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The role of mitomycin antibiotics in the chemotherapy of solid tumors.

作者信息

Sartorelli A C

出版信息

Biochem Pharmacol. 1986 Jan 1;35(1):67-9. doi: 10.1016/0006-2952(86)90559-9.

DOI:10.1016/0006-2952(86)90559-9
PMID:2416320
Abstract
摘要

相似文献

1
The role of mitomycin antibiotics in the chemotherapy of solid tumors.丝裂霉素类抗生素在实体瘤化疗中的作用。
Biochem Pharmacol. 1986 Jan 1;35(1):67-9. doi: 10.1016/0006-2952(86)90559-9.
2
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.
3
Role of NADPH:cytochrome c reductase and DT-diaphorase in the biotransformation of mitomycin C1.还原型辅酶Ⅱ：细胞色素c还原酶和DT-黄递酶在丝裂霉素C1生物转化中的作用
Cancer Res. 1984 Dec;44(12 Pt 1):5638-43.
4
Modification of the metabolism and cytotoxicity of bioreductive alkylating agents by dicoumarol in aerobic and hypoxic murine tumor cells.双香豆素对需氧和缺氧小鼠肿瘤细胞中生物还原烷基化剂代谢及细胞毒性的影响
Cancer Res. 1989 Jun 15;49(12):3310-3.
5
Mitomycin C is not metabolized by but is an inhibitor of human kidney NAD(P)H: (quinone-acceptor)oxidoreductase.丝裂霉素C不是人肾NAD(P)H:(醌受体)氧化还原酶的代谢产物，而是其抑制剂。
Cancer Chemother Pharmacol. 1988;22(2):126-30. doi: 10.1007/BF00257309.
6
Exploring the mechanistic aspects of mitomycin antibiotic bioactivation in Chinese hamster ovary cells overexpressing NADPH:cytochrome C (P-450) reductase and DT-diaphorase.探索在过表达NADPH：细胞色素C（P - 450）还原酶和DT - 黄递酶的中国仓鼠卵巢细胞中丝裂霉素抗生素生物活化的机制方面。
Adv Enzyme Regul. 1998;38:111-33. doi: 10.1016/s0065-2571(97)00009-5.
7
Caffeine, aminoimidazolecarboxamide and dicoumarol, inhibitors of NAD(P)H dehydrogenase (quinone) (DT diaphorase), prevent both the cytotoxicity and DNA interstrand crosslinking produced by 5-(aziridin-1-yl)-2,4-dinitrobenzamide (CB 1954) in Walker cells.
Biochem Pharmacol. 1989 Nov 15;38(22):4137-43. doi: 10.1016/0006-2952(89)90695-3.
8
Relationship between the antioxidant enzyme DT-diaphorase and tumor response to mitomycin C treatment.抗氧化酶DT-黄递酶与肿瘤对丝裂霉素C治疗反应之间的关系。
Basic Life Sci. 1988;49:713-6. doi: 10.1007/978-1-4684-5568-7_113.
9
Increased sensitivity of quinone resistant cells to mitomycin C.对醌耐药的细胞对丝裂霉素C的敏感性增加。
Cancer Lett. 1989 Jun;45(3):173-6. doi: 10.1016/0304-3835(89)90073-6.
10
Chemotherapeutic attack of hypoxic tumor cells by the bioreductive alkylating agent mitomycin C.生物还原烷基化剂丝裂霉素C对缺氧肿瘤细胞的化疗攻击。
Adv Enzyme Regul. 1985;23:291-307. doi: 10.1016/0065-2571(85)90053-6.

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3
Stereoselective synthesis of complex polycyclic aziridines: use of the Brønsted acid-catalyzed aza-Darzens reaction to prepare an orthogonally protected mitomycin C intermediate with maximal convergency.
立体选择性合成复杂的多环氮丙啶：使用布朗斯特酸催化的氮杂达参反应制备最大收敛性的具有正交保护的丝裂霉素 C 中间体。
Chem Commun (Camb). 2011 Apr 7;47(13):3975-7. doi: 10.1039/c0cc05734g. Epub 2011 Feb 24.
4
Effects of photochemically activated alkylating agents of the FR900482 family on chromatin.FR900482家族光化学活化烷基化剂对染色质的影响。
Chem Biol. 2007 May;14(5):553-63. doi: 10.1016/j.chembiol.2007.04.004.
5
Effect of hyperthermia on the activity of 1-[(4'-hydroxy-2'-butenoxy)methyl]-2-nitroimidazole, which is cytotoxic to hypoxic cells.热疗对1-[(4'-羟基-2'-丁烯氧基)甲基]-2-硝基咪唑活性的影响，该物质对缺氧细胞具有细胞毒性。
Cancer Chemother Pharmacol. 1993;31(6):455-8. doi: 10.1007/BF00685035.
6
Hypoxia and drug resistance.缺氧与耐药性。
Cancer Metastasis Rev. 1994 Jun;13(2):139-68. doi: 10.1007/BF00689633.
7
Activation mechanisms to chemical toxicity.化学毒性的激活机制。
Arch Toxicol. 1987;60(1-3):5-15. doi: 10.1007/BF00296939.
8
Characterization of radiation resistant hypoxic cell subpopulations in KHT sarcomas. (II). Cell sorting.KHT肉瘤中耐辐射缺氧细胞亚群的特征分析。（II）细胞分选。
Br J Cancer. 1988 Sep;58(3):296-300. doi: 10.1038/bjc.1988.207.
9
Mitomycin C is not metabolized by but is an inhibitor of human kidney NAD(P)H: (quinone-acceptor)oxidoreductase.丝裂霉素C不是人肾NAD(P)H:(醌受体)氧化还原酶的代谢产物，而是其抑制剂。
Cancer Chemother Pharmacol. 1988;22(2):126-30. doi: 10.1007/BF00257309.
10
Enhancement of chemotherapy and nitroimidazole-induced chemopotentiation by the vasoactive agent hydralazine.血管活性药物肼苯哒嗪增强化疗及硝基咪唑诱导的化学增敏作用
Br J Cancer. 1990 Sep;62(3):348-53. doi: 10.1038/bjc.1990.295.