Detection of HBV, PCNA and GST-π in hepatocellular carcinoma and chronic liver diseases

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:liongliong558
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AIM TO investigate the change of HBV DNA,PCNA and GST-in chronic liver disease and hepatocellular carcinoma(HCC).METHODS:Hepatitis B surface antigen(HBsAg),proliferatingcell nuclear antigen(PCNA)and glutathione S-transferases(GST-π)were detected by immunohistochemical staining andHBV DNA was detected by in situ hybridization(ISH)informalin-fixed and paraffin-embedded sections with a totalof 111 specimens of chronic hepatitis,liver cirrhosis,paratumorous tissue,HCC and normal liver tissue.RESULTS:The positive rates of HBsAg and HBVDNA were62.5 %(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 and45.0 %(14/31)and 64.3 %(9/14)in HCC.The positiveHBVDNA granules in chronic hepatitis,liver cirrhosis and theparatumorous tissue were more intense than that in HCC.The positive rates of PCNA and GST-πwere 34.8 %(8/23)and 25.0 %(4/16)in chronic hepatitis,73.7 %(14/19)and17.6 %(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-πin the paratumorous tissue was significantly higher than thatin the liver cirrhosis without tumor(P<0.05),but same asthat in HCC(P>0.05).CONCLUSION:The HBV infection may increase expressionof PCNA and GST-π.The paratumor cirrhosis may be asequential lesion of precancerous cirrhosis around HCC. AIM TO investigate the change of HBV DNA, PCNA and GST-in chronic liver disease and hepatocellular carcinoma (HCC). METHODS: Hepatitis B surface antigen (HBsAg), proliferating cell nuclear antigen (PCNA) and glutathione S-transferases (GST- were detected by immunohistochemical staining and HBV DNA was detected by in situ hybridization (ISH) informalin-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-πwere 34.8% (8/23) and 25.0% (4/16) in chronic hepatitis, 73.7% (14/19) and17.6% (3/17) in liver cirrh †, 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-πin the paratumorous tissue was significantly higher than that of the liver cirrhosis without tumor (P <0.05), but same asthat in HCC (P> 0.05) .CONCLUSION: The HBV infection may increase expressionof PCNA and GST-π.The paratumor cirrhosis may be asequential lesion of precancerous cirrhosis around HCC.
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