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丝裂霉素C单独及与X射线联合对体内EMT6小鼠乳腺肿瘤的影响。

Effects of mitomycin C alone and in combination with X-rays on EMT6 mouse mammary tumors in vivo.

作者信息

Rockwell S

出版信息

J Natl Cancer Inst. 1983 Oct;71(4):765-71.

PMID:6413743
Abstract

The effects of mitomycin C alone and in combination with radiation on the cells of EMT6 mouse mammary tumors in BALB/cKaRw mice were examined. At doses near the toxic level, approximately 98% of the tumor cells were killed by a single injection of mitomycin C. Both proliferating and quiescent cells and both hypoxic and aerobic cells were killed by the drug. Cytotoxicity with mitomycin C occurred rapidly and was apparently complete within 30 minutes after injection of the drug . No evidence was found for repair of potentially lethal mitomycin C damage or sublethal mitomycin C damage by the tumor cells. Mitomycin C and radiation in combination produced an additive cytotoxicity; neither agent was found to alter significantly the shape of the dose-response curve for the other agent. The cytotoxicity of mitomycin C and radiation in combination depended on the sequence and timing of the treatments; additive toxicities were obtained when mitomycin C was given just after, just before, or up to 24 hours before irradiation, but the combination was less effective when mitomycin C was given 2-12 hours after irradiation.

摘要

研究了丝裂霉素C单独及联合辐射对BALB/cKaRw小鼠EMT6小鼠乳腺肿瘤细胞的影响。在接近毒性水平的剂量下,单次注射丝裂霉素C可杀死约98%的肿瘤细胞。增殖细胞和静止细胞、缺氧细胞和好氧细胞均被该药物杀死。丝裂霉素C的细胞毒性迅速发生,在注射药物后30分钟内显然完全发挥作用。未发现肿瘤细胞对潜在致死性丝裂霉素C损伤或亚致死性丝裂霉素C损伤进行修复的证据。丝裂霉素C与辐射联合产生相加性细胞毒性;未发现一种药物能显著改变另一种药物的剂量反应曲线形状。丝裂霉素C与辐射联合的细胞毒性取决于治疗的顺序和时间;当丝裂霉素C在照射后、照射前或照射前24小时内给药时,可获得相加毒性,但当丝裂霉素C在照射后2至12小时给药时,联合治疗效果较差。

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Effects of mitomycin C alone and in combination with X-rays on EMT6 mouse mammary tumors in vivo.丝裂霉素C单独及与X射线联合对体内EMT6小鼠乳腺肿瘤的影响。
J Natl Cancer Inst. 1983 Oct;71(4):765-71.
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引用本文的文献

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J Cancer Res Clin Oncol. 1996;122(1):21-6. doi: 10.1007/BF01203069.
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Mechanism of differential sensitivity of human bladder cancer cells to mitomycin C and its analogue.人膀胱癌细胞对丝裂霉素C及其类似物的差异敏感性机制
Br J Cancer. 1994 Feb;69(2):242-6. doi: 10.1038/bjc.1994.46.
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Characterization of variant and parental-cross-protective immunity to immunogenic variants of a murine fibrosarcoma using the local adoptive transfer assay.
使用局部过继转移试验对小鼠纤维肉瘤免疫原性变体的变异和亲本交叉保护性免疫进行表征。
Cancer Immunol Immunother. 1989;30(4):219-26. doi: 10.1007/BF01665008.
4
Modulation of the antineoplastic efficacy of mitomycin C by dicoumarol in vivo.双香豆素对丝裂霉素C体内抗肿瘤疗效的调节作用。
Cancer Chemother Pharmacol. 1989;24(6):349-53. doi: 10.1007/BF00257440.
5
Deficient activation by a human cell strain leads to mitomycin resistance under aerobic but not hypoxic conditions.人类细胞系的激活缺陷在有氧而非缺氧条件下导致丝裂霉素耐药。
Br J Cancer. 1989 Mar;59(3):341-6. doi: 10.1038/bjc.1989.67.
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Inhibition of mitomycin C's aerobic toxicity by the seleno-organic antioxidant PZ-51.硒有机抗氧化剂PZ - 51对丝裂霉素C有氧毒性的抑制作用。
Cancer Chemother Pharmacol. 1991;28(3):228-30. doi: 10.1007/BF00685517.