The vascular network of tumours--what is it not for?
It is becoming almost a dogma that tumours cannot grow beyond 1-2 mm(3) unless they are supported by a rich vascular supply 1. It is true that tumours promote angiogenesis and that highly vascularized carcinomas have, in general, a more aggressive clinical course than carcinomas of low vascularization 23. However, a study of intratumoral angiogenesis reveals that the newly formed vessels are commonly deprived of those structural qualities that would allow them to perform an optimal oxygenation function 3. Thus, most tumours, irrespective of their angiogenic status, behave as if they were 'hypoxic', urging (via angiogenic mediators) for, what would look paradoxical at first sight, more defective angiogenesis. It is hypothesized that tumour cells can grow into solid neoplasms by exploiting the host's pre-existing vessels, without the need for new blood vessel formation. Neovascularization, however, may be important for tumours with an exophytic pattern of growth as these, by their very nature, lose the host's sheltering stroma. Shifting to anaerobic glycolysis and activation of anti-apoptotic pathways are complementary mechanisms for tumour cell survival and growth. Besides, continuous and indiscriminate production of a defective vascular network ensures an increased metastatic potential since the newly formed intratumoral vessels, simulating venular-like spaces, are easily permeable to tumour cells, facilitating metastases.
D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D017209:Apoptosis; D002196:Capillaries; D004730:Endothelium, Vascular / Q000473:pathology; D006801:Humans; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000098:blood supply* / Q000188:drug therapy / Q000473:pathology; D009389:Neovascularization, Pathologic
D020533:Angiogenesis Inhibitors