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

A method is reported for the study of early phases of neovascularization in syngeneic murine tumors and human tumor xenografts in nude mice. Using this method, the effect of irradiation of tumor cells or tumor bed on tumor angiogenesis was studied. Tumor cells were injected intradermally in the abdominal skin flap, which was reopened at 2-day intervals to quantify newly formed blood vessels at the site of tumor cell injection. Both tumor cell injection and blood vessel counting were performed under a dissecting microscope. Using three syngeneic murine tumors and two clones of a human colonic adenocarcinoma, it was observed that new blood vessels started appearing within a few days after tumor cell injection and that this event preceded measurable tumor growth. The number of blood vessels increased exponentially for several days but then their further growth slowed. The extent of angiogenesis depended on the tumor type and the number of tumor cells injected. The exposure of the skin flap to ionizing radiation prior to tumor cell injection reduced neovascularization. We further observed that heavily irradiated tumor cells retained their ability to induce angiogenic response and that lymphoid cells (peritoneal exudate and spleen cells) could also elicit an angiogenic response, although it is weaker than the response elicited by tumor cells. Thus this method is suitable for quantification and kinetics of early phases of tumor angiogenesis in individual mice bearing transplants of syngeneic tumors or human tumor xenografts, and it can be useful for investigating various regulators of tumor angiogenesis.
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PMID:An intradermal assay for quantification and kinetics studies of tumor angiogenesis in mice. 170 92

This study was undertaken to reveal the neovascularization at early stages of splenic autografts three-dimensionally, to illustrate the differences between it and tumor angiogenesis, and to establish its origin. Early vascular formation after transplantation of the rat spleen or Walker tumor into the major omentum was examined by using a video macroscope, vascular casting methods and the organ culture technique. A complex vascular network layer (vascular cortex) was first formed beneath the capsule of an autograft; later, vascular buds grew from this network toward the necrotic center. They anastomosed and changed into a form resembling withered twigs (vascular medulla). Tumor angiogenesis did not present such morphological features and was characterized by capillary loop formation with a columnar vertex resembling an "inverted V". This fundamental structure did not change throughout angiogenesis except for dilation and irregularity of vascular diameter. The organ culture technique demonstrated that the preliminary vasculature was formed in splenic autografts by regeneration of preexisting vessels in the graft and not by invading capillaries. Transmission electron microscopy showed that the cells present had characteristics of sinus endothelial cells. These results suggest that preexisting sinus endothelial cells rearrange themselves after devascularization and reconstruct a new vasculature that anastomoses with the penetrating capillaries. This mechanism establishes vascular circulation at an early stage, and accelerates regeneration of the splenic autograft before complete necrosis.
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PMID:Morphological analysis of neovascularization at early stages of rat splenic autografts in comparison with tumor angiogenesis. 172 29

Vascular permeability factor (VPF) is a highly conserved 34-42-kD protein secreted by many tumor cells. Among the most potent vascular permeability-enhancing factors known, VPF is also a selective vascular endothelial cell mitogen, and therefore has been called vascular endothelial cell growth factor (VEGF). Our goal was to define the cellular sites of VPF (VEGF) synthesis and accumulation in tumors in vivo. Immunohistochemical studies were performed on solid and ascites guinea pig line 1 and line 10 bile duct carcinomas using antibodies directed against peptides synthesized to represent the NH2-terminal and internal sequences of VPF. These antibodies stained tumor cells and, uniformly and most intensely, the endothelium of immediately adjacent blood vessels, both preexisting and those newly induced by tumor angiogenesis. A similar pattern of VPF staining was observed in autochthonous human lymphoma. In situ hybridization demonstrated VPF mRNA in nearly all line 10 tumor cells but not in tumor blood vessels, indicating that immunohistochemical labeling of tumor vessels with antibodies to VPF peptides reflects uptake of VPF, not endogenous synthesis. VPF protein staining was evident in adjacent preexisting venules and small veins as early as 5 h after tumor transplant and plateaued at maximally intense levels in newly induced tumor vessels by approximately 5 d. VPF-stained vessels were also hyperpermeable to macromolecules as judged by their capacity to accumulate circulating colloidal carbon. In contrast, vessels more than approximately 0.5 mm distant from tumors were not hyperpermeable and did not exhibit immunohistochemical staining for VPF. Vessel staining disappeared within 24-48 h of tumor rejection. These studies indicate that VPF is synthesized by tumor cells in vivo and accumulates in nearby blood vessels, its target of action. Because leaky tumor vessels initiate a cascade of events, which include plasma extravasation and which lead ultimately to angiogenesis and tumor stroma formation, VPF may have a pivotal role in promoting tumor growth. Also, VPF immunostaining provides a new marker for tumor blood vessels that may be exploitable for tumor imaging or therapy.
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PMID:Distribution of vascular permeability factor (vascular endothelial growth factor) in tumors: concentration in tumor blood vessels. 194 Aug 5

An understanding of the mechanisms responsible for tumor-associated edema involves the elucidation of the role played by a number of intra-related processes. These include (i) the permeability of new tumor microvessels that are associated with tumor angiogenesis; (ii) alterations in microvascular permeability due to factors secreted by tumor cells; (iii) immunological mechanisms and (iv) increased microvessel permeability associated with inflammation. The rationale for a role for inflammatory processes in tumor-associated edema has been outlined and the role of non-steroidal anti-inflammatory drugs in modulating experimental and human tumor-associated edema has been explored.
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PMID:Mechanisms of tumor-associated edema: a review. 219 88

Tumor angiogenesis is a very important process for growth and proliferation of most solid tumors. It insures the delivery of feeding molecules as well as the elimination of degradation products and allows tumoral cells to escape from the primary tumor site and the further establishment of metastases. Tumor neovascularisation is the result of a cascade of events primarily related to the properties of endothelial cells of capillaries. The main steps are: a) degradation of capillary basal lamina and destruction of the surrounding tissues, b) endothelial cell proliferation and c) endothelial cell migration towards the tumor site. A number of substances either synthetic or of natural origin are known to stimulate one of the above mentioned steps and/or to induce the production of factors which, in turn, stimulate one or several steps of the cascade. Such molecules can also be synthesized by tumoral cells; indeed they have often been evidenced in the fluids surrounding the tumor site. Many factors remain to be identified and their mechanism of action wait to be elucidated. However, it is already clear that several molecules are involved in the various steps of tumor angiogenesis. They display a coordinated sequential action and their synthesis is induced and controlled by the tumor itself. Amongst others, the following molecules play a role in tumor angiogenesis: degradative enzymes, E-prostaglandins, specific oligopeptides, fibronectin and heparin. Furthermore, several metal cations are also involved in tumor angiogenesis.
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PMID:[Tumor angiogenesis]. 242 24

Implantation of human renal adenocarcinoma in the rabbit cornea has resulted in new vascular growth from the limbus toward the tumor implant. This suggests that renal adenocarcinoma elaborates tumor angiogenesis factor (TAF) which stimulates endothelial cell growth. Such a substance could conceivably be responsible for the luxuriant vascularity of most renal adenocarcinomas. Conversely, absence or diminished secretion of TAF may be responsible for the hypovascular papillary renal adenocarcinomas and their recognized relatively benign clinical behavior.
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PMID:Detection of tumor angiogenesis factor in adenocarcinoma of kidney. 242 3

The release of prostaglandins from tumor cells seems to play an important role in tumor angiogenesis, in which platelet-derived factors may be also included. Administration of prostaglandin synthetase inhibitors reduces the growth of both experimental and human malignant tumors. One explanation may be reduced tumor vascularization, as observed in microangiographic studies of experimental transplantable tumors. A similar effect was observed after induced thrombocytopenia. A number of angiogenesis stimulating factors have been isolated from tumors during recent years. Factors released from host cells in the tumor area (e.g., mast cells, macrophages) with similar properties may also contribute to tumor vascularization. This seems to make stimulation of tumor angiogenesis to a rather complicated cascade of events, about which more must be learned before efficient inhibition of tumor vascularization can be attained. The target cell for angiogenesis stimulation, the endothelial cell, seems increasingly important as an object for future studies.
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PMID:Tumor angiogenesis inhibition by prostaglandin synthetase inhibitors. 242 14

We analysed the growth pattern of metastases in C3H-mice produced by i.v. injection (tail vein) of tumor cell suspensions of mammary carcinoma HB. Although the ordinary Gompertz equation generally corresponds well to tumor growth in animals and men, we found it inadequate to describe the growth of lung metastases in our model. The morphometric analysis and growth kinetics (LI/GF) of the metastases show a biphasic pattern. The first phase is characterized by a strictly avascular growth and nutrition by diffusion, the second phase is initiated by tumor angiogenesis. To analyze these observations we developed a new mathematical equation which fits particularly well to the metastatic growth curve. We conclude that the present model is appropriate for the analysis of tumor angiogenesis, especially to study factors, which influence the development of a tumor specific vascular system.
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PMID:A mathematical model for metastatic growth illustrated by in vivo and in vitro growth of a transplantable mammary carcinoma in mice. 242 82

The growth of five different kinds of human choriocarcinoma cell lines in vitro was quite alike. However, two distinct types of rapid and slow growth were observed in tumors grown in the hamster cheek pouch. The rapidly grown tumor tissues (BeWo, JEG-3, and NUC-1) involved significantly large numbers of blood vessels per microscopic field, as compared to slowly grown ones (SCH and HM). The vascular response was assayed using cell-free crude tumor angiogenesis factors (TAF) on chorioallantoic membrane (CAM) of the chick embryo. In all cell lines TAF activity correlated well with the extent of tumor growth in vivo. Gel filtration analysis showed that relatively high-molecular-weight (more than 10,000) factors could induce neovascularization in the both assays using CAM and rabbit cornea. These results suggest that a heterogeneity of TAF activity is present among human choriocarcinoma cell lines and tumor growth in xenograft depends on the secretion of TAF by the tumor cells themselves.
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PMID:Tumor angiogenesis activity of human choriocarcinoma cells grown in vitro. 243 Aug 62

The effect of tumor necrosis factor (TNF) on the tumor-induced endothelial migration was evaluated with the use of a phagokinetic track assay. TNF from both ddy mice and Japanese albino rabbits (sp act, 3-5 X 10(5) U/mg, respectively) was found to inhibit the migration of bovine capillary endothelial (BCE) cells stimulated by factors from tumor cells, such as the medium conditioned with mouse sarcoma 180 cells or human meningioma extract. These TNF preparations, however, did not affect the spontaneous migration of the BCE cells. When mouse TNF was further fractionated by polyacrylamide gel electrophoresis, only TNF-positive fractions showed an inhibitory activity on the tumor-induced endothelial motility. Moreover, monoclonal antibody against rabbit TNF completely neutralized its migration-inhibitory activity. These findings indicate that the observed inhibitory effect of TNF preparations on the endothelial motility evoked by tumor is exclusively ascribed to the function of TNF. This activity presumably is involved in the suppression of tumor angiogenesis in vivo.
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PMID:Inhibition of tumor-induced migration of bovine capillary endothelial cells by mouse and rabbit tumor necrosis factor. 243 5


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