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المستخلص
Hepatitis C virus (HCV) related liver damage is linked to an increased risk of hepatocellular carcinoma. Although-the mechanisms of hepatocarcinogenesis remain unclear, the presence of cirrhosis and ongoing necroinflammatory activity from chronic hepatitis appear to be the strongest risk factors.
In normal liver, most hepatocytes are in a resting stage (GO) but in setting of chronic hepatitis, cirrhosis and HCC, there is increased hepatocellular proliferation. In cirrhosis, hepatocytes enter the cell cycle and proliferate because of several factors including response to cell injury, loss of intact reticulin framework, altered intrahepatic microvasculature and abnormalities in intercellular communications. Cell population that continue to undergo replicative cycles under conditions of oxidative stress may be associated with P53 gene mutations. AlsoHCV core protein may
interact with cellular genes such as P53 or may induce P53 overexpression in relation to liver necrosis and inflammation.
Aim of this work was to study the proliferative activity of hepatocytes in chronic hepatitis C lesions and to determine whether P53 may be expressed in a precocious stage ofHeV related liver damage by using immunohistochemical staining for Ki-67 proliferating antigen and P53 tumor suppressor gene protein.