Angiogenesis is the process by which new blood vessels are formed. Cancer cells appear to be able to kick start this process, ensuring that such cells receive a continual supply of oxygen and other nutrients.

Normal tissues of the body have blood vessels running through them that deliver oxygen from the lungs. Cells must be close to the blood vessels to get enough oxygen for them to survive. New blood vessels are formed during the development of embryos, during wound repair and during the female reproductive cycle. An expanding tumour requires new blood vessels to deliver adequate oxygen to the cancer cells, and thus exploits these normal physiological processes for its benefit. To do this, the cancer cells acquire the ability to orchestrate production of new vasculature by activating the 'angiogenic switch'. In doing so, they control non-cancerous cells that are present in the tumour that can form blood vessels by reducing the production of factors that inhibit blood vessel production, and increasing the production of factors that promote blood vessel formation.

The process is triggered by signaling from tumour cells in a phase of rapid growth so that during tumour progression the angiogenic switch is activated, to remain turned on. The mechanism is associated with oxygen deprived cells at the centre of the tumour that become hypoxic and activate hypoxic stress. This event leads to HIF accumulation that induces the expression of target genes including vascular endothelial growth factor (VEGF).  VEGF and VEGF receptor tyrosine kinases 2 (VEGFR-2) are signaling proteins that control the angiogenic switch to play a central role in angiogenesis. VEGF and VEGF-R2 are often upregulated in human cancers.

Accordingly, anti-angiogenic therapeutic strategies based on VEGF/VEGFR pathway inhibition were initiated. Despite anti-VEGF/VEGFR targeted treatment, anti-angiogenic patient resistance was subsequently recognised and attributed to the presence and utilization of redundant and compensatory signaling pathways to recruit vasculature. To name a few compensatory pathways involved in tumour angiogenesis, the platelet-derived growth factor (PDGF) and PDGF receptor (PDGFR) and fibroblast growth factor (FGF) and FGF receptor (FGFR) pathways were identified and clinical observations showed elevated plasma levels of PDGF and FGF.

As such finding “the most important target” as an anti-angiogenic strategy may however be challenging as the tumour environment is highly diverse, consist of many different cell types, and redundancies in signaling pathways, all of which contribute to tumour angiogenesis.

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