Abstract
The capacity to induce neovascularization was compared in normal, preneoplastic, and neoplastic mouse mammary tumors from strains with a high incidence of tumors (C3H, C3H-Avy, C3H-AvyfB) by implantation of small biopsy fragments on the iris surface in New Zealand White rabbits. Proliferation of iris blood vessels was studied by: 1) direct, in vivo slit-lamp stereomicroscopy and fluorescein angiography; 2) filling of the microvasculature with colloidal carbon; and 3) histologic examination. Ninety percent of mammary tumor implants elicited iris neovascularization after 48-72 hours, regardless of their histologic classification or the presence or absence of mammary tumor virus. Corticosteroid treatment reduced immediate postoperative inflammation (12-36 hr) but did not abolish subsequent growth of new vessels. Necrotic tumor fragments failed to elicit any neovascular response. In contrast, only 6% of normal tissues from resting mammary glands caused any vasoproliferation. Hormone-stimulated mammary tissues from pregnant and lactating mice exhibited a transient neovascular capacity that was lost during postweaning involution. Of the implants from premalignant hyperplastic alveolar nodules (HAN's), 30% produced a pattern of vessel growth similar to that of tumor implants. D-1 line (HAN outgrowth) tissues, which have a predicted low incidence of tumors, induced significantly fewer neovascular responses (P less than 0.002) than morphologically and biochemically similar D-2 line tissues, which have a predicted high incidence of tumors. These data suggest that the capacity to induce neovascularization is acquired during malignant progression of mouse mammary tissues; therefore, demonstration of this property may be useful in the identification of those intermediate populations most at risk for neoplastic transformation.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have