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Tumor vasculature endothelial cells expressing proangiogenic genes are specialized endothelial cells found within the blood vessels of tumors. Unlike normal tissue endothelium, these cells exhibit an altered phenotype characterized by upregulation of proangiogenic factors such as VEGFA, PDGF, FGFs, ANGPT2, and their receptors including VEGFR2 and PDGFR. This results in a persistent "angiogenic switch," driving continuous formation of new blood vessels that support rapid tumor growth by supplying oxygen and nutrients while removing waste products. These activated endothelial cells also interact with other components of the tumor microenvironment—such as pericytes, macrophages (notably via IL‑8), smooth muscle cells, and cancer cells—through direct contact or secretion of cytokines. Their dysregulated signaling is essential for pathological angiogenesis in cancer but also contributes to metastasis by increasing vascular permeability and facilitating circulating tumor cell extravasation[1]. Note: The target name refers to a cell population defined by gene expression profile, not a single molecular entity or receptor; thus it is not strictly canonical as a drug target but represents an important therapeutic focus in antiangiogenic cancer therapy[1].
Inhibition of VEGF signaling to block angiogenesis and reduce blood supply to tumors[1]
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