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Description
Monoclonal antibody 1837-46 reacts with endostatin, a 20 kDa C-terminal fragment of collagen XVIII. Endostatin is able to evoke non-uniform response for proliferation, cell mount and migration of entothelial cells, with different endostatin binding characteristic, leads to the assumption that endostatin effect is strongly dependent from endothelial cell type. Furthermore endostatin inhibits angiogenesis and tumor growth in vivo by inducing apoptosis in endothelial cells. The local delivery of endostatin seems to specifically affect tumor-associated microvessels by reduction of the vessel density, diameter and functionality. Tumor cell migration and invasion was greatly reduced in the endostatin treated animals. Endostatin is non-toxic and does not induce acquired drug resistance and has therefore become a potent new therapy strategy in solid neoplasias. This therapy appear to have high potential not only for the treatment of gliomas, the most common brain tumours, but also of other tumours. The ability of endostatin to inhibit neoangiogenesis is mediated, at least in part, by Zn2+ binding and elastase processing. Widespread endostatin expression was found in elastic fibers in vessel walls and in some other basement membrane zones. Endostatin is released by neurons to accumulate in amyloid plaques in Alzheimer's disease.