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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
2008-8-1
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pubmed:abstractText |
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.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-10348350,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-10353739,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-10428802,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-10611230,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-10629559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-10945637,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-11021964,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-11506499,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-11734594,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-11830541,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-12163454,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-12781365,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-14601095,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-14699054,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-14710228,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-14732715,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-15197773,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-15448004,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-15538740,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-15613447,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-15655558,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-15863030,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-16061909,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-16220297,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-16721364,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-16822847,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-16867222,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-16927306,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-16951141,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-17084840,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-17132227,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-17237035,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-17440072,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-17607666,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-17898861,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-8622701,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18670643-8663044
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/FGFR4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Fibroblast Growth Factor 2,
http://linkedlifedata.com/resource/pubmed/chemical/HIP1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Fibroblast Growth...
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1476-5586
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
847-56
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:18670643-DNA-Binding Proteins,
pubmed-meshheading:18670643-Disease Progression,
pubmed-meshheading:18670643-Fibroblast Growth Factor 2,
pubmed-meshheading:18670643-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:18670643-Genetic Variation,
pubmed-meshheading:18670643-Humans,
pubmed-meshheading:18670643-Ligands,
pubmed-meshheading:18670643-Male,
pubmed-meshheading:18670643-Phosphorylation,
pubmed-meshheading:18670643-Polymorphism, Genetic,
pubmed-meshheading:18670643-Prostatic Neoplasms,
pubmed-meshheading:18670643-RNA, Messenger,
pubmed-meshheading:18670643-Receptor, Fibroblast Growth Factor, Type 4
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pubmed:year |
2008
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pubmed:articleTitle |
Altered fibroblast growth factor receptor 4 stability promotes prostate cancer progression.
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pubmed:affiliation |
Department of Pathology, Baylor College of Medicine and Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX 77030, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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