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, J. F. Modiano

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)618-632
Number of pages15
JournalVeterinary pathology
Issue number5
StatePublished - Sep 2005

Bibliographical note

Funding Information:
The authors wish to thank owners and veterinarians who contributed cases, and especially Drs. Michelle Ritt and Frank Coons for diligent follow-up information, Dr. Shairaz Baksh for assistance with construct design, Drs. Baksh, Robert Strange, Robert Sclafani, Michelle Ritt, and Robert Weiss for review of the manuscript and helpful discussions. This work was supported in part by grants 1626, 2025, and 2254 from the AKC Canine Health Foundation (to JFM, SCH, MB), 1R55CA86432 from the NCI (to JFM), and a grant from the Monfort Family Foundation (to the University of Colorado Cancer Center).

Copyright 2008 Elsevier B.V., All rights reserved.


  • Canine
  • Endothelial cells
  • Hemangiosarcoma
  • Mutations
  • PTEN
  • Tumor progression

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