Chronic HBV, and HCV, are the most important risk factors in the development of HCC (Tornai 2010) in agreement with the present results. Egypt has the highest prevalence of HCV worldwide, and has rising rates of HCC (Lehman and Wilson 2009). Prevalence of HBV, and HCV were reported 25.9%, and 78.5% among HCC cases respectively (Severi et al. 2010).
HCC in previous studies confirmed wide international variation risks (Franceschi and Raza 2009). Multiple non-viral factors have been implicated in the development of HCC (Soliman et al. 2010). Approximately, 10% of HCC patients were reported negative for both HBV markers and antibodies to HCV (Kusakabe et al. 2007). In the current work, a higher rate 13.87% of non-B non-C was detected, while Abe et al. (2008) reported increasing ratio from 17.8% in 2000 to 28.6% in 2006 in Japan. This difference in prevalence, between Egypt, and Japan could be attributed to the difference in environmental risks, and the higher prevalence of HCV in Egypt.
In the current study, no significant difference was detected between non-B non-C HCC, and those of viral-association, as regard to age, or gender in agreement with previous reports (Asahina et al. 2010, and Yeh and Chen 2010). Some difference could be attributed to the nature of work making men more exposed to more risks, and/or the intensity of these risks.
According to our knowledge, there are no previous reports for non-B non-C HCC in our region, but reports of exposure to chemicals in HCV-associated HCC were reported. Chemicals can induce hepatic carcinogenesis through direct hepatotoxicity, inducing oxidative stress, and/or causing steatohepatitis (Angulo 2002), which seems to have a cumulative effect.
In our study, serum total iron binding capacity, ceruloplasmin, and antinuclear antibody were detected in average values in non-B non-C HCC patients. This could exclude the role of iron, copper and auto immunity in hepatic carcinogenesis of this group.
In the current study, anti-p53 showed insignificant difference between both HCC groups of patients, suggesting the presence of non-viral onchogens in non-B non-C HCC patients. This could agree with previous results, with high percentage of positivity of anti-p53 antibodies in Egyptian healthy subjects (Attallah et al. 2009, and Gadelhak et al. 2009). They mentioned that tumor suppressor genes may play a role in the puzzle of hepatic carcinogenesis. The finding of P53 antibodies in sera of individuals who are at high risk of cancer, as workers exposed to chemicals indicates that they have onchogenic potential, and promising in the early detection of cancer. Expressions were more pronounced in patients with HCC more than patients with liver cirrhosis, which could be of clinical importance for early diagnosis. This could be explained by interactions of chemical carcinogens, and genetic variations, are possible in HCC (Zhang 2010).
Alpha fetoprotein showed significantly lower levels in non-B non-C HCC, as compared to patients with viral-associated HCC in agreement with a previous report (Yamagishi et al. 2004), as tumors were detected of almost solitary, and of small sizes. High ratios of sensitivity, specificity, PPV, NPV and accuracy test of anti P53 antibody positive patients which could suggest clinical significance in non-B non-C HCC patients.