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Results for “Sarcoma, Yoshida”

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PubMed1977

Antitumor activity of protoplast membrane from group A streptococcus.

Cytoplasmic membrane of Group A streptococcus has been obtained by treatment of the cells with a phage-associated lytic enzyme to dissolve the streptococcal cell wall, followed by shocking osmotically. The protoplast membrane fraction (PMF) remained as a distinct homogeneous structure in the electron micrograph and analysis showed a low rhamnose content. Febrile response produced by PMF was very slightly exhibited or not at all. PMF showed weak suppression against the growth of rat Yoshida sarcoma cells in culture and inhibition of [3H]-uridine incorporation into the sarcoma cells in vitro. In vivo antitumor experiments demonstrated that PMF has a mild inhibiting effect against mouse Ehrlich ascites carcinoma, though there was not observed a definite correlation between survival rate and dose level. Antitumor activity of PMF was thermo-labile and was strikingly abolished by treatment with a bacterial enzyme, Nagarse, but not so much by alpha-chymotrypsin.

Animals↗

PubMed1987

Amino acid sequence of a less-cytotoxic basic polypeptide (LCBP) isolated from the venom of the Indian cobra (Naja naja).

A less-cytotoxic polypeptide, designated as LCBP, was isolated from the venom of Naja naja by gel filtration on Sephadex G-50 followed by CM-cellulose chromatography. The cytotoxicity toward Yoshida sarcoma cells and lethal toxicity toward mice of LCBP were both one order of magnitude lower than that of cytotoxins and that of toxin A, respectively. LCBP is a single polypeptide consisting of 61 amino acid residues with four intramolecular disulfide linkages, and the amino acid sequence is the same as that of cardiotoxin-like basic polypeptide (CLBP) isolated from the venom of Naja naja atra. This is the first time that the same polypeptides were isolated from different cobra venoms.

Amino Acid Sequence↗

PubMed1978

Transfer of immunity by transfer of bone marrow cells: a requirement for T lymphocytes and sensitivity to cyclophosphamide.

Thymectomized, lethally irradiated mice reconstituted with bone marrow cells (TIR mice) from normal donors succumbed after i.p. challenge with xenogeneic (rat) Yoshida ascites sarcoma (YAS) given 1 month after irradiation and reconstitution. YAS rejection and production of YAS-antibodies was induced in TIR mice by a single i.v. injection of normal syngeneic spleen cells given 1 day after the tumor. Purified splenic T lymphocytes also induced YAS rejection in TIR mice, but splenic B lymphocytes did not affect progressive tumor growth. Tumor was also rejected in TIR mice that had been reconstituted with bone marrow cells from YAS-immune donors. The sera of these TIR mice did not contain tumor antibodies between reconstitution and YAS challenge, but a high YAS-antibody titer was present after YAS challenge and rejection. Immunofluorescence did not reveal any dramatic differences in the spleen and bone marrow content of T and B lymphocytes of TIR mice reconstituted with cells from normal donors and those reconstituted with cells from the YAS-immunized donors. Transfer of YAS-resistance was abolished when the bone marrow cells from immunized donors were treated with Thy 1.2 antiserum and complement, or when bone marrow donors were injected with cyclophosphamide 1 day after immunization. Cyclophosphamide was also shown to induce strong and specific suppression of YAS-antibody production in normal mice.

Animals↗

PubMed1987

Phase I clinical trial of methylene dimethane sulfonate.

Methylene dimethane sulfonate is the first member of the homologous series of straight-chain diol sulfonates. It was selected for phase I testing because of high activity in the rat Yoshida sarcoma system and a possible novel site of alkylation due to its small molecular size. Methylene dimethane sulfonate was administered as a rapid iv bolus infusion to 39 patients at doses ranging from 14 to 225 mg/m2. Nausea and vomiting were not severe but total alopecia occurred in the majority of patients at doses greater than 100 mg/m2. The dose-limiting toxic effect was thrombocytopenia, which was cumulative with lower, more prolonged nadirs following successive courses. The median time to platelet count nadir was 21 days, with recovery by 35 days. A minor response was seen in one patient with an adenocarcinoma of the lung. The recommended dose for phase II studies is 125 mg/m2 for patients who have received prior chemotherapy and 150 mg/m2 for those who have not, in an every 35-day schedule.

Adult↗

PubMed1985

Synthesis, toxicity, and therapeutic efficacy of 4-amino-N-(2'-aminophenyl)-benzamide: a new compound preferentially active in slowly growing tumors.

The present paper describes 4-amino-N-(2'-aminophenyl)benzamide (GOE1734) with regard to synthesis; toxicity in mice, rats, and dogs; and differential therapeutic efficacy in slowly and rapidly proliferating rat tumors. GOE1734, an analog of a group of compounds known for other than antitumor effects with relatively simple N-acyl-O-phenylenediamine structure, is characterized by a low bacterial mutagenic potential after in vitro metabolic activation and DNA-DNA crosslinking activity after in vivo treatment. Maximum tolerated doses in rats and dogs amount to 4 and 1 mg/kg, respectively. High growth-inhibiting efficacy was obtained in intratibially implanted osteosarcoma, in methylnitrosourea-induced primary mammary carcinoma, and in acetoxymethyl-methylnitrosamine-induced colorectal adenocarcinoma. GOE1734 proved to be ineffective in transplanted Yoshida sarcoma and Walker 256 carcinosarcoma when single or multiple doses were administered at dose levels that were moderately toxic or not toxic. Some antitumor effects were observed in L5222 leukemia after ip transplantation, but no effect could be observed after ic implantation or in vitro incubation and subsequent retransplantation of these cells. Since the latter three rat tumors are characterized by relatively short tumor volume doubling times (0.5-2 days), whereas the first three grow slower (tumor volume doubling time, 11-19 days), the remarkable differential antitumor activity of GOE1734 in fast and slowly growing malignancies is striking.

Animals↗

PubMed1985

Amino acid sequence of a cardiotoxin-like basic polypeptide (CLBP) with low cytotoxic activity isolated from the venom of the Formosan cobra (Naja naja atra).

A cardiotoxin-like basic polypeptide, designated as CLBP, was isolated from the venom of Naja naja atra by gel filtration on Sephadex G-50 followed by CM-cellulose chromatography. The cytotoxicity toward Yoshida sarcoma cells and lethal toxicity toward mice of CLBP were both one-order lower than those of cardiotoxins and cobrotoxin, respectively. CLBP is a single polypeptide consisting of 61 amino acid residues with four intramolecular disulfide linkages. The amino acid sequence of CLBP shows a high degree of homology with those of cardiotoxins from the same venom, but differs in the 19 to 23 positions.

Amino Acid Sequence↗

PubMed1979

Characterization of rat hepatoma glucosamine 6-phosphate synthase and its relation to liver and fetal forms.

Glucosamine 6-phosphate synthase (EC 5.3.1.19) purified from various rat tissues by a procedure involving chromatography on diethylaminoethyl Sephadex and hydroxylapatite were characterized by means of isoelectric focusing. The non-hepatic isozyme, previously reported to be present in Yoshida sarcoma, has a pI of 4.1 and is distinguished from the hepatic isozyme, with a pI of 5.0. The pI 4.1 form is the major one in all of the fast-growing, transplantable hepatomas studied. Although not detectable in 19-day fetal liver or normal adult liver, the pI 4.1 form has been observed in the whole 12-day fetus and adult brain as almost the sole form of glucosamine 6-phosphate synthase.

Animals↗

PubMed1981

Metabolism of pyrimidine nucleotides in various tissues and tumor cells from rodents.

The metabolism of pyrimidine nucleotides in various tissues and tumor cells of rodents was investigated. Ribonucleoside diphosphate reductase, thymidine monophosphate kinase and DNA polymerase (alpha, beta) were specifically localized in tumor cells, i.e., the activities of these enzymes in tumor cells were at least three times higher than those in normal tissues, including rapidly growing tissues, such as bone marrow, thymus, and spleen. The activities of deoxycytidine monophosphate deaminase and all the nucleoside kinase were high not only in tumor cells, but also in rapidly growing normal tissues, so that these enzymes are unsuitable as targets for cancer chemotherapy. The tissue distribution of other enzymes, including orotate phosphoribosyltransferases, cytidine triphosphate synthetase, thymidine monophosphate synthase, nucleoside phosphorylases and cytidine deaminase had no relation with the cell growth rate. AH130 tumor cells and the thymus showed specific increases in the activities of enzymes involved in de novo DNA synthesis. In contrast, Yoshida sarcoma and bone marrow showed high activities of enzymes in the salvage pathway of DNA synthesis, which suggested that the two tumors have different patterns of nucleotide metabolism.

Animals↗

PubMed1984

Amino acid sequence of cytotoxin IIa isolated from the venom of the Indian cobra (Naja naja).

A cytotoxic basic polypeptide, designated as cytotoxin IIa, was purified to homogeneous state from the venom of the Indian cobra (Naja naja) by a combination of gel filtration on Sephadex G-50, CM-cellulose chromatography, and fast protein liquid chromatography. Cytotoxin IIa is a single polypeptide consisting of 60 amino acid residues with four intramolecular disulfide linkages. The toxin showed high cytotoxicity toward Yoshida sarcoma and ascites hepatoma cells as did cytotoxins I and II isolated from the same venom. Analysis of the amino acid sequence revealed that cytotoxin I, IIa, and II are highly homologous in their primary structures and that cytotoxin IIa differs from cytotoxin I only in having Phe 25 and Val 52 in place of Tyr 25 and Glu 52 residues.

Amino Acid Sequence↗

PubMed1981

Reduced antitumor and immune-adjuvant activities of the sub-cellular fractions from Group A Streptococcus.

The sub-cellular fractions from Group A streptococcus (Su-strain) were prepared, and their antitumor and biological activities were examined. The cell wall fraction (CWF) and the protoplast membrane fraction (PMF) were slightly effective in retarding the growth of Ehrlich ascites carcinoma in outbred ddY mice when either fraction was used in combination with 5-FU. The cytoplasmic particle fraction (CPF) and the cytoplasmic soluble fraction (CSF), however, were not effective. In the B6D2F1 mice-L 1210 leukemia system, none of the subcellular fractions were beneficial even when combined with 5-FU. Further, the antitumor effect of OK-432 was completely abolished by disruption of the preparation, indicating that antitumor activity of OK-432 may depend on the structural integrity of the cocci in the preparation. Despite the general lack of anti-tumor activity in the mouse systems, the subcellular fractions, including those of OK-432, inhibited the growth of Yoshida sarcoma cells in culture and the uptake of [2H]-UR and [3H]-TdR by L 1210 cells in vitro. The immunopotentiating activities of these fractions, however, were demonstrated to be markedly diminished as compared with those of OK-432 and heated Su-cocci (60 degrees C, 30 min). The present study, therefore, shows that the decreased antitumor activity of the subcellular fractions closely correlate to the decrease of their immunopotentiating activities.

Adjuvants, Immunologic↗

PubMed1982

Molecular transformation of tumor adenylosuccinate synthetase and characteristics of its converting factor.

The properties of adenylosuccinate synthetase [inosine monophosphate:L-aspartate ligase (guanosine 5'-diphosphate-forming) EC 6.3.4.4]) of rat Yoshida sarcoma ascites tumor cells changed during purification. The isoelectric points (pI) of the crude and purified enzymes were 5.0 and 5.9, respectively. The Km values of the crude enzyme for inosine monophosphate, aspartate, and guanosine 5'-triphosphate were calculated to be 99 +/- 1 (S.E.), 870 +/- 40, and 27 +/- 2 microM, respectively, while those of the purified enzyme were 410 +/- 10, 980 +/- 50, and 69 +/- 5 microM, respectively. These data indicate that the crude enzyme should be more effective for activity than the purified one. It was found that the change in pI occurred during diethylaminoethyl cellulose column chromatography and that, during this step a compound, named pI-converting factor (ICF), was separated from the enzyme molecule. On addition of ICF, the pI of the purified enzyme changed from 5.9 to 5.0, indicating that the pI conversion was dependent on ICF and was reversible. ICF was nondialyzable, heat stable, and partly precipitated with 1 N perchloric acid but was not affected by 1 N KOH. It was partially degraded by DNAse I. These results suggest that ICF is a DNA-like compound.

Adenylosuccinate Synthase↗

PubMed1982

Antitumor effect and structure-activity relationship of asterriquinone analogs.

Asterriquinone (ARQ), a metabolic product from Aspergillus terreus IFO 6123, showed an inhibitory effect on some transplantable animal tumors, Ehrlich carcinoma, ascites hepatoma AH13 and mouse P388 leukemia, but had little or no effect on Yoshida sarcoma, ascites hepatoma AH109A and mouse L1210 leukemia. ARQ also inhibited the growth of HeLa cells in monolayer culture. Although metabolic products from Aspergillus terreus var. africanus IFO 8835 were almost ineffective against Ehrlich carcinoma, some chemically modified ARQ-like compounds were found to have potent inhibitory activity against the growth of the carcinoma in mice. The presence of free hydroxyl groups in the benzoquinone moiety and the number and position of tert-, iso-pentenyl, or both pentyl groups seem to be important in relation to the antitumor activity.

Animals↗

PubMed1993

Inhibition by oxonic acid of gastrointestinal toxicity of 5-fluorouracil without loss of its antitumor activity in rats.

The possibility of decreasing the gastrointestinal (GI) toxic effects of 5-fluorouracil (5-FU) on the digestive tract such as its injury of cells and induction of diarrhea, without reducing its antitumor activity, was investigated in rats. Oxonic acid was found to inhibit the phosphorylation of 5-FU to 5-fluorouridine-5'-monophosphate catalyzed by pyrimidine phosphoribosyl-transferase in a different manner from allopurinol in cell-free extracts and intact cells in vitro. On p.o. administration of 5-FU (2 mg/kg) and a potent inhibitor of 5-FU degradation to Yoshida sarcoma-bearing rats, oxonic acid (10 mg/kg) was found to inhibit the formation of 5-fluorouridine-5'-monophosphate from 5-FU and its subsequent incorporation into the RNA fractions of small and large intestine but not of tumor and bone marrow tissues. This selective inhibition of 5-FU phosphorylation in the GI tract was due to the much higher concentrations of oxonic acid in GI tissues than in other tissues and the blood. On p.o. administration with the 5-FU derivative, UFT, which is a combined form of 1 M tegafur and 4 M uracil and usually administered p.o. to cancer patients in Japan, oxonic acid (10-50 mg/kg) markedly reduced injury of GI tissues and/or severe diarrhea without influencing the antitumor effect of UFT. These findings suggest that coadministration of oxonic acid suppresses the GI toxicity of 5-FU and its derivatives without affecting their antitumor activity and thus prolongs the life span of cancer-bearing rats.

Administration, Oral↗

PubMedDate not supplied

[Biologic effects and possible therapeutic use of the granulocyte-macrophage colony-stimulating factor. Modern treatment of leukopenia].

This review is a brief overview of recent advances in biology as well as in potential clinical application of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF). Biologically active rhGM-CSF is a recombinant human protein expressed in Escherichia coli. GM-CSF is produced by nontransformed (T-lymphocytes, trophoblasts, keratinocytes, osteoblasts, tracheal epithelial cells, renal mesangial cells, endothelial cells, macrophages, fibroblasts, smooth muscle cells) and transformed (murine plasmocytoma, bladder carcinoma HIBY cell line, anaplastic carcinoma of the gall bladder, Yoshida sarcoma cell line, HC3T3-osteoblast cell line) cells. RhGM-CSF increases the number of circulating neutrophils, monocytes and eosinophils and increases chemotactic, microcidal killing and cytotoxic activity of monocytes and granulocytes. The present clinically relevant uses of rhGM-CSF two general areas: restoration of haematopoietic dysfunction by raising cell counts from suppressed to normal levels, and augmentation of host defence against infection. Thus, rhGM-CSF reduces risk of infections. In addition, rhGM-CSF may increase tumour cell destruction in some malignant diseases. RhGM-CSF produces dose-dependent toxicity consisting of myalgic fever, fluid retention and serosal effusions.

Granulocyte-Macrophage Colony-Stimulating Factor↗

PubMed1994

[Pharmacokinetics and changes of reduced folate levels in tumor after administration of cisplatin].

Cisplatin acts as a biochemical modulator of 5-FU to increase the intracellular concentration of reduced folates. To determine the optimum schedule for administering cisplatin as a 5-FU modulator, we analyzed pharmacokinetics of platinum and changes of reduced folate levels in the tumor following administration of cisplatin in Yoshida sarcoma-bearing rats. Clinical kinetics of cisplatin was also investigated. The reduced folate level in the tumor was temporarily increased 2-1.6 fold of the control level 1-2 hours after the rapid injection of cisplatin (4 mg/kg). The folate level 2 hours after the rapid injection of cisplatin increased dose-dependently within the dose of 1mg/kg and reached to the plateau with the doses of 1, 2, 4, 8 mg/kg, although the platinum concentration in plasma and tumor increased linearly correlated with the dose of cisplatin. These findings suggest the modulatory effect through rapid injection of cisplatin is transiently exerted only in the early phase, and not dose-dependently but limitatively with the dose of 1 mg/kg or more. Therefore, repeated administration with low dose or continuous infusion of cisplatin simultaneous with 5-FU derivatives is desirable for combination chemotherapy. Clinically, the minimum effective dose of cisplatin as a modulator was thought to be 10-20 mg/body judging from experimental as well as clinical kinetic study of cisplatin.

Animals↗

PubMed1993

Microvascular mechanisms of change in tumor blood flow due to angiotensin II, epinephrine, and methoxamine: a functional morphometric study.

To elucidate the microvascular mechanisms of change in tumor blood flow elicited by vasopressors, a functional morphometric study of the s.c. microcirculation within a rat transparent chamber was performed. Arteriolar vessels were classified centripetally (a2-a5) according to Strahler's method. Arteriolar pressure in each segment both under normotension and under hypertension induced by angiotensin II, epinephrine, or methoxamine was measured using a microocclusion technique. Vasoconstriction was estimated by changes in vessel diameters. In addition, tissue blood flow of the subcutis and s.c. tumor (LY80, a variant of Yoshida sarcoma) under the same conditions was measured with the hydrogen clearance method. By comparing the sites of the greatest pressure drop and the vasoconstriction induced by each vasopressor, we assessed the sites of vascular resistance (VR) which showed increases due to these vasopressors. The greatest VR increase elicited by angiotensin II occurred across a2 vessels. On the other hand, the sites of VR increase due to epinephrine were in a3 vessels and larger vessels upstream from a3 arterioles. The VR increase induced by methoxamine was much smaller than that induced by epinephrine. We conclude that the fact that the sites of increased VR differ with each vasopressor is the primary reason that various vasopressors have been found to produce different changes in tumor blood flow.

Angiotensin II↗

PubMed1993

Therapeutic tumor-specific cell cycle block induced by methionine starvation in vivo.

The ability to induce a specific cell cycle block selectively in the tumor could have many uses in chemotherapy. In the present study we have achieved this goal of inducing a tumor-specific cell cycle block in vivo by depriving Yoshida sarcoma-bearing nude mice of dietary methionine. Further, we demonstrate that methionine depletion also causes the tumor to eventually regress. The antitumor effect of methionine depletion resulted in the extended survival of the tumor-bearing mice. The mice on the methionine-deprived diets maintained their body weight for the time period studied, indicating that tumor regression was not a function of body weight loss. The data reported here support future experiments utilizing methionine depletion as a target for tumor-selective cell cycle-dependent therapy.

Animals↗

PubMed1993

[Experimental study on antitumor effect of cisplatin-microcapsule].

CDDP-microcapsule (CDDP-mc) was prepared in the search for method for administering anti-cancer agents and has been examined for its properties, vital reaction and antitumor effect. In the present study, the results of the examination and possibility of application of CDDP-mc are reported. 1) It took 48 hours for CDDP to be released from the microcapsule into saline. 2) CDDP-mc size is 80-200 microns, and it contains 0.645mg of CDDP per mg of microcapsule. It was available as a drug enabling us to introduce a high concentration of CDDP into tumor tissue. 3) The side effects of CDDP-mc on animals (rabbit and rat) were more limited than those of ordinary CDDP solution and slight, especially for intraperitoneal or local injection. Intraarterial infusion of CDDP-mc, however, causes transitory palsy of the treated lower extremity probably due to embolism. 4) Its intraperitoneal administration was much more effective than the ordinary CDDP solution against Yoshida's sarcoma implanted in rats. 5) The subcutaneous administration of CDDP-mc was more effective compared to ordinary solution of CDDP. 6) The above results suggested that CDDP-mc is clinically applicable to the treatment of ovarian cancer and uterine cancer when administered intraperitoneally and locally (intra-tumor).

Animals↗