[Angiogenesis and tumor progression in melanoma]

Angiogenesis is defined as the formation of new blood capillaries from preexisting vessels. It takes place in physiological and pathological conditions, such as cancer. Tumor angiogenesis depends on the release of angiogenic growth factors by tumor cells and infiltrating inflammatory cells, and from the extracellular matrix following degradation by tumor proteases. Human melanoma progresses through different steps: nevocellular nevi, dysplastic nevi, in situ melanoma, radial growth phase melanoma (Breslow index < or = 0.75 mm), vertical growth phase melanoma (Breslow index > 0.75 mm), and metastatic melanoma. In agreement with progression, it acquires a rich vascular network, whereas an increasing proportion of tumor cells express the laminin receptor, which enables their adhesion to the vascular wall. Hence, both phenomena favour tumour cell extravasation and metastases. Melanocytic cells produce and release Fibroblast Growth Factor-2 (FGF-2), mainly in the steps of dysplastic nevus and melanoma in vertical growth phase. Melanoma cells also secrete the Vascular Endothelial Growth Factor (VEGF), in parallel with the switch from the radial to the vertical growth phase and the metastatic phase. It is becoming clear that anti-angiogenic agents will interfere with or block melanoma progression.