Abstract
The growth and metastasis of solid tumors are dependent on the ability of tumor cells to induce angiogenesis [1]. Angiogenesis, the formation of new blood vessels from pre-existing ones, involves endothelial cell proliferation, motility, and tubular differentiation. It is known that tumor cells can secrete a variety of angiogenic factors, such as basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), to stimulate angiogenesis. Tumor cells also produce angiogenesis inhibitors such as thrombospondin and angiostatin to control angiogenesis. The balance between angiogenesis stimulators and inhibitors determines the angiogenicity of tumor cells [2]. Acquisition of the ability to stimulate angiogenesis by tumor cells is an integral part of tumorigenesis. Activated oncogenes, such as ras, or inactivated tumor suppressor genes, such as p53, not only increase mitogenesis and prevent apoptosis in tumor cells, but also lead to the development of an angiogenic phenotype [for review,.3].
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Nie, D. et al. (1999). Platelet-Type 12-Lipoxygenase Regulates Angiogenesis in Human Prostate Carcinoma. In: Honn, K.V., Marnett, L.J., Nigam, S., Dennis, E.A. (eds) Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury, 4. Advances in Experimental Medicine and Biology, vol 469. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4793-8_90
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DOI: https://doi.org/10.1007/978-1-4615-4793-8_90
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