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• W2000233490 abstract "Lactoferrin (Lf) systemically suppresses tumor growth and metastasis by unknown mechanisms. We have studied the effect of orally administered iron-unsaturated bovine Lf on angiogenesis induced by VEGF(165) and IL-1-alpha in adult rats using the mesenteric-window angiogenesis assay. VEGF(165) is a major angiogenic factor in most, if not all, tumors and other angiogenesis diseases of clinical relevance. A number of objective angiogenesis variables were analyzed using microscopic morphometry and image analysis. Lf treatment significantly inhibited the VEGF(165)-mediated response in terms of microvessel spatial extension, overall vascularity and incidence of crossover. The response to IL-1-alpha decreased significantly only in terms of microvessel crossover. In vitro, Lf exerted an antiproliferative effect on endothelial cells. To our knowledge, Lf is the first endogenous protein that has been shown to be antiangiogenic following oral administration. The oral administration of Lf thus appears to be of potential interest as an antiangiogenesis treatment modality in the clinical setting. Since tumor growth is angiogenesis dependent, the extensive therapeutic potential warrants further study to elucidate the mechanisms responsible for the angiostatic effect of Lf." @default.
• W2000233490 created "2016-06-24" @default.
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• W2000233490 date "2001-01-15" @default.
• W2000233490 modified "2023-10-14" @default.
• W2000233490 title "Orally administered bovine lactoferrin systemically inhibits VEGF165‐mediated angiogenesis in the rat" @default.
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• W2000233490 doi "https://doi.org/10.1002/1097-0215(200002)9999:9999<::aid-ijc1024>3.3.co;2-k" @default.
• W2000233490 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11146451" @default.
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