O^6-甲基鸟嘌呤-DNA甲基转移酶在食管癌患者的表达及临床意义

目的 探讨DNA修复蛋白O6-甲基鸟嘌呤-DNA甲基转移酶(MGMT)在老年食管癌患者的表达及临床意义.方法 采用免疫组织化学方法检测57例食管癌标本和20例正常食管组织中MGMT的表达,并分析其与临床病理特征之间的关系.结果 MGMT在食管癌表达的阳性率(49.1%)明显低于正常组织(85.0%,P＜0.01).侵及外膜层、有淋巴结转移、Ⅲ+Ⅳ期的食管癌患者MGMT阳性率明显低于未侵及外膜层、无淋巴结转移、Ⅰ+Ⅱ期患者(P＜0.05).MGMT在食管癌表达的阳性率在年龄、性别、分化程度、肿瘤部位组间无明显差异(P＞0.05).结论 MGMT在食管癌的表达与浸润深度、淋巴结转移和临床分期有关,可作为判断食管癌预后的指标.     

MGMT和ERCC1在胃癌及癌前病变中的表达及意义

目的探讨DNA损伤修复基因产物O6-甲基鸟嘌呤-DNA甲基转移酶（MGMT）与切除修复交叉互补基因1（ERCC1）的表达,及其与胃癌发生及生物学行为的关系。方法采用免疫组化SP法检测MGMT和ER-CC1的表达情况,并与临床病理特征相比较。结果 MGMT蛋白在轻度异型增生胃黏膜的表达率高于早期胃癌及进展期胃癌,ERCC1在正常胃黏膜的表达率高于早期胃癌及进展期胃癌。MGMT表达与胃癌分化程度、淋巴结转移有关,ERCC1与分化程度、浸润深度、淋巴结转移有关。胃癌中MGMT表达与ERCC1表达呈正相关。结论 MGMT、ERCC1可能在胃癌发生中起重要作用,有可能成为判断胃癌生物学行为的有用指标。     

Ⅲ～Ⅳ级胶质瘤组织中MGMT、TopoⅡα、P-gp的表达变化及意义

目的 观察Ⅲ～Ⅳ级胶质瘤组织中O6甲基鸟嘌呤-DNA甲基转移酶(MGMT)、拓扑异构酶Ⅱα (TopoⅡα)和P-糖蛋白(P-gp)的表达变化,并探讨其意义.方法 采用免疫组织化学法检测36例Ⅲ～Ⅳ级胶质瘤、24例Ⅰ～Ⅱ级胶质瘤及10例正常脑组织中的MGMT、TopoⅡα及P-gp.结果 高级别胶质瘤组织中MGMT、TopoⅡα、P-gp阳性率分别为72.2%、50.0%、66.7%,Ⅰ～Ⅱ级胶质瘤中分别为29.2%、33.3%、25.0%,正常脑组织中分别为10%、0、0,三者两两比较,P均＜0.01.相关分析表明,Ⅲ～Ⅳ级胶质瘤组织中MGMT与P-gp、TopoⅡα与P-gp有关,r分别为0.444、0.478.结论 高级别胶质瘤中MGMT、TopoⅡα、P-gp表达增高,可根据其表达情况制定个体化的化疗方案.     

Ⅲ～Ⅳ级胶质瘤组织中MGMT、TopoIIa、P—gP的表达变化及意义

目的观察III～Ⅳ级胶质瘤组织中O 6甲基鸟嘌呤-DNA甲基转移酶（MGMT）、拓扑异构酶Ⅱ仪（Topo11d）和P-糖蛋白（P-gp）的表达变化,并探讨其意义。方法采用免疫组织化学法检测36例Ⅲ～Ⅳ级胶质瘤、24例I～Ⅱ级胶质瘤及10例正常脑组织中的MGMT、Topo IIa及P—gp。结果高级别胶质瘤组织中MGMT、TopoIIa、P—gp阳性率分别为72．2％、50．0％、66．7％,I～Ⅱ级胶质瘤中分别为29．2％、33．3％、25．0％,正常脑组织中分别为10％、0、0,三者两两比较,P均〈0．01。相关分析表明,Ⅲ～Ⅳ级胶质瘤组织中MGMT与P—gp、TopIIa与P—gp有关,r分别为0．444、0．478。结论高级别胶质瘤中MGMT、TopoIId、P—gp表达增高,可根据其表达情况制定个体化的化疗方案。     

DNA-PKcs蛋白和MGMT蛋白在肝癌组织中的表达及意义

目的探讨DNA依赖蛋白激酶催化亚单位（DNA—PKcs）和O^6-甲基鸟嘌呤-DNA甲基转移酶（MGMT）在肝癌发生、发展中的作用及临床应用价值。方法应用免疫组化方法检测DNA—PKcs蛋白和MGMT蛋白在68份肝癌组织（肝癌组）和10份正常肝脏组织（对照组）中的表达情况,采用X^2检验及Spearman秩和相关检验分析结果。结果肝癌组及对照组DNA—PKcs蛋白表达阳性率分别为85％和10％,MGMT蛋白表达阳性率分别为40％和90％（P均〈0．05）;两者表达具有负相关性（r=-0．475,P〈0．05）。结论DNA-PKcs和MGMT在肝癌发生、发展中起重要作用：有望作为肿瘤标记物、基因靶点等用于肝癌的诊治。     

脑胶质瘤MGMT基因表达及启动子甲基化与患者临床预后关系的观察．

目的 探讨O6-甲基鸟嘌呤-DNA甲基转移酶（MGMT）基因表达及启动子甲基化与脑胶质瘤患者临床预后的关系。方法 选取郑州大学人民医院神经外科2007年4月至2009年4月收治的同意接受脑胶质瘤个体化综合治疗且有完整病历资料的患者78例,根据脑胶质瘤MGMT基因表达及启动子甲基化情况分组,术后均采用同步放化疗,观察患者近期疗效、无进展生存时间及安全性,比较各组间疗效。两组间均数比较采用独立样本t检验,计数资料采用R×C表χ2检验,采用Kaplan-Meier方法绘制生存曲线,并采用Log-rank检验对其生存曲线进行分析。结果 MGMT基因启动子甲基化状态与MGMT蛋白表达呈负相关（r=-0.514,P〈0.05）。MGMT基因启动子甲基化组近期客观疗效明显优于MGMT基因启动子非甲基化组（χ2=47.890,P=0.000）;MGMT蛋白低表达组近期客观疗效明显优于MGMT蛋白高表达组（χ2=30.032,P=0.000）。MGMT基因启动子甲基化患者生存期明显长于非甲基化组（χ2=21.405,P〈0.05）,MGMT蛋白低表达患者生存期明显长于MGMT蛋白高表达组（χ2=18.643,P〈0.05）;MGMT基因启动子甲基化组客观有效率81.0%（34/42）优于MGMT蛋白低表达组74.4%（29/39）。患者均未出现明显不良反应。结论 脑胶质瘤MGMT基因表达及启动子甲基化与患者应用尼莫司汀＋替莫唑胺会师化疗同步适行放疗治疗预后密切相关,且MGMT甲基化对判断恶性胶质瘤患者预后吻合性更高,为临床制订有效的个体化疗方案提供参考。     

人脑胶质瘤组织中耐药相关基因蛋白MGMT、Topo-Ⅱ、GST-π、P-gp的表达变化及意义

目的观察人脑胶质瘤组织中耐药相关基因蛋白O6-甲基鸟嘌呤-DNA-甲基转移酶（MGMT）、拓扑异构酶（Topo-Ⅱ）、谷胱甘肽转移酶（GST-π）、P-糖蛋白（P-gp）的表达变化,并探讨其临床意义。方法采用免疫组化法检测330例人脑胶质瘤组织及20例正常脑组织中的MGMT、Topo-Ⅱ、GST-π、P-gp蛋白。结果正常脑组织中MGMT、Topo-Ⅱ、GST-π、P-gp均无表达,人脑胶质瘤组织中MGMT、Topo-Ⅱ、GST-π、P-gp的阳性表达率分别为43.9%、24.3%、49.8%、48.2%;MGMT的表达与胶质瘤病理分级无关（P〉0.05）,Topo-Ⅱ、GST-π、P-gp的表达与胶质瘤病理分级有关（P均〈0.05）。结论人脑胶质瘤组织中不同程度地表达耐药相关基因蛋白MGMT、Topo-Ⅱ、GST-π、P-gp,可据此制订个体化的胶质瘤化疗方案。     

O^6-甲基鸟嘌呤-DNA甲基转移酶基因多态性与新疆哈萨克族食管癌易感性关系的研究

目的 为探讨O6-甲基鸟嘌呤-DNA甲基转移酶(MGMT)基因多态性与新疆哈萨克族食管癌易感性的关系. 方法 运用病例-对照研究的方法,PCR-RFLP技术检测新疆哈萨克族食管癌51例及非癌对照109例的MGMT 84C>T和MGMT 135G>T单核苷酸多态(SNPs)的基因型. 结果 MGMT 84C>T位点的三种基因型CC,CT,TT,在哈萨克族食管癌中所占比例分别为76.5%(39/51) 、17.6%(9/51) 、5.9%(3/51),对照组分别为77.0%(84/109)、18.3%(20/109)、4.6%(5/109),两组间分布差异不显著(P=0.938,P>0.05);MGMT 135G>T位点的三种基因型GG,GT,TT,在哈萨克族食管癌中所占比例分别为90.2%(46/51)、7.8%(4/51)、2.0%(1/51),对照组分别为82.6%(90/109)、16.5%(18/109)、0.9%(1/109),两组间分布差异不显著(P=0.295,P>0.05);MGMT 84C>T位点和MGMT 135G>T位点联合分析,在食管癌组0突变等位基因与1-4突变等位基因所占比例分别为68.6%(35/51)、31.4%(16/51);对照组分别为:63.3%(69/109)、36.7%(40/109),两组间分布差异也不显著(P=0.511,P>0.05). 结论 MGMT 84C>T和MGMT 135G>T SNPs与哈萨克族食管癌易感性可能无关联.     

DNA修复酶和热休克蛋白70在乳腺癌中表达的意义

目的 探讨DNA修复酶和热休克蛋白70(HSP70)在乳腺癌中的表达及临床意义.方法 采用免疫组织化学(SP)法检测6-氧-甲基鸟嘌呤-DNA甲基转移酶(MGMT)和HSP70在59例乳腺癌组织和26例乳腺腺瘤组织中的表达.结果 乳腺癌中MGMT和HSP70阳性表达率显著高于乳腺腺瘤(P＜0.05);MGMT在乳腺癌中的表达与组织学类型、部位及淋巴结转移有统计学意义;HSP70在乳腺癌中的表达与组织学类型及淋巴结有无转移有统计学意义(P＜0.05).结论 MGMT和HSP70与乳腺癌的发生密切相关,检测MGMT和HSP70对乳腺癌的早期诊断、治疗及预后有重要意义.     

O(6)-methylguanine DNA methyltransferase activity in diabetic patients

In the present study, we evaluated O(6)-methylguanine-DNA methyltransferase (MGMT) activity in diabetic patients. The study was performed on 27 patients with Type 1 diabetes, and 42 with Type 2 diabetes. Patients with complications were excluded from the study. 36 non-diabetic volunteers, non-smokers who do not consume alcoholic beverage, were chosen from the medical staff as control subjects. MGMT activity was measured by the transfer of radiolabeled methyl groups from a prepared methylguanine-DNA substrate to the enzyme fraction of leukocyte extract. Leukocyte MGMT activity was significantly reduced in both Type 1 and Type 2 diabetes patients as compared with control subjects (P<0.001). The present study demonstrates decreased MGMT activity in leukocytes from patients with Type 1 and Type 2 diabetes.     

非小细胞肺癌DNA甲基转移酶及基因p53表达与预后的关系

Objective To investigate the expression and role of O~6-methylguanine DNA methyltransferas(MGMT) and p53 in non-small cell lung cancer(NSCLc)and the association with prognosis. Methods Immunohistochemical method was used to investigate the expression of MGMT and p53 in NSCLC specimens from 110 cases and in 20 cages of benign lung diseases as the control.The association of their expression with the prognosis of the 110 patients was evaluated. Results The positive expression of MGMT in NSCLC and benign lung diseases was 41.8%(46/110)and 80%(16/20)(x2=9.89,P<0.05),respectively.The positive expression of p53 in NSCLC and benign lung diseases were 56.4%(62/110)and 0%(0/20)(x2=21.551,P<0.05),respectively.There was a significant association between expression of MGMT with smoking,and lymph node metastasis (x2=12.107,P<0.05;x2=6.512P<0.05).There was also a significant association between expression of p53 with smoking and lymph node metastasis(x2=6.330,P<0.05;x2=7.909,P<0.05).A negative correlation was observed between the expression of MGMT and that of p53 protein in NSCLC(R_S=-0.592,P<0.05).The 5-year survival rate and median survival time of 110 cages was 10.9%(12/110),and(30.4±0.6)months.In 46 cases with positive expression of MGMT the 5-year survival rate was 0%(0/110)and median survival was(25.9±0.4)months,which were lower than those in the 64 patients with negative expression of MGMT [18.8%(12/64),(32.4 ±0.7)months],Log rank test x2=23.569,P<0.05.in the 62 patients with positive expression of p53.the 5-year survival rate and modian survival were 4.8%(3/62)and(30.4±1.2)months,which were lower than those in the 48 cases with negative expression of p53[18.8%(9/48),(30. 5± 1.1 ) months], Log rank test X2 =5. 521, P <0. 05. Conclusion The loss of expression of MGMT may lead to activation of the wild-type p53. They may participate in lung carcinomatosis, and may predict prognosis in patients with NSCLC.     

非小细胞肺癌DNA甲基转移酶及基因p53表达与预后的关系

Objective To investigate the expression and role of O~6-methylguanine DNA methyltransferas(MGMT) and p53 in non-small cell lung cancer(NSCLc)and the association with prognosis. Methods Immunohistochemical method was used to investigate the expression of MGMT and p53 in NSCLC specimens from 110 cases and in 20 cages of benign lung diseases as the control.The association of their expression with the prognosis of the 110 patients was evaluated. Results The positive expression of MGMT in NSCLC and benign lung diseases was 41.8%(46/110)and 80%(16/20)(x2=9.89,P<0.05),respectively.The positive expression of p53 in NSCLC and benign lung diseases were 56.4%(62/110)and 0%(0/20)(x2=21.551,P<0.05),respectively.There was a significant association between expression of MGMT with smoking,and lymph node metastasis (x2=12.107,P<0.05;x2=6.512P<0.05).There was also a significant association between expression of p53 with smoking and lymph node metastasis(x2=6.330,P<0.05;x2=7.909,P<0.05).A negative correlation was observed between the expression of MGMT and that of p53 protein in NSCLC(R_S=-0.592,P<0.05).The 5-year survival rate and median survival time of 110 cages was 10.9%(12/110),and(30.4±0.6)months.In 46 cases with positive expression of MGMT the 5-year survival rate was 0%(0/110)and median survival was(25.9±0.4)months,which were lower than those in the 64 patients with negative expression of MGMT [18.8%(12/64),(32.4 ±0.7)months],Log rank test x2=23.569,P<0.05.in the 62 patients with positive expression of p53.the 5-year survival rate and modian survival were 4.8%(3/62)and(30.4±1.2)months,which were lower than those in the 48 cases with negative expression of p53[18.8%(9/48),(30. 5± 1.1 ) months], Log rank test X2 =5. 521, P <0. 05. Conclusion The loss of expression of MGMT may lead to activation of the wild-type p53. They may participate in lung carcinomatosis, and may predict prognosis in patients with NSCLC.     

非小细胞肺癌DNA甲基转移酶及基因p53表达与预后的关系

目的 探讨DNA修复酶O6-甲基鸟嘌呤DNA甲基转移酶(MGMT)及抑癌基因p53在非小细胞肺癌(NSCLC)中的表达及其与预后的关系. 方法 采用免疫组织化学SP法检测110例NSCLC患者及20例肺部良性病变患者术后肺组织中MGMT及p53的表达,并观察110例NSCLC根治术后患者的生存期. 结果 110例NSCLC患者及20例肺良性病变患者组织中MGMT蛋白阳性表达率分别为41.8%(46/110)和80%(16/20),p.53蛋白的阳性表达率分别为56.4%(62/110)和0%(0/20)例,MGMT蛋白表达与淋巴结转移及吸烟史相关(x2值为12.107和6.512,均P<0.05),p53蛋白表达亦与淋巴结转移及吸烟史相关(X2值为6.330和7.909,均P<0.05),MGMT和p53蛋白表达呈负相关(Rs=-0.592,P<0.05).110例患者的5年生存率为10.9%(12/110),中位生存期为(30.4±0.6)个月;46例MGMT表达阳性的患者5年生存率为0%(0/110),中位生存期为(25.9±0.4)个月,均低于64例MGMT表达阴性患者的5年生存率(18.8%,12/64)和中位生存期[(32.4±0.7)个月],差异有统计学意义(x2=23.569,P<0.05).62例053表达阳性患者的5年生存率为4.8%(3/62),中位生存期为(30.4±1.2)个月,均低于48例p53表达阴性患者的5年生存率(18.8%,9/48)和中位生存期[(30.5±1.1)个月],差异有统计学意义(x2=5.521,P<0.05). 结论 NSCLC患者体内MGMT表达缺失可能与突变型p53的表达水平有关,且与肺癌的发生、发展及预后相关.     

DNA甲基转移酶1在胰腺癌组织中的表达及其临床意义

目的 探讨DNA甲基转移酶1(DNMT1)在胰腺癌组织中的表达及其临床意义.方法 收集手术切除的30例胰腺癌组织和配对癌旁组织.采用实时定量PCR法检测DNMT1 mRNA的表达;免疫组织化学法检测DNMT1蛋白的表达;分析胰腺癌组织DNMT1蛋白表达强度与临床病理参数之间的关系.结果 胰腺癌组织中DNMT1 mRNA的表达量为2.32(1.17～5.17),显著高于配对癌旁组织的0.78(0.07～3.14,P＜0.05).胰腺癌组织中导管细胞DNMT1蛋白表达阳性率为(54.5±21.2)%,显著高于癌旁组织(10.9±15.0)%的表达阳性率(P＜0.01).以胰腺癌导管细胞DNMT1阳性率54.5%为界,分为高表达组(19例)和低表达组(11例).DNMT1表达强度和临床分期(x2=6.897,P=0.029)、淋巴结转移(x2=4.739,P=0.029)、神经浸润与否(x2=5.44,P=0.020)相关,而与年龄、性别、肿瘤位置、肿瘤大小、肿瘤分化、血清CEA和CA19-9浓度无关.结论 胰腺癌组织DNMT1 mRNA和蛋白表达明显增加,DNMT1蛋白表达强度与胰腺癌的侵袭力、淋巴结转移和神经浸润相关.     

表皮生长因子受体在老年大肠癌中的表达及临床意义

目的探讨表皮生长因子受体（EGFR）在老年大肠癌组织中的表达及其临床意义.方法采用免疫组化SABC法对87例大肠癌、14例大肠炎性黏膜和26例大肠腺癌样息肉进行检测。结果 EGFR在大肠炎性黏膜、腺瘤样息肉和大肠癌中阳性率分别为21.43%、46.15%和54.02%，其中RGFR在炎性黏膜中表达率明显低于腺瘤样息肉和大肠癌（P〈0.05）；EGFR表达与大肠癌浸润深度和淋巴结转移有相关性（P〈0.05）。结论：EGFR过度表达，在老年大肠癌的发生过程中可能起重要作用；检测EGFR对于指导临床治疗和判断预后有重要意义。     

Protection of hematopoietic cells against combined O6-benzylguanine and chloroethylnitrosourea treatment by mutant forms of O6-methylguanine DNA methyltransferase

This report demonstrates that expression of the P140A O6-methylguanine DNA methyl transferase (MGMT) mutant via retrovirus-mediated gene transfer leads to significant, but modest, resistance of cells to both 6-benzylguanine (6-BG) depletion and treatment with 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU). Expression of the P140A/G156A double mutant appeared to be associated with reduced or unstable protein in hematopoietic cells.     

老年大肠癌中PCNA和C-erbB-2的表达及意义

目的：检测ＰＣＮＡ和Ｃ－ｅｒｂＢ－２在老年大肠癌中的表达及其意义。对３３例老年大肠癌的石蜡切片标本进行免疫组化染色。结果ＰＣＮＡ和Ｃ－ｅｒｂＢ－２在３３例大肠癌中的阳性率分别为６６．７％和６０．６％;ＰＣＮＡ和Ｃ－ｅｒｂＢ－２的表达与癌组织的分化程度及临床分期有明显相关性（Ｐ〈０．０１）,淋巴结转移组中二者的表达明显高于无转移组（Ｐ〈０．０１）。结论ＰＣＮＡ和Ｃ－ｅｒｂＢ－２过高表达者预后不良,Ｐ     

Overexpression of DNA methyltransferase 1 and its biological significance in primary hepatocellular carcinoma

AIM： To explore the relationship between DNA methyltransferase 1 （DNMT1） and hepatitis B virus （HBV）-related hepatocellular carcinoma （HCC） and its biological significance in primary HCC. METHODS： We carried out an immunohistochemical examination of DNMT1 in both HCC and paired nonneoplastic liver tissues from Chinese subjects. DNMT1 mRNA was further examined in HCC cell lines by real-time PCR. We inhibited DNMT1 using siRNA and detected the effect of depletion of DNMT1 on cell proliferation ability and cell apoptosis in the HCC celt line SMMC-7721. RESULTS： DNMT1 protein expression was increased in HCCs compared to histologically normal nonneoplastic liver tissues and the incidence of DNMT1 immunoreactivity in HCCs correlated significantly with poor tumor differentiation （P = 0.014）. There were more cases with DNMT1 overexpression in HCC with HBV （42.85%） than in HCC without HBV （28.57%）. However, no significant difference in DNMT1 expression was found in HBV-positive and HBV-negative cases in the Chinese HCC group. There was a trend that DNMT1 RNA expression increased more in HCC cell lines than in pericarcinoma cell lines and normal liver cell lines. In addition, we inhibited DNMT1 using siRNA in the SMMC-7721 HCC cell line and found depletion of DNMT1 suppressed cells growth independent of expression of proliferating cell nuclear antigen （PCNA）, even in HCC cell lines where DNMT1 was stably decreased. CONCLUSION： The findings implied that DNMT1 plays a key role in HBV-retated hepatocellular tumorigenesis. Depletion of DNMT1 mediates growth suppression in SMMC-7721 cells.     

Repair of DNA lesion O 6-methylguanine in hepatocellular carcinogenesis

Evidence from both experimental carcinogenesis and studies in human cirrhotic liver suggest that defective repair of the promutagenic DNA base lesion,O⁶-methylguanine, is a factor in the multistep process of hepatocellular carcinogenesis. Ubiquitous environmental alkylating agents such as N-nitroso compounds can produce O⁶-methylguanine in cellular DNA. Unrepaired,O⁶-methylguanine can lead to the formation of G → A transition mutations, a known mechanism of human oncogene activation and tumour suppressor gene inactivation. Combined treatment of rodents with an agent producing O⁶-methylguanine in DNA, and an agent promoting cell proliferation, leads to development of hepatic nodules and hepatocellular carcinoma (HCC), cell division, hence DNA replication, being required for the propagation of tumorigenic mutation(s) in hepatocyte DNA. The paramount importance of O⁶-methylguanine in hepatocellular carcinogenesis is indicated by the observation that transgenic mice engineered to have increased hepatic levels of repair enzyme O⁶-methylguanine-DNA methyltransferase (MGMT) are significantly less prone to hepatocellular carcinogenesis following alkylating agent treatment. Cirrhosis is a universal risk factor for development of human HCC, and a condition that is characterized by increased hepatocyte proliferation as a result of tissue regeneration. Levels of the human repairing enzyme for O⁶-methylguanine were found to be significantly lower in cirrhotic liver than in normal tissue. In accord with findings from animal models, this suggested a mechanism in which persistence of O⁶-methylguanine due to defective DNA repair by MGMT, together with increased hepatocyte proliferation, might lead to specific gene mutation(s) and hepatocellular carcinogenesis. Screening for the presence and persistence of O⁶-methylguanine in human DNA presently involves formidable technical difficulty. Indications are that such limitations might be overcome by the use of an ultrasensitive method such as immuno-polymerase chain reaction (PCR). This approach should allow parallel measurement of DNA adduct and repair enzyme in routine liver biopsy samples. It might also enable investigation of O⁶-methylguanine in human genes specifically associated with hepatocellular carcinogenesis. Given the wide variation in human MGMT levels observed between individuals, tissues, and cells, this technology should be adapted to permit the ultrasensitive localisation and measurement of adducts and repairing enzyme in liver biopsy tissue sections. Ability to ultrasensitively measure O⁶-methylguanine, and its repair enzyme, should prove valuable in the risk assessment of cirrhotic patients for developing hepatocellular carcinoma.