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Journal of Heredity Advance Access originally published online on October 26, 2005
Journal of Heredity 2005 96(7):764-765; doi:10.1093/jhered/esi121
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© The American Genetic Association. 2005. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

RAS Gene Hot-Spot Mutations in Canine Neoplasias

A. Richter, H. Murua Escobar, K. Günther, J. T. Soller, S. Winkler, I. Nolte, and J. Bullerdiek

From the Centre for Human Genetics, University of Bremen, Leobener Strasse ZHG, 28359 Bremen, Germany (Richter, Murua Escobar, Günther, Soller, Winkler, and Bullerdiek); and Small Animal Clinic, School of Veterinary Medicine, Bischofsholer Damm 15, 30173 Hanover, Germany (Murua Escobar and Nolte)

Address correspondence to Dr. Jörn Bullerdiek at the address above, or e-mail: bullerd{at}uni-bremen.de.

Point mutations in the cellular homologues HRAS, KRAS2, and NRAS of the viral Harvey and Kirsten rat sarcoma virus oncogenes are commonly involved in the onset of malignancies in humans and other species such as dog, mouse, and rat. Most often, three particular hot-spot codons are affected, with one amino acid exchange being sufficient for the induction of tumor growth. While RAS genes have been shown to play an important role in canine tumors such as non-small lung cell carcinomas, data about RAS mutations in canine fibrosarcomas as well as KRAS2 mutations in canine melanomas is sparse. To increase the number of tumors examined, we recently screened 13 canine fibrosarcomas and 11 canine melanomas for point mutations, particularly within the mutational hot spots. The results were compared to the already existing data from other studies about these tumors in dogs.


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