<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Dickerson, E B</style></author><author><style face="normal" font="default" size="100%">Thomas, R</style></author><author><style face="normal" font="default" size="100%">Fosmire, S P</style></author><author><style face="normal" font="default" size="100%">Lamerato-Kozicki, A R</style></author><author><style face="normal" font="default" size="100%">Bianco, S R</style></author><author><style face="normal" font="default" size="100%">Wojcieszyn, J W</style></author><author><style face="normal" font="default" size="100%">Breen, M</style></author><author><style face="normal" font="default" size="100%">Helfand, S C</style></author><author><style face="normal" font="default" size="100%">Modiano, J F</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Mutations of phosphatase and tensin homolog deleted from chromosome 10 in canine hemangiosarcoma.</style></title><secondary-title><style face="normal" font="default" size="100%">Veterinary pathology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Vet. Pathol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Amino Acid Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line</style></keyword><keyword><style  face="normal" font="default" size="100%">Dog Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Dogs</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Enzymologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Neoplastic</style></keyword><keyword><style  face="normal" font="default" size="100%">Hemangiosarcoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Sequence Data</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">PTEN Phosphohydrolase</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Homology, Amino Acid</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2005 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">42</style></volume><pages><style face="normal" font="default" size="100%">618-32</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">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.</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16145208?dopt=Abstract</style></custom1></record></records></xml>