The formation, progression, and metastasis of hepatocellular carcinoma are closely associated with multiple genetic mutations and cell signaling pathways, including abnormal growth factor activation, sustained activation of cell division signaling pathways, dysregulation of anti-apoptotic signaling pathways, and abnormal proliferation of neovascularization. Depending on the pathogenesis of the disease, appropriate targeted drug therapy is selected.
Gefitinib, one of our common targeted therapeutics, is a small molecule anilinoquinazol compound that reduces MAPK/ERK protein phosphorylation, arrests hepatocellular carcinoma cells in G1/S phase, and inhibits BcL-2 and BCL-X expression thereby inducing apoptosis in hepatocellular carcinoma cells.
Cetuximab, also a commonly used clinically targeted drug therapy, is an IgG1 monoclonal antibody that competitively inhibits the binding of EGFR and its ligands and blocks intracellular signaling pathways, thereby interfering with tumor growth and metastasis, inhibiting cellular repair and angiogenesis, and inducing apoptosis of cancer cells.
Thalidomide, with effects such as inhibition of angiogenesis, disease has antitumor potential. Different targeted drugs target different points, so it is important to be targeted when choosing targeted drug therapy.