Clinical and molecular impact of inhibition of IMP dehydrogenase activity by tiazofurin.

Clinical and molecular impact of inhibition of IMP dehydrogenase activity by tiazofurin.
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噻唑呋林抑制 IMP 脱氢酶活性的临床和分子影响。

DOI:
10.1016/0065-2571(89)90080-0
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发表时间:
1989
期刊:
Advances in enzyme regulation
影响因子:
--
通讯作者:
Tricot,GJ
Tricot,GJ
中科院分区:
--
文献类型:
--
作者:
Weber,G;Yamaji,Y;Olah,E;Natsumeda,Y;Jayaram,HN;Lapis,E;Zhen,WN;Prajda,N;Hoffman,R;Tricot,GJ

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从临床和分子水平探讨噻唑呋喃对IMP脱氢酶抑制的影响。1. 证据表明,IMP脱氢酶和鸟苷酸盐在癌细胞中肿瘤程序的表达中起着重要作用,与人类白血病细胞特别相关。2. 提出了期望噻唑呋喃对人髓细胞有影响的论据。3. 人类白血病细胞IMP脱氢酶的动力学与大鼠肝癌酶相似。4. 本研究为挽救在化疗中的作用和次黄嘌呤抑制鸟嘌呤挽救的作用提供了新的证据。5. 报道了噻唑呋喃和维甲酸在HL-60白血病细胞中的作用。6. 概述了噻唑呋喃和维甲酸对肝癌3924A细胞增殖和细胞毒性的影响。7. 研究了鸟嘌呤对噻唑呋喃和维甲酸诱导分化的影响。8. 为噻唑呋喃治疗患者未出现耐药性提供了生化基础。9. 推测证据表明,噻唑呋喃治疗可诱导患者白血病细胞分化。10. 本文综述了噻唑呋林诱导K-562细胞分化的分子生物学机制,认为噻唑呋林可能通过下调ras癌基因起作用,可能与临床治疗相关。
The impact of tiazofurin on inhibition of IMP dehydrogenase was discussed at the clinical and molecular levels. 1. Evidence was provided for the role of IMP dehydrogenase and guanylates in the expression of the neoplastic program in cancer cells with particular relevance to human leukemic cells. 2. The argument for expecting an impact of tiazofurin in human myelocytic cells was provided. 3. Similarity of the kinetics of human leukemic cell IMP dehydrogenase to the rat hepatoma enzyme was documented. 4. New evidence was provided for the role of salvage in chemotherapy and the function of hypoxanthine in inhibiting guanine salvage. 5. The action of tiazofurin and retinoic acid was reported in HL-60 leukemic cells. 6. The effect of tiazofurin and retinoic acid on proliferation and cytotoxicity was outlined for hepatoma 3924A cells. 7. The effect of guanine on induced differentiation by tiazofurin and retinoic acid was examined. 8. Biochemical basis was provided for the lack of development of resistance in patients treated with tiazofurin. 9. Presumptive evidence was provided that tiazofurin treatment induced differentiation of leukemic cells in the patients. 10. The molecular biology of tiazofurin-induced differentiation in K-562 cells was reviewed with the possible relevance to clinical treatment that tiazofurin might also act through down-regulation of ras oncogene.
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DOI: --
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