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Results for “SARCOMA, FIBROSARCOMA”

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At least 1,603 records · Page 89Linked to original sources
PubMed1979

Cell-associated proteases affect tumour cell migration in vitro.

The in vitro migratory activity of mouse fibrosarcoma cells in medium containing either foetal calf serum or normal human serum was studied. These 2 sera were studied because foetal calf serum contains high levels of protease inhibitor activity while human serum contains much less. The cells migrated actively in medium with foetal calf serum but migration was greatly inhibited in human serum-containing medium. When protease inhibitors such as soybean trypsin inhibitor, lima bean trypsin inhibitor and bovine pancreas trypsin inhibitor were added to human serum-containing medium cell migration was supported almost as effectively as in medium with foetal calf serum. Addition of epsilon-amino-n-caproic acid to human serum or depletion of the plasminogen from human serum did not enable it to support enhanced migration. epsilon-amino-n-caproic acid actually inhibited migration. A variant cell population with elevated levels of caseinolytic activity and elevated levels of activity against the substrate n-acetyl-DL-phenylalanine-beta-naphthyl ester (a substrate specific for chymotrypsin-like enzymes) was isolated from the parent cells. When the variant cells were compared to the parent cells regarding migratory activity in foetal calf serum or human serum-containing medium, the variant cells showed much less activity. Only a few, widely scattered variant cells migrated in the human serum-containing medium. These data suggest that a cell-associated factor interferes with the migration of the cells in medium with human serum. This factor apparently is neutralized in medium sontaining human serum to which protease inhibitors with antitrypsin activity have been added.

Animals↗
PubMed1975

A comparison of the effects of radiation on tumour growth delay and cell survival. The effect of radiation quality.

Measurements have been made of the effects of 250 kV X-rays and cyclotron produced neutrons on the delay in growth of a rat fibrosarcoma (RIB5C) and on tumour cell survival assayed in vitro after irradiation in vivo. For doses above 300 rads of neutrons the RBE for cell survival was greaer than that for tumour growth delay. This may be due to X rays causing a greater delay in cell proliferation than neutrons for a given level of cell survival. This would be the opposite effect to that found by BBarendsen and Broerse (1969), irradiating a rat rhabdomyosarcoma. Another possibility is that meassurements of cellular radio-sensitivity which involve removal of cells from their normal environment may lead to incorrect estimates of cell survival in situ. A plot of the RBE for growth delay against the reciprocal of the neutron dose indicated that the dose level at which the RBE became dependent on the fraction of hypoxic tumour cells was larger than that for cell survival, indicating a smaller "effective" hypoxic fraction than that estimated from the cell-survival curves.

Animals↗
PubMed1978

The therapeutic advantage of combined heat and X rays on a mouse fibrosarcoma.

The response of an experimental fibrosarcoma to combined heat and X rays has been assessed using delay in tumour regrowth. No thermal sensitization was observed for one hour of heating at 41.5 degrees C. A thermal enhancement ratio of 1.4 to 1.5 was seen for one hour of heating at 42.5 or 43.5 degrees C immediately after irradiation. The importance of the sequence and time interval between the two modalities was tested using a constant heat treatment of 42.5 degrees C for one hour. Heating was most effective when given after irradiation, with little change in TER for an interval of a half to six hours. When heat preceded the irradiation the pattern was more complex, with no sensitization at half, one, and six hours, but with a significant effect at two and three hours. The degree of sensitization often depended upon the X-ray dose, being lower below X-ray doses of about 20 Gy. The therapeutic advantage of the combined treatment was assessed by comparison with previously published results for skin reactions. No therapeutic benefit was found for treatments when heat and X-rays were separated by one hour or less. A therapeutic gain factor of about 1.3 was observed for heat given two to six hours after irradiation of this fibrosarcoma.

Animals↗
PubMed1980

Fractionation studies with combined X rays and hyperthermia in vivo.

The combined effects of single and fractionated doses of X rays and local heat were investigated using an experimental fibrosarcoma and normal mouse skin. Thermal enhancement ratios were measured from pairs of dose-response curves for both tumour and skin, and the therapeutic advantage of each treatment was then assessed by comparing the enhancement for tumour and skin. For single doses there was a therapeutic advantage when heat was applied three hours after X rays but not with heat applied immediately after irradiation. For two and five daily fractions with heat immediately after irradiation there was significantly less thermal sensitization in tumour than in skin; hence there was a therapeutic loss. When heat was applied at three hours after each fraction there was no thermal sensitization in either skin or tumour; the therapeutic ratio was therefore 1.0. The repair capacity of skin after fractionated X rays alone, or in combination with heat, was also investigated. Heat immediately after X rays caused a small decrease in the repair capacity between two fractions but no decreased repair capacity was observed with five fractions.

Animals↗
PubMed1981

Thermal resistance in a spontaneous murine tumour.

Resistance to subsequent hyperthermia as a result of prior heating was investigated using a spontaneous murine tumour implanted into the feet of C3H/Sed mice. Tumours were treated by immersing the tumour-bearing foot into a constant-temperature hot water bath set at 45.5 degrees C and were given single and split doses of heat. Response was assessed using a tumour-growth time assay. Three aspects of thermally-induced resistance were particularly considered: the time course of development and decay; the importance of the magnitude of the priming dose and the influence of the size of the tumour at the time of treatment. Substantial resistance was induced in this tumour by short priming doses at 45.5 degrees C, rising rapidly 1-2 days after the first treatment and then starting to decay. There was no significant difference in the kinetics of thermal resistance induced in tumours treated at 4mm and those treated at 8 mm in size, although the large tumours were more sensitive to single doses of heat. Increasing the magnitude of the priming dose of heat resulted in an increase in the magnitude of resistance to the second dose. The results of this study are compared with results of similar studies in this and other laboratories using murine normal tissues and cells in culture. Possible clinical implications are considered.

Animals↗
PubMed1983

The dielectric properties of normal and tumour mouse tissue between 50 MHz and 10 GHz.

Microwaves are currently being investigated as a method of inducing hyperthermia. Values of the relative permittivity and conductivity of mouse muscle and tumour tissues over the frequency range 50 MHz to 10 GHz at a temperature of 37 degrees C are reported. The data were obtained by using an on-line computer-based time-domain spectrometer. The tumour tissues were the RIF/1 and KHT fibrosarcomas sited in the hind leg muscle of C3H mice. A significant difference in the relative permittivity between the normal and tumour tissue was shown to exist at frequencies up to 200 MHz.

Animals↗
PubMedDate not supplied

A phase I clinical trial evaluating imatinib mesylate (Gleevec) in tumor-bearing cats.

A phase I clinical trial evaluating the toxicity of orally-administered imatinib mesylate was performed in 9 tumor-bearing cats. Imatinib is a small molecule, tyrosine kinase inhibitor, which selectively blocks the function of overexpressed proteins associated with various malignancies. Cats included in the study had diagnoses of fibrosarcoma, squamous cell carcinoma, and mast cell tumor, and each cat was staged using CBC and serum biochemistry; urinalysis, thoracic radiographs, and abdominal ultrasonography were performed in some cats. Most cats were treated previously by surgery, radiation therapy, chemotherapy, or some combination of these treatments. None of the cats received any concurrent chemotherapy. Six cats were treated with imatinib mesylate at 1-2 mg/kg PO q24h. Dose escalations were made to 2, 4, and 10 mg/kg PO q24h in 5 cats. Two cats started therapy at 10 mg/kg PO q24h, and 1 cat started therapy at 15 mg/kg PO q24h; all 3 cats remained at these dosages. No signs of toxicity, as evaluated by CBC and serum biochemistry, were noted in 8 of the 9 cats, and minimal gastrointestinal toxicity was observed. Due to the low frequency of adverse effects, further evaluation of imatinib is ongoing at a dosage of 10 mg/kg PO q24h.

Animals↗
PubMed1975

Correlation of in vitro immune response with clinical course of malignant neoplasia in dogs.

An attempt was made to quantify the host antitumor immune response in 16 dogs with progressively growing tumors by evaluating the in vitro reactivity of their lymph node or peripheral blood lymphocytes to their own tumor cells. Serum from dogs with the same histologic type of neoplasm inhibited allogenic lymphocyte cytotoxicity, whereas serum from normal dogs, and a dog clinically free of osteosarcoma 17 months after limb amputation, did not significantly block cell-mediated reactivity. Low ratios of sensitized lymphocytes to tumor cells often stimulated tumor cell growth in vitro. Autologous serum from dogs with progressively growing neoplasms appeared to potentiate the stimulation of tumor growth above a simple blocking of lymphocyte-mediated cytotoxicity. An attempt was made to correlate the in vitro immune reactivity of the dog to the clinical behavior of its neoplasm. There was fair to good correlation in 12 dogs and no correlation in the remaining 4 dogs.

Animals↗
PubMed1975

Malignant transformation of mouse cells by cigarette smoke condensate.

A low-nicotine cigarette smoke condensate, 12 fractions of the condensate, and a reconstituted sample were tested for their ability to induce transformation in the mouse cell line 3H/10T-1/2 CL-8. This cell line is noted for its remarkable low spontaneous rate of transformation. Both the crude condensate and the reconstituted sample as well as two specific fractions induced transformation in the mouse cells. These transformed cells produced fibrosarcomas when injected s.c. into antithymocyte serum-treated syngeneic mice.

Animals↗
PubMed1975

Carcinogenesis from polyurethans.

Seventeen polyurethans, containing various substituent groups, and a polyethylene were implanted i.p. in groups of male black Bethesda rats and were evaluated for carcinogenesis over a 2-year period. Thirteen of the polyurethans and the polyethylene were similarly studied in females. Tumor development in these animals was expressed in terms of the incidence in the at-risk population, and the tumorigenic latent period was approximated for each sample. Twenty months after implantation, the relative tumorigenicity (area under the corrected cumulative tumor mortality versus time curve) in the males ranged from 0 (for the unimplanted controls) to 6.18 (for Y-238); for female rats this range was 0.29 (for unimplanted controls) to 5.72 (for Y-238). Estimated latent periods in the males ranged from 5 months (for Y-304) to 16 months (for Y-303), and 22.5 months for the unimplanted controls; for the females, the range was from 9 months (for Y-290) to 13.5 months (for Y-217), and 14 months for the unimplanted controls. The relative tumorigenicity of each sample was also compared to its in vitro activation energy for thermal decomposition. These data are discussed in terms of solid-state versus chemical carcinogenesis.

Animals↗
PubMed1975

Accumulation of mononuclear cells in tumors with growth slowing and elevation in host splenic histidine decarboxylase activity following repeated tumor injections with bradykinin.

Repeated intratumor injections of SV-40 virus-induced and transplaned syngenic fibrosarcomsa in hamsters with bradykinin (BK) has produced markded slowing of tumor growth in comparison with control saline injections. Growth slowing was greatest when the injections were daily, with a decrease in growth slowing as injections became less frequent. The growth slowing also was dose dependent (greater with 250 mug BK injections than with 50 mug BK injections). BK-injected tumors, on histological study, were found to have marked infiltration with mononuclear cells. This was not encountered in noninjected or saline-injected tumors. Significant mononuclear cell infiltration of noninjected tumors was found in two tumor animals which had had one tumor injectecd with BK. Splenic histidine decarboxylase (HDC) activity was higher in BK tumor-injected animals than in saline tumor-injected animals. Splenic HDC activity was higher when studed nearer the period of daily intratumor injections. The findings of this study suggest a potential role of inportance for inter-related vasoactive substances which act as mediators of inflammation in the study and therapy of neoplasia.

Animals↗