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Transforming activity of DNA from rat liver tumors induced by the carcinogen methyl(acetoxymethyl)nitrosamine

M Goyette1, M Dolan, W Kaufmann

  • 1Department of Pathology and Laboratory Medicine, Brown University, Providence, Rhode Island 02912.

Molecular Carcinogenesis
|January 1, 1988
PubMed

Insights

Ras gene mutations are infrequent in rat liver cancer induced by methyl(acetoxymethyl)nitrosamine. Instead, other activated genes, not homologous to common oncogenes, drive tumor development and NIH 3T3 cell transformation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Hepatocarcinogenesis

Background:

  • Altered c-Ha-ras genes are common in mouse liver tumors.
  • Ras gene mutations are suspected drivers of carcinogenesis.

Purpose of the Study:

  • To investigate ras gene mutation frequency during rat liver carcinogenesis.
  • To identify activated oncogenes in methyl(acetoxymethyl)nitrosamine-induced rat liver tumors.

Main Methods:

  • Induction of rat liver tumors using methyl(acetoxymethyl)nitrosamine and phenobarbital.
  • DNA extraction from tumors and NIH 3T3 cell transfection assays.
  • Southern blot analysis to identify transforming genes in transfectants.

Main Results:

  • Six of eight tumor DNAs induced NIH 3T3 cell transformation.
  • Transforming activity was stable and tumorigenic in nude mice.
  • Ras gene family members (Ha, Ki, N), neu, myc, A-raf, v-raf, erbA, or erbB were not responsible for transformation.

Conclusions:

  • Ras gene alterations are infrequent in this rat hepatocarcinogenesis model.
  • Novel, non-ras oncogenes are activated during DMN-OAc-induced liver cancer.
  • These activated genes are capable of NIH 3T3 cell transformation.

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