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The association of hepato- cellular carcinoma (HCC) with hepatitis B virus (HBV), hepatitis C virus (HCV) and mycotoxins, especially aflatoxins, has been established. Mycotoxins are com- monly encountered by the consumption of mycotoxin-contaminated food by African and Asian populations. A number of mechanisms contribute to the high risk of HCC in individuals with both aflatoxin B 1 (AFB 1 )-DNA adducts and hepatitis B surface antigen (HBsAg), and a viral- chemical interaction has been confirmed. Among the various suggested mecha- nisms, oxidative stress exacerbates the co-exposure of aflatoxins and chronic hepatitis infections. This increases the rate of DNA unwinding, supercoiling and/ or overstretching. It is hypothesized that these processes are promoted by reac- tive oxygen/nitrogen species (ROS/RNS) generated during HBV or HCV infections, which allow aflatoxin metabolites to inter - calate between DNA strands with their hydroxyl radicals. The aflatoxin metab - olites may attack the ribose in the DNA backbone where the bases reside. These complex reactions result in modification of the energetics of DNA transcription and replication as well as a concomitant mutation in the p53 tumor suppressor gene. The hypothesis described here may generate novel ideas, which could lead to further hypothesis-driven experiments aimed at improving strategies for the pre- vention and treatment of HCC. BACKGROUND Hepatitis B Virus

hypothesis

Hepatocellular carcinoma: Putative interactive mechanism between aflatoxins and hepatitis viral infections implicating oxidative stress during the onset and progression of cance