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.