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Analysis of transforming genes in indirectly induced radiogenic thymomas in mice

O Niwa1, M Muto, F Suzuki

  • 1Department of Pathology, Hiroshima University, Japan.

Journal of Radiation Research
|December 1, 1991
PubMed

Insights

Radiation and chemical exposures induce mouse tumors through different oncogene pathways. While chemical carcinogens amplify the myc oncogene, radiation-induced tumors show K-ras activation and tumor suppressor gene inactivation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Oncogene expression is crucial in tumor development.
  • Understanding oncogene activation mechanisms in radiation-induced vs. chemically-induced mouse tumors is important.

Purpose of the Study:

  • To investigate oncogene expression and activation in mouse tumors induced by radiation and chemicals.
  • To differentiate the molecular mechanisms underlying radiation versus chemical carcinogenesis.

Main Methods:

  • Analysis of oncogene amplification (myc) and activation (K-ras) in various mouse tumors.
  • DNA analysis including loss of heterozygosity and minisatellite locus analysis in radiogenic thymomas.
  • Transfection of cellular DNA into Golden hamster cells to identify activated oncogenes.

Main Results:

  • Chemically induced sarcomas showed myc oncogene amplification.
  • Radiation-induced thymomas exhibited loss of heterozygosity and activated K-ras oncogene.
  • Indirectly induced radiogenic thymomas lacked mouse ras oncogenes, suggesting spontaneous activation of unknown oncogenes.

Conclusions:

  • Chemically induced tumors primarily involve myc amplification.
  • Radiation carcinogenesis involves complex mechanisms including K-ras activation and tumor suppressor gene inactivation.
  • Indirectly induced radiation tumors may arise from spontaneous activation of unidentified oncogenes.

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