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Copper stimulates the proliferation and migration of endothelial cells and is required for the secretion of several angiogenic factors by tumour cells. Copper chelation decreases the secretion of many of these factors. Serum copper levels are upregulated in many human tumours and correlate with tumour burden and prognosis. Copper chelators reduce tumour growth and microvascular density in animal models. New orally active copper chelators have enabled clinical trials to be undertaken, and there are several studies ongoing. A unifying mechanism of action by which copper chelation inhibits endothelial cell proliferation and tumour secretion of angiogenic factors remains to be elucidated, but possible targets include copper-dependent enzymes, chaperones, and transporters.

Original publication

DOI

10.1007/s10911-006-9003-7

Type

Journal article

Journal

J mammary gland biol neoplasia

Publication Date

10/2005

Volume

10

Pages

299 - 310

Keywords

Animals, Biological Transport, Copper, Disease Models, Animal, Endothelial Cells, Humans, Models, Biological, Models, Chemical, Molybdenum, Neoplasms, Neovascularization, Pathologic, Prognosis, Up-Regulation