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1
Biochemical basis for the enhanced toxicity of deoxyribonucleosides toward malignant human T cell lines.脱氧核糖核苷对恶性人T细胞系毒性增强的生化基础。
Proc Natl Acad Sci U S A. 1979 May;76(5):2430-3. doi: 10.1073/pnas.76.5.2430.
2
Purinogenic immunodeficiency diseases: selective toxicity of deoxyribonucleosides for T cells.嘌呤生成性免疫缺陷疾病：脱氧核糖核苷对T细胞的选择性毒性。
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3
Biochemical basis for differential deoxyadenosine toxicity to T and B lymphoblasts: role for 5'-nucleotidase.脱氧腺苷对T和B淋巴母细胞产生不同毒性的生化基础：5'-核苷酸酶的作用
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本文引用的文献

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Sensitivity of cultured human lymphoblasts (CCRF-CEM cells) to inhibition by thymidine.培养的人淋巴母细胞（CCRF-CEM细胞）对胸苷抑制作用的敏感性。
Exp Cell Res. 1966 Sep;43(2):512-4. doi: 10.1016/0014-4827(66)90079-6.
2
A rapid quantitative determination of deoxyribonucleoside triphosphates based on the enzymatic synthesis of DNA.基于DNA酶促合成的脱氧核糖核苷三磷酸快速定量测定。
Biochim Biophys Acta. 1969 Feb 18;174(2):585-90. doi: 10.1016/0005-2787(69)90288-3.
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Heterogeneity of 5'-nucleotidase activity in lymphocytes in chronic lymphocytic leukemia.慢性淋巴细胞白血病淋巴细胞中5'-核苷酸酶活性的异质性
J Clin Invest. 1973 May;52(5):1297-300. doi: 10.1172/JCI107298.
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Workshop on severe combined immunological deficiency disease and adenosine deaminase deficiency. Albany, New York, on October 1, 1973.重度联合免疫缺陷病与腺苷脱氨酶缺乏症研讨会。1973年10月1日于纽约州奥尔巴尼市召开。
Clin Immunol Immunopathol. 1974 Nov;3(2):301-3. doi: 10.1016/0090-1229(74)90016-6.
5
Childhood lymphoblastic lymphoma, a cancer of thymus-derived lymphocytes.儿童淋巴细胞白血病，一种源自胸腺淋巴细胞的癌症。
Cancer Res. 1974 Mar;34(3):521-5.
6
Rosette-forming human lymphoid cell lines. I. Establishment and evidence for origin of thymus-derived lymphocytes.形成玫瑰花结的人淋巴细胞系。I. 胸腺衍生淋巴细胞起源的建立及证据。
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7
Epstein-barr virus-negative human malignant T-cell lines.爱泼斯坦-巴尔病毒阴性的人类恶性T细胞系
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8
Deoxynucleotide-polymerizing enzymes in normal and malignant human cells.正常和恶性人类细胞中的脱氧核苷酸聚合酶。
Cancer Res. 1974 May;34(5):1015-26.
9
Isolation and composition of human thymocyte plasma membrane.人胸腺细胞质膜的分离与组成
Biochim Biophys Acta. 1972 Jul 3;274(1):22-7. doi: 10.1016/0005-2736(72)90276-3.
10
The response in vitro, of continuous cultures of human lymphoblasts (CCRF-CEM cells) to chemotherapeutic agents.人淋巴母细胞（CCRF-CEM细胞）连续培养物对化疗药物的体外反应。
Biochem Pharmacol. 1967 Apr;16(4):659-74. doi: 10.1016/0006-2952(67)90078-0.

脱氧核糖核苷对恶性人T细胞系毒性增强的生化基础。

Biochemical basis for the enhanced toxicity of deoxyribonucleosides toward malignant human T cell lines.

作者信息

Carson D A, Kaye J, Matsumoto S, Seegmiller J E, Thompson L

出版信息

Proc Natl Acad Sci U S A. 1979 May;76(5):2430-3. doi: 10.1073/pnas.76.5.2430.

DOI:10.1073/pnas.76.5.2430
PMID:313056
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC383615/
Abstract

Human malignant T cell lines have high levels of deoxyribonucleoside phosphorylating activity and low levels of deoxyribonucleotide dephosphorylating activity. When incubated with deoxyadenosine or thymidine, the malignant T cell lines rapidly accumulate toxic concentrations of dATP and dTTP, respectively. This unusual pattern of deoxyribonucleotide metabolism renders the malignant T cells especially vulnerable to the toxic effects of deoxyribonucleosides and related analogues.

摘要

人类恶性T细胞系具有高水平的脱氧核糖核苷磷酸化活性和低水平的脱氧核糖核苷酸去磷酸化活性。当与脱氧腺苷或胸苷一起孵育时，恶性T细胞系会分别迅速积累有毒浓度的dATP和dTTP。这种脱氧核糖核苷酸代谢的异常模式使恶性T细胞特别容易受到脱氧核糖核苷及相关类似物的毒性作用影响。