Angiogenesis, antiangiogenesis

Tumor growth requires vascularization to be supplied by oxygen and nutritients. The vascular network could be different between tumors, even during the development of the same tumor (local and systemic spreading), from the occupation of already present vessels to the real angiogenesis (i.e, proliferation of endothelial cells). Moreover, the tumor cells can create channels, mimicking the normal vessels. This spectrum in morphology should be refl ected in the therapeutic response, in the effectiveness of antiangiogens, but the how is unknown. It is sure that acceptable clinical activity can be achieved only with combinations, both with traditional cytotoxic and targeting drugs.  The clinical advantage can be hampered by increased toxicity, demanding supportive actions. One of the key decisions is to select the proper therapy considering the patient and the tumor characteristics (today increasingly at molecular level) and predict the response to the therapy. Such (bio)markers are still missing, although intensive research trying the best. Since the main target of antiangiogenic drugs (today and tomorrow) the VEGF/R family, a useful marker is expected from them. The inhibition of angiogenesis is a logical step against the solid tumors and these steps slowly but steadily can improve the patients life-time, as well as their quality of life.