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VEGF angiogenesis

How tumours grow their own blood supply. Low oxygen makes cells release VEGF, which tells blood-vessel cells to sprout toward the tumour.

Hypoxia stabilises HIF-1α/HIF-2α, which induce VEGF-A. VEGF-A binds VEGFR2 on endothelial cells → PLCγ/PKC/MAPK and PI3K/AKT → proliferation, migration, and permeability. Tumour vessels are chaotic and leaky, causing hypoxia and impaired drug and immune-cell delivery. Bevacizumab neutralises VEGF-A; VEGFR TKIs (axitinib, cabozantinib, lenvatinib) block the receptor; 'vascular normalisation' at moderate doses improves immune infiltration, the rationale for IO-VEGF combinations and PD-1×VEGF bispecifics. VEGF also suppresses dendritic cell maturation and expands Tregs.

In one picture

A growing town (tumour) that keeps sending out road-building orders (VEGF). Anti-angiogenic drugs cancel the orders; at the right dose the roads that remain are straighter and better, so police (immune cells) and supplies (drugs) get in.

Diagram

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Light up a product:
HypoxiaHIF-1α / HIF-2αVEGF-AVEGFR2 (endothelium)PLCγ / MAPK / PI3KAngiogenesis, permeabilityImmune suppression (DC, T…activatesinhibitsdruggable target (click)hit by selected productescape route

How drugs attack it

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  • Bevacizumab, ramucirumab (antibodies)
  • VEGFR TKIs: axitinib, cabozantinib, lenvatinib, sunitinib
  • IO + VEGF combinations in RCC, HCC, endometrial cancer
  • PD-1×VEGF bispecifics: ivonescimab and successors
  • HIF-2α inhibitor belzutifan upstream in VHL-deficient RCC

Connected

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