs. The deletion polymorphisms of GSTM1 and GSTT1 genes are associated with reduced enzyme activity that influenced clinical outcomes of chemotherapeutic agents in breast cancer. However, there is limited information among Thai patients. This research aims to explore the frequency and role of GSTM1 and GSTT1 polymorphisms on survival among Thai patients with breast cancer. Methods: The retrospective cohort study was performed. Demographic data and clinicopathology characteristics were collected from hospital base registry data and medical records. A multiplex qualitative real-time PCR method was used to detect the presence or absence of the GSTM1 and GSTT1 gene in the genomic DNA samples of the participants. Results: The frequencies of the GSTM1 and GSTT1 null genotypes in 198 breast cancer patients were 65.70% and 33.30%, respectively. The overall survival at 1, 3 and 5 years were 95.00%, 83.00%, 71.00% respectively. The log rank test and Cox proportional hazards revealed a significant different in the 5-years overall survival according to lymph node metastasis and tumor stage (P = 0.014 and P < 0.001). No associations between overall survival and GSTM1 or GSTT1 genotype were found in single or combined genotypes analyses (P = 0.76 and P= 0.15). Conclusion: The results of our study provided the epidemiological information for prognostic of survival in breast cancer patients treated with chemotherapy.     

Polymorphisms in GSTM1, GSTTI and GSTP1 and nasopharyngeal cancer in the east of China: a case-control study

Aim: The study was performed to assess the potential role of GSTM1, GSTT1 and GSTP1 polymorphisms in the risk of nasopharyngeal cancer in Chinese population. Method: We collected 182 cases undergoing pathologic examination and 366 controls from the affiliated hospital of Medical College of Qingdao University from April 2006 to July 2010. Genotyping was based upon duplex polymerase-chain-reactions with the PCR-CTPP method. Results: More smokers were found in NPC patients than controls, and a higher IgA/VCA+ . Individuals carrying null GSTM1 and GSTT1 had 1.76 and 2.01 fold risk of NPC when compared with non-null genotypes, respectively. A non-significant increase risk of NPC was found in individuals with 1b/1b genotype when compared with 1a/1a genotype (OR=1.32, 95%CI=0.60-2.94). When compared with non-null GSTM1 and GSTT1 genotypes, the combination of null/null GSTM1 and GSTT1 genotypes showed moderate increased risk of NPC (OR=3.03, 95% CI=1.74-5.08). Conclusion: Our study provides evidence that genetic deletion of GSTM1 and GSTT1 may contribute to increased susceptibility to NPC in Chinese population, while GSTP1 may not. Our findings provide information relevant to the prevention of NPC.     

GSTT1, GSTM1 and GSTP1 genetic polymorphisms and interaction with tobacco, alcohol and occupational exposure in esophageal cancer patients from North India

Glutathione S-transferases(GSTs) are detoxification enzymes that provide critical defense against carcinogens. Our hypothesis was that altered frequencies of GST genotypes and environmental exposures might be associated with increased susceptibility for the development of esophageal cancer. A total of 100 esophageal cancer patients and 137 age and gender matched healthy controls were analyzed for GST polymorphisms. Frequencies of GSTT1 null, GSTM1 null and GSTP1 genotypes did not differ between patients and controls. However, a two-fold risk was observed for GSTM1 null genotype in adenocarcinoma (OR(odds ratio) 2.1; 95% CI(confidence intervals)=0.53-8.6). Further, we used a case only design to study gene-environment interactions in esophageal cancer. In patients with smoking habits, GSTM1 null and GSTP1 ile/ile genotype were at higher risk for esophageal cancer (OR 1.5; 95% CI=0.50-4.4 and OR 1.3; 95% CI=0.40-3.5), respectively. A moderate risk for cancer was observed from alcohol usage along with GSTM1 null(OR 1.3; 95% CI=0.50-3.6) and GSTP1 val/val genotypes(OR 1.2; 95% CI=0.20-5.7). Interaction of GST genotypes with occupational exposure did not affect risk for esophageal cancer. These findings suggest that genetic polymorphisms of GSTT1, GSTM1, and GSTP1 are not associated with higher risk of esophageal cancer. However, interaction of smoking or alcohol with GSTM1 null or GSTP1 ile/ile moderately increases the risk for esophageal cancer in North Indian population.     

Association Between GSTM1 Polymorphism and Nasopharyngeal Cancer Susceptibility: a Meta-analysis

Background/Aims: Glutathione S-transferase M1 (GSTM1) is a multifunctional enzyme that plays a criticalrole in the detoxification of varieties of carcinogenic metabolites. Many studies have been conducted to investigatethe association between GSTM1 polymorphism and nasopharyngeal cancer (NPC) risk, but the findings amongthose studies are inconsistent. To assess this relationship more precisely, we performed a meta-analysis of allavailable studies on the subject. Methods: Case-control studies were identified by searching Pubmed, Embase,ISI Web of Science, and Wanfang databases through September 6, 2012. We used the pooled odds ratio (OR)with its corresponding 95% confidence interval (95%CI) to evaluate the association of GSTM1 polymorphismwith NPC susceptibility. Subgroup analyses by pathological types, sex and smoking status were performed tofurther identify the association. Results: Overall, 11 published studies with 1,513 cases and 2,802 controls werefinally included into this meta-analysis according to the inclusion criteria. Meta-analysis of total studies showedthat the null genotype of GSTM1 was significantly associated with increased risk of NPC, when comparing withthe non-null genotype (OR=1.51, 95%CI=1.33-1.72, POR<0.001). The association was still statistically significantin subgroup analysis of patients with nasopharyngeal squamous cell carcinoma (OR=1.73, 95%CI=1.24-2.42,POR=0.001). Males with the null genotype of GSTM1 were more likely to subject to NPC than females. Inaddition, the association between the null genotype of GSTM1 and NPC risk was strongest in individuals withexposure to smoking. Sensitivity analysis by sequential omission of any individual studies one at a time furtherdemonstrated the significant association. Conclusions: The findings suggest that the null genotype of GSTM1 isa risk factor for NPC, and there is a gene- smoking interaction in this association     

Association of Glutathione-S-Transferases M1 and T1 Deletional Variants with Development of Oral Squamous Cell Carcinoma: A Study in the South-East of Iran

Background: The role of genetic polymorphisms in genes of Glutathione-S-transferases (GST) enzymes in susceptibilityto oral cavity cancers is controversial. Oral Squamous Cell Carcinoma (OSCC) is the most common oral cavity neoplasm.Aimed to evaluate the potential impacts of two well-known null variants residing in the gene encoding GSTM1 andGSTT1 enzymes of OSCC patients in the southeast of Iran. Methods: In a case-control design, 113 individuals (50OSCC patients, and 63 healthy subjects) were included. DNA was extracted using paraffin-embedded tissues. GSTgenotyping was carried out using multiplex PCR. Results: In 113 participants, 41 (36.3%) and 72 (63.7%) were malesand females respectively. No significant difference was recognized for distribution of GSTM1 (P=0.11) and GSTT1(P=0.28) null genotypes between OSCC patients (58%, and 24% respectively) and healthy controls (42.9% and 15.9%respectively). Also, no significant difference was noted regarding the frequency of GSTM1 null genotype in differenthistological grades, however, those patients with more aggressive disease (poorly differentiated or grade III) revealedwith a significantly higher ratio (66.7%) of GSTT1 null genotype (P=0.002). The highest odds ratio for OSCC was relatedto combined null genotypes for GSTM1 and GSTT1 (OR=2.5, 95% CI: 0.7-9.2), however, this was not statisticallysignificant finding (P=0.15). Conclusion: Null genotypes polymorphisms were more common in OSCC than healthyindividuals. GSTT1 null genotype may be an important genetic factor in the progression of OSCC.