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@ARTICLE{Bielesch:309981,
      author       = {S. Bielesch and I. Vogel and S. Nokodian and J. Moeller and
                      A. Blechschmidt and V. Hecht and V. Kuentzel and K. Thiedig
                      and M. Schwab and O. Schilling and H. Bronger$^*$ and M.
                      Kiechle and V. Magdolen and T. Dreyer$^*$},
      title        = {{K}eratin 19 as a prognostic marker and contributing factor
                      of metastasis and chemoresistance in high-grade serous
                      ovarian cancer.},
      journal      = {Molecular oncology},
      volume       = {nn},
      issn         = {1574-7891},
      address      = {Hoboken, NJ},
      publisher    = {John Wiley $\&$ Sons, Inc.},
      reportid     = {DKFZ-2026-00407},
      pages        = {nn},
      year         = {2026},
      note         = {epub},
      abstract     = {High-grade serous ovarian cancer (HGSOC) is the most
                      prevalent and lethal subtype of epithelial ovarian cancer
                      (EOC), characterised by extensive peritoneal metastasis. The
                      intermediate filament keratin 19 (KRT19) has been linked to
                      tumour progression and chemoresistance in various cancers.
                      However, its role varies across tumour types and remains
                      unclear for HGSOC. We evaluated KRT19 protein expression in
                      199 HGSOC patients and correlated findings with clinical
                      outcomes. In vitro, we assessed the effects of KRT19 on
                      tumour-associated mechanisms, including proliferation,
                      migration, adhesion, and spheroid formation. A xenograft
                      mouse model was used to assess tumour burden in vivo.
                      Publicly available datasets enabled in silico validation.
                      KRT19 was significantly overexpressed in HGSOC, and high
                      expression was associated with reduced overall survival. In
                      vivo, KRT19-overexpression increased peritoneal tumour
                      burden. In vitro and ex vivo, KRT19 induced a hybrid
                      epithelial phenotype through enhanced epithelial-mesenchymal
                      plasticity (EMP), promoting adhesion, migration, and
                      spheroid integrity, thereby potentially supporting
                      metastatic processes. Further, KRT19 could contribute to
                      paclitaxel resistance. Altogether, KRT19 represents a
                      potential independent prognostic marker and therapeutic
                      target to inhibit metastatic dissemination.},
      keywords     = {chemoresistance (Other) / epithelial–mesenchymal
                      plasticity (Other) / keratin 19 (Other) / ovarian cancer
                      (Other)},
      cin          = {MU01},
      ddc          = {610},
      cid          = {I:(DE-He78)MU01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41714116},
      doi          = {10.1002/1878-0261.70227},
      url          = {https://inrepo02.dkfz.de/record/309981},
}