Chronic hepatitis B virus (HBV) infection is the most frequent risk factor for development of hepatocellular carcinoma (HCC) worldwide. Studies of the molecular genetics and pathophysiology of HCC suggest that there are significant differences in the allelic imbalance, genome copy number, and gene expression patterns of HBV-induced HCC as compared to HCCs from other causes, which are presumably reflected to differences in the mode of presentation and outcomes of HBV-induced HCCs. Unique features of HBV-induced carcinogenesis include the role of HBV DNA integration in carcinogenesis and the powerful synergism between HBV and dietary aflatoxins in the pathogenesis of HCC. A more complete understanding of the biology of HBV-induced HCCs may reveal well-defined differences in the molecular pathways that regulate growth of these HCCs and allow better-targeted approaches to prevention and therapy of HBV-induced HCCs. This review will attempt to summarize the current knowledge about carcinogenic pathways in HBV-induced HCCs, review the agents currently in development for targeted therapy of HCCs, and propose potentially novel approaches to therapy of HBV-induced HCC.
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- - Key DNA repair mechanisms, especially those involving the NEIL1 enzyme, play a significant role in preventing these mutations and limiting cancer progression, with deficiencies in NEIL1 potentially leading to increased cancer risk.
- - Research focused on genetic variations of NEIL1 found three variants (A51V, P68H, and G245R) that affect its ability to repair DNA, with A51V showing sensitivity to temperature changes which could impact its function in humans.
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Explanation: The most important risk factors for HCC are Hepatitis B Virus (HBV) infection, Hepatitis C Virus (HCV) infection, excessive consumption of alcohol and exposition to aflatoxin B1.
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