In the present study, liver function tests were significantly elevated whereas log-HCV titer was significantly lower in HCC patients (p < 0.001) when compared to PNALT and CLD patients. In agreement with our findings, HCC group had learn more the highest values (86.3%) for various concurrently-measured liver function tests, significant higher values of AST/ALT, ALT, AST (each, p < 0.001) than cirrhotic patients as previously reported . On the other hand, HCV levels were markedly higher in non-cancerous liver than in HCC (p = 0.001) . Moreover, comparing HCV titers of four HCC isolates and surrounding cirrhotic liver tissues in two anti-HCV
positive patients; the copy numbers of HCV-RNA were 1 × 106 and 4 × 106/gm wet weight of HCC, and 8 × 107 and 3.2 × 108/gm wet weight of cirrhotic liver tissues from patient-1 and -2, respectively . The present study showed that men had higher log-HCV RNA titer than that detected in women; then, a strong
evidence is provided in favour of a higher HCV clearance rate in women compared with that in men . Fas (APO-1 or CD95) is a cell-surface receptor that transduces apoptotic signals from Fas ligand (Fas-L) . Apoptosis is tightly regulated throughout a variety of mechanisms, one of which is postulated to be the production of soluble forms of Fas (sFas) that normally HDAC inhibitor binds to Fas-L, thus blocking the signaling of the membrane-bound form Etomidate of Fas. Peripheral blood mononuclear cells in HCV infection exhibit decreased susceptibility to Fas-L induced cell death. This may signify a mean by which HCV escapes immune surveillance; however, it would be worth a further investigation on this phenomenon. The sFas appeared to increase in advanced stages of HCV-induced liver disease, as a result of host-related immunological factors . In the present series, the mean values of sFas were significantly higher in HCC patients compared to the other groups (p < 0.001). This could be explained by the role of sFas in the inhibition of apoptosis, progression to end stage liver damage, and subsequent development of HCC. Similarly, a significant
elevation of serum levels of sFas in HCC patients compared with liver cirrhosis and healthy control was previously reported . Previous studies [47, 48] have reported mRNA encoding secreted sFas in a number of hepatitis and HCC cases indicating that sFas may function as an inhibitor of the Fas/Fas-L system and escape of tumor cells from immune surveillance may then occur. In chronic hepatitis, sFas was correlated with the severity of disease  and its expression can illustrate the mechanism of liver injury caused by death receptors throughout the multistep process of fibrosis/carcinogenesis. So, the increased incidence of HCC is correlated not only with the higher degree of hepatic DMXAA fibrosis, but also with the lower expression of Fas protein .