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@ARTICLE{Saini:276368,
      author       = {M. Saini$^*$ and L. Schmidleitner and H. D. Moreno and E.
                      Donato$^*$ and M. Falcone$^*$ and J. M. Bartsch and V.
                      Vogel$^*$ and R. Würth$^*$ and N. Pfarr and E. Espinet$^*$
                      and M. Lehmann and M. Königshoff and M. Reitberger$^*$ and
                      S. Haas$^*$ and E. Graf and T. Schwarzmayr and T.-M. Strom
                      and S. Spaich and M. Sütterlin and A. Schneeweiss and W.
                      Weichert$^*$ and G. Schotta and M. Reichert$^*$ and N. Aceto
                      and M. Sprick$^*$ and A. Trumpp$^*$ and C. H. Scheel and C.
                      Klein$^*$},
      title        = {{R}esistance to mesenchymal reprogramming sustains clonal
                      propagation in metastatic breast cancer.},
      journal      = {Cell reports},
      volume       = {42},
      number       = {6},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2023-01077},
      pages        = {112533},
      year         = {2023},
      note         = {DKFZ-ZMBH Alliance / #EA:A010#LA:A010# / 2023 Jun
                      27;42(6):112533},
      abstract     = {The acquisition of mesenchymal traits is considered a
                      hallmark of breast cancer progression. However, the
                      functional relevance of epithelial-to-mesenchymal transition
                      (EMT) remains controversial and context dependent. Here, we
                      isolate epithelial and mesenchymal populations from human
                      breast cancer metastatic biopsies and assess their
                      functional potential in vivo. Strikingly, progressively
                      decreasing epithelial cell adhesion molecule (EPCAM) levels
                      correlate with declining disease propagation.
                      Mechanistically, we find that persistent EPCAM expression
                      marks epithelial clones that resist EMT induction and
                      propagate competitively. In contrast, loss of EPCAM defines
                      clones arrested in a mesenchymal state, with concomitant
                      suppression of tumorigenicity and metastatic potential. This
                      dichotomy results from distinct clonal trajectories
                      impacting global epigenetic programs that are determined by
                      the interplay between human ZEB1 and its target GRHL2.
                      Collectively, our results indicate that susceptibility to
                      irreversible EMT restrains clonal propagation, whereas
                      resistance to mesenchymal reprogramming sustains disease
                      spread in multiple models of human metastatic breast cancer,
                      including patient-derived cells in vivo.},
      keywords     = {CP: Cancer (Other) / EMT (Other) / EPCAM (Other) / GRHL2
                      (Other) / ZEB1 (Other) / breast cancer (Other) / intratumor
                      heterogeneity (Other) / metastasis (Other)},
      cin          = {A010 / HD01 / MU01},
      ddc          = {610},
      cid          = {I:(DE-He78)A010-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)MU01-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37257449},
      doi          = {10.1016/j.celrep.2023.112533},
      url          = {https://inrepo02.dkfz.de/record/276368},
}