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This presentation discusses the importance of VEGF and angiogenesis in lung cancer
development, as supported by pre-clinical and clinical data, and explores the
relationship between lung cancer prognosis and VEGF overexpression.

The hyperpermeable nature of VEGF-induced vasculature allows fluid to leak from tumour vessels into the interstitium. The resulting high interstitial pressure can impede the delivery of therapeutic agents from the bloodstream to tumour cells.

Angiogenesis, the process of new blood vessel formation, is vital to the growth of
malignant tumours. VEGF is the predominant regulator of tumour angiogenesis,
thereby affecting tumour growth and metastasis.

The moment at which a tumour begins to overexpress pro-angiogenic factors, such as
VEGF, is generally referred to as the angiogenic switch. The switch overwhelms the
balance of pro- and anti-angiogenic factors, facilitating tumour growth.

Tumour neovascularisation is required in the progression of cancer from small,
localised neoplasms to larger, growing and potentially metastatic tumours.
Tumours acquire an independent blood supply by expressing growth factors.

The binding of VEGF to its receptors on the surface of endothelial cells activates
intracellular tyrosine kinases, triggering multiple downstream signals that promote
angiogenesis.