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Tumor-associated endothelial cell antigens refer to a heterogeneous group of molecules upregulated or uniquely expressed on the surface of endothelial cells within the tumor microenvironment[1][4][2]. These markers distinguish tumor vasculature from normal endothelium and include proteins involved in angiogenesis (such as VEGFR2, CD105), immune regulation (such as PD-L1), cell adhesion (VCAM-1), and extracellular matrix remodeling (MMP2, MMP11)[1][4][2][3][6]. Tumor-associated endothelial cells (TECs) demonstrate increased metabolic activity, transcriptional heterogeneity, and altered barrier function, which support tumor growth, metastasis, and immune evasion[1][2][4]. Because these cells and their antigens play a central role in tumor angiogenesis, immune modulation, and therapy resistance, they are considered promising – though highly complex – targets for anti-cancer therapies, especially angiogenesis inhibitors and immunomodulators[6][3][2]. Targeting these antigens can impact tumor vascularization, immune cell infiltration, and response to treatments, but clinical development is challenged by resistance mechanisms, phenotypic heterogeneity, and overlap with markers on normal vasculature[1][4]. **Note:** - The term "Tumor-associated endothelial antigens" is **not a single molecular target** but describes a class or set of markers. Many are proteins such as VEGFR2, CD105, or PD-L1 that can serve as individual targets. For structured data, further specification of which antigen or marker is intended is necessary[4][6][1]. - This entry is marked **is_incorrect: true** because it names a population class (multiple potential antigens, not a single molecule) and is not a precise, standard molecular target.
Inhibition of VEGF/VEGFR signaling, Modulation of immune checkpoint pathways (e.g., PD-L1/PD-1), Interference with angiogenesis
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