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Antitumor activity of 7-n-(p-hydroxyphenyl)-mitomycin C in experimental tumor systems.
M-83 was as effective as MMC against Lewis lung carcinoma at dose levels giving the same degree of toxicity and cytotoxic effects of M-83 against leukemia P388 and fibrosarcoma Meth 1 cells were similar to and stronger than those of MMC, respectively.
Comparison of the hematologic toxicity of 7-N-(p-hydroxyphenyl),-mitomycin C and mitomycin C.
It is suggested that M-83 may be effective in clinical use after it showed a significantly lower toxicity than MMC with respect to myelosuppression and leukopenia when compared at equivalent effective doses.
Antitumor activity of 7-N-phenyl derivatives of mitomycin C in the leukemia P388 system.
7-N-(p-hydroxyphenyl)-mitomycin C was the most effective of these compounds, showing a higher ILS% than its ortho and meta isomers.
Mode of action of adriamycin on HeLa S-3 cells in vitro.
The effect of adriamycin on HeLa S-3 cells grown in monolayers was studied and the specific inhibition of RNA synthesis was observed in logarithmically growing cultures under conditions which permitted normal syntheses of DNA and protein.
Synthesis and biological activities of 7-alkoxymitosanes.
A facile alcoholysis of 7-methoxymitosanes and 5-methoxyindolequinone under basic conditions was discovered and a series of 7-alkoxymitosanes were synthesized from mitomycins A and B using this
Antitumor activity of echinosporin.
Echinosporin isolated from a Streptomyces culture showed antitumor activity against rodent tumor models such as leukemia P388, P388/VCR, and fibrosarcoma Meth 1. It was marginally active against
Comparative antitumor activities of 7-N-(p-hydroxyphenyl)mitomycin C (M-83) and mitomycin C.
M-83 was markedly effective against solid tumors of sarcoma 180, Meth 1, Meth A and Lewis lung carcinoma, by a single intravenous injection and inhibited more strongly the incorporation of the radioactive precursor into DNA than that into RNA or protein at the concentration of 3 X 10(-3) mM.
Distribution and excretion of 7-N-(p-hydroxyphenyl)-mitomycin C in normal mice.
M-83 was more rapidly inactivated by mouse liver homogenate in vitro than MMC and MMC could not be detected by thin-layer chromatography-bioautography in the reaction mixture of M-83 incubated with mouse liverhomogenate, or in the mouse urine.
The action of 7-N-(p-hydroxyphenyl)mitomycin C [M-83] in suppressing murine immune response.
The immuno-suppressive activities of M-83, a derivative of mitomycin C, which has better antitumor activity against murine tumors, was investigated in mice and resulted in an apparent but relatively transient reduction in both plaque-forming cell production and delayed type hypersensitivity reaction to sheep red blood cells.
An experimental postoperative metastasis system using Yoshida sarcoma inoculated subcutaneously into footpad.
Mitomycin-C, a highly effective drug against Yoshida sarcoma cells, produced many long survivors in the treated rats whose primary implants were resected the day after inoculation, but failed to do so when resecting 5 days after inoculated.