Abstract | BACKGROUND: METHODS: In the present study, we developed a novel ara-G-resistant variant (CEM/ ara-G) of human T- lymphoblastic leukemia cell line CCRF-CEM, and elucidated its mechanism of ara-G resistance. The cytotoxicity was measured by using the growth inhibition assay and the induction of apoptosis. Intracellular triphosphate concentrations were quantitated by using HPLC. DNA synthesis was evaluated by the incorporation of tritiated thymidine into DNA. Protein expression levels were determined by using Western blotting. RESULTS: CONCLUSIONS: An ara-G-resistant CEM variant was successfully established. The mechanisms of resistance included reduced drug incorporation into nuclear DNA and antiapoptosis.
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Authors | Takahiro Yamauchi, Kanako Uzui, Rie Nishi, Hiroko Shigemi, Takanori Ueda |
Journal | BMC cancer
(BMC Cancer)
Vol. 14
Pg. 547
(Jul 29 2014)
ISSN: 1471-2407 [Electronic] England |
PMID | 25070259
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antineoplastic Agents
- Arabinonucleosides
- 9-arabinofuranosylguanine
- nelarabine
- DNA
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Topics |
- Antineoplastic Agents
(metabolism, pharmacology)
- Apoptosis
(drug effects)
- Arabinonucleosides
(metabolism, pharmacology)
- Cell Line, Tumor
- DNA
(metabolism)
- DNA Replication
(drug effects)
- Drug Resistance, Neoplasm
(drug effects)
- Humans
- Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
(genetics, pathology)
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