% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Rao:305608,
      author       = {S. V. Rao and L. Young and D. Cheeseman and S. Flynn and N.
                      Krebs and D.-L. Couturier and S. Mack and R. Brais and J.
                      Temple and A. Smith and E. Papachristou and C. Pelicano and
                      C. S. R. Chilamakuri and K. Herka and H. Baba and L.
                      Farah$^*$ and P. F. Cheung$^*$ and J. Siveke$^*$ and S.
                      Guerrier and L. Insolia and M. Gill and E. Archer Goode and
                      S. Kupczak and Y. Cheng and G. Borsari and D. Jodrell and C.
                      D'Santos and A. Russell and B. T. Grünwald and E. Serrao
                      and I. Chernukhin and J. S. Carroll},
      title        = {{T}ranscription factor switching drives subtype-specific
                      pancreatic cancer.},
      journal      = {Nature genetics},
      volume       = {nn},
      issn         = {1061-4036},
      address      = {London},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DKFZ-2025-02258},
      pages        = {nn},
      year         = {2025},
      note         = {epub},
      abstract     = {Emerging evidence suggests that lineage-specifying
                      transcription factors control the progression of pancreatic
                      ductal adenocarcinoma (PDAC). We have discovered a
                      transcription factor switching mechanism involving the
                      poorly characterized orphan nuclear receptor HNF4G and the
                      putative pioneer factor FOXA1, which drives PDAC
                      progression. Using our unbiased protein interactome
                      discovery approach, we identified HNF4A and HNF4G as
                      reproducible, FOXA1-associated proteins, in both preclinical
                      models and Whipple surgical samples. In the primary tumor
                      context, we consistently find that the dominant
                      transcription factor is HNF4G, where it functions as the
                      driver. A molecular switch occurs in advanced disease,
                      whereby HNF4G expression or activity decreases, unmasking
                      FOXA1's transcriptional potential. Derepressed FOXA1 drives
                      late-stage disease by orchestrating metastasis-specific
                      enhancer-promoter loops to regulate the expression of
                      metastatic genes. Overall survival is influenced by HNF4G
                      and FOXA1 activity in primary tumor growth and in
                      metastasis, respectively. We suggest that the existence of
                      stage-dependent transcription factor activity, triggered by
                      molecular compartmentalization, mediates the progression of
                      PDAC.},
      cin          = {ED01},
      ddc          = {570},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41168397},
      doi          = {10.1038/s41588-025-02389-7},
      url          = {https://inrepo02.dkfz.de/record/305608},
}