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At least 451 records · Page 25Linked to original sources

PubMed1988

Characterization of human soft tissue sarcomas in nude mice. Evidence for histogenic properties of malignant fibrous histiocytomas.

Twenty-two human sarcomas were grafted subcutaneously into nude mice. Twelve tumors grew successfully. Nine of these 12 tumors had an aneuploid DNA content, whereas only 1 of 10 nonsuccessful tumors was aneuploid. The 12 sarcomas included two leiomyosarcomas, two malignant schwannomas, one synovial sarcoma, and seven malignant fibrous histiocytomas (MFHs). With light and electron microscopic and immunolabeling studies the original and xenografted tumors (the latter for at least two generations) were histopathologically compared. The xenografted leiomyosarcomas showed ultrastructurally a more pronounced leiomyodifferentiation, and one of the malignant schwannomas a more pronounced schwannian differentiation. The second malignant schwannoma and the synovial sarcoma, however, remained unchanged. Five storiform pleomorphic MFHs expressed features that were not observed in the original tumors. Tumor cells of three of these xenografted sarcomas showed leiomyogenic differentiation (filamentous densities, pinocytotic vescicles, and desmin immunoreactivity), whereas cells of the two others demonstrated schwannian differentiation (long cytoplasmic processes, basal lamina). A xenografted myxoid MFH and a pleomorphic MFH gave rise to pleomorphic sarcomas composed of undifferentiated cells. It appeared that under transplantation conditions tumor cells of storiform pleomorphic MFH can differentiate into various directions.

Animals↗

PubMed1979

Lymphocytic infiltration in murine tumors.

Histologic grading of the histiolymphocytic reaction in nodules of T241 or B16 murine tumors in 94 C57BL/6J mice was performed at various time intervals post-inoculation. The infiltrate occurring in the first four days was generally sparse and no significant difference was observed between two different dose control inocula, suggesting a weak primary localization. Comparison between control inocula, and challenge inocula in mice harboring the same tumor for 10 days, showed a somewhat denser infiltrate initially in the challenge inocula. Despite the immunogenicity of these tumors, as shown by concomitant immunity, lymphocytic infiltration was generally sparse, consistent with an hypothesis of deficient localization of immunocompetent cells at tumor sites.

Animals↗

PubMed1986

[Studies of the antitumor activity and enzymology of 2'-deoxy-5-fluorouridine (FdUrd) derivatives].

The antitumor activity and enzymology of 2'-deoxy-3', 5'-bis-O-(4-methoxyphenoxycarbonyl)-5-fluoro-3-(4-n-Propoxybenz oyl uridine (FF-707) were examined. It was found that stability in small intestine homogenate of FF-707 was higher than that of FF-705 [2'-deoxy-3', 5'-O-diacetyl-5-fluoro-3-(3 methylbenzoyl) uridine]. Reduction of the tumor weight was greater in mice bearing sarcoma-180 and rats bearing Yoshida sarcoma treated with the oral administration of FF-707 than that FF-705. The relationship between the antitumor activity and the inhibition of thymidylate synthase after the oral administration of FF-707 was examined. The extent of the inhibition of thymidylate synthase seemed to be parallel to that of the inhibition of the tumor growth.

Animals↗

PubMed1987

[BOF-A1 and BOF-A2, new 5-FU degradation-inhibitory agents].

2, 6-Dihydroxy-3-cyano pyridine (CNDP) was found from the study of inhibitory effects of pyrimidine and pyridine derivatives on 5-FU degradation catalyzed by dihydrouracil dehydrogenase. CNDP, a new inhibitor on 5-FU degradation was 300 times more effective than uracil. Co-administration of an equi-molar CNDP with some fluorinated pyrimidine preparations potentiated their antitumor activity. Tegafur (FT-207) and EM-FU in combination with CNDP were found most effective. This potentiation was exhibited not only to 5-FU derivatives but also to FdUrd and its derivatives. BOF-A1 and BOF-A2, new compounds combined with CNDP were markedly active against mouse sarcoma 180 and rat Yoshida sarcoma.

Animals↗

PubMed1988

Inhibition of tumor high-energy phosphate metabolism by insulin combined with rhodamine 123.

The purpose of this study was to determine whether the energy metabolism of an experimental rodent sarcoma was selectively depressed by the combination of inhibition of glycolysis and respiration. In vivo phosphorus-31 nuclear magnetic resonance spectroscopy was used to monitor the response of tumor or brain high-energy phosphate compounds to insulin hypoglycemia, rhodamine 123, or both agents in fasting rats with subcutaneous methylcholanthrene-induced sarcomas. Insulin or rhodamine 123 alone produced a similar 50% to 60% reduction in tumor adenosine triphosphate (ATP) concentration compared with controls injected with saline solution (p less than 0.05, one-way analysis of variance [ANOVA]). The combination of insulin plus rhodamine 123 resulted in a 90% reduction of tumor ATP concentration, which was significantly different from the effect of either agent alone (p less than 0.05, one-way ANOVA). Brain phosphocreatine and ATP concentrations were unchanged by these agents. Administration of dimethyl sulfoxide (DMSO)/glycerol, the vehicle for rhodamine, produced a 35% reduction of tumor ATP, which was similar to the effect of insulin alone but significantly different from rhodamine. The combination of DMSO/glycerol plus insulin hypoglycemia resulted in a 70% reduction in tumor ATP, which was significantly elevated compared with the combination of rhodamine plus insulin. Glucose deprivation induced by insulin, and combined with the inhibition of oxidative phosphorylation, produces an additive depression of tumor energetics. The drug vehicle DMSO/glycerol significantly depresses tumor energy metabolism, presumably because of its DMSO component, which may explain the previously reported antineoplastic efficacy of this solvent. Combinations of inhibitors directed at different points of tumor metabolism produced an enhanced depression of tumor energetics, whereas host tissue was protected.

Adenosine Triphosphate↗

PubMed1986