AIM: To investigate the change of HBV DNA, PCNA and GST-pi in chronic liver disease and hepatocellular carcinoma (HCC). METHODS: Hepatitis B surface antigen (HBsAg), proliferating cell nuclear antigen (PCNA) and glutathione S-transferases (GST-pi) were detected by immunohistochemical staining and HBV DNA was detected by in situ hybridization (ISH) in formalin-fixed and paraffin-embedded sections with a total of 111 specimens of chronic hepatitis, liver cirrhosis, paratumorous tissue, HCC and normal liver tissue. RESULTS: The positive rates of HBsAg and HBVDNA were 62.5 %(15/24) and 75.0 %(12/16) in chronic hepatitis, 64.0 %(16/25) and 83.3 %(15/18) in liver cirrhosis, 72.7 %(16/22) and 85.7 %(12/14) in the paratumorous tissu and 45.0 %(14/31) and 64.3 %(9/14) in HCC. The positive HBVDNA granules in chronic hepatitis, liver cirrhosis and the paratumorous tissue were more intense than that in HCC. The positive rates of PCNA and GST-pi were 34.8 %(8/23) and 25.0 %(4/16) in chronic hepatitis, 73.7 %(14/19) and 17.6 %(3/17) in liver cirrhosis, 86.7 %(13/15) and 53.3 %(8/15) in the paratumorous tissue, 100 %(15/15) and 60.0 %(9/15) in HCC, respectively, and the positive rate of GST-pi in the paratumorous tissue was significantly higher than that in the liver cirrhosis without tumor (P<0.05), but same as that in HCC (P>0.05). CONCLUSION: The HBV infection may increase expression of PCNA and GST-pi. The paratumor cirrhosis may be a sequential lesion of precancerous cirrhosis around HCC.
AIM: To investigate the change of HBV DNA, PCNA and GST-pi in chronic liver disease and hepatocellular carcinoma (HCC). METHODS: Hepatitis B surface antigen (HBsAg), proliferating cell nuclear antigen (PCNA) and glutathione S-transferases (GST-pi) were detected by immunohistochemical staining and HBV DNA was detected by in situ hybridization (ISH) in formalin-fixed and paraffin-embedded sections with a total of 111 specimens of chronic hepatitis, liver cirrhosis, paratumorous tissue, HCC and normal liver tissue. RESULTS: The positive rates of HBsAg and HBVDNA were 62.5 %(15/24) and 75.0 %(12/16) in chronic hepatitis, 64.0 %(16/25) and 83.3 %(15/18) in liver cirrhosis, 72.7 %(16/22) and 85.7 %(12/14) in the paratumorous tissu and 45.0 %(14/31) and 64.3 %(9/14) in HCC. The positive HBVDNA granules in chronic hepatitis, liver cirrhosis and the paratumorous tissue were more intense than that in HCC. The positive rates of PCNA and GST-pi were 34.8 %(8/23) and 25.0 %(4/16) in chronic hepatitis, 73.7 %(14/19) and 17.6 %(3/17) in liver cirrhosis, 86.7 %(13/15) and 53.3 %(8/15) in the paratumorous tissue, 100 %(15/15) and 60.0 %(9/15) in HCC, respectively, and the positive rate of GST-pi in the paratumorous tissue was significantly higher than that in the liver cirrhosis without tumor (P<0.05), but same as that in HCC (P>0.05). CONCLUSION: The HBV infection may increase expression of PCNA and GST-pi. The paratumor cirrhosis may be a sequential lesion of precancerous cirrhosis around HCC.
Authors: W Marwoto; U A Miskad; N C Siregar; R A Gani; U Boedihusodo; S Nurdjanah; P Boedi; H A Hasan; N Akbar; H M Noer; Y Hayashi Journal: Kobe J Med Sci Date: 2000-10
Authors: Alison A Evans; Gang Chen; Eric A Ross; Fu-Min Shen; Wen-Yao Lin; W Thomas London Journal: Cancer Epidemiol Biomarkers Prev Date: 2002-04 Impact factor: 4.254