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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0017337,
umls-concept:C0027627,
umls-concept:C0040690,
umls-concept:C0185117,
umls-concept:C0332307,
umls-concept:C0334227,
umls-concept:C0346647,
umls-concept:C0597357,
umls-concept:C0599946,
umls-concept:C1749467,
umls-concept:C2911684
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pubmed:issue |
3
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pubmed:dateCreated |
2002-12-6
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pubmed:abstractText |
Pancreatic ductal adenocarcinoma (PDAC) is a deadly malignancy that frequently metastasizes and that overexpresses transforming growth factor-beta s (TGF-beta s). To determine whether TGF-beta s can act to enhance the metastatic potential of PDAC, PANC-1 human pancreatic cancer cells were transfected with an expression construct encoding a soluble type II TGF-beta receptor (sT beta RII) that blocks cellular responsiveness to TGF-beta 1. When injected s.c. in athymic mice, PANC-1 clones expressing sT beta RII exhibited decreased tumor growth in comparison with sham-transfected cells and attenuated expression of plasminogen activator inhibitor 1 (PAI-1), a gene associated with tumor growth. When tested in an orthotopic mouse model, these clones formed small intrapancreatic tumors that exhibited a suppressed metastatic capacity and decreased expression of plasminogen activator inhibitor 1 and the metastasis-associated urokinase plasminogen activator. These results indicate that TGF-beta s act in vivo to enhance the expression of genes that promote the growth and metastasis of pancreatic cancer cells and suggest that sT beta RII may ultimately have a therapeutic benefit in PDAC.
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pubmed:grant |
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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/Plasminogen Activator Inhibitor 1,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transforming Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/Serine Proteinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/TGFB1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Tgfb1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta1,
http://linkedlifedata.com/resource/pubmed/chemical/Urokinase-Type Plasminogen Activator,
http://linkedlifedata.com/resource/pubmed/chemical/transforming growth factor-beta...
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1535-7163
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
161-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12467210-Animals,
pubmed-meshheading:12467210-Blotting, Northern,
pubmed-meshheading:12467210-Carcinoma, Pancreatic Ductal,
pubmed-meshheading:12467210-Female,
pubmed-meshheading:12467210-Gene Expression,
pubmed-meshheading:12467210-Genetic Vectors,
pubmed-meshheading:12467210-Humans,
pubmed-meshheading:12467210-Mice,
pubmed-meshheading:12467210-Mice, Nude,
pubmed-meshheading:12467210-Neoplasm Transplantation,
pubmed-meshheading:12467210-Pancreatic Neoplasms,
pubmed-meshheading:12467210-Plasminogen Activator Inhibitor 1,
pubmed-meshheading:12467210-Protein-Serine-Threonine Kinases,
pubmed-meshheading:12467210-Receptors, Transforming Growth Factor beta,
pubmed-meshheading:12467210-Serine Proteinase Inhibitors,
pubmed-meshheading:12467210-Signal Transduction,
pubmed-meshheading:12467210-Transfection,
pubmed-meshheading:12467210-Transforming Growth Factor beta,
pubmed-meshheading:12467210-Transforming Growth Factor beta1,
pubmed-meshheading:12467210-Tumor Cells, Cultured,
pubmed-meshheading:12467210-Urokinase-Type Plasminogen Activator
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pubmed:year |
2002
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pubmed:articleTitle |
Soluble type II transforming growth factor-beta receptor attenuates expression of metastasis-associated genes and suppresses pancreatic cancer cell metastasis.
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pubmed:affiliation |
Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Biological Chemistry, and Pharmacology, University of California, Irvine, California 92697, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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