Angela Coxon

TL;DR: In this paper, the authors showed that specific Ang2 inhibition may represent an effective anti-angiogenic strategy for treating patients with solid tumors, and they showed that anti-Ang2 therapy also prevented VEGF-stimulated neovascularization in a rat corneal model of angiogenesis.

TL;DR: Oral administration of AMG 706 potently inhibited VEGF-induced angiogenesis in the rat corneal model and induced regression of established A431 xenografts and had no significant effects on body weight or on the general health of the animals.

TL;DR: AMG 176 is a potent, selective, and orally bioavailable MCL1 inhibitor that induces a rapid commitment to apoptosis in models of hematologic malignancies and the synergistic combination of AMG 176 and venetoclax is synergistic in acute myeloid leukemia (AML) tumor models and in primary patient samples at tolerated doses.

TL;DR: It is concluded that inhibition of Ang2 slows tumor growth by limiting the expansion of the tumor vasculature by sprouting angiogenesis, in a manner that is complemented by concurrent inhibition of VEGF and leads to reduced proliferation and increased apoptosis of tumor cells.

TL;DR: Findings are consistent with a model whereby inhibition of Ang2 leads to normalization of tumor blood vessels by permitting the unopposed action of Ang1, but decreases tumor vascularity primarily by blocking Ang2 actions.