Showing papers on "Angiogenesis published in 1979"

Angiogenesis in the Mouse Cornea

Abstract: We have developed a method that permits analysis of neovascular responses in the mouse cornea. Using this method we have demonstrated that both allogeneic lymphocytes and a variety of tumors can induce angiogenesis, but that only the latter appear capable of eliciting secondary capillary sprouting.

Fibrin Gel Investment Associated With Line 1 and Line 10 Solid Tumor Growth, Angiogenesis, and Fibroplasia in Guinea Pigs. Role of Cellular Immunity, Myofibroblasts, Microvascular Damage, and Infarction in Line 1 Tumor Regression

Abstract: Line 1 and line 10 tumors became invested in a fibrin-gel cocoon within hours after transplantation to the subcutaneous spaces of unsensitized syngeneic inbred Sewall Wright strain 2 guinea pigs. The fibrin gel comprised more than 80% of the line 1 tumor mass and, after day 3, became organized and was subsequently replaced by fibrous connective tissue, which gave the tumor the appearance of a scirrhous carcinoma. A cellular infiltrate of lymphocytes and basophils developed at the periphery of line 1 tumors after day 8, and tumors regressed by day 13. The fibrin gel investing the highly malignant line 10 tumors accounted for less than 10% of the tumor mass and persisted without fibrous organization as a tumor grew progressively and invaded adjacent tissues. These data provide new and potentially important insights into the biology of solid tumor growth and the mechanisms of immunologic tumor rejection. Envelopment of tumors in a fibrin gel created an anatomic barrier separating the tumors from the host. Neovascularization mimicking that about line 1 and line 10 tumors was induced by sc fibrin implants; these data suggest that activation of the clotting and/or fibrinolytic systems by tumor cells may itself provide sufficient stimulus for induction of tumor angiogenesis without requiring a separate tumor angiogenesis factor. The scirrhous pattern of growth characteristic of line 1 tumors apparently was achieved by organization of an abundant fibrin gel. Line 1 tumor regression did not for the most part involve direct contacts between tumor cells and any type of inflammatory cell, including macrophages; rather, tumor destruction was effected by ischemic necrosis secondary to widespread microvascular injury. The mechanisms of such injury are uncertain, but tumor rejection was correlated with evidence of developing cellular immunity and anatomic associations between lymphocytes and myofibroblasts. Further experiments will be necessary before these findings can be generalized to other tumor systems.

Nature of the Stimulus Leading to Lymphocyte-Induced Angiogenesis

Abstract: Experiments are described that characterize the nature of the stimulus leading to lymphocyte-induced angiogenesis (LIA), a reaction previously shown to reflect a local in vivo graft- vs -host reaction. The studies demonstrate that circulating cells of the host animals provide the stimulation essential for activation of donor lymphocytes and that the major allogeneic stimulus in congenic lines of mice is correlated with I-region disparity, primarily associated with I A -controlled determinants. The results are readily compartible with the hypothesis that is proposed that LIA is in large part the consequence of the release of soluble mediators or lymphokines that may act either directly on endothelial cells or indirectly by activating macrophages, which in turn generate the vascular reaction.

Tumor angiogenesis activity in clonal cells transformed by bovine adenovirus type 3.

Abstract: Four different sets of clonal cells transformed by bovine adenovirus type 3 and its oncogenic DNA fragments, and their clonal normal counterparts, were tested for tumor angiogenesis activity. The activity was assayed by measuring the host-mediated vascular response of a chorioallantoic membrane to the cell suspension separated from the vascular bed by a Millipore filter. Angiogenesis activity due to inflammation reaction was prevented by using corticosteroids. All of the transformed cells tested induced strong vascular responses as compared with their corresponding clonal normal cells. Cell dose and time dependency for the expression of the activity were also shown.