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Analysis of mechanism of carcinogenesis in uterine cervix of K5 E2F1 transgenic mice

Research Project

Project/Area Number 15591755
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Obstetrics and gynecology
Research InstitutionEhime University

Principal Investigator

MATSUMOTO Takashi  Ehime University, School of Medicine, Instructor, 医学部, 助手 (20346670)

Co-Investigator(Kenkyū-buntansha) UEDA Norifumi  Ehime University, School of Medicine, Professor, 医学部, 教授 (30030886)
ITO Masaharu  Ehime University, School of Medicine, Professor, 医学部, 教授 (10136731)
Project Period (FY) 2003 – 2004
Project Status Completed (Fiscal Year 2004)
Budget Amount *help
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2004: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2003: ¥1,900,000 (Direct Cost: ¥1,900,000)
KeywordsUterine cervical cancer / Animal model / Transgenic mice / E2F1 / Tumorigenesis
Research Abstract

The "high-risk" human papilloma viruses (HPVs), such as HPV-16 and-18, are found in 80-90% of invasive cancers of the uterine cervix. However, HPV-infection appears to be insufficient for carcinogenesis, because most lesions in human cervical squamous epithelium containing high-risk HPVs do not progress to invasive carcinoma. Furthermore, several researchers reported that HPV or E6/E7 transgenic mice developed cervical intraepithelial neoplasias, but not invasive cancers. These evidences suggested that the other genetic alterations in addition to HPV-infection might be also important for cervical carcinogenesis. Recently, we have established a lot of transgenic mice using specific keratin promoters, which developed various epithelial tumors including skin, prostate and gallbladder. In our more recent studies, the squamous epithelium of uterine cervix expressed K1, K5 and K14, and the reserve cells at the squamo-columnar junction had K5 expression. These results suggested that target ge … More nes might be overexpressed in uterine cervix of transgenic mice using specific keratin promoters. In this study, we analyzed female genital tract from our various transgenic mice, and finally we found that K5 E2F1 transgenic mice developed cancer of the uterine cervix. E2F1, as well as keratin 5, was overexpressed in the squamous epithelium of uterine cervix and cancer tissues from K5 E2F1 transgenic mice. In general, as requirements of an ideal adequate animal model of cancer, the tumors developing in such a model must display a reasonable degree of similarity with human cancer. Cervical cancers from K5 E2F1 transgenic mice were similar to human cervical cancers as follows: i)They were squamous cell carcinomas. ii)They developed from similar precursor lesions, cervical intraepithelial neoplasias (CINs). iii)They were metastasizing to pelvic lymph nodes.These data suggest that K5 E2F1 transgenic mice appear to be an exellent animal model for analysis of carcinogenesis of uterine cervix. Less

Report

(3 results)
  • 2004 Annual Research Report   Final Research Report Summary
  • 2003 Annual Research Report
  • Research Products

    (8 results)

All 2004 2003 Other

All Journal Article (6 results) Publications (2 results)

  • [Journal Article] Development of transgenic mice that inducibly express an active form of c-Src in the epidermis.2004

    • Author(s)
      Takashi Matsumoto et al.
    • Journal Title

      Molecular Carcinogenesis 40

      Pages: 189-200

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Annual Research Report 2004 Final Research Report Summary
  • [Journal Article] Development of transgenic mice that inducibly express an active form of c-Src in the epidermis2004

    • Author(s)
      Takashi Matsumoto, Kaoru Kiguchi, Jianghong Jiang, Steve Carbajal, Lynnsie Ruffino, Linda Beltran, Xiao-Jing Wang, Dennis R Roop, John DiGiovanni
    • Journal Title

      Mol Carcinog 40

      Pages: 189-200

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Tumor formation in mice with conditional inactivation of Brca1 in epithelial tissues2003

    • Author(s)
      Thomas R Berton, Takashi Matsumoto et al.
    • Journal Title

      Oncogene 22

      Pages: 5415-5426

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Targeted expression of c-src in epidermal basal cells leads to enhanced skin tumor promotion, malignant progression, and metastasis2003

    • Author(s)
      Takashi Matsumoto et al.
    • Journal Title

      Cancer Research 63

      Pages: 4819-4828

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Tumor formation in mice with conditional inactivation of Brca1 in epithelial tissues2003

    • Author(s)
      Thomas R Berton, Takashi Matsumoto, Angustias Page, Claudio J Conti, Chu-Xia, Deng, Jose L Jorcano, David G Johnson
    • Journal Title

      Oncogene 22

      Pages: 5415-5426

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Overexpression of c-src in epidermal basal cells of transgenic mice leads to enhanced skin tumor promotion, malignant progression, and metastasis2003

    • Author(s)
      Takashi Matsumoto, Jianghong Jiang, Kaoru Kiguchi, Lynnsie Ruffino, Steve Carbajal, Linda Beltran, David Bol, Michael P Rosenberg, John DiGiovanni
    • Journal Title

      Cancer Res 63

      Pages: 4819-4828

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Publications] Thomas R Berton, Takashi Matsumoto et al.: "Tumor formation in mice with conditional inactivation of Brca1 in epithelial tissues"Oncogene. 22. 5415-5426 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] Takashi Matsumoto et al.: "Targeted expression of c-src in epidermal basal cells leads to enhanced skin tumor promotion, malignant progression, and metastasis"Cancer Research. 63. 4819-4828 (2003)

    • Related Report
      2003 Annual Research Report

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Published: 2003-04-01   Modified: 2016-04-21  

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