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。     

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。     

鸟氨酸氨甲酰基转移酶/丙氨酸氨基转移酶和甲胎蛋白联合检测在肝细胞癌中的诊断价值

目的：研究鸟氨酸氨甲酰基转移酶／丙氨酸氨基转移酶（OCT／ALT）比值和甲胎蛋白（AFP）联合检测对肝细胞癌的诊断价值。方法：测定61例肝细胞癌、49例慢性肝炎、45例肝硬化和51名健康体检者血清OCT／ALT比值和AFP水平，应用受试者工作特征曲线（ROC）进行评价。结果：肝细胞癌组血清OCT／ALT和AFP水平高于对照组、肝炎组和肝硬化组，差异有统计学意义（P〈0．05）。血清OCT／ALT和AFP的ROC曲线下面积分别为0．808和0．758。OCT／ALT的最优截断点约为3．2，灵敏度和特异度为68．3％和90．3％。AFP的最优截断点约为400ng／ml，灵敏度和特异度分别为60．7％和80．0％。结论：通过ROC曲线评价，在肝细胞癌的诊断中，血清OCT／ALT和AFP联合检测优于两项指标的单独检测。     

外周血甲胎蛋白mRNA的检测及其临床意义

目的：寻找肝细胞癌微小转移的标志物。方法：用巢式反转录聚合酶链反应（Nested-RT-PCR）技术检测６５例肝细胞癌,２１例非肝癌的恶性肿瘤,22例慢性乙型肝炎或肝硬化患者及21例健康志愿者外周静脉血中的甲胎蛋白（AFP）mRNA,结果：AFR－mRNA在健康志愿者,非肝癌恶性肿瘤患者外周血中均为阴性,在肝细胞癌组外周血中AFR－mRNA的检出率（44／65,67．7％）明显高于慢性乙型肝炎或肝硬化组（2／22,9．1％,P＜0．01）。AFR－mRNA检出率与临床分期、门静脉癌栓、肝外转移显著相关。在12例血清AFP＜25μg/L的肝癌患者血中,7例（58．3％）可检出AFR－mRNA.结论：AFR－mRNA可作为血循环中有肝癌细胞或肝细胞的标志物,在肝癌患者,阳性预示有血源性转移的可能,并且AFR－mRNA对血清AFP阴性或低值的肝癌患者能起到补充诊断作用。     

慢性乙型肝炎病毒感染与p16INK4A基因启动子甲基化关系的研究

目的探讨慢性乙型肝炎病毒(HBV)感染对p16INK4A基因启动子甲基化的影响及其在HBV相关肝细胞癌(HCC)形成中的作用。方法选取23例HBV相关HCC癌及癌旁组织、25例慢性乙型肝炎肝穿刺组织,采用甲基化特异性PCR(MSP)检测p16INK4A基因启动子的甲基化状态;免疫组化EnVision二步法测定肝组织内HBsAg、HBcAg、HBeAg和HBx蛋白的表达;荧光实时定量PCR检测肝组织HBV DNA含量;PCR扩增和直接测序检测HBV x基因变异。结果癌组织p16INK4A基因启动子甲基化阳性率(47.83%)明显高于癌旁组织(17.39%),慢性乙型肝炎患者p16INK4A基因启动子甲基化阳性率(36.00%)与癌组织、癌旁组织差异无统计学意义。在癌旁组织和慢性乙型肝炎, p16INK4A基因启动子甲基化者HBx蛋白表达中位数分别为3.000和0.250,明显高于非甲基化者(0.500和0.000),但在癌组织中,HBx蛋白的表达与p16INK4A基因启动子甲基化状态无关。HBsAg、HBcAg、组织HBV DNA含量和x基因突变均与p16INK4A基因启动子甲基化状态无关。结论在癌前病变中,p16INK4A基因启动子甲基化与HBx蛋白高表达有关,HBx蛋白可能通过诱导p16INK4A基因启动子甲基化而使该抑癌基因失活,在HBV相关HCC形成中起重要作用。     

乙肝病毒基因产物和HSP70在肝炎相关性肝癌发生中的作用

目的：探讨乙肝病毒基因产物（HBsAg，HBcAg，HBxAg）和热休克蛋白70（hot shock protein70．HSP70）在乙型肝炎相关性肝癌中的表达及其在肝细胞癌变中的作用。方法：采用组织芯片技术和免疫组织化学染色方法对152例乙型肝炎相关肝细胞肝癌组织、78例乙型肝炎后肝硬化组织中HSP70、HBsAg、HBcAg和HBxAg的表达情况进行检测。结果：与乙型肝炎后肝硬化相比，在乙型肝炎相关性肝癌组织中HBsAg表达显著降低（P=0．000），HBcAg表达显著增高（P=0．000），HBxAg显著增高（P=0．005），HSP70呈现高表达（P=0．000）；相关分析结果显示．HSP70的表达和HBcAg的表达呈显著正相关（P=0．009），而和HBxAg的表达未显示相关性（P=-0．673）。结论：乙肝病毒抗原成分HBcAg、HBxAg以及HSP70参与在乙型肝炎相关性肝癌的发生过程，HBcAg可能通过增加HSP70的表达而参与肝癌的发生。     

外周血glypican-3 mRNA的检测及其临床意义

目的：寻找肝细胞癌微小转移的标志物。方法：用巢式逆转录聚合酶链反应（nested-RT-PCR）技术检测60例肝细胞癌、20例非肝癌的恶性肿瘤、20例慢性乙型肝炎、20例肝硬化患者和20例健康志愿者外周静脉血中的glypican-3mRNA。结果：Glypiean-3mRNA在健康志愿者、非肝癌恶性肿瘤、慢性乙型肝炎、肝硬化组患者的外周血中均为阴性；在肝细胞癌组外周血中glypican-3的检出率为80％（48／60）。Glypican-3检出率与临床分期、门静脉癌栓、肝外转移明显相关（P〈0．05）。在12例血清AFP〈25μg／L的肝癌患者血中，8例（66．7％）可检出glypican-3。结论：Glypican-3可作为血循环中有肝癌细胞的标志物，在肝癌患者中阳性预示有血源性转移的可能；并且glypican-3对血清AFP阴性或低值的肝癌患者能起到辅助诊断作用。     

肝细胞癌组织中乙型肝炎病毒和丙型肝炎病毒的检测

目的检测肝细胞癌（hepatocellular carcinoma，HCC）组织中乙型病毒性肝炎（virus hepatitis type B）表面抗原（HB—sAg）和丙型病毒性肝炎（virus hepatitis type C）核心抗原（HCVAg）的表达。方法应用免疫组织化学法检测78例HCC及癌旁肝组织HBsAg和HCVAg的表达。同时比较患者的HBsAg和HCVAg血清学检测结果。结果HCC及癌旁肝组织中HBsAg和HCVAg阳性及HBsAg和HCVAg双重阳性表达率分别为9.1％、6．4％、2．6％和80．8％、44．9％、29．5％。HCC与癌旁肝组织HBsAg和HCVAg阳性及HBsAg和HCVAg双阳性表达率相互比较有非常显著性差异（P〈0．01）。合并肝硬化组和无肝硬HCC组中HCC与癌旁肝组织HBsAg和HCVAg阳性、HBsAg及HCVAg双阳性表达率相互比较也有非常显著性差异（P〈0．01）。HCC的HBsAg和HCVAg血清学检测的结果与手术标本HBsAg和HCVAg免疫组织化学检测的结果相吻合。结论HCC的发生与HBV和HCV的感染密切相关。     

环氧化酶-2在肝细胞癌及癌旁肝硬化中表达及意义

[ 目的]探讨环氧化酶2（COX-2）在肝细胞癌（HCC）、癌旁肝硬化和正常肝组织中的表达及其意义。[方法]应用免疫组织化学法检测30例HCC石蜡包埋组织、25例癌旁肝硬化组织及10例正常肝组织标本中COX-2的表达情况，分析其与肝细胞癌临床病理特征间的联系。[结果]COX-2蛋白在HCC、癌旁肝硬化中表达阳性率分别为70．0％和92．O％，显著高于在正常肝组织中的20．0％（P〈0．05）．而COX-2在癌旁肝硬化组织中的表达高于HCC组织。COX-2蛋白在分化好HCC中的表达显著高于分化差的HCC（P〈0．05），转移组中COX-2蛋白表达显著高于无转移组（P〈0．01）；而COX-2蛋白的表达与肿瘤大小、有无包膜及AFP水平无关。[结论]COX-2蛋白在肝细胞癌、癌旁肝硬化组织中高表达，表明COX-2可能在肝细胞癌的发生、发展过程中起着重要作用。     

肝细胞癌临床病理学特征与p53蛋白表达的关系

应用免疫组织化学技术检测29例肝细胞癌（肝癌）和23例肝硬化标本中突变型p53蛋白的表达，并探讨后者与肝癌临床病理学特征之间的关系。结果：肝癌突变型p53蛋白表达阳性率为70％（20／29），癌旁组织阳性率为60％（18／29），肝硬化组织阳性率为30％（7／23），有血管侵犯的12例肝癌变变型p53蛋白表达均为阳性，而无血管侵犯的17例中仅8例为阳性（P＜0．05）；突变型p53蛋白阳性组血清甲胎蛋白（AFP）明显高于阴性组（8370±4764ng／ml比98．7±64．3ng／ml，P＜0．05）。提示：P53蛋白表达在肝硬化时即发生了异常；p53蛋白异常可能是AFP基因被激活的原因之一；p53蛋白异常有利于肝癌向门静脉转移。     

Association of human hepatocellular carcinoma and cirrhosis with hepatitis B virus surface and core antigens in the liver.

Paraffin sections of livers obtained at autopsy from 50 cases of hepatocellular carcinoma (HCC), 58 cases of cirrhosis and 54 cases of other miscellaneous liver disorders (controls) were stained for both surface (HBsAg) and core (HBcAg) components of hepatitis B virus (HBV) by immunoperoxidase and immunofluorescence techniques and rigidly controlled for antigen specificity, and in addition stained by orcein for HBsAg. The material was collected from different regions of India and adequate amounts of tissue were examined in most specimens to overcome possible sampling error caused by random distributions of the antigens in liver. HBsAg was detected in 94% of HCC, 71% of cirrhosis and only 2% of control livers, while HBcAg was found in 22%, 31% and none respectively. Antigen positivity seems to be directly related to the amount of tissue examined. Peroxidase staining detected smaller amounts of HBcAg than fluorescence and was also much more convenient for identifying the antigen. Both antigens were present in 9 of 41 HCC cases, 12 of 39 cirrhosis and none of 25 controls. Most of these livers contained 1+ HBsAg and 1+ to 2+ HBcAg, an antigen expression pattern suggestive of a carrier state or, rarely, of mild chronic liver disease. Among all livers tested, HBsAg alone was present in 48, both antigens were found in 21, and HBcAg alone in none. HBsAg was seen inside tumour cells in four cases, but no tumour showed HBcAg. Most HCC was associated with cirrhosis (92%) and antigen-positive cirrhosis had a higher chance of harbouring HCC than antigen-negative disease. HBsAg was detected in all four non-cirrhotic livers associated with HCC, while two of these also had HBcAg. Active cirrhosis was very frequently associated with HBsAg. These results and the overwhelming evidence of sero-logical and epidemiological studies from various parts of the world suggest a strong association of the hepatitis B virus with HCC. The possible ways in which the two could be related are discussed.     

Immunohistochemical study on HBsAg, HBcAg and AFP in 104 patients with small liver cancer

HBsAg, HBcAg and AFP in small liver cancer (less than or equal to 5 cm) and adjacent non-neoplastic liver tissue were assayed by peroxidase-antiperoxidase (PAP) method. The positive rates of HBsAg, HBcAg and AFP in liver cancer tissue were 13.8% (9/65), 9.2% (6/65) and 75.0% (42/56), while those in the uninvolved liver tissue were 93.3% (97/104), 46.2% (48/104), 66.1% (37/56), respectively. 3.6% (2/56) of cancer tissue and 33.9% (19/56) of unaffected liver tissue were found to have these three markers simultaneously. Pathologically all showed chronic hepatitis changes, and 66.3% (69/104) of them had cirrhosis. The development of liver cancer may be associated with HBV/DNA integration, but it does not rule out the possibility of HBV replication in the canceration. The phenotype patterns of HBAg possess variable clinical significance and HBV replication affects the long time survival of the patients with liver cancer. The results show that both cancer foci and their surrounding tissue could secrete AFP, and the AFP positive rate in liver cancer with negative sero-AFP is 30% (3/10). The sensitivity of assaying HBsAg in PAP method was 1.4 times as high as that of R-PHA or orcein stain. Small liver cancer is a valuable material to the study of human liver cancer.     

Iron, ferritin, hepatitis B surface and core antigens in the livers of Chinese patients with hepatocellular carcinoma

Surgically resected specimens, consisting of tumor and adjacent non-neoplastic liver tissue, were obtained from 40 patients with primary liver cancer at Zhong Shan Hospital, Shanghai Medical University, the People's Republic of China, between March 1983 and July 1984. All were hepatocellular carcinomas (HCC), one being admixed with cholangiocarcinoma. The relationship of hepatitis B virus (HBV) markers with iron and ferritin was evaluated in liver tissues from patients with primary liver cancers. The serum HBsAg (Hepatitis B surface antigen) positive rate was 80.0% (32/40). Cirrhosis was observed in 97.5% (39/40). HBsAg was identified in 82.5% (33/40) of uninvolved liver, and 35.0% (14/40) of HCC tissues (P less than 0.001). HBcAg (hepatitis B core antigen) was detected in 25.0% (10/40) of liver, and 7.5% (3/40) of HCC tissues (P less than 0.05). Stainable iron was found in 65.0% (26/40) of unaffected livers, and 10.0% (4/40) of HCC tissues (P less than 0.001). Ferritin was demonstrated in 75% (30/40) of non-neoplastic liver, and 40% (16/40) of HCC tissues (P less than 0.001). Twenty-two of 33 HCC patients (66.7%) with HBsAg positive cells in their livers also showed stainable iron. Of 16 patients positive for ferritin in HCC cells, iron was found in only two. Iron was found in nine of ten patients with HBcAg in non-neoplastic hepatocytes (P = 0.056); a finding compatible with the hypothesis that iron accumulates in cells replicating HBV. The other results indicate that: immunohistologic ferritin in HCC is not due to increased stainable iron; tumor cells may produce ferritin; polyclonal antibodies to human liver ferritin react better with non-neoplastic hepatocytes than with HCC cells; the high prevalence of HBsAg and cirrhosis in HCC suggests that HBV plays a major etiologic role in hepatocarcinogenesis in China; and one case of HCC is attributed to Schistosoma japonicum infestation via cirrhosis.     

Liver cell dysplasia in cirrhosis. A serologic and immunohistochemical study

Liver cell dysplasia (LCD) was investigated for hepatitis B virus (HBV) markers, alpha-fetoprotein (AFP) and ferritin by serologic and immunohistochemical methods in 101 patients with cirrhosis. LCD was found in 30 cases (29.7%), with the highest incidence in cases of posthepatitic cirrhosis (67%). In the group of dysplastic cirrhosis (DC) 46.6% of the patients had active HBV infection (hepatitis B surface antigen [HBsAg] serum positivity) compared with 7% of the patients with nondysplastic cirrhosis (NDC) (P less than 0.01). The mean serum AFP concentration was significantly raised in the DC group compared with that in the NDC group (P less than 0.05). In seven patients with LCD at the initial biopsy, the histologic followup showed the persistence of LCD in all cases, and the development of hepatocellular carcinoma (HCC) in three cases. In serologic HBsAg-positive cases, dysplastic cells, at variance with the surrounding liver parenchyma, were almost always negative for tissue HBsAg, and always negative for tissue hepatitis B core antigens (HBcAg). AFP was never detected in either normal or dysplastic cells. Ferritin was found in all cases, but dysplastic foci displayed a lesser amount of this protein. These serologic and immunohistochemical data strongly suggest a preneoplastic significance of LCD. The importance of monitoring cirrhotic patients with LCD and particularly those with HBV infection and/or increased AFP levels with more aggressive follow-up is also stressed.     

A prospective study on the development of hepatocellular carcinoma from liver cirrhosis with persistent hepatitis B virus infection

We made a prospective study on the development of hepatocellular carcinoma (HCC) in patients with liver cirrhosis with hepatitis B virus infection from April, 1973 to December, 1977. Seven out of 30 patients (23%) with hepatitis B surface antigen (HBsAg)-positive cirrhosis developed HCC. On the other hand, only 5.9% of the patients with HBsAg-negative liver cirrhosis developed HCC. These patients were classified into three groups according to their anti-HB core (anti-HBc) titers. When the anti-HBc titer, expressed as a dilution of serum, was 2(10) or more (Group I), 20-24% of the liver cirrhosis patients developed HCC either with or without a detectable amount of HBs Ag present in the sera. When the anti-HBc titer was 2(9) or less (Group II), only 0-5.7% developed HCC. There was no significant difference between this and the anti-HBc and HBsAg-negative group (Group III), which was 4.4%. In five individual cases from group I, HBsAg was detected in serum, and in biopsies of liver cells, before HCC could be detected by angiography and/or rising levels of alphafetoprotein (AFP). In all of these cases, the anti-HBc titer was higher than 2(10) throughout the observation period, even before the development of HCC. These findings indicate that active virus proliferation in chronic hepatitis B virus infection precedes the development of HCC as indicated by a higher anti-HBc titer. Therefore we have prepared these studies to show the pathogenic role of hepatitis B virus in the development of hepatocellular carcinoma.     

人类肝癌发生过程中cyclinD1和CDK4及p16蛋白的表达

目的研究肝细胞癌(HCC)发生过程中细胞周期调控因子cyclinD1、CDK4和p16蛋白表达及其意义。方法应用免疫组织化学SP染色法检测正常肝组织、慢性肝炎、肝硬化、癌周肝硬化和肝癌组织中cyclinD1、CDK4和p16蛋白表达。对免疫组化结果进行计算机图象定量分析。结果cyclinD1、CDK4和p16蛋白的阳性单位(positive unit,PU)和面数密度(area number density,NA)从慢性肝炎(PU分别为39.4、41.0和33.3;NA分别为236.7、272.7和237.4)、肝硬化(PU分别为40.8、45.2和43.6;NA分别为313.8、354.6和322.9)、癌周肝硬化(PU分别为55.5、59.4和54.4;NA分别为481.9、488.9和432.6)到肝癌(PU分别为59.6、63.7和58.1;NA分别为549.2、587.7和451.3)表达逐渐增强。癌周肝硬化和肝癌组织中cyclinD1、CDK4、p16的表达明显高于慢性肝炎和肝硬化(P值分别为0.034、0.020、0.030、0.007、0.003和0.005),但癌周肝硬化和肝癌组织之间差异无统计学意义,P值分别为0.433、0.535和0.447。慢性肝炎和肝硬化中cy-clinD1、CDK4、p16阳性信号主要定位于胞核,而癌周肝硬化和HCC中主要定位于胞质。p16与HCC的分化程度有关,但未发现cyclinD1、CDK4与肿瘤分化程度之间有相关性。结论cyclin-细胞周期蛋白依赖性激酶(CDKs)-细胞周期蛋白依赖性激酶抑制因子(CKIs)调控网络中,相关调控因子的异常可能参与了HCC的发生、发展。cyclinD1、CDK4的过度表达可能是肝癌发生过程中的早期事件。在HCC的发生过程中p16高表达可能是细胞周期正反馈调控的结果,在HCC的发生中可能属于早期事件,而p16表达下降或缺失可能是肝癌发生过程中的晚期事件。     

整合型HBVDNA前C区突变和p53基因突变与肝细胞癌发生的关系

背景与目的:乙型肝炎病毒 (hepatitis B virus, HBV)的慢性感染是肝细胞癌 (hepatocellular carcinoma, HCC)发生的主要危险因素,但其确切的作用机理还不清楚.本研究拟探讨整合型 HBV 前 C区突变、 p53基因突变与 HCC发生的关系,以期更好地了解 HCC发生的分子机理.方法 :应用聚合酶链反应技术( PCR)和聚合酶链反应-单链构象多态 (single strand conformation polymorphism analysis of polymerase chain reaction products, PCR SSCP) 技术对 28例肝癌组织、 25例癌旁肝硬化组织、 12例肝硬化组织和 15例正常肝组织标本内的整合型 HBV DNA及其前 C区基因突变和肝细胞 p53基因突变进行检测分析.结果:( 1)正常肝组织、肝硬化组织、癌旁肝硬变组织和肝癌组织中整合 HBV DNA 阳性率分别为 6.66%、 66.67%、 96.43% 和 96.43%,正常肝组织与其它三组间阳性率差异有非常显著性( P< 0.005); (2)4组整合型 HBV DNA前 C区突变率分别为 0%、 25.00% 、 48.15% 和 70.37%, 4组间的突变率差异有显著性( P< 0.05); ( 3)肝癌组织的 p53基因突变率( 57.14%)明显高于肝硬化组( 16.67%) (P< 0.05);( 4)不同肝组织中 p53基因突变率与整合 HBV DNA 阳性率、 HBV前 C区基因突变率呈正相关.结论:在肝细胞癌的发生、发展中整合 HBV DNA及其前 C区基因突变和 p53基因突变可能起协同作用.     

Hepatocellular Carcinoma and its Early Detection by AFP Testing in Mongolia

Liver cancer is one of the leading causes of cancer death in Mongolia. Since 1982-1986 , when HCC became themost frequent cancer among the Mongolian population, the rate has been increasing continuously. In the period2000-2005 years 35.3%of all newly registered cancer cases were liver cancers, with an incidence rate of 51.3 per100,000 population. Compared to the previous 5 year period, the rate increased by 11%. The objective here was toanalyze hepatitis B (HBV) and C virus (HCV)-related HCC cases and to evaluate the possibility of tumor marker(AFP) testing for early detection in Mongolia. Sera from a total of 513 patients with chronic liver diseases, livercirrhosis and HCC were analyzed for liver function (ALAT, ASAT) and hepatitis virus markers (HBsAg, anti-HCV).Sera from 316 patients were also examined for alpha-fetoprotein (AFP) levels. The overall incidence of HBsAg oranti-HCV were very high ( 95.3%) among all patients. Some 33.5% (66/197) of patients with HCC were positive forHBsAg and 45.2% (89/197) for anti-HCV. Moreover, 17.3% ( 34/197) of HCC patients demonstrated co-infectionwith HBV and HCV. AFP levels were elevated in 4.6% (11/238) and 29.5% (23/78) of chronic hepatitis and cirrhosispatients, respectively. In HCC cases, 84.3% (166) of patients had increased level of AFP ranging from 32ng/ml tomore than 400 ng/ml. We conclude that HBV/HCV infection is the main factor related to development of HCC inMongolia and that testing for AFP serum levels is a useful tool for early detection and diagnosis.