Cellular actions and signaling by endostatin. Crit Rev Eukaryot Gene Expr 2002;12(3):175-91
Date
11/27/2002Pubmed ID
12449342Pubmed Central ID
PMC3270378DOI
10.1615/critreveukaryotgeneexpr.v12.i3.20Scopus ID
2-s2.0-0037584218 (requires institutional sign-in at Scopus site) 20 CitationsAbstract
The malignant transformation of a normal cell into a cancer cell requires no vasculature. Growth of solid tumors, however, requires angiogenesis to provide oxygen and nutrients to support cell proliferation. The switch from an avascular to a vascular phenotype is typically associated with acceleration of tumor growth. Antiangiogenic therapy, starving a tumor of its blood supply, is an attractive addition to the anticancer armamentarium. Animal tests of antiangiogenic therapy have shown remarkable potential. Initial human trials have proven antiangiogenic therapy to be remarkably nontoxic. Numerous antiangiogenic agents have been isolated as proteolytic fragments of endogenous polypeptides of the extracellular matrix. Endostatin was the first such antiangiogenic protein described and its potent antitumor effects in mice have generated wide interest. This review summarizes recent advances in endostatin biology and highlights new results on the cellular and subcellular mechanisms of endostatin action.
Author List
Ramchandran R, Karumanchi SA, Hanai J, Alper SL, Sukhatme VPAuthor
Ramani Ramchandran PhD Professor in the Pediatrics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Angiogenesis InhibitorsAnimals
Cell Transformation, Neoplastic
Collagen
Endostatins
Humans
Neovascularization, Pathologic
Neovascularization, Physiologic
Peptide Fragments
Receptors, Cell Surface
Signal Transduction