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Epidermal Growth Factor and Transforming Growth Factor-Alpha-Associated Overexpression of Cyclin D1, Cdk4, and C-Myc During Hepatocarcinogenesis in Helicobacter Hepaticus-Infected a/Jcr Mice

  1. Author:
    Ramljak, D.
    Jones, A. B.
    Diwan, B. A.
    Perantoni, A. O.
    Hochadel, J. F.
    Anderson, L. M.
    1. Year: 1998
  2. Journal: Cancer Research
    1. 58
    2. 16
    3. Pages: 3590-3597
  4. Type of Article: Article
  1. Abstract:

    Helicobacter hepaticus is a new bacterial species that is homologous to Helicobacter pylori, a human gastric carcinogen. H. hepaticus causes chronic active hepatitis, with progression to hepatocellular tumors. We hypothesized that chronic up-regulation of epidermal growth factor (EGF), transforming growth factor-alpha, and nuclear oncogenes (cyclin D1 and c-Myc), all known to transform by overexpression, might contribute to tumorigenesis. Livers from mice that were 6-18 months old mere analyzed, including nonneoplastic and preneoplastic tissues and turners, along with age-matched controls, by immunohistochemistry and immunoblotting. EGF and transforming growth factor-cr mere increased at the earliest stage, with a further increase in EGF in tumors. Cyclin D1, cyclin-dependent kinase 4, and c-Myc were strongly increased in all infected livers, with even greater increases in tumors. An increase in cyclin D1/cyclin-dependent kinase 4 complex was also demonstrated in tumors, and its functionality mas confirmed by an increase in the hyperphosphorylated:hypophosphorylated retinoblastoma protein ratio. Our findings suggest a possible cooperation of growth factors, cell cycle proteins, and transcription factors during the development of H. hepaticus-associated liver tumors and may have relevance to human cancers associated with bacterial, viral, or parasitic infections. [References: 40]

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