title: [Expression of GST-pi and HBV infection in hepatocellular carcinoma].
abstract: OBJECTIVE
  The expression of glutathione S-transferases(GST-pi) might abnormally increase in many carcinogenesis, and the alteration of GST-pi preceded than that alteration of cell morphology. This study was designed to investigate the expression of glutathione S-transferases (GST-pi) and its relationship with hepatitis B virus (HBV) infection in hepatocellular carcinoma (HCC).
  
  
  METHODS
  Hepatitis B surface antigen (HBsAg), Hepatitis B core antigen (HBcAg), and GST-pi were detected by immunohistochemical staining and HBV DNA was detected by in situ hybridization (ISH) in total 86 samples of chronic hepatitis, liver cirrhosis, paratumor cirrhosis, HCC, and normal liver tissue.
  
  
  RESULTS
  The positive expression rates of HBsAg, HBcAg, and HBV DNA were 61.9% (13/21), 42.9% (9/21), and 75.0% (12/16) in chronic hepatitis; 64.0% (16/25), 36.0% (9/25), and 83.3% (15/18) in liver cirrhosis; 72.7% (16/22), 61.1% (11/18), and 85.7% (12/14) in the paratumor cirrhosis, as well as 45.0% (14/31), 50.0% (14/28) and 64.3% (9/14) in HCC. HBV DNA positive granules in chronic hepatitis, liver cirrhosis, and the paratumor cirrhosis were more and stronger than that in HCC, respectively. The positive expression rates of GST-pi were 25.0% (4/16), 17.6% (3/17), 53.3% (8/15), and 60.0% (9/15) in chronic hepatitis, liver cirrhosis, the Paratumor cirrhosis, and HCC, respectively. The positive rate of GST-pi in the paratumor cirrhosis was significantly higher than that in the liver cirrhosis without tumor (P < 0.05), but the same as in HCC (P > 0.05).
  
  
  CONCLUSIONS
  Most of the HCC cases were closely associated with chronic hepatitis and liver cirrhosis of HBV infection. The HBV infection may increase expression of GST-pi. The paratumor cirrhosis may be a sequential lesion of precancerous cirrhosis around HCC.
authors.affiliation: Department of Pathology, Kunming Medical College, Kunming 650031, P. R. China. WYCSLJ@public.km.yn.cn
authors.forename: Li-juan
authors.initials: LJ
authors.lastname: Shen
authors.forename: Zong-ji
authors.initials: ZJ
authors.lastname: Zhang
authors.forename: Hua-xian
authors.initials: HX
authors.lastname: Zhang
authors.forename: Wei-bo
authors.initials: WB
authors.lastname: Yang
authors.forename: Run
authors.initials: R
authors.lastname: Huang
mesh_terms: D006528:Carcinoma, Hepatocellular / Q000201:enzymology / Q000209:etiology* / Q000382:microbiology; D004279:DNA, Viral / Q000032:analysis; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase / Q000032:analysis*; D006509:Hepatitis B / Q000150:complications*; D006512:Hepatitis B Core Antigens / Q000032:analysis; D006514:Hepatitis B Surface Antigens / Q000032:analysis; D006801:Humans; D007527:Isoenzymes / Q000032:analysis*; D008113:Liver Neoplasms / Q000201:enzymology / Q000209:etiology* / Q000382:microbiology
chemical_list: D004279:DNA, Viral; D006512:Hepatitis B Core Antigens; D006514:Hepatitis B Surface Antigens; D007527:Isoenzymes; C496556:GSTP1 protein, human; D051549:Glutathione S-Transferase pi; D005982:Glutathione Transferase