Published online Mar 15, 2003. doi: 10.3748/wjg.v9.i3.459
Revised: August 16, 2002
Accepted: August 23, 2002
Published online: March 15, 2003
AIM: To investigate the change of HBV DNA, PCNA and GST-π in chronic liver disease and hepatocellular carcinoma (HCC).
METHODS: Hepatitis B surface antigen (HBsAg), proliferating cell nuclear antigen (PCNA) and glutathione S-transferases (GST-π) 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-π 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-π 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-π. The paratumor cirrhosis may be a sequential lesion of precancerous cirrhosis around HCC.