• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to project page

2007 Fiscal Year Final Research Report Summary

Inhibition of radiation-induced DNA dsbs repair by inducing misrejoining and its clinical application

Research Project

Project/Area Number 18591378
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Radiation science
Research InstitutionChiba University

Principal Investigator

ITO Hisao  Chiba University, Graduate School of Med, Professor (20095574)

Co-Investigator(Kenkyū-buntansha) KAWATA Tetsuya  Chiba University, Graduate School of Med, Associate Prof (60234077)
UNO Takashi  Chiba University, Graduate School of Med, Associate Prof (30302540)
ISOBE Koichi  Chiba University, Hospital, Associate Prof (80334184)
Project Period (FY) 2006 – 2007
KeywordsATM / siRNA / radiation damage / chromosome aberration
Research Abstract

The purpose of this study was to inhibit repair of radiation-induced DNA damages in malignant cells by using siRNA for ATM gene and other chemical components. To achieve this purpose, we designed in-vitro and in-vivo experiments. When exponentially growing normal and cancer cells were treated with sIRNA for ATM gene, radiation-sensitivity was enhanced. However, when non-cycling normal cells (GO) cells were treated with siRNA before irradiation, no significant change in sensitivity was observed, suggesting that siRNA may not work on non-cycling cells. To study the effect of siRNA in vivo, Hela cells (human uterine cancer cells) was transplanted to Balb/c nu/nu mice. After two weeks, ATM siRNA (12 nM) was injected directly and 24 - 72 hour later tumors were irradiated with X-rays. It was found that the maximum effect was observed when siRNA was injected around 48 hour before irradiation. Lb study synergistic effect of ATMsiRNA with radiation, mice tumors were irradiated with 4 Gy per day up to total dose of 20 Gy. During this treatment, siRNA was injected twice, I.e, 24 hour before irradiation and after second irradiation. The tumor volume was compared with non-treated mice. It was found after 21 day, tumor size was found to increase up to 6.5 times for non-irradiated mice, 4.5 times for only irradiation group and 3 times for mice treated with siRNA with irradiation. Further study was underway by using ATM specific inhibitor to understand the function of ATM gene for radiation-repair pathway.

  • Research Products

    (4 results)

All 2008 2007

All Journal Article (2 results) Presentation (2 results)

  • [Journal Article] 粒子線照射された線維芽細胞における染色体異常の細胞周期依存性に関する研究2008

    • Author(s)
      川田哲也、伊東久夫、他
    • Journal Title

      重粒子がん治療装置等共同利用研究報告書 平成19年版

      Pages: 77-79

    • Description
      「研究成果報告書概要(和文)」より
  • [Journal Article] Comparison of G1 and G2 phase chromosome aberrations in human fibroblasts exposed to low- or high-LET radiations2008

    • Author(s)
      Kawata, T., Hisao, Ito., et. al.
    • Journal Title

      2007 Annual report of the research project with heavy ions at NIRS-HIMAC

      Pages: 77-79

    • Description
      「研究成果報告書概要(欧文)」より
  • [Presentation] Inhibition of ATM may induce high frequency of misrepair in normal and AT heterozygous fibroblast cells.2007

    • Author(s)
      川田哲也、伊東 久夫 他
    • Organizer
      International Congress of Radiation Research
    • Place of Presentation
      米国サンフランシスコ
    • Year and Date
      20070708-12
    • Description
      「研究成果報告書概要(和文)」より
  • [Presentation] Inhibition of ATM may induce high frequency of Misrepair in normal and AT heterozygous fibroblast cells2007

    • Author(s)
      Kawata T, Ito H, et. al.
    • Organizer
      ICRR (International Congress of Radiation Research)
    • Place of Presentation
      San Francisco, USA
    • Year and Date
      20070708-12
    • Description
      「研究成果報告書概要(欧文)」より

URL: 

Published: 2010-02-04  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi