Angiogenesis is a clinically validated target in cancer. For example, the anti-angiogenic drug Avastin (also known as Bevacizumab), a monoclonal antibody which targets the angiogenic glycoprotein VEGF-A, has been in clinical use for treating a variety of cancers over the past decade. However, the clinical benefit of anti-angiogenic drugs for cancer has in general been modest. Hence we require a more complete understanding of the molecular mechanisms driving tumour angiogenesis to identify improved therapeutic strategies based on targeting growth of tumour blood vessels. Furthermore, remodelling of lymphatic vessels (e.g. lymphangiogenesis, lymphatic enlargement and lymphatic invasion) also contributes to tumour progression, particularly in regards to metastatic spread to lymph nodes and, potentially, to distant organs. Members of the VEGF family, such as VEGF-C and VEGF-D, play key roles in controlling the remodelling of both blood vessels and lymphatics in development, cancer and cardiovascular diseases. In this presentation I will explore molecular mechanisms of VEGF-C and VEGF-D activation in tumours and signalling pathways used by these growth factors to promote angiogenesis and lymphatic remodelling in cancer. These mechanisms involve molecular targets for novel biological therapeutics (some already in clinical trials) designed to achieve more comprehensive anti-angiogenic effects in cancer, and to restrict the metastatic spread of tumour cells via blood vessels and lymphatics.