الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Hepatocellular carcinoma (HCC) is the most common primary cancer of the liver (8090% of primary hepatic carcinomas) approximately one million deaths each year, predominantly in the underdeveloped and developing countries. HBV and HCV infection, the cell proliferation and the expression of the apoptosisrelated genes (Bcl2 and p53) have been suggested to be important factors in the genesis of HCC. Thus, this study was suggested to study the incidence of viral infection in HCC and its relationship with the expression of p53 and Bcl2 protein antigens. METHODS: This study was performed on 45 patients (30 males and 15 females) diagnosed as HCC cytologically and histopathologically. All patients were screened for the level of serum alfafetoprotein (AFP) using the enzymeimmunoassay (EIA) and tested for hepatitis B surface antigen (HBsAg) and for hepatitis C virus antibodies (antiHCV) using the enzymelinked immunosorbent assay (ELISA) in addition to routine liver function tests. p53 and Bcl2 antigens were studied in serum using ELISA. Further investigations were performed by special staining and immunohistochemical staining including eosin and hematoxylin, silver staining (AgNOR), p53 and Bcl2 antigens. RESULTS: It was found that the high prevalence of serum p53 antigen concentration and p53 immunostaining seemed to correlate with HCC grade suggesting that mutant p53 seems to intervene in the progress of HCC through various grades of increasing malignancy. The expression of Bcl2 protein was inversely proportional with the HCC grade thus, Bcl2 may be abnormally expressed in some hepatocellular carcinomas especially in those with low grade. Bcl2 was remarkably upregulated in HCC patients with immunopositive p53, but was downregulated in patients with immunonegative p53. This finding is supported by the positive linear correlation we found between serum Bcl2 and serum p53 concentrations (P<0.05) in the present study. These results suggest that Bcl2 and p53 expression are seemed to be proportionally correlated in HCC cases. The present study also showed that p53 and Bcl2 protein overexpression, detected in serum and tissues, in HCC patients positive for hepatitis B or C or both was greater as compared to that observed in negative patients. Furthermore, the overexpression of these two proteins in serum and tissues was more frequently associated with HBV infection than HCV infection. CONCLUSION: hepatitis B virus and hepatitis C virus may be involved in hepatocarcinogenesis in patients with HCC. These viral infections may be responsible, at least in a part, for the mutational change in the p53 gene and may affect the expression of the Bcl2 protein in HCC patients.