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ESTABLISHMENT OF MODELS OF PRECANCEROUS OR CANCEROUS CELLS BY ONCOGENIC TRANSFORMATION OF NORMAL KERATINOCYTES FROM NORMAL HUMAN ORAL CAVITIES

Research Project

Project/Area Number10557186
Research Category

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

Allocation TypeSingle-year Grants
Section展開研究
Research Field Surgical dentistry
Research InstitutionTOKYO MEDICALAND DENTAL UNIVERSITY

Principal Investigator

SAKAI Eiki  Graduate School, Tokyo Medical and Dental University, Research Associate, 大学院・医歯学総合研究科, 助手 (60292976)

上田 晶義(1998)  医科歯科大, 歯学部, 助手 (00272609)

Co-Investigator(Kenkyū-buntansha) 平野 泰正  東京医科歯科大学, 歯学部, 助手
Project Period (FY) 1998 – 2000
Project Status Completed(Fiscal Year 2000)
Budget Amount *help
¥12,400,000 (Direct Cost : ¥12,400,000)
Fiscal Year 2000 : ¥1,800,000 (Direct Cost : ¥1,800,000)
Fiscal Year 1999 : ¥3,400,000 (Direct Cost : ¥3,400,000)
Fiscal Year 1998 : ¥7,200,000 (Direct Cost : ¥7,200,000)
KeywordsORAL CANCER / TELOMERASE / N0RAMAL HUMAN KERATINOCYTE / 口腔粘膜上皮角化培養細胞 / テロメテーゼ / ヒト口腔粘膜由来初代培養細胞 / 変異型p53癌抑制遺伝子 / H-ras / SV40 large T / TERT / 口腔粘膜 / ヒト正常粘膜角化細胞 / p53癌抑制遺伝子変異 / アデノウイルスベクター / mRNAサプトラクション法
Research Abstract

We studied these themes shown below.
(1) Expression of telomerase activity between cell lines established from human oral squamous cell carcinomas and primary cultured keratinocytes from noraml oral cavities
(2) Expression of telomerase activity between oral squamous cell carcinoma tissues, leukoplakias and normal mucosa from oral cavities
We detected high telomerase activity in all cell lines though 2cell lines showed statistically lower activity than others. But the reasons or the genetical difference for example, expression level of protein of p53, p16 and EGFR still remain unclear. In 6 cell lines, we reported previously mutation of p53 or H-ras, we found that both pathway of p53 and Rb were disrupted samely as shown by Winberg et al.
We detected telomerase activity in 77% of oral squamous cell carcinoma tissues and 47% of leukoplakias while all normal tissues showed no telomerase activity. The activity of the carcinoma tissues showed higher than these of leukoplakias. Furthermore, we detected telomerase activity in 47% of leukoplakias, in spite of almost all lekoplakias we analized showed slight dysplasia. It might suggests that telomerase is activated and cells itself start to gain the ability of immortalization even in the early stage of precancer.

Report

(4results)
  • 2000 Annual Research Report   Final Research Report Summary
  • 1999 Annual Research Report
  • 1998 Annual Research Report

Research Products

(6results)

All Other

All Publications

  • [Publications] 島本裕彰: "口腔扁平上皮癌および白板症におけるテロメラーゼ活性"口腔病学会雑誌. 第68巻第1号. 125-133 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] 中島雄介: "B-mybおよびE2F2プロモーターの転写抑制配列に結合する因子とE2F/Rbファミリータンパク質の相互作用"口腔病学会雑誌. 第65巻第2号. 172-188 (1997)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Hiroaki Shimamoto: "Telomerase Activity in Oral Squamous Cell Carcinoma and Leukoplakias"THE JOURANAL OF THE ST0MAT0L0GICAL SOCIETY, JAPAN. 68(1). 125-133 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Yusuke Nakajima: "Interaction of E2F/Rb Family Members with Factor Binding to Co-repressor Eletnent on B-myb and E2F1 Promoters"THE JOURANAL OF THE STOMATOL0GICAL SOCIETY, JAPAIN. 65(2). 172-188 (1997)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] 島本裕彰: "口腔扁平上皮癌および白板症におけるテロメレーゼ活性"口腔病学会雑誌. 第68巻第1号. 125-133 (2001)

    • Related Report
      2000 Annual Research Report
  • [Publications] 中島雄介: "B-mybおよびE2F2プロモーターの転写抑制配列に結合する因子とE2F/Rbファミリータンパク質の相互作用"口腔病学会雑誌. 第65巻第2号. 172-188 (1998)

    • Related Report
      2000 Annual Research Report

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Published : 1998-04-01   Modified : 2016-04-21  

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