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Protection against human papillomavirus type 16-E7 oncogene- induced tumorigenesis by in vivo expression of dominant- negative c-jun

  1. Author:
    Young, M. R.
    Farrell, L.
    Lambert, P.
    Awasthi, P.
    Colburn, N. H.

  2. Author Address

    NCI, Basic Res Lab, POB B, Frederick, MD 21702 USA NCI, Basic Res Lab, Frederick, MD 21702 USA Univ Wisconsin, Sch Med, Dept Pathol, McArdle Lab Canc Res, Madison, WI 53706 USA SAIC Frederick, Lab Anim Sci Program, Frederick, MD USA Young MR NCI, Basic Res Lab, POB B, Frederick, MD 21702 USA
    1. Year: 2002
  2. Journal: Molecular Carcinogenesis
    1. 34
    2. 2
    3. Pages: 72-77
  4. Type of Article: Article
  1. Abstract:

    Expression of the human papillomavirus (HPV) type 16 E6 and E7 gene products is a risk factor for human cervical carcinogenesis as well as skin and oral carcinogenesis. Expression of the HPV-16 E7 gene in mouse skin induces hyperplasia and enhances tumor promotion. Expression of dominant-negative c-jun (TAM67) in the mouse skin protects mice from 7,12-dimethylbenz[a]anthracene (DMBA)/12-O- tetradecanoylphorbol-13-acetate (TPA)-induced papillomagenesis without blocking mitogen-induced hyperproliferation. To determine the role of activator protein-1 (AP-1) in HPV-induced cancer, we crossed HPV-16 E7 mice with TAM67 mice and analyzed the effects of DMBA/TPA on tumor promotion. We showed that expression of TAM67 protected mice from HPV-16 E7-enhanced tumorigenesis, suggesting AP-1 as a target for prevention of HPV-induced cancer. Published 2002 Wiley-Liss, Inc.(dagger)

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