RT Journal Article SR Electronic T1 Vessel Cooption, Regression, and Growth in Tumors Mediated by Angiopoietins and VEGF JF Science JO Science FD American Association for the Advancement of Science SP 1994 OP 1998 DO 10.1126/science.284.5422.1994 VO 284 IS 5422 A1 Holash, J. A1 Maisonpierre, P. C. A1 Compton, D. A1 Boland, P. A1 Alexander, C. R. A1 Zagzag, D. A1 Yancopoulos, G. D. A1 Wiegand, S. J. YR 1999 UL http://science.sciencemag.org/content/284/5422/1994.abstract AB In contrast with the prevailing view that most tumors and metastases begin as avascular masses, evidence is presented here that a subset of tumors instead initially grows by coopting existing host vessels. This coopted host vasculature does not immediately undergo angiogenesis to support the tumor but instead regresses, leading to a secondarily avascular tumor and massive tumor cell loss. Ultimately, however, the remaining tumor is rescued by robust angiogenesis at the tumor margin. The expression patterns of the angiogenic antagonist angiopoietin-2 and of pro-angiogenic vascular endothelial growth factor (VEGF) suggest that these proteins may be critical regulators of this balance between vascular regression and growth.