Deoxycytidine Kinase-Mediated Toxicity of Deoxyadenosine Analogs toward Malignant Human Lymphoblasts in vitro and toward Murine L1210 Leukemia in vivo

An inherited deficiency of adenosine deaminase (adenosine aminohydrolase, EC 3.5.4.4) produces selective lymphopenia and immunodeficiency disease in humans. Previous experiments have suggested that lymphospecific toxicity in this condition might result from the selective accumulation of toxic deoxya... Ausführliche Beschreibung

1. Person: Carson, Dennis A.
Weitere Personen: Wasson, Donald B. verfasserin; Kaye, Jonathan verfasserin; Ullman, Buddy verfasserin; Martin, David W. verfasserin; Robins, Roland K. verfasserin; Montgomery, John A. verfasserin
Quelle: in Proceedings of the National Academy of Sciences of the United States of America Vol. 77, No. 11 (1980), p. 6865-6869
Weitere Artikel
Format: Online-Artikel
Sprache: English
Veröffentlicht: 1980
Beschreibung: Online-Ressource
Schlagworte: research-article
Medical Sciences
Adenosine Deaminase
Chemotherapy
Online Zugang: Volltext
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100 1 |a Carson, Dennis A. 
245 1 0 |a Deoxycytidine Kinase-Mediated Toxicity of Deoxyadenosine Analogs toward Malignant Human Lymphoblasts in vitro and toward Murine L1210 Leukemia in vivo  |h Elektronische Ressource 
300 |a Online-Ressource 
520 |a An inherited deficiency of adenosine deaminase (adenosine aminohydrolase, EC 3.5.4.4) produces selective lymphopenia and immunodeficiency disease in humans. Previous experiments have suggested that lymphospecific toxicity in this condition might result from the selective accumulation of toxic deoxyadenosine nucleotides by lymphocytes with high deoxycytidine kinase levels and low deoxynucleotide dephosphorylating activity. The present experiments were designed to determine if deoxyadenosine analogs which are not substrates for adenosine deaminase might similarly be toxic toward lymphocytes and lymphoid tumors. Two such compounds, 2-chlorodeoxyadenosine and 2-fluorodeoxyadenosine, at concentrations of 3 nM and 0.15 μ M, respectively, inhibited by 50% the growth of human CCRF-CEM malignant lymphoblasts in vitro. Each was phosphorylated in intact cells by deoxycytidine kinase, accumulated as the nucleoside triphosphate, and inhibited DNA synthesis more than RNA synthesis. Both deoxynucleosides had significant chemotherapeutic activity against lymphoid leukemia L1210 in mice. 
653 |a research-article 
653 |a Medical Sciences 
653 |a Adenosine Deaminase 
653 |a Chemotherapy 
700 1 |a Wasson, Donald B.  |e verfasserin  |4 aut 
700 1 |a Kaye, Jonathan  |e verfasserin  |4 aut 
700 1 |a Ullman, Buddy  |e verfasserin  |4 aut 
700 1 |a Martin, David W.  |e verfasserin  |4 aut 
700 1 |a Robins, Roland K.  |e verfasserin  |4 aut 
700 1 |a Montgomery, John A.  |e verfasserin  |4 aut 
773 0 8 |i in  |t Proceedings of the National Academy of Sciences of the United States of America  |d Washington, DC : National Acad. of Sciences  |g Vol. 77, No. 11 (1980), p. 6865-6869  |q 77:11<6865-6869  |w (DE-601)JST069399220  |x 0027-8424 
856 4 1 |u https://www.jstor.org/stable/9662  |3 Volltext 
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951 |a AR 
952 |d 77  |j 1980  |e 11  |h 6865-6869 

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