pubmed-article:17097565 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0042172 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0678222 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0302600 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0872097 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C1522484 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0079419 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0036525 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0181586 | lld:lifeskim |
pubmed-article:17097565 | lifeskim:mentions | umls-concept:C0205417 | lld:lifeskim |
pubmed-article:17097565 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:17097565 | pubmed:dateCreated | 2006-11-13 | lld:pubmed |
pubmed-article:17097565 | pubmed:abstractText | Metastatic disease is the primary cause of death in breast cancer, the most common malignancy in Western women. Loss of E-cadherin is associated with tumor metastasis, as well as with invasive lobular carcinoma (ILC), which accounts for 10%-15% of all breast cancers. To study the role of E-cadherin in breast oncogenesis, we have introduced conditional E-cadherin mutations into a mouse tumor model based on epithelium-specific knockout of p53. Combined loss of E-cadherin and p53 resulted in accelerated development of invasive and metastatic mammary carcinomas, which show strong resemblance to human ILC. Moreover, loss of E-cadherin induced anoikis resistance and facilitated angiogenesis, thus promoting metastatic disease. Our results suggest that loss of E-cadherin contributes to both mammary tumor initiation and metastasis. | lld:pubmed |
pubmed-article:17097565 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17097565 | pubmed:language | eng | lld:pubmed |
pubmed-article:17097565 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17097565 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17097565 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17097565 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17097565 | pubmed:month | Nov | lld:pubmed |
pubmed-article:17097565 | pubmed:issn | 1535-6108 | lld:pubmed |
pubmed-article:17097565 | pubmed:author | pubmed-author:CardiffRobert... | lld:pubmed |
pubmed-article:17097565 | pubmed:author | pubmed-author:PeterseJohann... | lld:pubmed |
pubmed-article:17097565 | pubmed:author | pubmed-author:DerksenPatric... | lld:pubmed |
pubmed-article:17097565 | pubmed:author | pubmed-author:JonkersJosJ | lld:pubmed |
pubmed-article:17097565 | pubmed:author | pubmed-author:BernsAntonA | lld:pubmed |
pubmed-article:17097565 | pubmed:author | pubmed-author:KrimpenfortPa... | lld:pubmed |
pubmed-article:17097565 | pubmed:author | pubmed-author:GriffioenArja... | lld:pubmed |
pubmed-article:17097565 | pubmed:author | pubmed-author:ZevenhovenJoh... | lld:pubmed |
pubmed-article:17097565 | pubmed:author | pubmed-author:LiuXiaolingX | lld:pubmed |
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pubmed-article:17097565 | pubmed:author | pubmed-author:SaridinFranci... | lld:pubmed |
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pubmed-article:17097565 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17097565 | pubmed:volume | 10 | lld:pubmed |
pubmed-article:17097565 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17097565 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17097565 | pubmed:pagination | 437-49 | lld:pubmed |
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pubmed-article:17097565 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:17097565 | pubmed:articleTitle | Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis. | lld:pubmed |
pubmed-article:17097565 | pubmed:affiliation | Division of Molecular Biology, Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands. | lld:pubmed |
pubmed-article:17097565 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17097565 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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