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Human hepatocellular carcinoma (HCC) cells are malignant hepatocytes that constitute the primary form of liver cancer, typically arising in the context of chronic liver disease or cirrhosis [2, 17]. These cells are characterized by a complex genomic landscape and the dysregulation of multiple signaling pathways, including those involved in cell growth (Raf/MEK/ERK), survival (PI3K/Akt/mTOR), and angiogenesis (VEGF/VEGFR) [2, 11]. While HCC cells themselves are not a single molecular target, they harbor numerous proteins—such as receptor tyrosine kinases and immune checkpoint ligands—that are the focus of modern systemic therapies [1, 8]. Therapeutic approaches often utilize multikinase inhibitors like sorafenib or combination immunotherapies such as atezolizumab and bevacizumab to inhibit tumor proliferation and modify the immunosuppressive microenvironment [1, 4]. However, treatment remains challenging due to significant tumor heterogeneity and the frequent presence of underlying liver dysfunction, which impacts the safety and efficacy of therapeutic interventions [14, 17].
Multi-kinase inhibition (targeting VEGFR, PDGFR, FGFR, and Raf), immune checkpoint inhibition (PD-1/PD-L1 and CTLA-4), and VEGF neutralization to inhibit tumor proliferation and angiogenesis [1, 2, 4, 8].
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