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Tumor-feeding vasculature refers to the specialized network of blood vessels that tumors recruit and develop to sustain their metabolic demands (National Cancer Institute, 2023). These vessels are essential for providing oxygen and nutrients while removing metabolic waste, thereby facilitating tumor progression and metastasis (Carmeliet & Jain, Nature, 2011). Unlike healthy blood vessels, tumor-associated vasculature is characterized by structural abnormalities, including high permeability, irregular branching, and a lack of distinct pericyte coverage (PubMed, PMID: 17039111). This system is a major focus of therapeutic intervention, primarily through the use of anti-angiogenic agents and vascular disrupting agents (VDAs) (StatPearls, 2023). Anti-angiogenic drugs, such as bevacizumab, work by inhibiting signaling pathways like the VEGF axis to prevent the formation of new vessels. Conversely, VDAs target the existing, fragile endothelial lining of tumor vessels to cause rapid vascular collapse and central tumor necrosis. Clinical challenges associated with targeting this system include the development of resistance and significant side effects like hypertension and impaired wound healing. Despite these challenges, modulating the tumor-feeding vasculature remains a fundamental strategy in treating various solid tumors.
Therapeutic strategies targeting the tumor-feeding vasculature include anti-angiogenesis, which inhibits the growth of new vessels by blocking pro-angiogenic signaling such as the VEGF/VEGFR pathway (National Cancer Institute, 2023), and vascular disruption, which selectively destroys existing tumor vessels by targeting the cytoskeleton of tumor endothelial cells to cause vessel occlusion (PubMed, PMID: 17039111).
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