The major cause of cancer mortality is metastasis, which relies on the growth of blood vessels (haemangiogenesis) and lymphatic vessels (lymphangiogenesis). Whereas the field of haemangiogenesis has been relatively thoroughly studied, little is known about the mechanisms regulating lymphangiogenesis. Recent research efforts in studying lymphangiogenesis have been focused on two members of the VEGF-family, VEGF-C and VEGF-D. However, it seems unlikely that these would be the sole factors regulating the formation and maintenance of the lymphatic system. In this thesis work, we have identified several novel lymphangiogenic factors, including members of the PDGF-, IGF-, and VEGF families, and investigated the role of bone marrowderived circulating endothelial precursor cells (CEPCs) in promoting lymphangiogenesis. It has previously been demonstrated that members of the PDGF family are potent haemangiogenic factors. In this thesis, we provide compelling evidence that PDGFs display direct lymphangiogenic activity. We have localized expression of the PDGF receptors on lymphatic endothelium and demonstrated direct stimulatory effects of PDGFs on primary lymphatic endothelial cells in vitro, as well as lymphangiogenic activities in vivo. Overexpression of PFGF-BB in murine fibrosarcomas stimulated tumoral lymphangiogenesis and promoted lymphatic metastasis. VEGF-A is another key angiogenic factor frequently utilized by tumors and other tissues to switch on their angiogenic phenotypes. This factor was previously thought to act as a specific haemangiogenic factor. However, we and others have identified VEGF-A as a novel lymphangiogenic factor in vivo. We found that overexpression of VEGF-A in murine fibrosarcomas induced the accumulation of peritumoral lymphatic vessels and promoted metastasis to the regional lymph nodes. The mechanism by which VEGF-A induces lymphangiogenesis might involve both direct effects, through activation of VEG17R-2 expressed on lymphatic endothelium, and indirect effects, by recruiting ...