Source:http://linkedlifedata.com/resource/pubmed/id/17178895
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
24
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pubmed:dateCreated |
2006-12-20
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pubmed:abstractText |
Activated growth factor receptor tyrosine kinases (RTK) play pivotal roles in a variety of human cancers, including breast cancer. Ron, a member of the Met RTK proto-oncogene family, is overexpressed or constitutively active in 50% of human breast cancers. To define the significance of Ron overexpression and activation in vivo, we generated transgenic mice that overexpress a wild-type or constitutively active Ron receptor in the mammary epithelium. In these animals, Ron expression is significantly elevated in mammary glands and leads to a hyperplastic phenotype by 12 weeks of age. Ron overexpression is sufficient to induce mammary transformation in all transgenic animals and is associated with a high degree of metastasis, with metastatic foci detected in liver and lungs of >86% of all transgenic animals. Furthermore, we show that Ron overexpression leads to receptor phosphorylation and is associated with elevated levels of tyrosine phosphorylated beta-catenin and the up-regulation of genes, including cyclin D1 and c-myc, which are associated with poor prognosis in patients with human breast cancers. These studies suggest that Ron overexpression may be a causative factor in breast tumorigenesis and provides a model to dissect the mechanism by which the Ron induces transformation and metastasis.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0008-5472
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pubmed:author |
pubmed-author:BeaumanShirelyn RSR,
pubmed-author:CollinsMargaret HMH,
pubmed-author:KaderSarah ASA,
pubmed-author:LeonisMike AMA,
pubmed-author:PathrosePetersonP,
pubmed-author:PeaceBelinda EBE,
pubmed-author:ThobeMeganM,
pubmed-author:ToneyKenyaK,
pubmed-author:WaltzSusan ESE,
pubmed-author:ZinserGlendon MGM
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
66
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
11967-74
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17178895-Animals,
pubmed-meshheading:17178895-Cloning, Molecular,
pubmed-meshheading:17178895-Female,
pubmed-meshheading:17178895-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:17178895-Humans,
pubmed-meshheading:17178895-Hyperplasia,
pubmed-meshheading:17178895-Mammary Glands, Animal,
pubmed-meshheading:17178895-Mammary Neoplasms, Animal,
pubmed-meshheading:17178895-Mice,
pubmed-meshheading:17178895-Mice, Transgenic,
pubmed-meshheading:17178895-Neoplasm Metastasis,
pubmed-meshheading:17178895-Receptor Protein-Tyrosine Kinases
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pubmed:year |
2006
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pubmed:articleTitle |
Mammary-specific Ron receptor overexpression induces highly metastatic mammary tumors associated with beta-catenin activation.
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pubmed:affiliation |
Department of Surgery, University of Cincinnati College of Medicine and Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45267, 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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