吡唑呋喃菌素的临床、生物学及生化效应 - Suppr

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Clinical, biological, and biochemical effect of pyrazofurin.

作者信息

Cadman E C, Dix D E, Handschumacher R E

出版信息

Cancer Res. 1978 Mar;38(3):682-8.

PMID:272228

Abstract

摘要

相似文献

Clinical, biological, and biochemical effect of pyrazofurin.吡唑呋喃菌素的临床、生物学及生化效应

Cancer Res. 1978 Mar;38(3):682-8.

Pyrazofurin enhancement of 5-azacytidine antitumor activity in L5178Y and human leukemia cells.吡唑呋喃增强5-氮杂胞苷对L5178Y细胞和人白血病细胞的抗肿瘤活性。

Cancer Res. 1978 Dec;38(12):4610-7.

Metabolism and cytotoxicity of 5-azacytidine in cultured Novikoff rat hepatoma and P388 mouse leukemia cells and their enhancement by preincubation with pyrazofurin.5-氮杂胞苷在培养的诺维科夫大鼠肝癌细胞和P388小鼠白血病细胞中的代谢与细胞毒性及其与吡唑呋林预孵育后的增强作用

Cancer Res. 1978 Aug;38(8):2458-66.

Selective inhibition of pyrimidine synthesis and depletion of nucleotide pools by N-(phosphonacetyl)-L-aspartate.N-（膦酰乙酰基）-L-天冬氨酸对嘧啶合成的选择性抑制及核苷酸库的耗竭

Cancer Res. 1979 Aug;39(8):3089-94.

Pharmacological and biochemical effects of pyrazofurin in humans.吡唑呋喃在人体中的药理和生化作用。

Cancer Res. 1977 Jul;37(7 Pt 1):2043-9.

Uridine and cytidine metabolism following inhibition of de novo pyrimidine synthesis by pyrazofurin.吡唑呋喃抑制嘧啶从头合成后尿苷和胞苷的代谢

Biochim Biophys Acta. 1980 Oct 17;609(3):372-82. doi: 10.1016/0005-2787(80)90111-2.

[L-asparaginase--first specific cytostatic].[L-天冬酰胺酶——首个特异性细胞生长抑制剂]

Arzneimittelforschung. 1968 Nov;18(11):1380-6.

Effect of methylthioinosine on nucleotide concentrations in L5178Y cells.甲硫肌苷对L5178Y细胞中核苷酸浓度的影响。

Cancer Res. 1973 Jul;33(7):1711-5.

Inhibition of pyrimidine metabolism in myeloid leukemia cells by triazole and pyrazole nucleosides.三唑和吡唑核苷对髓系白血病细胞嘧啶代谢的抑制作用。

Biochem Pharmacol. 1990 Feb 1;39(3):455-62. doi: 10.1016/0006-2952(90)90050-u.

Pyrazofurin metabolism, enzyme inhibition, and resistance in L5178Y cells.吡唑呋喃在L5178Y细胞中的代谢、酶抑制作用及耐药性。

Cancer Res. 1979 Nov;39(11):4485-90.

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Trypanosoma brucei (UMP synthase null mutants) are avirulent in mice, but recover virulence upon prolonged culture in vitro while retaining pyrimidine auxotrophy.布氏锥虫（UMP 合酶缺失突变体）在小鼠中无致病性，但在体外长时间培养后恢复致病性，同时保留嘧啶营养缺陷型。

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