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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2007-8-13
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pubmed:abstractText |
Progression of non-small-cell lung cancer (NSCLC) to metastasis is poorly understood. Two genetic approaches were used to evaluate the role of adherens junctions in a C-RAF driven mouse model for NSCLC: conditional ablation of the cdh1 gene and expression of dominant-negative (dn) E-cadherin. Disruption of E-cadherin caused massive formation of intratumoral vessels that was reversible in the early phase of induction. Vascularized tumors grew more rapidly, developed invasive fronts, and gave rise to micrometastasis. beta-catenin was identified as a critical effector of E-cadherin disruption leading to upregulation of VEGF-A and VEGF-C. In vivo, lung tumor cells with disrupted E-cadherin expressed beta-catenin target genes normally found in other endodermal lineages suggesting that reprogramming may be involved in metastatic progression.
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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/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/CDH1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cadherins,
http://linkedlifedata.com/resource/pubmed/chemical/Luciferases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-raf,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A,
http://linkedlifedata.com/resource/pubmed/chemical/beta Catenin,
http://linkedlifedata.com/resource/pubmed/chemical/vascular endothelial growth factor...
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1535-6108
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
145-59
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17692806-Adenocarcinoma,
pubmed-meshheading:17692806-Adenoma,
pubmed-meshheading:17692806-Adherens Junctions,
pubmed-meshheading:17692806-Animals,
pubmed-meshheading:17692806-Apoptosis,
pubmed-meshheading:17692806-Biological Markers,
pubmed-meshheading:17692806-Cadherins,
pubmed-meshheading:17692806-Carcinoma, Non-Small-Cell Lung,
pubmed-meshheading:17692806-Cell Adhesion,
pubmed-meshheading:17692806-Cells, Cultured,
pubmed-meshheading:17692806-Disease Progression,
pubmed-meshheading:17692806-Endoderm,
pubmed-meshheading:17692806-Endothelium, Vascular,
pubmed-meshheading:17692806-Fluorescent Antibody Technique,
pubmed-meshheading:17692806-Genes, Dominant,
pubmed-meshheading:17692806-Immunoblotting,
pubmed-meshheading:17692806-Immunoprecipitation,
pubmed-meshheading:17692806-In Situ Nick-End Labeling,
pubmed-meshheading:17692806-Luciferases,
pubmed-meshheading:17692806-Lung Neoplasms,
pubmed-meshheading:17692806-Mice,
pubmed-meshheading:17692806-Mice, Knockout,
pubmed-meshheading:17692806-Mice, Transgenic,
pubmed-meshheading:17692806-Neoplasm Invasiveness,
pubmed-meshheading:17692806-Neovascularization, Pathologic,
pubmed-meshheading:17692806-Proto-Oncogene Proteins c-raf,
pubmed-meshheading:17692806-RNA, Messenger,
pubmed-meshheading:17692806-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:17692806-Signal Transduction,
pubmed-meshheading:17692806-Vascular Endothelial Growth Factor A,
pubmed-meshheading:17692806-beta Catenin
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pubmed:year |
2007
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pubmed:articleTitle |
Disruption of tumor cell adhesion promotes angiogenic switch and progression to micrometastasis in RAF-driven murine lung cancer.
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pubmed:affiliation |
Institut für Medizinische Strahlenkunde und Zellforschung, Universität Würzburg, Versbacher Strasse 5, 97078, Würzburg, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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