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in vitro manipulation of genes relevant to oncogenesis

Research Project

Project/Area Number 06454608
Research Category

Grant-in-Aid for General Scientific Research (B)

Allocation TypeSingle-year Grants
Research Field Human genetics
Research InstitutionMedical Institute of Bioregulation, Kyushu University

Principal Investigator

SASAZUKI Takehiko  Medical Institute of Bioregulation, Kyushu University, Professor, 生体防御医学研究所, 教授 (50014121)

Co-Investigator(Kenkyū-buntansha) YAMAMOTO Ken  Medical Institute of Bioregulation Kyushu University, Assistant Professor, 生体防御医学研究所, 助手 (60274528)
FUKUI Yoshinori  Medical Institute of Bioregulation Kyushu University, Assistant Professor, 生体防御医学研究所, 助手 (60243961)
KAMIKAWAJI Nobuhiro  Medical Institute of Bioregulation Kyushu University, Assistant Professor, 生体防御医学研究所, 助手 (90224659)
TANIGUCHI Shunichiro  Sinshu University, School of Medicine Professor, 医学部, 教授 (60117166)
木村 彰方  九州大学, 生体防御医学研究所, 助教授 (60161551)
Project Period (FY) 1994 – 1995
Project Status Completed (Fiscal Year 1995)
Budget Amount *help
¥7,000,000 (Direct Cost: ¥7,000,000)
Fiscal Year 1995: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1994: ¥4,300,000 (Direct Cost: ¥4,300,000)
KeywordsColon cancer cell lines / homologous recombination / K-ras gene / 大腸癌細胞株 / 血管内皮増殖因子 / K-ras / P53 / 相同組み換え
Research Abstract

We have established the colon cancer cell lines in which the mutated K-ras gene was replaced by the normal K-ras gene, using homologous recombination. The comparative analyzes between these cell lines and the parental cell lines made it feasible to directly assess the role of the mutated K-ras gene in oncogenesis. As compared with the parental cell lines, the cell lines which lack the expression of the mutated K-ras gene showed the remarkable induction of C-fos and C-jun expression by the serum stimulation and the suppression of vascular endothelial growth factor (VEGF) production. These observations indicate that the mutated K-ras gene is involved in the suppression of the immediate early genes expression and the production of VEGF.Our strategy could be applied to clarify the role of the mutation in other oncogenes and tumor suppressor genes in oncogenesis.

Report

(3 results)
  • 1995 Annual Research Report   Final Research Report Summary
  • 1994 Annual Research Report
  • Research Products

    (5 results)

All Other

All Publications (5 results)

  • [Publications] J. Rak et al.: "Mutant ras oncogenes upregulate VEGF/VPF expression: Implications for induction and inhibition of tumor angiogenesis" Cancer Research. 55. 4575-4580 (1995)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] J.Rak, Y.Mitsuhashi, L.Bayko, J.Filmus, S.Shirasawa, T.Sasazuki, and R.S.Curbel: "Mutant ras oncogenes upregulate VEGF/VPF expression : Implications for induction and inhibition of tumor angiogenesis" Cancer Research. vol.55. 4575-4580 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] J. Rak: "Mutant ras oncogenes upregulate VEGF/VPF expression: Implications for induction and inhibition of tumor angiogenesis" Cancer Research. 55. 4575-4580 (1995)

    • Related Report
      1995 Annual Research Report
  • [Publications] Rae SM.Yeung: "Human CD4-major histocompatibility complex class II(DQW6) transgenic mice in an endogenous CD4/CD8-deficient background:Reconstitution of phenotype and human restrieted function." J.Exp.Med.180. 1911-1920 (1994)

    • Related Report
      1994 Annual Research Report
  • [Publications] Yamamoto K.: "Functional interaction between human histocompatibility leukocyte antigen (HLA)class II and mouse CD4 molecule in antigen tecognition by T cells in HLA-DR and DQ transgenic mice." J.Exp.Med.180. 165-171 (1994)

    • Related Report
      1994 Annual Research Report

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Published: 1994-04-01   Modified: 2016-04-21  

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