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@ARTICLE{Tenhagen:130658,
      author       = {M. Tenhagen and S. Klarenbeek and T. M. Braumuller and I.
                      Hofmann$^*$ and P. van der Groep and N. Ter Hoeve and E. van
                      der Wall and J. Jonkers and P. W. B. Derksen},
      title        = {p120-{C}atenin {I}s {C}ritical for the {D}evelopment of
                      {I}nvasive {L}obular {C}arcinoma in {M}ice.},
      journal      = {Journal of mammary gland biology and neoplasia},
      volume       = {21},
      number       = {3-4},
      issn         = {1573-7039},
      address      = {Dordrecht [u.a.]},
      publisher    = {Springer Science + Business Media B.V},
      reportid     = {DKFZ-2017-05736},
      pages        = {81 - 88},
      year         = {2016},
      abstract     = {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.},
      cin          = {A190},
      ddc          = {570},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27411687},
      pmc          = {pmc:PMC5159444},
      doi          = {10.1007/s10911-016-9358-3},
      url          = {https://inrepo02.dkfz.de/record/130658},
}