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| Home > Publications database > p120-Catenin Is Critical for the Development of Invasive Lobular Carcinoma in Mice. > print |
| 001 | 130658 | ||
| 005 | 20240228143452.0 | ||
| 024 | 7 | _ | |a 10.1007/s10911-016-9358-3 |2 doi |
| 024 | 7 | _ | |a pmid:27411687 |2 pmid |
| 024 | 7 | _ | |a pmc:PMC5159444 |2 pmc |
| 024 | 7 | _ | |a 1083-3021 |2 ISSN |
| 024 | 7 | _ | |a 1573-7039 |2 ISSN |
| 024 | 7 | _ | |a altmetric:9919002 |2 altmetric |
| 037 | _ | _ | |a DKFZ-2017-05736 |
| 041 | _ | _ | |a eng |
| 082 | _ | _ | |a 570 |
| 100 | 1 | _ | |a Tenhagen, Milou |b 0 |
| 245 | _ | _ | |a p120-Catenin Is Critical for the Development of Invasive Lobular Carcinoma in Mice. |
| 260 | _ | _ | |a Dordrecht [u.a.] |c 2016 |b Springer Science + Business Media B.V |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1521188975_1730 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Loss of E-cadherin expression is causal to the development of invasive lobular breast carcinoma (ILC). E-cadherin loss leads to dismantling of the adherens junction and subsequent translocation of p120-catenin (p120) to the cytosol and nucleus. Although p120 is critical for the metastatic potential of ILC through the regulation of Rock-dependent anoikis resistance, it remains unknown whether p120 also contributes to ILC development. Using genetically engineered mouse models with mammary gland-specific inactivation of E-cadherin, p120 and p53, we demonstrate that ILC formation induced by E-cadherin and p53 loss is severely impaired upon concomitant inactivation of p120. Tumors that developed in the triple-knockout mice were mostly basal sarcomatoid carcinomas that displayed overt nuclear atypia and multinucleation. In line with the strong reduction in ILC incidence in triple-knockout mice compared to E-cadherin and p53 double-knockout mice, no functional redundancy of p120 family members was observed in mouse ILC development, as expression and localization of ARVCF, p0071 or δ-catenin was unaltered in ILCs from triple-knockout mice. In conclusion, we show that loss of p120 in the context of the p53-deficient mouse models is dominant over E-cadherin inactivation and its inactivation promotes the development of basal, epithelial-to-mesenchymal-transition (EMT)-type invasive mammary tumors. |
| 536 | _ | _ | |a 311 - Signalling pathways, cell and tumor biology (POF3-311) |0 G:(DE-HGF)POF3-311 |c POF3-311 |f POF III |x 0 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
| 700 | 1 | _ | |a Klarenbeek, Sjoerd |b 1 |
| 700 | 1 | _ | |a Braumuller, Tanya M |b 2 |
| 700 | 1 | _ | |a Hofmann, Ilse |0 P:(DE-He78)0c4543046185361a644540fee0dad8b1 |b 3 |u dkfz |
| 700 | 1 | _ | |a van der Groep, Petra |b 4 |
| 700 | 1 | _ | |a Ter Hoeve, Natalie |b 5 |
| 700 | 1 | _ | |a van der Wall, Elsken |b 6 |
| 700 | 1 | _ | |a Jonkers, Jos |b 7 |
| 700 | 1 | _ | |a Derksen, Patrick W B |b 8 |
| 773 | _ | _ | |a 10.1007/s10911-016-9358-3 |g Vol. 21, no. 3-4, p. 81 - 88 |0 PERI:(DE-600)1483136-3 |n 3-4 |p 81 - 88 |t Journal of mammary gland biology and neoplasia |v 21 |y 2016 |x 1573-7039 |
| 909 | C | O | |o oai:inrepo02.dkfz.de:130658 |p VDB |
| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 3 |6 P:(DE-He78)0c4543046185361a644540fee0dad8b1 |
| 913 | 1 | _ | |a DE-HGF |l Krebsforschung |1 G:(DE-HGF)POF3-310 |0 G:(DE-HGF)POF3-311 |2 G:(DE-HGF)POF3-300 |v Signalling pathways, cell and tumor biology |x 0 |4 G:(DE-HGF)POF |3 G:(DE-HGF)POF3 |b Gesundheit |
| 914 | 1 | _ | |y 2016 |
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| 915 | _ | _ | |a JCR |0 StatID:(DE-HGF)0100 |2 StatID |b J MAMMARY GLAND BIOL : 2015 |
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