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At least 19 recordsLinked to original sources

PubMed1978

Studies on Crocker sarcoma 180 under the effect of alkylating agents. IV. Morphological studies of sarcoma 180 during treatment with the antitumour drug cytoxan.

The effect of one massive dose of cytoxan (150 mg/kg), as an alkylating agent, on the morphology of sarcoma 180 cells was followed after 1, 3, 6, 12, 24, 48, 96, 120, and 168 h. After 1 h the cells of treated tumour showed clumping and a decrease in their size. In addition, statistical analysis manifested significant decrease in all phases of mitotic figures. All mitotic figures were completely stopped after 3 h from cytoxan treatment. After 6 and 12 h from cytoxan treatment the hyaline degenerations became more marked in the treated tumour tissue. Chromosomal bridge formation, nuclei aberrations and polynuclear cells were more prominent in 24, 48, and 96 h from cytoxan treatment. Increase in the nuclear size and hyaline degeneration were observed in treated section of 120 and 168 h.

Alkylating Agents↗

PubMed1978

Detection of induced resistance in short-term-tests. Adriamycin-resistant sarcoma 180.

By treatment of the sarcoma 180 (ascites) with adriamycin over 30 passages in NMRI mice, an adriamycin-resistant tumor cell line was developed. The resistance could be detected both in animal experiments and in the short-term test. In spite of treatment of the sarcoma 180 with triaziquone over 50 passages, no resistance could be detected against triaziquone either in the in vitro test or in animal experiments. The necessary criterion for a pretherapeutic test of sensitivity or resistance--a good correlation between in vivo and in vitro results--was fulfilled in all experiments carried out.

Animals↗

PubMed1976

Adenosine phosphyorylase activity as distinct from inosine-guanosine phosphorylase activity in Sarcoma 180 cells and rat liver.

Adenosine phosphorylase (EC 2.4.2.-) activity present in Sarcoma 180 cells grown in culture and in rat liver, is shown to be distinct from inosine-guanosine phosphorylase by several criteria: (a) treatment of Sarcoma 180 cell extract with p-chloromercuribenzoate inhibited the two activities to a different extent, (b) adenine selectively protected the adenosine phosphorylase activity of Sarcoma 180 and rat liver extract against heat inactivation, while hypoxanthine selectively protected inosine-guanosine phosphorylase activity, (c) at nearly saturating substrate concentrations and using Sarcoma 180 extract, the rates of ribosylation of a mixture of adenine + hypoxanthine or adenine + guanine, but not of hypoxanthine + guanine, were found to be almost equal to the sum of their individual rates as measured separately, (d) inosine selectively inhibited the ribosylation of hypoxanthine and guanine catalysed by Sarcoma 180 and rat liver extract while 2-chloroadenosine selectively inhibited the ribosylation of adenine and N6-furfuryladenine, (e) pH vs. activity curves were similar with hypoxanthine or guanine as the substrate but they were markedly different from the curve with adenine as the substrate. The potential role of adenosine phosphorylase activity in vivo is discussed.

Adenine↗

PubMed1978

Effect of immunoglobulin G on membrane-bound enzyme activity of sarcoma 180 cells.

Changes in the activity of membrane bound ATPase of Sarcoma 180 cells caused by immunoglobulin G (IgG) of anti-Sarcoma 180 was investigated in relation to the incorporation of amino acid by the cells. Enzymatic activity of ATPase was increased up to 160% of the original activity upon incubation of the cell with IgG. Kinetic studies showed that IgG did not change the affinity of this enzyme for the substrate, but exerted influence upon catalytic efficiency of the enzyme. The rate of incorporation of leucine into Sarcoma 180 cells was also affected by IgG, as observed in the effect of IgG on the enzymatic reaction of the cells.

Animals↗

PubMed1977

Entry of mRNA into polyribosomes during recovery from starvation in mouse sarcoma 180 cells.

Starvation in mouse sarcoma 180 cells leads to a block in initiation of protein synthesis which results in the conversion of polysomes to 80-S ribosomes. The mRNA is released as nucleoprotein particles. Addition of nutrients to the starved cell causes the rapid uptake of the mRNA into large polysomal structures. The ribosomes enter these structures more gradually, without much effect on the sedimentation profile of the labeled mRNA. The results indicate that the stored mRNA in starved cells is readily available for uptake into polysomes. They also suggest that the mRNA may be binding to components other than ribosomes during the initial stages of polysome formation.

Animals↗

PubMed1979

[Effect of UHF frequency on the growth of sarcoma 180].

Studies performed on mice transplanted sarcoma 180 subcutaneously indicated that the UHF-field of non-thermogenic intensity in multiple (5-10 fold) total irradiation inhibits the tumor growth (T = 60%) and produces a 1.5 times increase of an average survival in tumor-bearing animals. It is suggested that there is a direct relationship between the increased antiblastic function of the body and a stimulating effect of the UHF-field on the immune response in animals.

Animals↗

PubMed1978

Optimization of high-dose methotrexate with leucovorin rescue therapy in the L1210 leukemia and sarcoma 180 murine tumor models.

An analysis of dose and schedule dependence of calcium leucovorin rescue during high-dose methotrexate therapy of ascitic forms of l1210 leukemia and Sarcoma 180 is reported. Schedules with very delayed "low-dose" leucovorin rescue following lethal doses of methotrexate were highly effective in preventing toxicity and achieved a pronounced antitumor effect in both ascites tumor models. Best results were obtained on a schedule of methotrexate (400 mg/kg s.c.) followed 16 to 20 hr later by calcium leucovorin (12 mg/kg s.c.) given once every 2 hr for a total of 5 doses. Progressive increases in the calcium leucovorin dosage on any schedule reduced both toxicity and the antitumor effect of methotrexate in each model. Following a single course of therapy, essentially no toxicity was observed, and the antitumor effects were 2-fold (L1210 leukemia) and 4-fold (Sarcoma 180) greater than a single, maximally tolerated dose (24/kg s.c.) methotrexate alone. An increase in the methotrexate dosage to 800 mg/kg s.c. with or without an increase in calcium leucovorin dosages on the same schedule did not appreciably increase the antitumor effect observed. Two courses of high-dose methotrexate (400 mg/kg s.c.) with leucovorin rescue (24 mg/kg s.c. 16, 20, and 24 hr after drug) given with an 8-day interval between courses doubled the total antitumor effect in each model with no substantial increase in toxicity and gave long-term survivors with Sarcoma 180. The results, overall, are in close agreement with prior prediction for schedule and dose dependence made on the basis of related pharmacokinetic and biochemical studies in murine tumor models reported from this laboratory.

Animals↗

PubMed1979

[Use of carminomycin in combination with UHF hyperthermia in the therapy of sarcoma 180].

It was found that combined treatment of sarcoma 180 with local U. H. F.-hyperthermia and carminomycin resulted in the tumor growth inhibition by more than 90 per cent, which was much higher than the effect of every agent alone. The thermochemotherapy allowed a decrease in the dose of the antibiotic without decreasing the antitumor effect. The U. H. F.-hyperthermia has an independent tumorolytic effect and promotes selective accumulation of carminomycin by the tumor.

Animals↗

PubMed1977

Experimental chemotherapy with 5-arylpyrimidine antifolates: Further studies on toxicity and the responsiveness of ascitic, solid, and intracranial sarcoma 180 to DDMP and DDMP with citrovorum factor.

Multiple-dose toxicity of the 5-arylpyrimidine DDMP showed marked seasonal variation and sex dependence in BD2F1 mice. Considerable therapeutic activity against the ascitic, solid, and intracranial forms of Sarcoma 180 was demonstrated. Antitumor effects were highly schedule and dose dependent at a limited number of doses between 16 and 40 mg/kg. Antitumor activity (increase in lifespan) was approximately twofold greater against the ascitic tumor compared to the intracranial tumor at each dose level. The use of citrovorum factor rescue appeared to improve the therapeutic index of DDMP against intracranial Sarcoma 180 on specific multiple-dose schedules. Citrovorum factor rescue did not result in a greater initial antitumor effect of DDMP against the solid Sarcoma 180, but the effect was maintained for a longer period of time by allowing an increase in the number of doses which could be administered without toxicity.

Animals↗

PubMed1979

In vivo cell cycle synchronization of the murine sarcoma 180 tumor following alternating periods of hydroxyurea blockade and release.

The durations of the cell cycle intervals of the murine Sarcoma 180 tumor were determined by computer analysis of the fraction-labeled mitosis curve following tritiated thymidine administration. This tumor has a usual total cell cycle duration of 19.6 hr, a DNA synthetic time of 8.3 hr, and a growth fraction of 1. Approximately 38% of cells are in S phase at one time. Hydroxyurea (HU) infusions (i.v.) at 1.17 mg/hr into tumor-bearing mice rapidly inhibit tumor DNA synthesis. Following a 5-hr HU infusion, 58% of all tumor cells are in S phase, and maximal tumor mitotic rates after release of the HU blockade are double control rates. HU was infused for 5 hr, followed by 7 hr of Ringer's solution, and then another 5 hr of HU. Following this 2-cycle blockade, 70% of tumor cells are in S phase, predominantly in early S phase and at the G1-S junction. After release, peak mitotic rates are 2.5 times control. The duration of the intermitotic time of the tumor following HU infusion is less than the total cell cycle time of control tumor. Cycles of HU infusion and release, timed according to the predetermined duration of the cell cycle intervals, will synchronize significant increments of S phase or mitotic cells of the Sarcoma 180 tumor during predictable periods of time.

Animals↗

PubMed1976

[Effect of alkylating chemical substances on the activity and molecular heterogeneity of mouse sarcoma 180 nucleoside phosphate kinases].

The fractionation of extracts from sarcoma 180 cells was carried out on DEAE-cellulose following the administration to tumor-bearing mice of one of chloroctyl amino-phenildioxan derivatives. The tumor regression was noted more than in 50 per cent. It was found that the tumor regression, caused by this alkylating agent, results in marked changes in the fractionation pattern of thymidilatkinases. The origin of these changes is being discussed.

Alkylating Agents↗

PubMed1975

[Utilization of rubidium 86 for humoral cytotoxicity tracing of sarcoma 180].

86Rb has been used as a tracer for Sarcoma 180 ascitic cells in a humoral cytotoxicity system, and compared with the trypan blue dye exclusion method. In as little as five minutes after contact with antiserum and complement, about 90 p. cent of the isotope has gone from the cells, with a significant difference between controls and experimentals. There is a good correlation between 86Rb and trypan blue dye exclusion results. The only pitfall is a relative fragility of cells during the centrifugation stages of the two washings.

Animals↗

PubMed1976

Regulation of folate reductase synthesis in sensitive and methotrexate-resistant sarcoma 180 cells. In vitro translation and characterization of folate reductase mRNA.

A highly specific assay for folate reductase mRNA activity from Sarcoma 180 cells was developed using the rabbit reticulocyte lysate protein synthesizing system. Quantitation of in vitro folate reductase synthesis was accomplished by direct immunoprecipitation from lysate reactions. The in vitro labeled folate reductase was synthesized in a linear response to a wide range of RNA concentrations, migrated as a single prominent radioactive species upon polyacrylamide gel electrophoresis, and was indistinguishable from authentic 14C-labeled folate reductase on the basis of molecular weight and immunotitration with anti-folate reductase gamma-globulin. The assay was used to quantitate folate reductase mRNA activity in various cell lines and under several conditions known to affect folate reductase synthesis. These included (a) sensitive and methotrexate-resistant Sarcoma 180 cells, (b) two lines of resistant cells having different relative rates of folate reductase synthesis, (c) growth of methotrexate-resistant cells in the absence of methotrexate, and (d) growth phase. The results indicate that the relative rate of folate reductase synthesis in each case can be explained solely by the level of translatable folate reductase mRNA. The use of poly(U)-Sepharose and sucrose gradient fractionation procedures indicated that folate reductase mRNA contains poly(A) and has a sedimentation coefficient of approximately 14 S. These two fractionation steps were combined to achieve an approximately 90-fold purification of folate reductase mRNA over total cytoplasmic RNA.

Animals↗

PubMed1978

Anionic polymers and biological activities. Effects of some new polycarboxylic acids on the ascitic sarcoma 180 in mice.

Eleven new polymeric carboxylic acids with widely different solubilities in water have been synthesized. The activities of these polymers against the ascitic sarcoma 180 tumor of mice and their acute toxicities in mice have been compared with molecular parameters of the polymers such as molecular weights, charge densities, and abilities to complex calcium and magnesium ions. The maximum effectiveness of these polymers against ascitic sarcoma 180 of mice is greatest for those polymers having fewer carboxyl groups ionized at pH 7. Toxicities are lower for polymers having more carboxyl groups ionized at pH 7.

Acrylates↗

PubMed1978

Nitrogen analogues of 1,4-benzoquinones. Activities against the ascitic sarcoma 180 of mice.

Compounds having the basic structure N-(R)-substituted ring-substituted 4-iminocyclohexadienone have been synthesized and tested as antitumor agents against the ascitic sarcoma 180 tumor in Swiss mice. Among these compounds, the dimethylindoanilines [R = 4-(CH3)2NC6H4] are most stable in water at pH 7.0 and at 25 degrees C, the oximes (R = oh) are less stable, and the N-halo compounds (R = Br and Cl) are least stable. The N-halo derivatives have the highest redox potentials under the conditions used, the greatest effect against ascitic sarcoma 180 in Swiss mice, and the greatest acute toxicity when injected ip in the Swiss mice. Discriminant analysis of the results indicates that substituents with positive values of F and negative values of pi increase the antitumor activities, whereas those with positive values of sigma and R should lower the toxicity. The redox potential, a molecular parameter, is the best single variable for discriminating between the groups based on antitumor activities.

Animals↗

PubMed1977

Lethal and sublethal effects of hydroxyurea in relation to drug concentration and duration of drug exposure in sarcoma 180 in vitro.

The lethal and sublethal effects of hydroxyurea were studied in Sarcoma 180 in vitro in relation to drug concentration and drug exposure duration using cloning methods, radioautography, and flow microfluorometry. It was shown that postperturbation changes in radioautographic labeling intensity reflected real changes in the rate of DNA synthesis in individual cells. The data suggest that both the lethal and sublethal effects of hydroxyurea are dependent on the rate of DNA synthesis. These findings have important implications for the interpretation of DNA content distributions under perturbation conditions and for the development of drug treatment regimens that are based on cell kinetics.

Animals↗

PubMed1975

[Sensitivity tests of malignant tumours against cytostatic agents in vitro and in vivo/studies on the mouse sarcoma 180 (author's transl)].

The effects of ten different substances on the mouse sarcoma 180 have been compared using in vivo and in vitro test systems. The size of the tumours was taken as a measure of the success of the therapy in animal experiments. The in vitro effects were estimated by measuring the incorporation of radioactively labelled uridine in tumour cell suspensions from solid tumours, in ascites tumours and in tissue culture. Similar results were obtained using all three in vitro test systems. Four substances (daunomycin, fluoruracil, actinomycin D, adriamycin) exhibited activity both in vivo and in vitro, whereas five substances (cytosinarabinoside, methotrexate, ibenzmethyzin, triaziquone, bleomycin) showed no activity in any of the test systems used. With podophyllic acid ethyl hydrazide, however, no correlation between in vivo and in vitro effects was observed. Studies on the influence of the cytostatic agents on the rate of transport of uridine into the cells showed that podophyllic acid ethyl hydrazide strongly reduced the permeability of the cells to radioactive uridine.

Animals↗

PubMed1978

Carcinostatic effect of aliphatic aldehydes and aldehyde dehydrogenase activity in Ehrlich carcinoma, Sarcoma 180, and Yoshida AH 130 hepatoma.

The antitumor activity of 2,3-dihydroxybutyraldehyde on Ehrlich carcinoma, Sarcoma 180, and Yoshida AH 130 hepatoma, as well as the aldehyde dehydrogenase activity in these tumors, was studied. 2,3-Dihydroxybutyraldehyde at nontoxic doses (500 mg/kg body weight i.p. daily for 7 days) slowed down the growth of solid and ascites tumors in mice. The treatment completely prevented the development of Yoshida ascites hepatoma in several rats. 2,3-Dihydroxybutyraldehyde, although it did not influence the growth of Ehrlich carcinoma transplanted in the brain of mice, significantly decreased in the lungs of these animals the number of viable tumour cells that derived from the primary tumor. All the tested tumors, which were sensitive to the action of 2,3-dihydroxybutyraldehyde, were virtually devoid of aldehyde dehydrogenase activity. These results suggest a possible relationship between the lack of this enzyme activity and the antitumor activity of aliphatic aldehydes.

Aldehyde Oxidoreductases↗