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@ARTICLE{Zhou:282686,
      author       = {X. Zhou and J. An and R. Kurilov$^*$ and B. Brors$^*$ and
                      K. Hu and T. Peccerella and S. Roessler and K. Pfütze$^*$
                      and A. Schulz$^*$ and S. Wolf$^*$ and N. Hohmann and D.
                      Theile and M. Sauter and J. Burhenne and S. Ei and U. Heger
                      and O. Strobel and S. T. Barry and C. Springfeld and C.
                      Tjaden and F. Bergmann and M. Büchler and T. Hackert and F.
                      Fortunato and J. P. Neoptolemos and P. Bailey},
      title        = {{P}ersister cell phenotypes contribute to poor patient
                      outcomes after neoadjuvant chemotherapy in {PDAC}.},
      journal      = {Nature cancer},
      volume       = {4},
      number       = {9},
      issn         = {2662-1347},
      address      = {London},
      publisher    = {Nature Research},
      reportid     = {DKFZ-2023-01832},
      pages        = {1362-1381},
      year         = {2023},
      note         = {#EA:B330# / 2023 Sep;4(9):1362-1381},
      abstract     = {Neoadjuvant chemotherapy can improve the survival of
                      individuals with borderline and unresectable pancreatic
                      ductal adenocarcinoma; however, heterogeneous responses to
                      chemotherapy remain a significant clinical challenge. Here,
                      we performed RNA sequencing (n = 97) and multiplexed
                      immunofluorescence (n = 122) on chemo-naive and
                      postchemotherapy (post-CTX) resected patient samples
                      (chemoradiotherapy excluded) to define the impact of
                      neoadjuvant chemotherapy. Transcriptome analysis combined
                      with high-resolution mapping of whole-tissue sections
                      identified GATA6 (classical), KRT17 (basal-like) and
                      cytochrome P450 3A (CYP3A) coexpressing cells that were
                      preferentially enriched in post-CTX resected samples. The
                      persistence of GATA6hi and KRT17hi cells post-CTX was
                      significantly associated with poor survival after
                      mFOLFIRINOX (mFFX), but not gemcitabine (GEM), treatment.
                      Analysis of organoid models derived from chemo-naive and
                      post-CTX samples demonstrated that CYP3A expression is a
                      predictor of chemotherapy response and that CYP3A-expressing
                      drug detoxification pathways can metabolize the prodrug
                      irinotecan, a constituent of mFFX. These findings identify
                      CYP3A-expressing drug-tolerant cell phenotypes in residual
                      disease that may ultimately inform adjuvant treatment
                      selection.},
      cin          = {B330 / HD01 / B340 / W190},
      ddc          = {610},
      cid          = {I:(DE-He78)B330-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)B340-20160331 / I:(DE-He78)W190-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37679568},
      doi          = {10.1038/s43018-023-00628-6},
      url          = {https://inrepo02.dkfz.de/record/282686},
}