![]() ![]() In these models, VEGFR-2 was selectively expressed in tumor endothelial cells. Combination therapy reprogrammed the immune microenvironment by increasing cluster of differentiation 8–positive (CD8 +) cytotoxic T cell infiltration and activation, shifting the M1/M2 ratio of tumor-associated macrophages and reducing T regulatory cell (Treg) and chemokine (C-C motif) receptor 2–positive monocyte infiltration in HCC tissue. ![]() However, dual anti-PD-1/VEGFR-2 therapy significantly inhibited primary tumor growth and doubled survival in both models. ![]() Specific blockade of vascular endothelial receptor 2 (VEGFR-2) using a murine antibody significantly delayed primary tumor growth but failed to prolong survival, while anti-PD-1 antibody treatment alone conferred a minor survival advantage in one model. We recapitulated these clinical outcomes using orthotopic-grafted or induced-murine models of HCC. Combining PD-1 blockade with antiangiogenesis has shown promise in substantially increasing the fraction of patients with HCC who respond to treatment, but the mechanism of this interaction is unknown. Activation of the antitumor immune response using programmed death receptor-1 (PD-1) blockade showed benefit only in a fraction of patients with hepatocellular carcinoma (HCC).
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June 2023
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