VEGF — Tumour Blood Vessel Growth

Vascular Endothelial Growth Factor represents a family of signalling proteins—most notably VEGF-A—that regulate angiogenesis, the growth of new blood vessels from existing vasculature. Under normal physiological conditions, VEGF aids embryonic development, tissue repair, and collateral vessel growth following ischaemia.

In malignant tumours, rapid growth creates areas deprived of oxygen (hypoxia). This triggers cells to upregulate hypoxia-inducible factors, which prompt massive release of VEGF. VEGF binds to receptors (VEGFR) on nearby endothelial cells, causing them to proliferate, migrate, and form leaky, disorganised capillary networks that feed the neoplasm.

Discovering VEGF led to a transformative class of drugs known as anti-angiogenic therapies. By interrupting the VEGF signalling pathway, these medicines can halt the development of new tumour vessels and normalise existing ones, improving chemotherapy delivery. Understanding your VEGF status clarifies why medications targeting blood supply are part of your regimen.

VEGF itself is rarely measured as an everyday clinical blood test because circulating levels fluctuate. Instead, pathologists identify VEGFR expression in tumour samples through immunohistochemistry, or assess genomic alterations in related pathways (such as VHL gene alterations in kidney cancer) that cause chronic VEGF oversecretion.

VEGF plays a prominent role in highly vascular malignancies, including renal cell carcinoma (kidney cancer), colorectal cancer, epithelial ovarian cancer, glioblastoma, non-small cell lung cancer, and hepatocellular carcinoma (liver cancer).

Anti-angiogenic drugs target this pathway directly. Monoclonal antibodies like bevacizumab bind directly to circulating VEGF, preventing receptor interaction. Small-molecule tyrosine kinase inhibitors, such as sunitinib, sorafenib, and lenvatinib, block the internal VEGFR receptor. Common side effects include high blood pressure and protein in the urine.