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http://purl.uniprot.org/citations/18670643http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18670643http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18670643http://www.w3.org/2000/01/rdf-schema#comment"Fibroblast growth factor receptor 4 (FGFR-4) is expressed at significant levels in almost all human prostate cancers, and expression of its ligands is ubiquitous. A common polymorphism of FGFR-4 in which arginine (Arg(388)) replaces glycine (Gly(388)) at amino acid 388 is associated with progression in human prostate cancer. We show that the FGFR-4 Arg(388) polymorphism, which is present in most prostate cancer patients, results in increased receptor stability and sustained receptor activation. In patients bearing the FGFR-4 Gly(388) variant, expression of Huntingtin-interacting protein 1 (HIP1), which occurs in more than half of human prostate cancers, also results in FGFR-4 stabilization. This is associated with enhanced proliferation and anchorage-independent growth in vitro. Our findings indicate that increased receptor stability and sustained FGFR-4 signaling occur in most human prostate cancers due to either the presence of a common genetic polymorphism or the expression of a protein that stabilizes FGFR-4. Both of these alterations are associated with clinical progression in patients with prostate cancer. Thus, FGFR-4 signaling and receptor turnover are important potential therapeutic targets in prostate cancer."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.org/dc/terms/identifier"doi:10.1593/neo.08450"xsd:string
http://purl.uniprot.org/citations/18670643http://purl.org/dc/terms/identifier"doi:10.1593/neo.08450"xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/author"Cai Y."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/author"Cai Y."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/author"Ren C."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/author"Ren C."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/author"Yu W."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/author"Yu W."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/author"Ittmann M.M."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/author"Ittmann M.M."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/name"Neoplasia"xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/name"Neoplasia"xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/pages"847-856"xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/pages"847-856"xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/title"Altered fibroblast growth factor receptor 4 stability promotes prostate cancer progression."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/title"Altered fibroblast growth factor receptor 4 stability promotes prostate cancer progression."xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/volume"10"xsd:string
http://purl.uniprot.org/citations/18670643http://purl.uniprot.org/core/volume"10"xsd:string