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Mutation of ras oncogene in di-isopropanolnitrosamine-induced rat thyroid carcinogenesis

Yoshihiko Kobayashi1, Akira Kawaoi, Ryohei Katoh

  • 1Fuji Biomedix Co., Ltd. Kobuchizawa Laboratories 10221, Kobuchizawa-cho, Kitakoma-gun, Yamanashi-ken, 408-0044, Japan.

Insights

K-ras gene mutations are frequent in rat thyroid nodules induced by di-isopropanolnitrosamine (DIPN). This ras gene mutation appears to be an early event in thyroid tumorigenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Thyroid tumorigenesis involves complex genetic alterations.
  • The role of ras gene mutations in chemically induced thyroid tumors requires further elucidation.

Purpose of the Study:

  • To investigate the incidence and role of K-ras gene mutations in rat thyroid lesions induced by di-isopropanolnitrosamine (DIPN).

Main Methods:

  • DNA extraction from rat thyroid lesions.
  • Microdissection-Polymerase Chain Reaction-Direct Sequencing (MD-PCR-DS) for mutation analysis.

Main Results:

  • K-ras gene mutation (G-A transition at codon 12) was detected in 75% of nodular lesions.
  • Mutations were absent in diffuse hyperplastic and pre-nodular lesions.
  • Mutation incidence correlated with DIPN administration method (serial vs. single injection).

Conclusions:

  • K-ras mutation is a significant factor in DIPN-induced rat thyroid tumorigenesis.
  • K-ras mutation may represent an early event in this process.

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