he onset of angiogenesis is believed to be an early event in tumorigenesis and may facilitate tumor progression and metastasis. Several growth factors with angiogenic activity have been described. These include fibroblast growth factor (FGF), platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF). Like VEGF, several PlGF variants have been shown to arise from alternative mRNA splicings. Evidence has suggested VEGF to be an obligatory component in PlGF signaling. While VEGF homodimers and VEGF/PlGF heterodimers function as potent mediators of mitogenic and chemotactic responses in endothelial cells, PlGF homodimers are effectual only at extremely high concentrations. Indeed, many of the physiological effects attributed to VEGF may actually be a result of VEGF/PlGF. VEGF and PlGF share a common receptor, Flt-1, and may also activate Flk-1/KDR.
