Angiogenic endothelial cells in tumor vasculature (TEC)

Angiogenic endothelial cells in tumor vasculature are a specialized population of endothelial cells that have been activated to form new blood vessels, a process essential for the growth and progression of solid tumors (Nature Rev. Cancer, 2008). These cells differ from normal, quiescent endothelial cells by their high rate of proliferation, increased permeability, and the expression of specific surface markers such as VEGFR-2, integrin αvβ3, and CD105 (US Pharmacist, 2010). In the tumor microenvironment, they are stimulated by pro-angiogenic factors like vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) released by cancer cells (PNAS, 2012). Therapeutic targeting of these cells, known as anti-angiogenic therapy, aims to inhibit the formation of new vessels or disrupt existing tumor vasculature to deprive the tumor of nutrients and oxygen (NIH, 2018). Common drugs targeting this system include bevacizumab, which neutralizes VEGF, and various tyrosine kinase inhibitors like sunitinib that block VEGFR signaling. While effective in many cancers, challenges include the development of resistance and safety concerns such as hypertension and impaired wound healing (Nature Rev. Cancer, 2008). Additionally, these cells are being explored as targets for selective drug delivery using nanocarriers like EndoTAG-1 (ResearchGate, 2018).

Other names

Tumor-associated endothelial cellsTumor vascular endothelial cellsActivated endothelial cellsTumor neovasculatureAngiogenic endothelial cells

Anti-angiogenic drugs target these cells by inhibiting the VEGF/VEGFR signaling pathway, which is the primary driver of endothelial cell activation and vessel formation in tumors. This blockade leads to the inhibition of endothelial cell proliferation and migration, the regression of immature tumor vessels, and the normalization of the remaining vasculature to improve drug delivery. Other approaches include targeting integrins (e.g., αvβ3) or using vascular disrupting agents that cause the rapid collapse of established tumor blood vessels.