| Susceptibility to cytosine arabinoside (Ara-C)-induced cytotoxicity in human leukemia cell lines. | |
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MedLine Citation:
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PMID: 15302096 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cytosine arabinoside (1-beta-d-arabinofuranosylcytosine; Ara-C) is the most important antimetabolite chemotherapeutic drug used for acute leukemia. We examined the difference in susceptibility to Ara-C-induced cell death among a number of typical human leukemia cell lines, NALM-6, MOLT-4, Jurkat, U937 and HL-60. NALM-6, which had a high expression level of p53, a tumor suppressor gene, was most susceptible to Ara-C. U937 and HL-60, with p53-null human leukemia cell lines were little affected by Ara-C. There was not always a correlation between susceptibility and the uptake of Ara-C. The production of reactive oxygen species (ROS) was increased in all leukemia cells. Pifithrin-alpha, a chemical inhibitor of wild-type p53, ameliorated the cytotoxicity of Ara-C in NALM-6 and MOLT-4, but not Jurkat, U937 or HL-60. Our data suggest that the mechanism of Ara-C-induced cell death is a common one, involving an increase in the production of ROS and p53-dependent cell death. |
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Authors:
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Syu-Ichi Kanno; Ayako Higurashi; Yurie Watanabe; Ai Shouji; Keiko Asou; Masaaki Ishikawa |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Toxicology letters Volume: 152 ISSN: 0378-4274 ISO Abbreviation: Toxicol. Lett. Publication Date: 2004 Sep |
Date Detail:
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Created Date: 2004-08-10 Completed Date: 2004-10-21 Revised Date: 2005-11-17 |
Medline Journal Info:
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Nlm Unique ID: 7709027 Medline TA: Toxicol Lett Country: Netherlands |
Other Details:
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Languages: eng Pagination: 149-58 Citation Subset: IM |
Affiliation:
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Department of Pharmacology and Toxicology, Cancer Research Institute, Tohoku Pharmaceutical University, 4-4-1 Komatsushima, Aoba-ku, Sendai 981-8558, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antimetabolites, Antineoplastic
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pharmacology* Apoptosis / drug effects Cell Line, Tumor Cell Nucleus / drug effects, pathology Cytarabine / metabolism, pharmacology* Dose-Response Relationship, Drug Gene Expression Regulation, Neoplastic / drug effects* Genes, p53 Humans Leukemia / drug therapy, genetics*, pathology RNA, Messenger / genetics, metabolism Reactive Oxygen Species / metabolism Reverse Transcriptase Polymerase Chain Reaction Tumor Suppressor Protein p53 / genetics, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Antimetabolites, Antineoplastic; 0/RNA, Messenger; 0/Reactive Oxygen Species; 0/Tumor Suppressor Protein p53; 147-94-4/Cytarabine |
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