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Tumor vascular endothelial cells (TECs) are the specialized cells that form the inner lining of blood vessels within a tumor microenvironment. Unlike normal endothelial cells, TECs are characterized by structural abnormalities, such as gaps between cells and a lack of a proper basement membrane, which contributes to high vascular permeability and inefficient blood flow [1][2]. They are highly proliferative and overexpress various pro-angiogenic receptors, most notably vascular endothelial growth factor receptors (VEGFRs), which drive the formation of new blood vessels to support tumor growth and metastasis [3]. Therapeutic targeting of TECs primarily involves anti-angiogenic agents that inhibit growth factor signaling or vascular disrupting agents (VDAs) that cause the rapid collapse of existing tumor vessels [4]. Because TECs are genetically distinct from normal endothelial cells and are directly accessible via the systemic circulation, they represent a critical target for cancer therapy, although treatment is often associated with systemic side effects like hypertension and impaired wound healing [5].
Inhibition of pro-angiogenic signaling pathways (primarily the VEGF/VEGFR and Ang/Tie2 axes), disruption of endothelial microtubule assembly leading to vascular collapse, and induction of endothelial cell apoptosis.
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