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Query: UMLS:C0027651 (tumor)
685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor angiogenesis factor (TAF) elicits a strong vasoproliferative response when implanted upon the chorioallantoic membrane (CAM) of the chick embryo. This response is first observed stereomicroscopically 2-3 days after implantation. A 40-fold increase in mast cell density is observed within the vicinity of this implant by 24 h. Mast cells that have been isolated from retired breeder Sprague-Dawley rats fail to evoke a vascular reaction when implanted on the CAM. An intermediate role for the mast cell in tumor angiogenesis is suggested.
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PMID:Mast cells and tumor angiogenesis. 6 25

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.
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PMID: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. 28 18

Capillary endothelial cells from rats, calves, and humans, have been carried in long-term culture. Bovine capillary endothelial cells have been cloned and maintained by serial passage for longer than 8 months. This prolonged culture was accomplished by using tumor-conditioned medium, gelatin-coated plates, and a method of enriching cells in primary culture. Cultured bovine capillary endothelial cells produce Factor VIII antigen and angiotensin-converting enzyme, but do not have Weibel-Palade bodies. Human cells do contain Weibel-Palade bodies. Capillary endothelial cells are distinguished from aortic endothelial cells by their requirement for conditioned medium. Bovine capillary endothelial cells in regular medium grow slowly with a mean doubling time of 67 hr and eventually die. In tumor-conditioned medium, these cells grow rapidly with a doubling time of 28 hr and continue to proliferate for as long as the tumor-conditioned medium is present. In contrast, bovine aortic endothelial cells grow as rapidly in regular medium as in tumor-conditioned medium. This method allows the production of pure capillary endothelial cells that may prove useful for studies of tumor angiogenesis, metastatic mechanisms, and the role of capillary endothelium in other pathologic states.
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PMID:Long-term culture of capillary endothelial cells. 29 37

The assembled evidence suggests that geometry plays an important role in regulation of cell growth, at least at two levels: (1) For non-transformed individual cells in culture, there may be a continuous range of shapes, from spherical all the way to extremely flat or extended, which correlates with increasing proliferative capacity or increasing ability to respond to serum growth factors. In other words, sensitivity to a variety of mitotic stimulators and growth factors may be modulated by cell conformation. Fully transformed cells appear to lose the modulating effect of shape, and thus are able to proliferate even when spherical. (2) For transformed cells which can grow in three-dimensional populations, the shape of the population itself eventually limits growth. The most likely mechanism is based upon the limiting effects of diffusion gradients of nutrients, oxygen and catabolites which build up across the surface of a three-dimensional population of cells. Tumor cells which are able to make tumour angiogenesis factor (TAF), induce new capillary blood vessels from the host. These vessels penetrate the tumor and permit further rapid growth. In this sense, tumor angiogenesis is a mechanism by which "successful" tumors escape the growth restriction imposed upon three-dimensional cell population by geometry [49].
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PMID:Influence of geometry on control of cell growth. 76 36

We tested fresh amelanotic and dry amelanotic melanoma tissue, gelatin, embryo and adult connective tissue, fresh and dry liver, fibrinogen, fibrin, pouch membrane, starch, dry hamster embryo and placental tissue, and glycogen in the transparent cheek pouch chamber of the Syrian hamster to explore the specificity of tumor angiogenesis and the mechanism that may selectively inhibit proliferation of blood vessels in the pouch membrane. Differences between the proliferations induced by tumor and normal tissues, various proteins, and polysaccharides were qualitative as well as quantitative. The glucocorticoid 6 alpha-methylprednisolone (MPS) decreased and sometimes totally inhibited the vascularization phenomenon. Dry tumor tissue induced capillary proliferation in seven of eight chambers 3 days after surgery; two of seven chambers of MPS-treated animals showed a reaction 10 days after the operation. MPS suppressed (in some cases only partially) capillary proliferation in chambers with implants of adult connective tissue, fresh liver, starch, or glycogen.
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PMID:Vascularization induced in the cheek pouch of the Syrian hamster by tumor and nontumor substances. 79 99

Adult rabbit retinal vessels underwent neovascularization in response to tumor implantation within the vitreous body. The neovascular response was presumably elicited by the tumor angiogenesis factor (TAF). The response of adult retinal vessels to an angiogenic stimulus raises the possibility that a similar substance may cause retinal neovascularization in humans, and that in normal conditions the vitreous may be able to suppress angiogenic activity.
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PMID:Experimental retinal neovascularization induced by intravitreal tumors. 86 66

Capillary proliferation induced by tumor is shown to be inhibited by neonatal scapular cartilage. Using the rabbit cornea as an assay, the cartilage implant decreased the rate of capillary growth, induced by tumor, by an average of 75%. Vascularization was prevented completely in 28% of tumors. The inhibitory effect of small cartilage implants operates over distances of up to 2.0 mm and displays a gradient from the cartilage source. The experiments suggest that the cartilage inhibitor does not antagonize tumor angiogenesis factor, but appears to inhibit capillary proliferation directly. The inhibitory material does not elicit an inflammatory response in either the rabbit cornea or in the chick chorioallantoic membrane. Thus with further purification, it may prove useful as a means of maintining tumor dormancy by "antiangiogenesis."
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PMID:Inhibition of tumor angiogenesis mediated by cartilage. 111 64

A "rod-shaped tubulated body" (tubular body) was first described by Weibel and Palade in the vascular endothelial cells of various organs in both man and animals. This is now considered to be an organelle specific to the endothelial cell, but its function is still unknown. Both in experimental and human pathology this organelle has been observed more often in either seemingly young or abnormal endothelial cells of the blood vessels in tissue regeneration, inflammation, brain tumors among others. This report deals with ultrastructural study of two surgical cases of cerebellar neoplasm, in which the vascular endothelium was examined for a tubular body. The first case was a 12-year-old boy with cerebellar hemangioblastoma, and the second a 36-year-old female who had a history of renal cell carcinoma removed approximately 5 years previously. Histological diagnosis of the cerebellar tumor in the latter case was indetermined, because a part of the tumor consisted of clear cells suggestive of clear cell carcinoma and another part of well developed endothelial cells and vascular channels apparently indicative of hemangioblastoma. The findings of the ultrastructural study were rather compatible with that of renal cell carcinoma metastatic to the cerebellum although inconclusive. The tubular body observed in the endothelial cells of those tumor vessels consisted of a membrane-limited round, oval or elongated shaped intracytoplasmic body which contained tubules of 170 to 200 A outer diameter with approximately 50 to 60 A thickness. The tubules were arranged mostly in a parallel fashion along their long axis. In the first type of tubular body they were embedded in a relatively pale matrix, and in the second their arrangement appeared to be more compact. The third tubular body, so far undescribed in human endothelial cells except in our previous communication, showed an irregularly and markedly enlarged matrix, surrounded by a limiting membrane which was occasionally observed connected with either a coated vesicle or cytoplasmic membrane. Abundant tubules were intermingled without showing a particular arrangement. Morphological and functional significance of the third type tubular body is unknown, but it might represent a pathological change of a tubular body in cerebellar neoplasms. These findings might give us some clues in understanding a tumor angiogenesis.
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PMID:[A specific organelle in the vascular endothelial cells of cerebellar neoplasms (author's transl)]. 123 7

Normal, viral transformed and tumor-derived cells grown in tissue culture and representing different species were tested for their ability to produce an extracellular tumor angiogenesis factor (TAF). TAF was assayed by measuring the host-mediated vascular response of the chorioallantoic membrane to TAF preparations. All of the viral transformed and tumor-derived cells tested, including SVT2, SVW126, Welker 256 rat carcinoma, B-16 mouse melanoma, human glioblastoma, and human meningioma cells, produced TAF. The potency of the TAF preparations, as measured by the number of cells needed to induce a positive vascular response on the chorioallantoic membrane, varied from cell line to cell line. The most potent cells tested were the glioblastoma and maningioma brain tumor cells. Since these brain tumors are found to be the most highly vascularized tumors in vivo, it was concluded that a correlation exists between the vascularity of a tumor in vivo and the potency of TAF in vitro. There was no detectable angiogenesis activity induced by density-inhibited BALB/c primary mouse embryo or early-passage human skin fibroblasts, even when relatively large numbers of cells were used to make a sample. However, density-inhibited BALB/c 3T3 aan W138 human embryonic lung fibroblasts, two cell lines widely regarded as demonstrating "normal" growth behavior in culture, produced TAF. From these and other observations, it was suggested that BALB/c 3T3 and W138 are not fully "normal" cells. Furthermore, it was suggested that the production of TAF is an early event in the cell transformation process that precedes the loss of density inhibition of growth in vitro.
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PMID:Tumor angiogenesis activity in cells grown in tissue culture. 124 90

In this paper we present a simple mathematical model that adequately accounts for at least the initial vasculature that is established in a melanoma transplant. It is assumed that the tumor produces a substance (tumor angiogenesis factor--TAF) that elicits capillary sprouts from the vascular bed of the host. These sprouts then invade the tumor along the gradient of TAF and cross-connect forming a vascular pathway that is similar to the experimental patterns observed in a hamster cheek pouch. This model is then extended to include the migration of loops. The rupture and formation of sprouts from these loops is assumed to depend on the strength of the stimulus (TAF). Under the assumption that the production of TAF is significantly reduced in a neighborhood of an established vessel, the network formed by the vessels in the tumor corresponds to the observed arboreal patterns.
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PMID:Model for initial vascular patterns in melanoma transplants. 127 14


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