rdf:type |
|
lifeskim:mentions |
umls-concept:C0026809,
umls-concept:C0036525,
umls-concept:C0042172,
umls-concept:C0079419,
umls-concept:C0181586,
umls-concept:C0205263,
umls-concept:C0205417,
umls-concept:C0302600,
umls-concept:C0678222,
umls-concept:C0683598,
umls-concept:C0872097,
umls-concept:C1522484
|
pubmed:issue |
5
|
pubmed:dateCreated |
2006-11-13
|
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.
|
pubmed:commentsCorrections |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Nov
|
pubmed:issn |
1535-6108
|
pubmed:author |
pubmed-author:BernsAntonA,
pubmed-author:CardiffRobert DRD,
pubmed-author:DerksenPatrick W BPW,
pubmed-author:EversBastiaanB,
pubmed-author:GriffioenArjan WAW,
pubmed-author:JonkersJosJ,
pubmed-author:KrimpenfortPaulP,
pubmed-author:LiuXiaolingX,
pubmed-author:PeterseJohannes LJL,
pubmed-author:SaridinFrancisF,
pubmed-author:VinkJacquelineJ,
pubmed-author:ZevenhovenJohnJ,
pubmed-author:van BeijnumJudy RJR,
pubmed-author:van der GuldenHannekeH
|
pubmed:issnType |
Print
|
pubmed:volume |
10
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
437-49
|
pubmed:meshHeading |
pubmed-meshheading:17097565-Animals,
pubmed-meshheading:17097565-Anoikis,
pubmed-meshheading:17097565-Breast Neoplasms,
pubmed-meshheading:17097565-Cadherins,
pubmed-meshheading:17097565-Carcinoma, Lobular,
pubmed-meshheading:17097565-Disease Models, Animal,
pubmed-meshheading:17097565-Female,
pubmed-meshheading:17097565-Gene Silencing,
pubmed-meshheading:17097565-Humans,
pubmed-meshheading:17097565-Mammary Glands, Human,
pubmed-meshheading:17097565-Mice,
pubmed-meshheading:17097565-Mice, Inbred BALB C,
pubmed-meshheading:17097565-Neoplasm Metastasis,
pubmed-meshheading:17097565-Neovascularization, Pathologic,
pubmed-meshheading:17097565-Skin Neoplasms,
pubmed-meshheading:17097565-Survival Rate,
pubmed-meshheading:17097565-Tumor Cells, Cultured,
pubmed-meshheading:17097565-Tumor Suppressor Protein p53
|
pubmed:year |
2006
|
pubmed:articleTitle |
Somatic inactivation of E-cadherin and p53 in mice leads to metastatic lobular mammary carcinoma through induction of anoikis resistance and angiogenesis.
|
pubmed:affiliation |
Division of Molecular Biology, Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|