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Cellular actions and signaling by endostatin. Crit Rev Eukaryot Gene Expr 2002;12(3):175-91

Date

11/27/2002

Pubmed ID

12449342

Pubmed Central ID

PMC3270378

DOI

10.1615/critreveukaryotgeneexpr.v12.i3.20

Abstract

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 VP

Author

Ramani Ramchandran PhD Professor in the Pediatrics department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Angiogenesis Inhibitors
Animals
Cell Transformation, Neoplastic
Collagen
Endostatins
Humans
Neovascularization, Pathologic
Neovascularization, Physiologic
Peptide Fragments
Receptors, Cell Surface
Signal Transduction
jenkins-FCD Prod-484 8aa07fc50b7f6d102f3dda2f4c7056ff84294d1d