Mutations of phosphatase and tensin homolog deleted from chromosome 10 in canine hemangiosarcoma.
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.
Dickerson
E B
EB
Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, USA.
Thomas
R
R
Fosmire
S P
SP
Lamerato-Kozicki
A R
AR
Bianco
S R
SR
Wojcieszyn
J W
JW
Breen
M
M
Helfand
S C
SC
Modiano
J F
JF
D000595:Amino Acid Sequence; D000818:Animals; D002460:Cell Line; D004283:Dog Diseases / Q000235:genetics*; D004285:Dogs; D015971:Gene Expression Regulation, Enzymologic; D015972:Gene Expression Regulation, Neoplastic; D006394:Hemangiosarcoma / Q000235:genetics* / Q000662:veterinary*; D008969:Molecular Sequence Data; D009154:Mutation / Q000235:genetics*; D051059:PTEN Phosphohydrolase / Q000737:chemistry / Q000235:genetics*; D017386:Sequence Homology, Amino Acid
D051059:PTEN Phosphohydrolase