1-beta-D-Arabinofuranosylcytosine is Cytotoxic in Quiescent Normal Lymphocytes Undergoing DNA Excision Repair

Material type: 文書・図像類

Author: Yamauchi, Takahiroほか

Publisher: Japanese Cancer Association

Publication date: 2002-12

Material Format: Digital

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Note (General)：: We have sought to clarify the potential activity of S-phase specific antileukemic agent 1--D-arabinofuranosylcytosine (ara-C), an inhibitor of DNA sy...

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Material Type: 文書・図像類
Title: 1-beta-D-Arabinofuranosylcytosine is Cytotoxic in Quiescent Normal Lymphocytes Undergoing DNA Excision Repair
Author/Editor: Yamauchi, Takahiro
Kawai, Yasukazu
Ueda, Takanori
Author Heading: Yamauchi, Takahiro
Kawai, Yasukazu
Ueda, Takanori
Publication, Distribution, etc.: Japanese Cancer Association
Publication Date: 2002-12
Publication Date (W3CDTF): 2002-12
Periodical title: Japanese journal of cancer research : Gann
No. or year of volume/issue: 93 12
Volume: 93
Issue: 12
Pages: 1334-1341
Text Language Code: eng
Subject Heading: ara-C
DNA repair
UV
BCNU
Comet assay
Target Audience: 一般
Note (General): We have sought to clarify the potential activity of S-phase specific antileukemic agent 1--D-arabinofuranosylcytosine (ara-C), an inhibitor of DNA synthesis, in quiescent cells that are substantially non-sensitive to nucleoside analogues. It was hypothesized that the combination of ara-C with DNA damaging agents that initiate DNA repair will expand ara-C cytotoxicity to non-cycling cells. The repair kinetics, which included incision of damaged DNA, gap filling by DNA synthesis and rejoining by ligation, were evaluated using the single cell gel electrophoresis (Comet) assay and the thymidine incorporation assay. When normal lymphocytes were treated with ultraviolet C or with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), the processes of DNA excision repair were promptly initiated and rapidly completed. When the cells were incubated with ara-C prior to irradiation or BCNU treatment, the steps of DNA synthesis and rejoining in the repair processes were both inhibited. ara-C-mediated inhibition of the repair processes was concentration-dependent, with the effect peaking at 10 μM. ara-C combined with these DNA repair initiators exerted the subsequent cytotoxicity, which was proportional to the extent of the repair inhibition in the presence of ara-C. In conclusion, ara-C was cytotoxic in quiescent cells undergoing DNA repair. This might be attributed to unrepaired DNA damage that remained in the cells thereby inducing lethal cytotoxicity. Or, alternatively, ara-C might exert its own cytotoxicity by inhibiting DNA synthesis in the repair processes. Such a strategy may be effective against a dormant subpopulation in acute leukemia that survives the chemotherapy.
Source: https://u-fukui.repo.nii.ac.jp/?action=repository_action_common_download&item_id=20281&item_no=1&attribute_id=22&file_no=1
https://u-fukui.repo.nii.ac.jp/?action=repository_action_common_download&item_id=20281&item_no=1&attribute_id=22&file_no=1
Access Restrictions: 限定公開
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 福井大学 : 福井大学学術機関リポジトリ