AuthOr’s VIew AuthOr’s VIew

Neoangiogenesis is the pathophysiological process whereby tumors stimulate the for-mation of novel blood vessels to support their growth and metastatic dissemina-tion. The production of pro-angiogenic factors including vascular endothelial growth factor (VEGF) by malignant cells robustly contributes to neoangiogenesis. In line with this notion, targeting pro-angiogenic factors or their receptors by means of specific anti-angiogenic agents has significantly improved the clinical course of several types of cancer in the last two decades. Two main classes of anti-angiogenic agents have been developed so far: small tyrosine kinase inhibitors (TKIs), which often target multiple pro-angiogenic signal receptors at the same time, and monoclonal antibodies, which generally operate by directly neutralizing pro-angiogenic factors. Thus, sunitinib— a TKI that inhibits vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), KIT and fms-related tyrosine kinase 3 (FLT3)—is nowadays employed for the treatment of metastatic renal cancer, while bevacizumab, an anti-VEGFA antibody, is currently used in metastatic colorectal carcinoma (CRC) patients. VEGFA/VEGFR2-targeted therapies prevent the VEGFA-induced proliferation of regulatory T cells in cancer Magali terme1,*, eric tartour1,2, and Julien taieb1,3,