Vessel cooption, regression, and growth in tumors mediated by angiopoietins and VEGF

In contrast with the prevailing view that most tumors and metastases begin as avascular masses, evidence is presented here that a subset of tumors ins tead initially grows by coopting existing host vessels. This coopted host v asculature does not immediately undergo angiogenesis to support the tumor b ut instead regresses, leading to a secondarily avascular tumor and massive tumor cell loss. Ultimately, however, the remaining tumor is rescued by rob ust angiogenesis at the tumor margin. The expression patterns of the angiog enic antagonist angiopoietin-2 and of pro-angiogenic vascular endothelial g rowth factor (VEGF) suggest that these proteins may be critical regulators of this balance between vascular regression and growth.