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Vet Pathol 42:618-632 (2005)
© 2005 American College of Veterinary Pathologists

Mutations of Phosphatase and Tensin Homolog Deleted from Chromosome 10 in Canine Hemangiosarcoma

E. B. Dickerson, R. Thomas, S. P. Fosmire, A. R. Lamerato-Kozicki, S. R. Bianco, J. W. Wojcieszyn, M. Breen, S. C. Helfand and J. F. Modiano

Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI (EBD, SCH); Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC (RT, MB); Integrated Department of Immunology and AMC Cancer Center, University of Colorado Health Sciences Center, Denver, CO (SPF, ARL-K, SRB, JFM); IHC Services, Smithville, TX (JWW); University of Wisconsin Comprehensive Cancer Center, Madison, WI (SCH); and University of Colorado Cancer Center, Denver, CO (JFM)

We examined the presence of phosphatase and tensin homolog deleted from chromosome 10 (PTEN) abnormalities that could contribute to the origin or progression of naturally occurring canine endothelial tumors (hemangiosarcoma). Our results document somatic point mutations or deletions encompassing the PTEN C-terminal domain in canine hemangiosarcoma that might provide cells a survival advantage within their microenvironment. This represents the first characterization of a naturally occurring, highly metastatic tumor with biologically significant mutations of PTEN in the C-terminal domain.

Key words: Canine; endothelial cells; hemangiosarcoma; mutations; PTEN; tumor progression.

Request reprints from J. F. Modiano, VMD, PhD, Integrated Department of Immunology and AMC Cancer Center, University of Colorado Health Sciences Center, 1600 Pierce Street, 2-Diamond Research Bldg., Denver, CO 80214 (USA). E-mail: modianoj{at}amc.org.




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