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Direct single gene mutational events account for radiation-induced intestinal adenoma yields in Apc(Min/+) mice

Michele Ellender1, John D Harrison, Alan A Edwards

  • 1National Radiological Protection Board, Chilton, Didcot, Oxon, OX11 ORQ, United Kingdom. michele.ellender@nrpb.org

Radiation Research
|April 27, 2005
PubMed

Insights

X radiation induces small intestinal tumors in Apc(Min/+) mice. Loss of the Apc+ gene is sufficient for adenoma initiation, without requiring genomic instability.

Area of Science:

  • Oncology
  • Genetics
  • Radiation Biology

Background:

  • Apc(Min/+) mice are a model for intestinal adenoma development.
  • X radiation is known to induce mutations and tumors.

Purpose of the Study:

  • To investigate the role of X radiation in inducing small intestinal tumors in Apc(Min/+) mice.
  • To determine if direct gene mutation or genomic instability drives adenoma initiation.

Main Methods:

  • Induction of tumors using X radiation in Apc(Min/+) mice.
  • Comparison of tumor incidence with literature data on radiation-induced mutation frequencies.

Main Results:

  • X radiation induced small intestinal tumors, primarily adenomas.
  • The incidence of radiation-induced adenomas supports the hypothesis that loss of Apc+ is sufficient for initiation.
  • Adenoma initiation rates were comparable to or lower than direct somatic gene mutation frequencies.

Conclusions:

  • Direct mutational loss of Apc+ is the sole requirement for intestinal adenoma initiation in this model.
  • Genomic instability is not necessary for adenoma initiation, though it may play a role in tumor progression.

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