Sequencing analysis of Ha‐, Ki‐, and N‐ras genes in rat urinary bladder tumors induced by N‐[4‐(5‐nitro‐2‐furyl)‐2‐thiazolyl]formamide (FANFT) and sodium saccharin

T. Masui, A. M. Mann, C. D. Borgeson, E. M. Garland, T. Okamura, H. Fujii, J. C. Pelling, Samuel Monroe Cohen

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Male F344 rats were fed N[4‐(5‐nitro‐2‐furyl)‐2‐thiazolyl]formamide (FANFT) for up to 4 wk, then given the basal diet with or without 5% sodium saccharin for up to 100 wk. In a previous study, we demonstrated point mutations in codons 12 and 61 of Ha‐ras gene among eleven transitional cell carcinomas (TCC), one undifferentiated carcinoma, and two sarcomas of the urinary bladder (Mol Carcinogen 3:210–215, 1990). In this study, Ha‐ras, Ki‐ras, and N‐ras sequences were examined by polymerase chain reaction (PCR) and direct DNA sequencing. The results confirm the point mutation in codon 61 (CAA to CGA in 5 TCCs and to CTA in one TCC) of the Ha‐ras gene. Mutation at codon 12 was not confirmed. No mutation was found in the Ki‐ras gene. Sequences of the N‐ras gene exons 1 and 2 were determined, and no mutations was detected. These results suggest the involvement of activated Ha‐ras gene, but not Ki‐N or N‐ras gene, in rat urinary bladder carcinogenesis induced by FANFT. Subsequent sodium saccharin administration did not affect the changes in Ha‐ras gene. ©1993 Wiley‐Liss, Inc.

Original languageEnglish (US)
Pages (from-to)225-233
Number of pages9
JournalTeratogenesis, Carcinogenesis, and Mutagenesis
Volume13
Issue number5
DOIs
StatePublished - 1993

Fingerprint

FANFT
Saccharin
Urinary Bladder Neoplasms
Rats
Tumors
Urinary Bladder
Genes
Codon
Transitional Cell Carcinoma
Point Mutation
Mutation
Polymerase chain reaction
Inbred F344 Rats
Nutrition
formamide
DNA Sequence Analysis
Sarcoma
Carcinogens
Exons
Carcinogenesis

Keywords

  • mutations
  • oncogenes
  • ras
  • rat urinary bladder carcinogenesis

ASJC Scopus subject areas

  • Oncology
  • Genetics
  • Toxicology
  • Genetics(clinical)
  • Health, Toxicology and Mutagenesis

Cite this

Sequencing analysis of Ha‐, Ki‐, and N‐ras genes in rat urinary bladder tumors induced by N‐[4‐(5‐nitro‐2‐furyl)‐2‐thiazolyl]formamide (FANFT) and sodium saccharin. / Masui, T.; Mann, A. M.; Borgeson, C. D.; Garland, E. M.; Okamura, T.; Fujii, H.; Pelling, J. C.; Cohen, Samuel Monroe.

In: Teratogenesis, Carcinogenesis, and Mutagenesis, Vol. 13, No. 5, 1993, p. 225-233.

Research output: Contribution to journalArticle

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abstract = "Male F344 rats were fed N[4‐(5‐nitro‐2‐furyl)‐2‐thiazolyl]formamide (FANFT) for up to 4 wk, then given the basal diet with or without 5{\%} sodium saccharin for up to 100 wk. In a previous study, we demonstrated point mutations in codons 12 and 61 of Ha‐ras gene among eleven transitional cell carcinomas (TCC), one undifferentiated carcinoma, and two sarcomas of the urinary bladder (Mol Carcinogen 3:210–215, 1990). In this study, Ha‐ras, Ki‐ras, and N‐ras sequences were examined by polymerase chain reaction (PCR) and direct DNA sequencing. The results confirm the point mutation in codon 61 (CAA to CGA in 5 TCCs and to CTA in one TCC) of the Ha‐ras gene. Mutation at codon 12 was not confirmed. No mutation was found in the Ki‐ras gene. Sequences of the N‐ras gene exons 1 and 2 were determined, and no mutations was detected. These results suggest the involvement of activated Ha‐ras gene, but not Ki‐N or N‐ras gene, in rat urinary bladder carcinogenesis induced by FANFT. Subsequent sodium saccharin administration did not affect the changes in Ha‐ras gene. {\circledC}1993 Wiley‐Liss, Inc.",
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