Showing papers on "Angiogenesis published in 1977"
TL;DR: The mitogenic effects of several untransformed and transformed cell lines on cloned ABAE cells and non-vascular endothelial cell controls are reported, establishing a cloned adult bovine aortic endothelial (ABAE) cell line which has maintained its endothelial properties for over 1 yr in culture.
Abstract: TUMOURS induce vascularisation into the neoplasm to provide needed cell nutrients and remove wastes1. The formation of tumour blood vessels seems to depend, in part, on the proliferation and movement of vascular endothelial cells which are, in turn, controlled by the secretion of tumour angiogenesis factor (TAP) (refs 2–4). Extracts of tumours2–4 and of established cell lines5 have TAF activity in vivo. But little is known about the molecular nature or mechanism of action of TAF. The proliferation, formation and integrity of vascular endothelium are also involved in normal host processes: wound healing, morphogenetic tissue rearrangements, as well as the prevention of various non-neoplastic diseases resulting from blood vessel wall injury depend on angiogenesis factors6. A convenient method to study angiogenesis and endothelial repair is with an in vitro endothelial cell system, but the lack of uniform, reliable cultured endothelial cell lines has delayed progress in this area. Most studies7–9 (with some exceptions10) have used uncloned vascular cells which are often slow growing and heterogeneous in cell type. We have recently established a cloned adult bovine aortic endothelial (ABAE) cell line which has maintained its endothelial properties for over 1 yr in culture, provided that fibroblast (growth factor (FGF) is present in the growth medium11. We report here the mitogenic effects of several untransformed and transformed cell lines on cloned ABAE cells and non-vascular endothelial cell controls.
49 citations
TL;DR: It is shown that isolated chondrocytes can inhibit the angiogenesis induced by lymphocytes in vivo, and their ability to do so depends on the ratio of chondROcytes to lymphocytes used.
Abstract: LYMPHOCYTE-induced angiogenesis (LIA) has been introduced by Sidky and Auerbach1 as a quantitative and sensitive assay for measuring cell-mediated immunity in vivo. In this assay immuno-competent lymphocytes are injected intradermally into allogeneic or semiallogeneic mice. A local graft versus host (GVH) reaction is therefore induced, resulting in new blood vessel formation. As early as the second day post-injection, this effect could be observed in a dose–response fashion dependent on the number of cells injected. The relationship of lymphocyte-induced angiogenesis to tumour-induced angiogenesis mediated by tumour–angiogenesis factor (TAF)2 remains theoretical. Folkman and others have demonstrated inhibition of TAF-induced angiogenesis by cartilage fragments3 or extracts4. In this study we show that isolated chondrocytes can inhibit the angiogenesis induced by lymphocytes in vivo. Their ability to do so depends on the ratio of chondrocytes to lymphocytes used.
21 citations
Journal Article•
TL;DR: Impregnation of the vasculature with ink was used to study microvascular changes induced in rats by liquid (ascites) and solid growth of W256 and Y-P388 tumours, and the nature and significance of neovascularization of tumours and their so-called "haemorrhagic" growth are discussed.
Abstract: Impregnation of the vasculature with ink was used to study microvascular changes induced in rats by liquid (ascites) and solid growth of W256 and Y-P388 tumour cells. Ascites fluid produced by both tumours was heavily blood-stained; the deep red colour of solid tumour deposits was similarly due to the presence of free blood. In both types of tumour growth this free blood was due to diapedesis of erythrocytes through tips of capillary sprouts which grow when neovascularization (angiogenesis) occurs in response to any suitable (non-neoplastic or neoplastic) stimulus. Ascites growth of these tumours induced profuse sprouting from the peritoneal capillaries; this sprouting, together with the "bleeding" it caused, were inhibited by local pre-irradiation of the peritoneal vasculature with X-rays before intraperitoneal inoculation of rats with the tumours. Similar angiogenesis with bleeding did not occur following inoculation with an allogeneic tumour in rats which had been previously immunized against the tumour. LI tumour cells (tumour cells lethally irradiated in vitro to destroy their proliferative integrity, but which remain metabolically active) also induced sprouts to grow in close proximity to the implanted LI cells, but heat-killed tumour cells caused no sprouting. The nature and significance of neovascularization of tumours and their so-called "haemorrhagic" growth are discussed.
20 citations
TL;DR: It is evident that at the stage in which disseminated tumor cells are not yet vascularized; they are not accessible and, thus, largely invulnerable to such anticancer drugs as may be presented in the circulating blood.
Abstract: To the Editor.— The disagreement between Moertel (236:1935, 1976) and Li (237:872, 1977) regarding the value of fluorouracil as an adjuvant agent can be reconciled if the factors of angiogenesis and selective solubilization of fluorouracil are taken into account. It is evident that at the stage in which disseminated tumor cells are not yet vascularized; they are not accessible and, thus, largely invulnerable to such anticancer drugs as may be presented in the circulating blood. Further, in the unvascularized state, only limited growth of the tumor mass occurs. 1 While angiogenesis renders the tumor accessible to anticancer drugs, at the same time it also promotes an exponential rate of malignant cell growth. 2 The tumor growth rate that occurs after even a relatively short period of vascularization is such as to make it problematic whether in the individual case fluorouracil will be able to selectively overcome the kinetics of cancer cell
2 citations