Angiogenesis disease

Carmeliet P (2005) Angiogenesis in life, disease and medicine. Nature 438(7070)... 

Erdmann et al. (2000) report the fabrication of devices for the localized delivery of salicylic acid from the poly(anhydride-co-ester)s mentioned in Section II.C. A unique feature of this drug delivery system is that the drug compound is part of the polymer backbone. Devices were implanted intraorally and histopathology was reported (Erdmann et al., 2000). Chasin et al. (1990) review fabrication and testing of implantable formulations for other drugs including angiogenesis inhibitors for treatment of carcinomas and bethanechol for the treatment of Alzheimer s disease. 

The antibody brings about its effect by inhibiting angiogenesis (the formation of new blood vessels), a process required to support tumour growth. Specifically, the antibody binds human vascular endothelial growth factor. This prevents the latter from binding to its cell surface receptor, a process central to triggering new blood vessel formation in both normal and diseased tissue. 

Folkman, J. (1995). Angiogenesis in cancer, vascular, rheumatoid and other disease. Nat. Med. 1, 27-431. 

The putative role of angiogenesis in chronic inflammatory diseases is the maintenance of the inflammatory state by allowing ongoing recruitment of inflammatory cells and by supplying nutrients and oxygen to proliferating inflamed tissue. The increased endothelial surface creates an enormous capacity for the production of cytokines, adhesion molecules, and other inflammatory stimuli [35]. 

In many chronic inflammatory diseases, angiogenesis can be identified in the inflamed lesions. For example, in rheumatoid arthritis extensive neovascularization is present in the inflamed synovium where it is one of the earliest histopathological findings [36]. Since in RA synoviocytes exhibit characteristics of tumour cells, including somatic mutations in key regulatory genes such as H-ras and the p53 tumour suppressor, RA can be viewed as a multicentric tumour-like mass that invades and destroys its local environment [37]. Concurrent increased endothelial cell turnover may contribute to microvascular dysfunction and thereby facilitate persistent synovitis. 

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