Vascular endothelial growth factor or VEGF is an important signal protein involved in angiogenesis. VEGF belongs to PDGF superfamily and has more than 10 isoforms (VEGF-121,VEGF-165,VEGF-189,VEGF-206, -B, -C, -D, -E, PIGF-I and PIGF-II), ranging in weight from 35-44 kDa. Each bind to a specific combination of endothelial cell surface ligands (known as VEGFR-1, -2 and -3). VEGF production can be induced in cells that are not receiving enough oxygen. When a cell is deficient in oxygen, it produces HIF, Hypoxia Inducible Factors, a transcription factor. HIF stimulates the release of VEGF, among other functions (including modulation of erythropoeisis). Circulating VEGF then binds to VEGF Receptors on endothelial cells, triggering a Tyrosine Kinase Pathway leading to angiogenesis.

VEGF has been implicated with poor prognosis in breast cancer. Numerous studies show a decreased OS and DFS in those tumors overexpressing VEGF. The overexpression of VEGF may be an early step in the process of metastasis, a step that is involved in the "angiogenic" switch. Although VEGF has been correlated with poor survival, its exact mechanism of action in the progression of tumors remains unclear.

VEGF is also released in rheumatoid arthritis in response to TNF-α, increasing endothelial permeability and swelling and also stimulating angiogenesis (formation of capillaries).

Once released, VEGF may elicit several responses. It may cause a cell to survive, move, or further differentiate. Hence, VEGF is a potential target for the treatment of cancer. The first anti-VEGF drug, a monoclonal antibody named bevacizumab, was approved in 2004.

Current studies show that VEGFs are not the only promoters of angiogenesis

Angiology | Growth factors

VEGF | 血管内皮生长因子