Sequencing of the Von Hippel-Lindau Gene in Canine Renal Carcinoma
Article first published online: 21 APR 2009
Copyright © 2009 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 23, Issue 3, pages 592–597, May/June 2009
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How to Cite
Pressler, B. M., Williams, L. E., Ramos-Vara, J. A. and Anderson, K. I. (2009), Sequencing of the Von Hippel-Lindau Gene in Canine Renal Carcinoma. Journal of Veterinary Internal Medicine, 23: 592–597. doi: 10.1111/j.1939-1676.2009.0310.x
- Issue published online: 19 MAY 2009
- Article first published online: 21 APR 2009
- Submitted October 31, 2008; Revised February 11, 2009; Accepted February 26, 2009.
- Cancer genes;
- Molecular biology;
- PCR assays;
- Renal neoplasia;
- Urinary tract
Background: Similarities in human and canine renal cell carcinoma (RCC) epidemiology and biologic behavior suggest that molecular mechanisms of tumorigenesis may be similar in both species. Approximately 75% of RCC in people are of the clear cell subtype, up to 85% of which are associated with mutation of the von Hippel-Lindau (VHL) gene. The canine VHL coding deoxyribonucleic acid (DNA) shares 90% identity with the human VHL gene.
Objective: To determine whether or not RCC in dogs are associated with VHL mutations, and if so determine the prevalence, type, and location of these mutations.
Animals: Thirteen dogs with RCC, 2 dogs with primary renal sarcomas, and 10 dogs without neoplastic kidney disease.
Methods: DNA was extracted from paraffin-embedded RCC tissue; DNA extracts from paraffin-embedded and snap-frozen nonneoplastic canine kidneys and canine whole blood were used as negative controls. Polymerase chain reaction and sequencing of the 3 VHL exons was performed, and results compared with the accessioned canine sequence.
Results: All VHL exons were amplified from 9 of 13 canine RCC samples, both renal sarcomas, 8 of 10 nonneoplastic kidney samples, and canine whole blood; only exon 2 could be amplified from 2 RCC samples. Mutations were not identified in any exons. A maximal prevalence of 33.6% for VHL mutations in canine RCC was determined.
Conclusion and Clinical Importance: Although similarities between canine and human RCC merit further investigation of the dog as a model for some subtypes of renal tumors, the lower prevalence of VHL mutations suggests that oncogenesis in these 2 species differs.