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The aberrant expression by the target genes of tumor supressor protein p53 in non- small cell lung cancer. A search for a new mechanism of carcinogenesis.

Research Project

Project/Area Number 08670647
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionTohoku University

Principal Investigator

EBINA Masahito  Tohoku University, Institute of Development, Aging and Cancer Instructor, 加齢医学研究所, 助手 (10280885)

Project Period (FY) 1996 – 1997
Project Status Completed (Fiscal Year 1997)
Budget Amount *help
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1997: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1996: ¥800,000 (Direct Cost: ¥800,000)
Keywordslung cancer / tumor supressor gene / p53 / p21Waf1 / Cip1 / MDM2 / GADD45 / Wafl / Cipl / Waf1 / CiPl
Research Abstract

While p53 overexpression is often associated with p53 mutaions, the abnormalities in downstream of p53 transactivation may also contribute to the overexpression and dysfunction of p53 protein. In this study, the expressions of p53, Mdm2, and p21WAF1/CIP1 were examined by immunohistochemistry, and the mutations of p21 and GADD45 were searched by PCR-SSCP in a cohort of 123 patients with NSCLC of all stages, incluging 71 primary lung tumors and 52 metastatic tumors. Sixty-three patients received potentially curative treatment (stages I,II and IIIA) and 60 patients palliative treatment (stages IIIB and IV). Of all tumors, 39% were positive for p53 (DO-7, Dako) and 18% were positive for Mdm2 (Ab-1, Oncogene Science). As for p21 (Ab-1, Oncogene Science), 75% of the tumors were negative while the rest of the tumors expressed variable amounts. While the expression of p53 and p21 was independent, Mdm2 appeared to be coexpressed with p53 (p2=0.013) and p21 (p2=0.001). In the patients treated with curarive intent, the probability of survival or development of metastases according to Kaplan-Meier method showed limited number of associations with p53 or Mdm2 expression. Cox proportional hazards model only associated the overexpression of p53 (p=0.0001) with shortened survival and the development of metastases in these patients. the results that no mutations were found in the coding region of p21 and GADD45, revealed the alterations of the p53 gene products are the main cause of the carcinogenesis. The heterogeneous expression of p53, Mdm2, and p21 in NSCLC suggested multiple mechanisms of transactivating or suppressing transactivation factors contributing to carcinogenesis.

Report

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

    (10 results)

All Other

All Publications (10 results)

  • [Publications] 海老名 雅仁, 他: "非小細胞性肺癌組織における癌抑制遺伝子p53とその標的遺伝子産物p21Waf1/Cip1の発現異常の病理学的比較及び臨床的意義" Proccedings of the Japanese Cancer Association. 55. 548- (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Ebina, M, et al.: "Abnormal expression of p53 and its down-regulating proteins in non-small cell lung cancer(NSCLC).A clinicopathologic study." Proccedings of the American Association for Cancer Research. 37. 567- (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Kanazawa, H, Ebina, M, et al.: "The immunohistochemical and genetic approach to the clonality of adenosquamous carcioma of the lung." Proccedings of the American Association for Cancer Research. 38. 327- (1997)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Ebina M,et al.: "Abnormal expression of p53 and its down-regulating proteins in non-small cell lung cancer (NSCLC). A clinicopathologic study." Proceedings of the American Association for Cancer Research. 37. 567 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Kanazawa H,Ebina M,et al.: "The immunohistochemical and genetic approach to the clonality of adenosquamous carcioma of the lung" Proceedings of the American Association for Cancer Research.38. 327 (1997)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Kanazawa H, Ebina M, et al.: "The immunohistochemical and genetic approach to the clonality of adenosquammous carcinoma of the lung." Proceedings of the American Association for Cancer Research. 38. 327- (1997)

    • Related Report
      1997 Annual Research Report
  • [Publications] 金澤裕信, 海老名雅仁, 他: "肺腺扁平上皮癌におけるclonality-免疫組織学的および遺伝子学的検討" 日本胸部疾患学会雑誌. 35. 297- (1997)

    • Related Report
      1997 Annual Research Report
  • [Publications] 金澤裕信, 海老名雅仁, 他: "肺腺扁平上皮癌の発生機序-免疫組織学的及び遺伝子学的検討" Proceedings of the Japanese Cancer Association. 56. 537- (1997)

    • Related Report
      1997 Annual Research Report
  • [Publications] 海老名 雅仁 他: "非小細胞肺癌組織における癌抑制遺伝子p53とその標的遺伝子の産物p21WAfl/CiPl, MDM2の発明異常の病理学的比較及び臨床的意義" Proceedings of the Japanese Cancer Association. 55. 548- (1996)

    • Related Report
      1996 Annual Research Report
  • [Publications] EBINA M, et al.: "Abnormal expression of p53 and its down-regulating Proteins in non-samll cell wing cancer (NSCLC). A clinicapathologital study" Proceedings of the American Association for Cancer Research. 37. 567- (1996)

    • Related Report
      1996 Annual Research Report

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

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