Different expression of hepatitis B surface antigen between hepatocellular carcinoma and its surrounding liver tissue, studied using a tissue microarray

被引:43
作者
Wang, Y
Wu, MC
Sham, JST
Tai, LS
Fang, Y
Wu, WQ
Xie, D
Guan, XY
机构
[1] Mil Med Univ 2, Eastern Hepatobilliary Surg, Shanghai, Peoples R China
[2] Univ Hong Kong, Dept Clin Oncol, Hong Kong, Hong Kong, Peoples R China
[3] Sun Yan Sen Univ Med Sci, Canc Inst, Guangzhou, Peoples R China
关键词
HbsAg; HBVS gene; hepatocellular carcinoma; tissue microarray; immunohistochemistry; viral integration;
D O I
10.1002/path.1150
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and is highly associated with chronic liver disease, including hepatitis B viral infection. In order to study the association between hepatitis B virus (HBV) infection and HCC development, tissue microarrays were used to detect the expression of hepatitis B surface antigen (HBsAg) in 194 HCCs and their surrounding liver tissues, using anti-HBsAg monoclonal antibody. The results showed that the expression of HBsAg is significantly lower in turnout tissue than in non-tumour tissue. Among the 138 cases with positive serum HBsAg, expression of HBsAg was more frequently detected in non-tumour tissue (103 cases, 75%) than in tumour tissue (11 cases, 8%,). RT-PCR and Southern blot analysis were performed to explore the mechanism of the decreased expression of HBsAg in tumour cells. The RT-PCR results showed that absence or decreased expression of the HBV S gene was detected in 3/15 (20%) and 6115 (40%) HCCs, respectively. Integration of HBV in 23 pairs of HCCs and their matched non-tumour liver tissues was studied by Southern blot. The results showed that the integrated HBV S gene sequence was detected in 19/23 tumours (83%) and 1/23 non-tumour tissues (4%), whereas the free replicative virus form was observed in 3/23 tumours (13%) and 14/23 non-tumour tissues (61%). These findings suggest that HBsAg-negative results in turnout tissues were directly related to HBV DNA insertion and provide new insights into the involvement of HBsAg in hepatocarcinogenesis. Copyright (C) 2002,John Wiley Sons, Ltd.
引用
收藏
页码:610 / 616
页数:7
相关论文
共 29 条
[1]   Putative role of hepatitis B virus X protein in hepatocarcinogenesis: Effects on apoptosis, DNA repair, mitogen-activated protein kinase and JAK/STAT pathways [J].
Arbuthnot, P ;
Capovilla, A ;
Kew, M .
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, 2000, 15 (04) :357-368
[2]  
BEASLEY RP, 1988, CANCER, V61, P1942, DOI 10.1002/1097-0142(19880515)61:10<1942::AID-CNCR2820611003>3.0.CO
[3]  
2-J
[4]   Epidemiology of primary liver cancer [J].
Bosch, FX ;
Ribes, J ;
Borràs, J .
SEMINARS IN LIVER DISEASE, 1999, 19 (03) :271-285
[5]   Molecular bases for the development of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) [J].
Bréchot, C ;
Gozuacik, D ;
Murakami, Y ;
Paterlini-Bréchot, P .
SEMINARS IN CANCER BIOLOGY, 2000, 10 (03) :211-231
[6]   Hepatitis B virus envelope variation after transplantation with and without hepatitis B immune globulin prophylaxis [J].
Carman, WF ;
Trautwein, C ;
vanDeursen, FJ ;
Colman, K ;
Dornan, E ;
McIntyre, G ;
Waters, J ;
Kliem, V ;
Muller, R ;
Thomas, HC ;
Mannis, MP .
HEPATOLOGY, 1996, 24 (03) :489-493
[7]  
CASELMANN WH, 1995, J HEPATOL, V22, P34
[8]   EXPRESSION OF INSULIN-LIKE GROWTH-FACTOR-II (IGF-II) IN HUMAN HEPATOCELLULAR CARCINOMAS - AN IMMUNOHISTOCHEMICAL STUDY [J].
DERRICO, A ;
GRIGIONI, WF ;
FIORENTINO, M ;
BACCARINI, P ;
LAMAS, E ;
DEMITRI, S ;
GOZZETTI, G ;
MANCINI, AM ;
BRECHOT, C .
PATHOLOGY INTERNATIONAL, 1994, 44 (02) :131-137
[9]  
FARA H, 1994, MOL CARCINOG, V9, P185
[10]  
Feitelson MA, 1999, J CELL PHYSIOL, V181, P188