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

The effect of "antiangiogenesis" therapy using cortisone acetate (CA) with or without heparin on tumor growth as well as in combination with chemotherapy was investigated. C3H mice were implanted intradermally with N-[4-(5-nitro-2-furyl)-thiazolyl]formamide induced undifferentiated transitional cell carcinoma, MBT-2, in the right flank. The treatment was initiated 9 to 10 days after tumor inoculation. Daily injections of CA (250 mg/kg s.c.) suppressed tumor growth significantly in a dose dependent fashion. Administration of heparin (Elkins-Sinn) at the concentration of 200, 400, or 1000 units/ml in drinking water for 3 to 6 days was neither additive nor detrimental to the effect of CA. Chemotherapy was combined with CA; 3 days of administration of 250 mg/kg of CA in tapering doses was used. The chemotherapeutic agent was injected once 24 h before the initial CA. Combinations of chemotherapy (Adriamycin, 2.5-7.5 mg/kg i.v; cisplatin, 3-9 mg/kg i.p.; cyclophosphamide, 50-150 mg/kg i.p.; cis-(diammino)(1,1-cyclobutanedicarboxylate)platinum(II) (JM-8), 60-150 mg/kg i.p.; mitomycin C, 3-4.5 mg/kg i.p.) with CA showed additive suppression of tumor growth. Mice tolerated chemotherapy alone, CA alone, and both in combination. CA combined with JM-8 was not tolerated. Mice tolerated 100 to 150 mg/kg of JM-8, whereas the addition of CA to JM-8 resulted in a 66% (6 of 9) to 89% (8 of 9) mortality rate. CA at a concentration of 5 and 25 micrograms/ml showed no direct cytotoxic activity against MBT-2 cells in vitro. However, 3 days of administration of 250 mg/kg of CA inhibited tumor angiogenesis generated by MBT-2 cells in C3H mice using a dorsal air sac assay. The data suggest that CA alone inhibits tumor angiogenesis in C3H mice and that antiangiogenesis therapy enhances the antitumor efficacy of chemotherapeutic agents without increasing host toxicity (except for JM-8).
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PMID:Efficacy of antitumor chemotherapy in C3H mice enhanced by the antiangiogenesis steroid, cortisone acetate. 244 60

Tumor angiogenic activity (TAA) from tumor angiogenesis factor (TAF), produced by 24 cell lines of various kinds of gynecologic tumors, was assayed onto chorioallantoic membranes (CAMs) of chick embryos. Methylcellulose (1%) pellets containing 1 x 10(7) cells were placed on 8-day-old postfertilized CAMs, and the grade of neovascularization was assayed 3 days after inoculation. Neovascularization occurred prominently in such cell lines, as HTBOA (poorly differentiated ovarian carcinoma), HUOCA-II (poorly differentiated clear cell adenocarcinoma), HWUA (poorly differentiated endometrial adenocarcinoma), and in HKUS (uterine cervical small cell carcinoma); however, neovascularization did not occur in SNK (uterine leiomyosarcoma line). The cell lines which secreted TAF showed high heterotransplantability in the nude mice and produced rapidly growing tumors which were rich in blood vessels. However, the SKN line which did not secret TAF was not transplantable. These results suggested that there was a close relationship among TAA, transplantability, and tumor growth rate.
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PMID:Tumor angiogenic activity of gynecologic tumor cell lines on the chorioallantoic membrane. 244 91

The development of permanent cell lines of human head and neck squamous cell carcinoma in culture has enabled these cell lines to be used to investigate the interaction of the tumor cells with bone. After the squamous carcinoma lines on fetal rat skulls were implanted the explants with their added tumor were maintained in long-term tissue culture by use of the procedures developed for growing these tumor cells. Results confirm direct interaction with the bone by the malignant cells. Specific surface and cytoplasmic markers have been demonstrated by use of monoclonal antibodies against the tumor cells. Furthermore, tumor angiogenesis without the addition of any endogenous endothelial components has been verified. Investigations into the degree of bone infiltration and susceptibility of these interacting tumor cells to various factors, radiation therapy, and chemotherapeutic agents have been carried out. The establishment of a model system for bony invasion by squamous cell carcinoma of the head and neck permits the investigation of the mechanism of tumor invasion and the study of various potential treatment modalities.
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PMID:An organ culture system designed to study interaction of fetal rat calvaria with human head and neck squamous cell carcinoma. 245 Dec 1

A model for the study of tumor angiogenesis within the rabbit brain is presented. Implantation of the VX2 carcinoma provides a reproducible tumor accompanied by angiogenesis. The authors report the sequential growth, histology, tumor neovascularization, and vascular permeability of this tumor following its intracerebral implantation. Tumor angiogenesis correlates with the rapid and logarithmic intracerebral tumor growth. The proliferation of blood vessels in the tumor and the organization of tumor cells around tumor vessels are described. Breakdown of the blood-brain barrier (detected by Evans blue leakage) starts in the early stages of tumor development and becomes prominent as the tumor vasculature and size increase. This model is useful for experimental studies of angiogenesis.
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PMID:Neovascularization and tumor growth in the rabbit brain. A model for experimental studies of angiogenesis and the blood-brain barrier. 245 89

The role of host mast cells in tumor-associated angiogenesis was investigated by comparing the angiogenic response of genetically mast-cell-deficient W/Wv mice and mast-cell-sufficient +/+ littermate mice to s.c. growing B16-BL6 tumors. The angiogenic response was found to be slower and initially less intense in W/Wv mice than in +/+ mice. Fewer W/Wv mice than +/+ mice developed spontaneous lung metastases and W/Wv mice exhibited fewer lung metastases per mouse. Bone-marrow repair of the mast-cell deficiency restored the angiogenic response of W/Wv mice and also restored the incidence of hematogenous metastases to approach that of +/+ mice. Differences in lymphatic metastasis were not detected between W/Wv and +/+ mice. These results demonstrate a role for mast cells in vivo during tumor angiogenesis, and suggest a role also for host mast cells in hematogenous metastasis.
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PMID:Mast-cell-deficient W/Wv mice exhibit a decreased rate of tumor angiogenesis. 245 91

The role of host-tumor interactions in tumor angiogenesis was studied in an id mouse model. Although many previous studies have described the effects of certain host factors (age, nutritional status, tumor location, etc.) on experimental tumor systems, the effects of these factors on tumor angiogenesis have not been reported. In preliminary studies we inoculated cloned tumor cells id into syngeneic mice and found positional differences in tumor growth that did not correlate with measured angiogenesis levels. In addition, while tumor growth was inhibited by radiation, tumor-induced (but not fibroblast-induced) angiogenesis was not. This id system may provide an assay not only for examining the effect of host factors on tumor angiogenesis, but also for elucidation of the mechanisms underlying neovascular induction and host response.
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PMID:Investigation of tumor angiogenesis in an id mouse model: role of host-tumor interactions. 245 11

Significant proliferation of capillaries with hyperplastic vascular endothelium is one of the characteristic histologic features of glioblastoma multiforme (GBM). It has been shown that the renin-angiotensin II cascade stimulates new vessel formation. The presence of renin in several types of highly vascularized neoplasm suggests that it may also be implicated in the mechanism of tumor angiogenesis. In order to study the possible relationship of renin to GBM, immunohistochemical search for human renin was carried out in ten instances of such a tumor. Eight of these cases demonstrated renin-containing neoplastic astrocytes, whereas seven cases of reactive gliosis and six cases of low-grade astrocytoma revealed no renin-containing cells. The immunostaining was not present after preabsorption of the renin antiserum with pure human renin or substitution of preimmune serum for the specific renin antiserum. Because it has also been demonstrated that a product of renin, angiotensin II, has angiogenic properties, it seems reasonable to postulate that renin, through angiotensin II, may play a role in the mechanism of GBM-associated neovascularization.
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PMID:Renin in glioblastoma multiforme and its role in neovascularization. 245 55

Tumor stroma formation results from the interaction of tumor cells and their products with the host and certain of its normal defense mechanisms, particularly the clotting and fibrinolytic systems. It is a process in which tumor cells render local venules and veins hyperpermeable with the result that fibrinogen and other proteins extravasate and clot, forming an extravascular crosslinked fibrin gel. Coagulation is mediated by an interaction between extravasated plasma clotting factors and tumor-associated and perhaps other tissue procoagulants. Parallel activation of the fibrinolytic system leads to substantial fibrin turnover, but fibrin nonetheless accumulates in amounts, variable from tumor to tumor, that are sufficient to provide a provisional stroma. This provisional stroma imposes on tumor cells a structure that persists even as tumor cells multiply and as the fibrin provisional stroma is replaced by mature connective tissue. The provisional fibrin stroma also serves to regulate the influx of macrophages, and perhaps other inflammatory cells, but at the same time, and in ways that are not fully understood, facilitates the inward migration of new blood vessels and fibroblasts, integral components of mature tumor stroma. Ascites tumors differ from solid tumors in that fibrin gel is not ordinarily deposited in body cavities and, as a result, there is no provisional stroma to impose an initial structure. Tumor stroma generation resembles the process of wound healing in many respects. However, it differs in the mechanism of its initiation, and in the apparent lack of a role for platelets. It also differs fundamentally in that invading tumor cells continually render new vessels hyperpermeable to plasma, thus perpetuating the cycle of extravascular fibrin deposition. In this sense, tumors behave as wounds that do not heal. Largely neglected in this review has been discussion of the numerous cytokines, mitogens, and growth factors that are widely believed to play important roles in tumor angiogenesis and wound healing; i.e., PDGF, FGF, EGF, TGF alpha, TGF beta, TNF, interferons, etc. This omission has been intentional, and for two reasons. First, these cytokines have already received considerable attention [100,123-128]. Second, it is not yet clear how closely the actions of these molecules, as described in vitro, relate to their functions in vivo. At present we are deluged with a surfeit of factors that have the capacity to induce new blood vessel formation in angiogenesis assays; these factors include not only peptides but lipids and even ions [126,129-131].(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathogenesis of tumor stroma generation: a critical role for leaky blood vessels and fibrin deposition. 246 81

The growth of the C3H mouse mammary tumor (MMT) is considered to be hormone independent. Medroxyprogesterone acetate (MPA) had no effect on the growth of transplanted autochthonous MMT or the colony-formation of MMT cells. The tumor angiogenesis factor (TAF) activity of tumor-extract prepared from C3H mouse with transplanted autochthonous MMT and injected with 0.67 mg of MPA (in vivo MPA group) and that prepared from the colony of MMT cells treated with 10(-6) M MPA (in vitro MPA group) was lower (100.0% and 9.8%) than those of the in vivo and in vitro cortisol groups (325.5% and 44.3%), and the in vivo and in vitro groups without treatment (393.5% and 46.8%), respectively. The fibroblast growth factor (FGF) activity of the in vivo and in vitro MPA groups was lower (23.7% and 2.7%) than those of the in vivo and in vitro cortisol groups (54.7% and 11.3%), and the in vivo and in vitro groups without treatment (49.6% and 11.3%), respectively. Therefore, MPA may reduce neovascularization induced by TAF and FGF, although it had no effect on the growth of this MMT, and it had a glucocorticoid action similar to that of cortisol.
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PMID:Inhibition of tumor angiogenesis activity in C3H mouse mammary tumor by medroxyprogesterone acetate. 246 26

More than 30% of the colony formation of dispersed tumor cells was inhibited by medroxyprogesterone acetate (MPA) in 2 out of 6 cases of endometrial cancer, in 1 out of 6 cases of cervical cancer, and in 3 out of 12 cases of ovarian cancer. The colony formation inhibited by MPA was not related to clinical stage or histological type. There was no significant difference in the tumor angiogenesis factor (TAF) activity of any case of endometrial, cervical and ovarian cancer between the cortisol-treated group and the controls. TAF activity was inhibited by MPA in 4 out of 6 cases of endometrial cancer, in 5 out of 6 cases of cervical cancer, and in 9 out of 12 cases of ovarian cancer. There was no significant difference in the fibroblast growth factor (FGF) activity of any case of endometrial, cervical and ovarian cancer between the cortisol-treated group and the controls. FGF activity was inhibited by MPA in 3 out of 6 cases of endometrial cancer, in 5 out of 6 cases of cervical cancer, and in 10 out of 12 cases of ovarian cancer. The cases in which the colony formation was inhibited by MPA were not related to the cases in which TAF or FGF activity was inhibited by MPA. Therefore, MPA may reduce neovascularization induced by TAF and FGF, and can depress secondary spreading of some endometrial, cervical and ovarian cancer via the mechanism of terminal process of secondary spreading, regardless of the presence of glucocorticoid actions similar to that of cortisol, and the reduction of cell proliferation.
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PMID:Inhibition of tumor angiogenesis activity by medroxyprogesterone acetate in gynecologic malignant tumors. 247 53


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