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Mutations in the VHL gene from potassium bromate-induced rat clear cell renal tumors

Yih-Horng Shiao1, Sonie I Kamata, Leeanne M Li

  • 1Laboratory of Comparative Carcinogenesis, National Cancer Institute at Frederick, National Institutes of Health, Frederick, MD, USA.

Cancer Letters
|October 3, 2002
PubMed

Insights

Potassium bromate induces rat kidney tumors similar to human clear cell renal carcinomas. However, the genetic basis differs, with VHL gene promoter mutations found in rats, unlike common VHL coding mutations in humans.

Area of Science:

  • Toxicology
  • Carcinogenesis
  • Molecular Biology

Background:

  • Potassium bromate (KBrO3) is a carcinogen and a drinking water disinfection byproduct.
  • Clear cell renal tumors, common in humans, are rare in animals but inducible by KBrO3 in F344 rats.
  • VHL gene mutations are frequent in human clear cell renal carcinomas.

Purpose of the Study:

  • To investigate VHL gene mutations in KBrO3-induced rat renal tumors.
  • To assess the relevance of these rat tumors for human health risk assessment.

Main Methods:

  • Microscopic examination of rat renal tumors.
  • DNA extraction and analysis of the VHL gene (coding and promoter regions).
  • Polymerase chain reaction-single strand conformation polymorphism and DNA sequencing.

Main Results:

  • Two of nine clear cell renal tumors had C to T mutations in the VHL promoter's Sp1 binding motif.
  • One untreated rat had a VHL promoter mutation outside the conserved core region.
  • VHL coding sequence mutations were rare, and absent in chromophilic tumors.

Conclusions:

  • KBrO3-induced rat renal tumors are morphologically similar to human tumors.
  • The genetic mechanisms of tumorigenesis differ between rat and human clear cell renal tumors.
  • VHL promoter mutations may play a role in KBrO3-induced rat renal carcinogenesis.

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