肝细胞肝癌和慢性肝病P53蛋白表达与乙型肝炎病毒感染的关系

目的：探讨肝细胞肝癌和慢性肝病P53蛋白表达与乙型肝炎病毒（HBV）感染的关系。方法：对慢性肝炎、肝硬化、癌旁肝硬化、肝细胞肝癌和正常肝组织共98例用免疫组化方法检测乙型肝炎表面抗原（HBsAg）、乙型肝炎核心抗原（HBcAg）和P53蛋白，用原位分子杂交方法检测HBV DNA。结果：慢性肝炎HBsAg阳性率为61.9%（13／21），HBcAg42.9%(9/21)，HBV DNA75.0%（12／16）；肝硬化HBsAg64.0%（16／25），HBcAg36.0%（9／25），HBV DNA83.3%（15／18）；癌旁肝硬化HBsAg72.7%（16／22），HBcAg61.1%（11／18），HBV DNA85.7%（12／14）；肝细胞肝癌HBsAg45.2%（14／31），HBcAg50.0%(14/28)，HBV DNA64.3%（9／14）。P53蛋白只在肝细胞肝癌组表达（27.9%,12/43)，其他组均不表达。结论：P53蛋白表达于肝细胞肝癌相对较晚的演进阶段，P53蛋白表达阳性率与HBV感染无相关性。     

DKK-1、DKK-2和GPC3蛋白在肝细胞癌组织中的表达及其临床意义

目的:探讨DKK-1、DKK-2和人磷脂酰肌醇蛋白聚糖3(glypican3,GPC3)蛋白在肝细胞癌组织中的表达及临床意义.方法:采用组织芯片联合免疫组织化学法检测DKK-1、DKK-2和GPC3蛋白在10例正常肝、12例肝硬化、57例肝细胞癌及癌旁肝组织中的表达差异,并分析其临床意义.结果: 免疫组织化学检测结果发现,DKK-1和DKK-2在肝细胞癌组织中阳性染色率分别为59.65%(34/57)和57.89%(33/57);GPC3只在肝细胞癌组织中表达,其阳性染色率为47.37%(27/57),而在正常肝、肝硬化及癌旁肝组织中均呈阴性表达.DKK-1与DKK-2阳性表达之间存在密切相关性(χ2=0.570, P=0.000),DKK-2与GPC3阳性染色之间也存在相关性(χ2=0.272, P=0.041).统计分析DKK-1、DKK-2及GPC3在肝细胞癌组织中阳性染色与肝癌患者性别、年龄、血清甲胎蛋白(α-fetoprotein,AFP)水平、乙肝表面抗原(hepatitis B surface antigen, HBsAg)、肿瘤大小、病理学分级、静脉浸润以及是否伴随肝硬化等的相关性,结果表明血清AFP水平与GPC3表达呈正相关(P=0.007),HBsAg与DKK-1表达呈正相关(P=0.037),DKK-1阳性染色与肝细胞癌组织分级存在相关性(P=0.014),与其他参数则无相关性.结论:GPC3在肝细胞癌组织的阳性染色率为47.37%,GPC3染色阴性的肝细胞癌组织中DKK-1和DKK-2双阳性染色率为40.00%,而GPC3(+)联合DKK-1(+)/DKK-2(+)/GPC3(-)可将肝细胞癌的免疫组织化学检出率提高至68.42 %(39/57),降低肝癌免疫组织化学检测中的假阴性率.     

乙型肝炎性原发性肝癌患者乙肝病毒DNA载量与免疫功能的相关性

目的:探讨乙型肝炎性原发性肝癌患者乙肝病毒DNA载量与免疫功能的相关性。方法:自2016年1月至2018年1月，连续性收集我院收治的乙型肝炎性原发性肝癌患者80例作为观察组，同期收集健康成人80例作为对照组，分析两组免疫功能差异。此外，测量观察组患者乙肝病毒DNA载量，分析乙肝病毒DNA载量与患者免疫功能的相关性。结果:与对照组比较，观察组CD4+T细胞含量显著降低(0.21±0.08 vs 0.29±0.09,P=0.000)；CD8+T细胞含量、Treg细胞含量增高［(0.29±0.07 vs 0.23±0.06,P=0.000)和(0.12±0.04 vs 0.08±0.03,P=0.000)］。Pearson线性相关性显示乙肝病毒DNA载量与CD4+T细胞含量负相关，与CD8+T细胞含量、Treg细胞含量、肿瘤直径显著正相关(P＜0.05)。与TNM分期为Ⅱ期的患者相比，Ⅲ期的患者乙肝病毒DNA载量显著增高［（6.16±1.51）×103 IU/ml vs （5.47±1.36）×103 IU/ml,P=0.035］。结论:乙型肝炎性原发性肝癌患者高水平乙肝病毒DNA载量与细胞免疫功能紊乱有关，与患者TNM分期和肿瘤直径有关。     

HSP90α和HSP90β在肝癌中共同上调表达

[目的]探讨热休克蛋白90α(HSP90α)和HSP90β在肝癌中的表达及意义.[方法]采用免疫组化法检测103例肝癌组织和79例非肝癌相关组织(正常肝组织,肝炎,肝硬化)中HSP90α和HSP90β的表达,并分析其与肝癌临床病理特征的关系.[结果]肝癌组织中,HSP90α和HSP90β的阳性表达率分别为82.52％和85.44％,均显著高于非癌组织(P＜0.05).HSP90α高表达与肝癌分化程度相关(P＜0.05),而与患者性别、病理类型、病理分期无关(P＞0.05).HSP90β高表达与肝癌分化程度和TNM分期相关(P＜0.05),而与患者性别、病理类型无关(P＞0.05).Spearman相关性分析显示,HSP90α和HSP90β在肝癌组织中协同表达(r=0.535,P＜0.001).[结论]HSP90α和HSP90β在肝癌组织中共同表达上调,可能可作为肝癌潜在的诊断和治疗靶点.     

肝细胞癌、肝硬化肝组织中的乙型肝炎核心抗原(HBcAg)

为研究肝细胞癌与乙型肝炎的关系,在探讨乙型肝炎表面抗原(HBsAg)在肝组织的分布规律的基础上,用免疫过氧化物酶间接法检测肝细癌和肝硬化的肝组织中乙型肝炎核心抗原(HBcAg)的存在情况。     

E-cadherin与粘着斑激酶在肝细胞癌组织中的表达及其临床意义

目的:探讨Ecadherin、粘着斑激酶在肝细胞癌中的表达及其临床病理意义。方法:应用免疫组化SP法检测42例肝细胞癌、13例正常肝细胞中Ecadherin、粘着斑激酶的表达。结果:1)Ecadherin在正常肝细胞、癌旁组织及肝癌组织中的阳性表达率分别为76.92%(10/13)、25.00%(24/32)、23.80%(10/42)。肝癌组织与前二组阳性表达率比较差异有统计学意义(P=0.010,P=0.000)。2)粘着斑激酶在正常肝细胞及癌旁组织中多数呈阴性表达,在肝癌细胞粘着斑激酶阳性表达率为71.42%(30/42),与前两组比较差异有统计学意义(P=0.000,P=0.001)。3)高侵袭转移组与低侵袭转移组间,Ecadherin阳性率分别为27.27%(6/22)和60.00%(12/20),组间差异有统计学意义,(P=0.033);粘着斑激酶阳性率分别为59.09%(13/22)和25.00%(5/20),组间差异有统计学意义(P=0.020)。结论:Ecadherin在肝癌细胞表达缺失、粘着斑激酶在肝癌细胞高表达与肝细胞癌的发生、侵袭和转移有关。     

HSP70和P27在食管鳞癌中的表达及意义

目的探讨热休克蛋白70(HSP70)和P27在食管鳞状细胞癌中表达的相关性。方法采用SP免疫组化染色法检测65例食管鳞癌组织、30例正常食管组织及30例癌旁组织中的HSP70和P27。结果正常食管上皮、癌旁组织、食管鳞癌中HSP70的阳性表达率分别是16.67%(5/30)、46.67%(14/30)、86.15%(56/65),正常食管上皮、癌旁组织及食管鳞癌中P27的表达率分别是96.67%(29/30)、53.33%(16/30)、41.54%(27/65)。在食管鳞癌中,HSP70和P27的表达呈负相关(rs=-0.541,P=0.000)。结论在食管癌中,P27可能随着HSP70表达的上调而下降,其表达率与多个临床病理指标相关。     

肝细胞癌组织XAF1表达及其临床意义的研究

目的:探讨XAF1在原发性肝细胞癌发生中的作用。方法:应用RT-PCR技术检测人胎肝细胞株LO2、人肝癌细胞株SMMC7721、HepG2和30例肝癌及其相应癌旁组织XAF1mRNA的水平,同时应用免疫组织化学方法及蛋白质印迹检测上述细胞株及组织中XAF1蛋白的表达。结果:人胎肝细胞株LO2检测到XAF1mR-NA和蛋白的表达,人肝癌细胞株SMMC7721、HepG2XAF1mRNA和蛋白的表达低。肝癌组织XAF1mRNA和蛋白表达较癌旁组织显著降低(mRNA:0.587±0.064,1.013±0.159,t=2.392,P=0.000;蛋白:43179±11412,95541±30153,t=3.532,P=0.000)。免疫组化染色显示,XAF1蛋白表达集中在肝细胞胞质和胞核中,表达下调的XAF1蛋白与原发性肝细胞癌患者病理分期有显著相关性。结论:XAF1mRNA及蛋白在肝癌组织及肝癌细胞系中表达水平降低,提示可能是促进肝细胞癌发生的一个重要因素。     

肝癌组织DLK1和Jagged1表达临床意义探讨

目的探讨DLK1和Jagged1在原发性肝细胞性肝癌组织中的表达情况,深入分析两者与肝癌临床病理资料的关系及其临床意义。方法收集2001-01-01-2009-10-30顺德第一人民医院病理科采用免疫组化SP法检查10例正常肝组织、50例肝炎、50例肝硬化和150例肝细胞性肝癌组织中DLK1和Jagged1的表达情况。结果 DLK1阳性表达率在正常肝组织为0(0/10)、肝炎组为6.00%(3/50)、肝硬化组为28.00%(14/50)、肝癌组为46.67%(70/150),四组间阳性率比较差异有统计学意义,χ2=34.38,P<0.05。正常肝组织和肝炎组,正常肝组织和肝硬化组,正常肝组织和肝癌组,肝硬化和肝癌组两两比较差异均无统计学意义,P值均>0.05。肝炎和肝硬化组(χ2=8.575,P=0.003),肝炎和肝癌组(χ2=26.757,P<0.001)两两比较差异均有统计学意义。Jagged1阳性表达率在正常肝组织中为40.00%(4/10)、肝炎组为40.00%(20/50)、肝硬化组为62.00%(31/50)、肝癌组为71.33%(107/150),四组间阳性率比较差异有统计学意义,χ2=17.92,P<0.05。正常肝组织和肝炎组,正常肝组织和肝硬化组,正常肝组织和肝癌组,肝炎组和肝硬化组,肝硬化组和肝癌组,两两比较差异均无统计学意义,P值均>0.05。肝炎组和肝癌组比较差异有统计学意义,χ2=15.885,P<0.001。DLK1表达与年龄有关(χ2=15.01,P<0.05),Jagged1表达与年龄(χ2=7.94,P<0.05)、分化程度(χ2=14.79,P<0.05)、HBsAg(χ2=4.53,P<0.05)和预后(χ2=3.92,P<0.05)有关。DLK1和Jagged1在肝细胞癌组织中表达密切相关,χ2=12.79,P<0.05。结论 DLK1和Jagged1的异常表达与肝癌的发生、发展和分化密切相关。     

热休克蛋白90α在不同转移潜能人肝癌细胞株及HBV相关性肝细胞癌患者血清中表达水平的临床研究

目的 探讨热休克蛋白90α(HSP90α)在不同转移潜能人肝癌细胞株及乙型肝炎病毒(HBV)相关性肝细胞癌患者血清中的表达水平.方法 收集HBV感染肝病患者60例和同期体检的健康受试者12例的血清样本,采用Western blot技术检测不同转移潜能人肝癌细胞株中HSP90α的表达水平,采用ELISA技术检测HBV相关性肝癌患者、良性肝病患者、健康受试者血清中HSP90α的表达水平,采用统计学方法分析HSP90α的表达水平与HBV相关性肝细胞癌患者临床病理特征的关系.结果 高转移潜能人肝癌细胞株MHCC97H细胞中HSP90α的表达水平明显高于无转移潜能人肝癌细胞株HepG2细胞,差异有统计学意义(t=13.375,P=0.001);肝癌组与良性肝病组患者血清中HSP90α的表达水平均明显高于健康受试者,差异有统计学意义(F=11.357,P=0.002;F=9.633,P=0.005),但肝癌组与良性肝病组患者血清中HSP90α的表达水平比较,差异无统计学意义(F=0.859,P=0.983);42例伴HBV慢性感染肝癌患者血清中HSP90α的表达水平与性别有关,其中,女性患者血清中HSP90α的表达水平高于男性患者,差异有统计学意义(F=4.729,P=0.039),但患者年龄、HBeAg是否为阳性、甲胎蛋白(AFP)浓度、HBV DNA及临床分期之间比较,差异无统计学意义(P﹥0.05).结论 HSP90α可成为抗癌治疗的新靶点,并为肝病的早期诊断、肝癌的侵袭转移、预后评估及科学治疗提供理论依据.     

Immunohistochemical assessment and prognostic value of hepatitis B virus X protein in chronic hepatitis and primary hepatocellular carcinomas usinganti-HBxAg monoclonal antibody

Hepatitis B virus (HBV) is the most meaningful risk factor in chronic hepatitis, cirrhosis and primary hepatocellular carcinoma (PHC). The hepatitis B virus X protein (HBxAg) is a multifunctional protein with many important functions in hepatocellular carcinogenesis. A monoclonal anti-HBxAg antibody was developed in our laboratory and characterized by different methods. Using this antibody HBxAg was detected in formaldehyde fixed paraffin embedded tissue sections of 72 liver biopsies from patients with acute hepatitis, chronic hepatitis, cirrhosis and primary hepatocellular carcinoma. The co-expression of hepatitis B surface antigen (HBsAg), hepatitis B core antigen (HBcAg) and HBxAg was compared. The histological and cytological localization of the detected HBxAg showed a characteristic distribution in different stages of HBV infection. Strong and diffuse nuclear reaction was detected in PHC cases in contrast to the focal, cytoplasmic and nuclear labeling in the acute and chronic B hepatitis cases. Our antibody seems to be a suitable prognostic marker for routine pathohistological diagnosis and for comparative pathological and epidemiological research on the development of PHC.     

IMMUNOHISTOCHEMICAL STUDY ON X ANTIGEN OF HBV (HBxAg) IN PRIMARY HEPATIC CARCINOMA

The specimens were from 110 patients with primary hepatic carcinoma. The formalin- fixed and paraffin-embedded sections were stained for HBxAg by ABC method and for HBsAg and HBcAg by PAP method. Of the 110 cases, 64 (58. 2%) showed HBxAg-positive reaction in tumor tissue, and 63 (78. 8%) of 80 cases displayed positive HBxAg in surrounding non-cancerous hepatic tissue. Among the 64 cases with positive HBxAg in tumor tissue, 15 (23. 4%) were associated with HBsAg and/or HBcAg, while in the 63 cases with positive HBxAg in non-tumor tissue, 45(71. 4%) were accompanied with HBsAg and/or HBcAg. These findings suggest a dose relationship between prlmay hepatic carcinoma and HBV infection. The high detection rate of HBxAg Indicates a very active expression of the Integrated HBV- DNA genome in the host cells. However, the action of HBxAg in pathogenesis of hepatocellular carcinoma remains to be further investigated.     

Hepatitis B x antigen in hepatitis B virus carrier patients with liver cancer.

Formalin-fixed, paraffin-embedded specimens from 110 cases of primary hepatocellular carcinoma were stained for hepatitis B x antigen (HBxAg), hepatitis B surface antigen (HBsAg), and hepatitis B core antigen (HBcAg). Eighty-four % of these patients were HBxAg positive in their tumor cells. Among the 110 cases studied, 80 had adjacent nontumorous tissue in the same block, and 65 of these nontumorous liver tissues stained positive for HBxAg (81%). HBsAg was positive in 19% of cases within tumor tissue and 61% in surrounding nontumorous tissue. HBcAg was positive in 11% of cases within tumor tissue and 26% in surrounding nontumorous tissue. These findings show that HBxAg is a common marker in the liver of patients with hepatitis B virus (HBV)-associated primary hepatocellular carcinoma and that it is closely associated with tumor cells in these individuals. In addition, the finding of HBxAg in the absence of detectable HBsAg and HBcAg in the liver tissues of many HBsAg carriers suggests that HBxAg could be expressed independent of HBV replication and implies that the synthesis of this antigen may be directed from integrated HBV DNA templates. The finding of HBxAg in the nucleus of hepatocytes from primary hepatocellular carcinoma patients with dysplasia, combined with the known trans-activating properties of HBxAg, implies that HBxAg plays one or more important roles in hepatocarcinogenesis. The finding of HBxAg in bile duct epithelium and cholangiocarcinoma tissues is compatible with the hypothesis that HBV may contribute to this other primary tumor type in the liver. Together, these results further implicate HBxAg in the pathogenesis of primary liver cancers.     

Immunohistochemical study on X antigen of HBV (HBxAg) in primary hepatic carcinoma]

Specimens of 110 cases of primary hepatic carcinoma were obtained from the pathological Laboratory of the First Teaching Hospital of the 4th Military Medical University, Xi'an. P. R. China. Sections from formalin-fixed and paraffin-embedded material were stained for HBxAg by ABC method and for HBsAg and HBcAg by PAP method. Among the 110 cases of primary hepatic carcinoma, 64 (58.2%) showed HBxAg-positive reaction in tumor tissue, and 63 (78.8%) of 80 cases of noncancerous surrounding hepatic tissue displayed HBxAg positivity. Among 64 HBxAg-positive cases in tumor tissue, 15 (23.4%) were associated with HBsAg and/or HBcAg and among 63 HBxAg-positive cases in non-tumor tissue, 45 (71.4%) were associated with HBsAg and/or HBcAg. These findings suggested a close relationship between primary hepatic carcinoma and HBV infection. The high detection rate of HBxAg indicates very active expression of the integrated HBV-DNA genome in the host cells. However, how does HBxAg act in pathogenesis of hepatocellular carcinoma remains to be further investigated.     

肝癌患者HBxAg与Fas/FasL表达的研究

目的：探讨肝癌患者肝组织中 ＨＢｘＡｇ与 Ｆａｓ／ＦａｓＬ的表达状况及血清中 ＨＢＶ Ｘ基因与 Ｆａｓ／ＦａｓＬ的水平。方法：用ＳＰ法对３４例肝癌组织ＨＢｘＡｇ、Ｆａｓ与ＦａｓＬ表达状况进行分析,用ＥＬＩＳＡ法对３０例肝癌、３２例肝硬化及２０例正常人血清ｓＦａｓ与 ｓＦａｓＬ含量进行分析,并用ＰＣＲ法对肝癌与肝硬化患者血清ＨＢＶ Ｘ基因表达进行检测。结果：ＨＢｘＡｇ、Ｆａｓ与ＦａｓＬ在肝癌表达的阳性率分别为９７．０６％、８５．２９％及１００％。阳性信号均主要位于胞浆,且三者可在同一癌组织的相同区域出现阳性染色,Ｒｅｄｉｔ分析示三者的阳性程度无统计学差异（Ｐ＞０．０５）。血清ｓＦａｓ在肝癌、肝硬化与正常人中的含量分别为（７２２．９７±３２１．１３）μｇ／Ｌ、（８０１．９０±４１９．９４）μｇ／Ｌ和（２２４．０７±１４８．２３）μｇ／Ｌ,其中肝癌与肝硬化组显著高于正常人（Ｐ＜ ０． ０１）;血清 ｓＦａｓＬ在肝癌、肝硬化与正常人中的含量分别为（１５２． ２７±７． ９９）μｇ／Ｌ、（ １６２． ９７±１２． ４０）μｇ／Ｌ和（１５４．９９± ６．９６）μｇ／Ｌ,其中肝硬化组含量高于肝癌与正常人（ Ｐ＜０．０１）。血清ＨＢＶ　Ｘ基     

肝细胞癌乙型肝炎病毒感染与人胎盘型谷胱甘肽S-转移酶的表达

背景与目的：许多肿瘤癌变过程中人胎盘型谷胱甘肽S－转移酶（glutathione S-transferases,GST-π）的表达会异常升高,其变化早于细胞的形态改变。探讨肝细胞癌乙型肝炎病毒（hepatitis B virus,HBV)感染与GST－π表达的关系。方法：对肝细胞癌和相关慢性肝病及正常肝组织共86例用免疫组化染色方法检测乙型肝炎表面抗原（hepatitis B surface antigen,HBsAg）、乙型肝炎核心抗原（hepatitis B core antigen,HBcAg）和GST－π,用原位分子杂交方法检测乙型肝炎病毒DNA（hepatitis B virus DNA,HBVDNA)。结果：HBsAg,HBcAg和HBVDNA的阳性率在慢性肝炎分别为61．9％（13／21）;42．9％（9／21）和75．0％（12／16）;在肝硬化分别为64．0％（16／25）,36．0％（9／25）和83．3％（15／18）;在癌旁肝硬化分别为72．7％（16／22）,61．1％（11／18）和85．7％（12／14）;在肝细胞癌分别为45．2％（14／31）,50．0％（14／28)和64．3％（9／14）。其中以癌旁肝硬化组阳性率最高。慢性肝炎、肝硬化和癌旁肝硬化HBVDNA阳性信号较肝细胞癌多而强。GST－π在慢性肝炎（25．0％,4／16）、肝硬化（17．6％,3／17）、癌旁肝硬化（53．3％,8／15）和肝细胞癌（60．0％,9／15）均有表达,但癌旁肝硬化组和肝细胞癌组阳性率明显增高,癌旁肝硬化（53．3％,8／15）和肝细胞癌（60．0％,9／15）均有表达,但癌旁肝硬化组和肝细胞癌组阳性率明显增高,癌旁肝硬化组与不伴肝癌的肝硬化组差异有显著性（P＜0．05）,与肝细胞癌组差异无显著性（P＞0．05）。结论：大多数肝细胞癌与HBV感染所致的慢性肝炎和肝硬化密切相关,HBV感染可能导致GST－π的表达升高。癌旁的肝硬化比不伴癌的肝硬化更具癌前病变的特点。     

乙型肝炎病毒感染与肝细胞癌发生的关系

目的：探讨乙型肝炎病毒（HBV）的可能致癌机理，方法：采用免疫组化和原位分子杂交方法，对慢性乙型肝炎，肝硬化，癌旁肝硬化，肝细胞癌和正常肝组织中的乙型肝炎表面抗原（HBsAg)，核心抗原（HBcAg),HBV,DNA和甲胎蛋白（AFP）水平进行检测。结果：HBsAg,HBcAg和HBV DNA的阳性率在慢性乙型肝炎组中分别为61．9％（13／21），42．9％（9／21），75．0％（12／16），在肝硬化组中分别为64．0％（16／25），36．0（9／25），83．3％（15／18），在癌旁肝硬化组中分别为72．7％（16／22），61．1％（11／18），85．7％（12／14），在肝细胞癌组中分别为45．2％（14／31），50．0％（14／28），64．3％（9／14），慢性乙型肝炎，肝硬化和癌旁肝硬化组中HBV DNA阳性信号较肝细胞癌多而,AFP主在癌旁肝硬化（33．3％，9／27）和肝细胞癌（43．6％，17／39）组中表达，而在慢性肝炎和肝硬化组中不表达，癌旁肝硬化与不伴肝癌的肝硬化有非常显著性差异（P＜0．01），结论：大多数肝细胞癌的发生与HBV感染所致的慢性乙型肝炎和肝硬化密切相关，癌旁肝硬化可能是癌前肝硬化在癌周的残留。     

启东地区鸭肝癌中人HBV变异体蛋白产物的表达

本文分析了启东鸭肝癌组织中人ＨＢＶ变异体的蛋白产物，用ＷｅｓｔｅｒｎＢｌｏｔ方法检测１２例启东鸭肝癌组织中人ＨＢｓＡｇ，ＨＢｃＡｇ的表达。９例标本检测到３５ｋｄ和（或）大于３５ｋｄ的ＨＢｓＡｇ。７例标本出现２４ｋｄ的ＨＢｃＡｇ。９例标本有ＨＢｘＡｇ的表达。其其分子量为１２ｋｄ和（或）２５ｋｄ。本文同时也分析了ＤＨＢＶ基因产物ＤＨＢｓＡｇ．７例鸭肝癌标本检测ＤＨＢｓＡｇ，４例阳性，分子量为４０ｋｄ。     

Expression and significance of Pre-S1 and Pre-S2 in human primary hepatic carcinoma (PHC)]

135 specimens of primary hepatic carcinoma (PHC) were formalin fixed and paraffin embedded and stained for Pre-S1, Pre-S2 and HBxAg by ABC method, for HBsAg and HBcAg by PAP method. The detection rates of Pre-S1 and Pre-S2 positive cases in cancerous tissues were 22.2% and 20.0%. The detection rates of Pre-S1 and Pre-S2 in non-cancerous liver tissues were 60.0% and 59.6%. The positive ratio of Pre-S1 and Pre-S2 in the same hepatoma was 16.3% and that in the same non-cancerous liver tissue was 55.6%. Among 135 cases of PHC, HBsAg, HBxAg and HBcAg positives in tumor tissues were 16.3%, 55.6% and 8.9%, respectively. Those in non-cancerous tissues were 59.6%, 78.8% and 24.2%. This study suggested that the detection rates of Pre-S1 and Pre-S2 positivity in hepatoma tissues were higher than those of HBsAg and HBcAg but lower than that of HBxAg. The frequency of positive Pre-S1 and Pre-S2 in non-cancerous liver tissues was similar to HBsAg, and slightly lower than that of HBxAg. S1 and S2 are considered new markers for HBV infection. Their antigens could play an important role in the pathogenesis of PHC.     

Double immunocytochemical staining for HBsAg and HBcAg in hepatocellular carcinoma and surrounding nontumorous liver tissue

A double immunocytochemical staining method was used to demonstrate HBsAg and HBcAg simultaneously in the same sections of 58 hepatocellular carcinomas. Several tumor cells contained both HBsAg and HBcAg. These results demonstrate that hepatitis B virus (HBV) DNA in tumor cells can simultaneously express both HBsAg and HBcAg and suggest the production of a complete virus by these cells. Cytoplasmic membranous HBcAg was found not only in well differentiated hepatocellular carcinoma but also in moderate and poorly differentiated hepatocellular carcinoma. The localization of HBcAg in tumor cells appears to be the same as that of surrounding nontumorous liver tissue.