4.2.1 Liver Cancer and Hepatitis

4.2.1 Liver Cancer and Hepatitis

The occurrence of liver cancer is closely related to hepatitis B virus infection, with over 80% of liver cancer tissues testing positive for hepatitis B virus markers. Moreover, the incidence of liver cancer significantly decreases after vaccination against hepatitis B. The following points explain the possible mechanisms by which long-term hepatitis B patients gradually develop liver cancer:

① Clinical Perspective: HBV infection leads to chronic hepatitis B, which then progresses to cirrhosis. The longer the duration of viral infection, the higher the risk of malignant transformation into liver cancer. In addition, the synergistic effects of unhealthy lifestyle habits such as smoking and drinking further increase the risk of liver cancer.

② Genetic Perspective: From a molecular standpoint, cancer development results from mutations caused by the combined action of tumor suppressor genes and oncogenes. This is not a single-gene expression but rather a process involving multiple genes working together. After HBV infection, genetic mutations in liver cells accumulate over time, eventually leading to liver cancer.

③ Biological Perspective: Among the gene expression products of HBV, only the HBVX protein contributes to the malignant transformation of liver cells. It acts as an inhibitor of proteases, suppressing the activity of caspase-3 during apoptosis, thereby blocking cell death and allowing uncontrolled cell growth. Additionally, HBVX protein can directly bind to the tumor suppressor gene P53, disrupting its structural and functional integrity—even if no mutation has occurred, it can render P53 non-functional. Furthermore, studies have found that before liver cancer develops, there are small peaks of aneuploidy, suggesting that high expression of HBVX protein can induce DNA synthesis, thus initiating the complex process of liver cancer development. Relevant literature also confirms that HBVX protein participates in activating cytokines expressed by liver cells, such as insulin-like growth factor-1, FASL, and vascular endothelial growth factor, all of which influence tumor formation and metastasis.