Alkylator-Induced DNA Excision Repair in Human Leukemia CCRF-CEM Cells In Vitro, Measured Using the Single-Cell Gel Electrophoresis (Comet) Assay

Material type: 文書・図像類

Author: Yamauchi, Takahiroほか

Publisher: 日本血液学会

Publication date: 2002-11

Material Format: Digital

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Note (General)：: The capacity to repair DNA damage is an important factor that affects the therapeutic outcome in cancer treatment. To clarify the cellular repair resp...

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Material Type: 文書・図像類
Title: Alkylator-Induced DNA Excision Repair in Human Leukemia CCRF-CEM Cells In Vitro, Measured Using the Single-Cell Gel Electrophoresis (Comet) Assay
Author/Editor: Yamauchi, Takahiro
Kawai, Yasukazu
Ueda, Takanori
Author Heading: Yamauchi, Takahiro
Kawai, Yasukazu
Ueda, Takanori
Publication, Distribution, etc.: 日本血液学会
Publication Date: 2002-11
Publication Date (W3CDTF): 2002-11
Periodical title: International Journal of Hematology
No. or year of volume/issue: 76 4
Volume: 76
Issue: 4
Pages: 328-332
Text Language Code: eng
Subject Heading: Alkylating agent
DNA excision repair
Drug resistance
Comet assay
Target Audience: 一般
Note (General): The capacity to repair DNA damage is an important factor that affects the therapeutic outcome in cancer treatment. To clarify the cellular repair response, we investigated the kinetics of DNA excision repair initiated by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in human leukemia CCRF-CEM cells at an exponential growth phase in vitro. Using the alkaline single-cell gel electrophoresis (comet) assay, we quantitated the repair kinetics as the amount of DNA single-strand breaks that were generated from the incision and were diminished by the rejoining in the repair process. CEM cells could initiate DNA excision repair in response to BCNU by starting an incision reaction. However, the incision capacity came to a plateau at a concentration of 80 to 1003M or after an incubation time of 90 to 120 minutes. When the cells were pulsed with 403M BCNU, the maximal incision occurred at the end of the incubation period, and the repair process was completed within 4 hours.When cells were treated with 1003M BCNU, the incised DNA was not rejoined at 4 hours, suggesting that the repair was not completed. Higher concentrations might surpass the cellular capacity for repair and would be associated with increased cell death. Evaluation of the repair process may provide a clue for therapeutic strategies to improve clinical efficacy if accelerated DNA repair is responsible for the drug resistance.
Source: https://u-fukui.repo.nii.ac.jp/?action=repository_action_common_download&item_id=20452&item_no=1&attribute_id=22&file_no=1
https://u-fukui.repo.nii.ac.jp/?action=repository_action_common_download&item_id=20452&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