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Experimental therapeutics for gastric cancer using adenovirus vectors

Research Project

Project/Area Number 08671476
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Digestive surgery
Research InstitutionNARA MEDICAL UNIVERSITY

Principal Investigator

YAMADA Yukishige (1998)  Nara Medical University, First Departmentof Surgery, Research Associate, 医学部, 助手 (50254496)

渡辺 明彦 (1996-1997)  奈良県立医科大学, 医学部, 講師 (80211671)

Co-Investigator(Kenkyū-buntansha) SAWADA Hidetomo  Nara Medical University, First Departmentof Surgery, Assistant professor, 医学部, 講師 (10206021)
山田 行重  奈良県立医科大学, 医学部, 助手 (50254496)
Project Period (FY) 1996 – 1998
Project Status Completed (Fiscal Year 1998)
Budget Amount *help
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
KeywordsGastric Cancer / Adenovirus Vector / アデノウィルスベクター / アデノウィルス
Research Abstract

1) EGER and c-met expression after EGFR and c-met antisense expressing adenovirus in gastric cancer cells
Following infection with EGFR or c-met antisense RNA-expressing adenovirus(Ad-EAS or Ad-MAS), the cell surface EGER or c-met protein levels of infected cancer cell were observed by immunocytological method resulting in that markedly reduction of these proteins respectively. These suppression was not observed in non-infection or beta-galactosidase expressing adenovirus(Ad-GAL) infected group.
2) The effect of Ad-EAS virus on the growth of gastric cancer cells in vitro and in vivo.
Following infection with EGFR antisense RNA-expressing adenovirus(Ad-EAS), the in vitro growth of Ad-EAS infected cells was significantly inhibited relative to control infected cells in 3 gastric cancer cell lines (AGS, KKLS, MKN28) studied here(p(]SY.di-substituted right.[)O.0002). In a nude mouse subcutaneous tumor system, in vivo tumor growth of MKN28 was significantly inhibited after Ad-EAS treatment, and the inhibition on the 48th day was 93% by volume compared to that of untreated controls.
3) The effect of Ad-MAS virus on cancer cell motility in gastric cancer cells.
After Ad-MAS virus infection, the cell motility of AGS (c-met expressing) and Hs746t (c-met overexpressing) were significantly inhibited in comparison with control groups. The inhibition rate compare to non-infection group were 88% in AGS and 45% in Hs746t, respectively. These motility inhibition was not observed in KKLS cell (c-met non-expressing).

Report

(4 results)
  • 1998 Annual Research Report   Final Research Report Summary
  • 1997 Annual Research Report
  • 1996 Annual Research Report
  • Research Products

    (4 results)

All Other

All Publications (4 results)

  • [Publications] H.Sawada: "Efficiency of gene transfer into human gastric carcinoma cells using adenovirus vector" Progress in Gastric Cancer Research. 677-681 (1997)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] T.Hirao: "Antisense EGFR Delivered by Adenoviral Vector Blocks Tumor Growth in Human Gastric Cancer" Cancer gene therapy. (in press). (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] H.SAWADA et.al.: "Efficiency of gene transfer into human gastric carcinoma cells using adenovirus vector" Progress in Gastric Cancer Research. 677-681 (1997)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] T.HIRAO , H.SAWADA, et.al.: "Antisense EGFR delivered by adenoviral vector blocks tumor growth in human gastric cancer." Cancer Gene Therapy. (in press). (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1998 Final Research Report Summary

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Published: 1996-04-01   Modified: 2016-04-21  

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