title: Tumor angiogenesis and anti-angiogenic therapies.
abstract: Angiogenesis, the development and growth of blood vessels, is a major topic of research which began in 1971 with Folkman's original hypothesis. Different mechanisms of blood vessel growth are sprouting and intussusceptive angiogenesis, vascular mimicry, and blood vessel cooption. Dis-regulated angiogenesis may result in numerous angiogenic diseases and is responsible for solid tumor growth and metastasis. Vascular endothelial cells are generally dormant in adult but in pathological conditions when tumors reach a size of about 0.2-2.0 mm in diameter, they become hypoxic and hindered in tumor growth in the lack of angiogenesis. During angiogenic switch pro-angiogenic factors predominate and result in angiogenesis and tumor progression. Angiogenesis switch leads to the increased production of vascular endothelial growth factor (VEGF) following up-regulation of the hypoxia-inducible transcription factor. The VEGF family comprises from VEGF (VEGF-A), VEGF-B, VEGF-C, VEGF-D, and placental growth factor (PlGF). The VEGF family of receptors consists of three protein-tyrosine kinases. Now, the most conventional approach for controlling tumor angiogenesis is blockade of the vascular endothelial growth factor (VEGF) pathway. The results of preclinical studies, substantial therapeutic effects of VEGF blockers have been stated in various types of human cancers, even in progressive or recurrent cancer cases.
authors.affiliation: Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran Department of Immunology, Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
authors.forename: Fatemeh Zare
authors.initials: FZ
authors.lastname: Shahneh
authors.forename: Behzad
authors.initials: B
authors.lastname: Baradaran
authors.forename: Fatemeh
authors.initials: F
authors.lastname: Zamani
authors.forename: Leili
authors.initials: L
authors.lastname: Aghebati-Maleki
mesh_terms: D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D000068258:Bevacizumab; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007211:Indoles / Q000627:therapeutic use; D009369:Neoplasms / Q000098:blood supply* / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D009389:Neovascularization, Pathologic; D000072483:Placenta Growth Factor; D011257:Pregnancy Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D011758:Pyrroles / Q000627:therapeutic use; D011799:Quinazolines / Q000627:therapeutic use; D040262:Receptors, Vascular Endothelial Growth Factor / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D000077210:Sunitinib; D042442:Vascular Endothelial Growth Factors / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism
chemical_list: D020533:Angiogenesis Inhibitors; D061067:Antibodies, Monoclonal, Humanized; D007211:Indoles; C000608036:PGF protein, human; D011257:Pregnancy Proteins; D011758:Pyrroles; D011799:Quinazolines; D042442:Vascular Endothelial Growth Factors; D000072483:Placenta Growth Factor; D000068258:Bevacizumab; D040262:Receptors, Vascular Endothelial Growth Factor; C500926:cediranib; D000077210:Sunitinib
keywords: Angiogenesis; VEGF; anti-angiogenic therapy; tumor angiogenesis