Abstract
Tumor growth relies on formation of a vascular supply. In 1971, Judah Folkman was the first to propose that in order to grow beyond 2–3 mm in size tumors required a new vascular network [16]. Subsequent research has confirmed that growth of a tumor, both at the primary site and metastases, is dependent on neoangiogenesis [17, 24]. This development of a new vasculature, angiogenesis, is normally regulated by both activators and inhibitors (Table 18.1). Tumors can produce some of these activators or down-regulate expression of inhibitors, therefore altering the balance in favor of an “angiogenic switch” [23]. In addition, the tumor-associated blood vessels differ from normal blood vessels in a number of ways: the capillary network is not organized, loose perivascular cells lead to a leaky basement membrane and tumor cells may become integrated into the new blood vessel [2]. There is recent evidence to suggest that anti-angiogenic therapy may also alter the abnormal tumor blood supply resulting in blood vessels which are more normal, allowing for improved tumor perfusion and better delivery of chemotherapy [34].
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Zakarija, A., Gradishar, W.J. (2011). Inhibitors of Tumor Angiogenesis. In: Minev, B. (eds) Cancer Management in Man: Chemotherapy, Biological Therapy, Hyperthermia and Supporting Measures. Cancer Growth and Progression, vol 13. Springer, Dordrecht. https://doi.org/10.1007/978-90-481-9704-0_18
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