SEARCH · PubMed Health

Results for “Sarcoma, Yoshida”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources

PubMed2000

[Tumor microcirculation and selective enhancement of drug delivery--clinical applications based on pathophysiological experiments].

Tumor tissue is composed of cancer cells (parenchyma) and tumor vessels (interstitium). Many investigators have pointed out that blood flow in tumors has a very inhomogenous distribution, and that this inhomogeneity in blood flow increases as tumors grew. This would be a certain cause of insufficient drug delivery to tumor tissues. Among the experimental evidence using Yoshida Sarcoma and Ascites Hepatomas, functional differences in microcirculation between tumor and normal tissues were found by Suzuki et al. (1977). Under hypertensive state induced by the continuous infusion of angiotensin II, tumor blood flow increased remarkably, while there was no change or decrease in blood flow in normal tissues such as the brain, bone marrow, liver and kidney. Moreover, the increase in blood flow in tumors was selective, as the mean blood pressure remained at the level of 150 mmHg. Increases were confirmed not only in many growing sites such as in the liver, muscle, subcutis, and even microfoci, but also in various kinds of xenografted human tumors and autochthonous tumors. Augmentation of the anti-tumor effects of angiotensin II-induced hypertension chemotherapy (IHC) for advanced gastric carcinoma was revealed in two randomized controlled trials (RCT-1 & 2) of collaborative study groups in Japan. The response rates were 42.9% vs 10.5% in RCT-1 and 31.3% vs 6.7% in RCT-2. The frequencies of toxicities were not statistically different. In the results of phase II studies from 1978 to 1994 (OPN-1) and 1995 to 1999 (OPN-2) for advanced gastric carcinoma (GC), the response rates were 37.9% and 35.7%. Down staging in which the conclusive stage score was lower than the score of the clinical stage, was observed in 8 out of 94 cases (19%) with primary lesions in total and in 30 patients (63%) receiving reduction surgery after IHC, since 1978. It is very important for exact evaluation after chemotherapy to understand or estimate the pathohistological changes in the tumor and its degenerated or repaired tissues, which present various clinical images. In the present study, the actual administered dose intensity of adriamycin (aDIadm) was 5.9 +/- 2.4 mg/sqm/w, and the ratio of aDIadm to the proposed DIadm of reported FAM/FAP schedules was 0.78 +/- 0.32. IHC with smaller DI could lead to a reduction in the accumulation of toxicities of anti-cancer drugs in the host. In conclusion, IHC might be applied to all kinds of tumors to enhance the chemotherapeutic effects through selective increase of drug delivery to tumors.

Animals↗

PubMed1975

An infallible method for producing ascitic fluid from solid tumours.

Notwithstanding all precautions, the methods usually applied for the transformation of solid tumours into the ascitic form, frequently fail. This must certainly be ascribed to the still existing, considerably high intercellular adhesion forces despite the fact that cancer cells generally show lack of adhesiveness due to their higher electrical charge in comparison with normal cells. Hagmar recently stipulated that particularly anionic detergents increase the negative surface charge of tumour cells, while cationic detergents drastically reduce or even reverse this charge. A series of comparative experiments were undertaken by us in order to study the influence of anionic, nonionic and amphoteric detergents on the production of ascitic fluid from macerates of Yoshida sarcoma and fibrosarcoma BUSP. This latter tumour was produced and maintained in our laboratory and resisted to all our attempts to produce the ascitic form. Heparin, in concentrations of 0,2, 0,4 and 1,0 mg/ml, was used as an example of an anionic detergent; Pluronic F-68 and phosphatidylcholine, both in concentrations of 1, 2, and 5 mg/ml, represent a nonionic and an amphoteric detergent, respectively. The obtained results clearly show a most favourable action of the applied surfactants: whereas the controls, in which the detergents were not applied, failed to produce ascitic fluid in, sometimes, considerable percentages (up to 100% in the case of BUSP) of the treated animals, not a single animal remained free of ascite when the injected macerate was pre-treated with the emulsifier. It should here be mentioned, however, that heparin in the highest concentration applied (1 mg/ml) caused lysis of the tumour cells impeding, thus, whatever formations of ascitic fluid.

Animals↗

PubMed1976

Two forms of thymidine kinase in normal and tumor tissues of animals.

The thymidine kinases extracted from the spleen of mice infected with Friend virus and from Yoshida sarcoma in rats were separated into two active peaks by diethylaminoethyl cellulose column chromatography, while those of normal tissues have been found to consist of only the first peak (P-1). The second peak (P-II) was also found in the enzyme from the extract of the spleen when the animals were treated by i.p. injections of 1-acetyl 2-phenylhydrazine. The two P-II peaks from tumor tissue and from spleen enlarged by anemia-inducing agents were indistinguishable on the chromatographic profile. On the other hand, the thymidine kinase extracted with Triton X-100 from a mitochondrial fraction of normal liver was found to consist of only one peak in the same position as the above P-II's on the chromatogram, but its faculty for deoxythymidine triphosphate inhibition was not identical to that of tumor tissue. This treatment with the detergent might cause dissociation of a certain component from the enzyme complex to make the extra peak (P-IIb), but it eventually shifts to P-II on the chromatogram.

Animals↗

PubMed1975

[Tumour inhibitory N-(bis--(2-chlorethyl)-aminomethyl)-urethanes (author's transl)].

The synthesis of N-[bis-(2-chlorethyl)-aminomethyl]-urethanes (I-VI) and N,N'-di[bis-(2-chlorethyl)-aminomethyl]-urea (VII) and their evaluation on the Yoshida sarcoma of the rat and on the sarcoma 180 of the mouse are described. The antitumor activity of I-VI is based on a reaction mechanism analogous to that of aromatic N-lost-derivatives.

Animals↗

PubMed1978

Accumulation of radioisotopes with tumor affinity. I. Uptake and excretion of 67Ga-citrate in malignant tumors and normal cells.

Using in vivo and in vitro experimental models, the uptake and excretion of 67Ga-citrate in tumor cells and normal cells were studied. The time-lapse accumulation of 67Ga in the tumor of rats bearing Yoshida sarcoma reached its peak 24 h after the administration of 67Ga and gradually decreased thereafter. However, the excretion of 67Ga from the tumor was less than that from normal lung. For culture cells in vitro, the uptake of 67Ga increased with lapse of contact time between 67Ga and the cells, but there was no distinct difference between the results of tumor cells and normal skin fibroblasts. The excretion of 67Ga from the cells tended to decrease with prolongation of the contact time, the excretion from tumor cell being only about 10% after a contact time of 24 h. This indicated a significant delay in excretion in comparison with that of normal skin fibroblasts. This delay in the excretion of 67Ga may be an important factor in the tumor accumulation of 67Ga.

Animals↗

PubMed1977

Characterization of pyrimidine nucleoside monophosphokinase in normal and malignant tissues.

It was found that there are two kinds of pyrimidine nucleoside, monophosphokinase deoxythymidine 5'-monophosphate-deoxyuridine 5'-monophosphate (dTMP-dUMP) kinase and cytidine 5'-monophosphate-deoxycytidine 5'-monophosphate-uridine 5'-monophosphate-doexyuridine 5'-monophosphate (CMP-dCMP-UMP-dUMP) kinase, and their molecular weights were calculated to be 46,000 and 26,000, respectively, by gel filtration. dTMP-dUMP kinase phosphorylated dTMP with a Km of 3.1 X 10(-5)M and dUMP with a Km of 7.7 X 10(-4) M. dTMP phosphorylation catalyzed by dTMP-dUMP kinase was inhibited competively by dUMP with a Ki of 2.0 X 10(-3) M. Similarly, phosphorylation of dUMP by this enzyme was inhibited competively by dTMP with a Ki of 2.5 X 10 (-5) M. CMP-dCMP-UMP-dUMP kinase of Yoshida sarcoma phosphorylated dUMP with a Km of 3.1 X 10(-3) M and dCMP with a Km of 7.1 X 10 (-4) M, but it did not phosphorylate dTMP. Phosphorylation of dUMP BY CMP-dCMP-UMP-dUMP kinase was inhibited competitively by DCMP and dTMP with Ki's of 6.9 X 10(-4) and 3.0 X 10(-3) M, respectively, and phosphorylation of dCMP was inhibited completely by dUMP a Ki of 2.2 X 10(-3) M. Relative Vmax activity of this enzyme was 345 nmoles/mg protein with dCMP and 127 nmoles/mg protein with dUMP.

Animals↗

PubMed1978

Motility of rat ascites hepatoma cells, with reference to malignant characteristics in cancer metastasis.

The motility of four strains of rat ascites tumor cells in an agar medium was studied quantitatively by means of time lapse cinematography. The motility of these cells differed characteristically with each strain. Yoshida sarcoma and AH-66F cells showed active locomotion and partial movement markedly, while AH-130 and AH-100B cells made no locomotion and only a slight movement.

Animals↗

PubMed1990

[Antitumor activities of orally administered 7-con-0-methylnogarol (TUT-7)].

We estimated antitumor activity of TUT-7 following p.o. administration using animal tumor models and human tumor xenografts. In mouse L 1210 leukemia system, antitumor activity of TUT-7 administered orally was as good as that by i.v. administration. Treatment involving schedules of every 4-days or daily administration was much more effective than single treatment. Therapiotic indices of this compound administered both p.o. or i.v. routes, were better than that of adriamycin administered i.v.. TUT-7 showed antitumor activities against various mouse tumors (L 1210 leukemia, P 388 leukemia, colon 38 adenocarcinoma, B 16 melanoma), LX-1 human tumor xenografts, and Yoshida sarcoma in rat. Base on above results, we concluded that oral administration is one of the useful route of TUT-7 administration.

Administration, Oral↗

PubMed1990

[Index of tumor response by in-vivo 31P-MRS--T1 effect as a new predicting index of therapeutic effects].

We observed the metabolism of the Yoshida sarcoma by in-vivo 31P-MRS, using two varieties of repetition time (TR), i.e., TR2s and TR10s. It was measured before the injection of 5FU and 4, 24, 48 hours after the injection. In the each time, PME/ATP ratio, intracellular pH, and TR10/TR2 ratio of PME which reflects the T1 value of PME, were calculated. TR10/TR2 ratio of PME decreased 4 and 24 hours after the injection of 5FU and recovered 48 hours after the injection to the same level before the injection. However decrease of PME/ATP ratio was not observed until 48 hours after the injection of 5FU, when apparent tumor regression appeared. These results suggested that the T1 value of PME decreased prior to the PME changes and when the PME decreased, the intracellular environment of PME recovered to the same state before the therapy. It was considered that the TR10/TR2 ratio of PME offers significant information different from the PME/ATP ratio. It is possible to use the TR10/TR2 ratio as a predicting index for the therapeutic effects.

Animals↗

PubMed1975

Induction of ornithine decarboxylase, tyrosine aminotransferase, and thymidine kinase by glucocorticoid in isolated, perfused liver after tumor inoculation.

A method for producing solid tumors in rat liver or spleen by local inoculation of Yoshida sarcoma or Hirosaki sarcoma was developed by careful selection of rat strains. After development of the tumor, the liver was isolated and perfused with a mixture of calf serum and fluorocarbon. Addition of corticoid hormone to the perfusion fluid induced tyrosine aminotransferase in normal tissue of the liver and to a lesser degree in the tumor tissue. Corticoid did not cause any detectable induction of thymidine kinase in normal tissue of the liver, but caused slight but definite induction of the enzyme in the tumor tissue. Ornithine decarboxylase was induced in the normal tissue by perfusion with serum alone, even without corticoid, but no enzyme induction was observed in the tumor tissue. The low level of this enzyme found in solid tumor tissue might be due to the fact that the enzyme was measured in the late period of tumor growth, because, in experiments with ascites tumor cells, higher enzyme activities were observed in the early period of growth.

Animals↗

PubMed1989

[Experimental studies on the antitumor effect of progesterone and enhancement of the therapeutic effect of anticancer drugs by progesterone--from the aspect of zinc metabolism].

Since zinc is essential for the proliferation of tumor cells, the growth of tumor cells is suppressed in the zinc deficient condition. Thus, administration of progesterone, which decreases zinc uptake of tumor cells, to tumor bearing rats may inhibit the tumor growth. From this aspect, the antitumor effect of progesterone alone, or in combination with various anticancer drugs was investigated in the rats bearing Yoshida sarcoma (YS) or ascites hepatoma 109A (AH 109 A). In YS bearing rats, a significant inhibition of the tumor growth in size was observed by progesterone, and a slight inhibition of the tumor growth in AH 109 A bearing rats. A decreased zinc content of YS cells was also observed in YS bearing rats given progesterone in comparison with that of control rats. In combination of progesterone and anticancer drugs, the antitumor effect of methotrexate or vincristine was markedly enhanced by progesterone in YS bearing rats.

Animals↗

PubMed1987

A new glucocorticoid receptor detected in host rat liver but not in various hepatomas.

Previously a new glucocorticoid receptor (Peak C), which eluted with 0.12 to 0.14 M NaCl from DEAE-cellulose column, was identified in addition to another receptor (Peak B), a classic type of glucocorticoid receptor, which eluted with 0.05 to 0.08 M NaCl. Peak C appeared after stress or injection of a high dose (20 micrograms/100 g body weight) of dexamethasone into rats. Peak C was also detected in the liver of rats bearing various tumors, but it was not found in malignant tumors (Yoshida sarcoma and Yoshida ascites hepatoma AH 130), a less malignant Yoshida ascites hepatoma (LY-5), or in minimal deviation-type hepatomas (Morris hepatomas 7316A and 7794A). The absence of Peak C in these tumors coincided with the inability of the glucocorticoid to induce tryptophan oxygenase in these tumors and in the liver of rats during early postnatal development. Peak B was consistently observed in various hepatomas and immature rat liver with capability to induce tyrosine aminotransferase. Thus Peak C appeared to be a highly differentiated type of glucocorticoid receptor mediating specific hormone actions and to be present in mature liver cells, but not in immature liver or tumor cells, even of the minimal deviation type.

Animals↗

PubMed1987

Wide distribution of rat hepatoma asialo GM1 and its different responses to anti-asialo GM1 antibody-mediated in vitro and in situ cell killing.

By means of TLC immunostaining with anti-asialo GM1 antiserum and conventional structural analyses including exoglycosidase treatment, permethylation and negative ion FABMS, asialo GM1 was found to be widely distributed in rat ascites hepatomas, AH130, AH109A, AH44, AH272, AH41C, AH60C, AH414, AH7974, AH66, AH66 alpha F, AH66F and AH13, and Yoshida sarcoma cells. However, reactivity of asialo GM1, when measured by flow cytometry and complement-mediated cytotoxicity assay with anti-asialo GM1 antiserum, was only observed on AH13 and AH66F, and did not necessarily correspond to the concentration of asialo GM1 on the cells, indicating a cryptic or unreactive nature of glycosphingolipids with respect to their antibodies. On the other hand, although rats injected with 10(7) cells of AH66F died within 7 days, treatment of the rats with anti-asialo GM1 antiserum was found to be effective for their cure or for prolonging their survival, indicating an in situ cytotoxic effect of antiserum. For the in situ cytotoxicity, the timing and period of injection and the dose of antiserum were found to be important.

Animals↗

PubMed1988

Levo-carnitine, its derivatives, and free fatty acids in serum, heart, liver, and muscle of both tumoral and alcoholic rats.

We present a comparative study of carnitine-related fatty acid metabolism in rats bearing a Yoshida sarcoma, in chronic alcoholic rats, and in control rats. Levels of levo-carnitine, acetylcarnitine, acylcarnitine, and free fatty acids were studied in serum and in different tissues--liver, heart, and skeletal muscle--of each group of rats. Chronic alcoholic rats showed high levels of free fatty acids and elevated levo-carnitine and acetylcarnitine levels relative to those of the controls. Biosynthesis of carnitine appeared to be increased, whereas fatty acid oxidation was depressed. Tumor-bearing rats also showed high levels of free fatty acids in both serum and tissues. However, levels of levo-carnitine were decreased in this group. It seems that the tumor not only utilizes the precursors of carnitine biosynthesis but also increases carnitine expenditure.

Alcoholism↗

PubMed1985

Antitumor spectrum of a new anthracycline, (2"R)-4'-O-tetrahydropyranyladriamycin, and effect on the cellular immune response in mice.

(2''R)-4'-O-Tetrahydropyranyladriamycin (THP), a new anthracycline antibiotic, showed stronger inhibition of the growth of L1210, CCMT (mouse mammary adenocarcinoma) and Yoshida sarcoma in rats than did adriamycin (ADM). The antitumor activity of THP against P388 and Meth-A (mouse fibrosarcoma) was equal or slightly superior to that of ADM. Moreover, THP was active against an ADM-resistant subline of P388. THP at the optimal effective dose against experimental tumors had no toxic effect on the cellular immune system in normal and tumor-bearing mice.

Adenocarcinoma↗

PubMed1985

The use of protein as a carrier of methotrexate for experimental cancer chemotherapy. I. Preparation of pea seed lectin-methotrexate derivative and the preliminary experiments.

A method of preparation of pea seed lectin-methotrexate derivative by means of hydroxy-succinimide ester of methotrexate was elaborated. Five moles of methotrexate was bound to one lectin mole on the average as verified by analysis. For the distribution study lectin was labeled with 131I. Labeled lectin was administered intravenously to Yoshida sarcoma bearing rats and its distribution in the organism was monitored. After 24 hours the labeled lectin was entrapped predominantly in the reticuloendothelial system but after 48 and 72 hours the accumulation was seen also in thyroid, urinary bladder and tumor (1/4 cases only). The discrepancy in distribution of lectin in the tumor has been discussed.

Animals↗

PubMed1979

Enhancement of the nuclear reactivity of alkylating agents by prednisolone.

We have compared the nuclear reactions of the alkylating agents chlorambucil, melphalan, and cyclophosphamide used alone, with those produced when the same drugs were used in combination with the corticosteroid prednisolone. Studies were performed in vivo in Wistar rats bearing ascites forms of either the Yoshida sarcoma or the Walker carcinosarcoma. Strains of both tumor lines, which were sensitive to alkylating agents, showed loss of condensed chromatin, increased phosphorylation of nuclear proteins, and increased DNA cross-linking after exposure to the alkylating agents alone; these changes were generally enhanced in the presence of prednisolone. When paired tumor lines which exhibited acquired resistance to alkylating agents were studied, no nuclear changes were detected when individual alkylating agents were given alone. However, in combination with prednisolone, each of the three alkylating agents produced loss of condensed chromatin, increased nuclear protein phosphorylation, and DNA cross-linking. These chromatin changes were associated with tumor cell death and may determine drug sensitivity in the tumors studied.

Alkylating Agents↗

PubMed1975

alpha-Fetoprotein detected in rat transplantable hepatomas by radioimmunoassay.

Production of rat alpha-fetoprotein by transplantable ascites hepatoma was studied by radioimmunoassay method. alpha-Fetoprotein was detected in sera from rats bearing 22 out of 50 ascites hepatoma cell lines that were previously negative for the presence of alpha-fetoprotein by the Ouchterlony test. alpha-Fetoprotein was also detected with high prevalency in Morris hepatomas and sublines of Yoshida sarcoma by this assay system.

Animals↗