rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2009-11-3
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pubmed:abstractText |
Endometrial cancer is the most common gynecological cancer. Estrogen-dependent endometrioid carcinoma is the most common type of endometrial cancer, and alterations in the expression of PTEN and K-ras have been associated with this disease. To study the roles of Pten and K-ras in endometrial cancer, we generated Pten ablation and oncogenic K-ras mutation in progesterone receptor positive cells (PR(cre/+)Pten(f/f)K-ras(G12D)). Double mutant mice dramatically accelerated the development of endometrial cancer compared to a single mutation of either gene. Histological analysis showed that all of the 1-month old double mutant female mice developed endometrial cancer with myometrial invasion. The expression of PR was downregulated in double mutant mice compared to a single mutation of either gene which resulted in decreased suppression of estrogen signaling. Therefore, these results suggest a synergistic effect of dysregulation of the Pten and K-ras signaling pathways during endometrial tumorigenesis.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:status |
PubMed-not-MEDLINE
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pubmed:issn |
1687-8450
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
2010
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
139087
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pubmed:year |
2010
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pubmed:articleTitle |
The Synergistic Effect of Conditional Pten Loss and Oncogenic K-ras Mutation on Endometrial Cancer Development Occurs via Decreased Progesterone Receptor Action.
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pubmed:affiliation |
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
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pubmed:publicationType |
Journal Article
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