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The tumor vascular supply plays a central role in cancer biology, as tumors require new blood vessels to grow and metastasize. This supply consists of a disorganized network of vessels formed through processes such as angiogenesis, vasculogenic mimicry, and vessel co-option. These vessels are typically immature, leaky, and structurally abnormal compared to normal tissue vasculature. Pro-angiogenic signaling molecules—especially vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and others—drive vessel formation. Targeting the tumor vascular supply with antiangiogenic agents is a major strategy in cancer therapy, but challenges remain due to vascular redundancy, adaptation, and the creation of an immunosuppressive tumor microenvironment. The heterogeneity of tumor vasculature is increasingly being used as a biomarker for patient stratification and therapeutic response prediction[1][2][3][4][5][7].
Inhibition of angiogenesis (blocking VEGF/VEGFR signaling, FGF, PDGF) Blockade of pro-angiogenic cytokines Functional disruption of newly formed tumor blood vessels Inhibition of vasculogenic mimicry
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