PROLONGED TUMOR DORMANCY BY PREVENTION OF NEOVASCULARIZATION IN VITREOUS

Abstract

Tumors release a diffusible substance that stimulates neovascularization. To study the neovascularization that occurs in diabetic retinopathy, [rabbit] V2 carcinomas and mouse ependymoblastomas were implanted into the vitreous of experimental animals. In the rabbit or dog vitreous, unlike previous sites, the tumors failed to stimulate neovascularization. The grew for weeks as small, unvascularized, 3-dimensional aggregates of cells. Explosive growth into a large, vascularized mass occurred when the avascular tumors reached the retinal surface. The vitreous proved to be a valuable model for observing the in vivo growth of small, solid tumors. Xenografts survived for months without evidence of immune rejection. The consequence of the prolonged avascular state is the restriction of tumor size. The normal vitreous may act to inhibit capillary proliferation. An understanding of the mechanism for maintaining the avascular state may lead to therapeutic blockade of neovascularization. This would be important in the management of diabetic retinopathy and neoplasia.