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@ARTICLE{Schlsser:300218,
      author       = {R. M. Schlösser and F. Krumbach and E. Corrales and G.
                      Andrieux and C. Preisinger and F. Liss and A. Golzmann and
                      M. Börries$^*$ and K. Becker and R. Knüchel and S. Garczyk
                      and B. Lüscher},
      title        = {{M}ultidimensional {OMIC}s reveal {ARID}1{A} orchestrated
                      control of {DNA} damage, splicing, and cell cycle in
                      normal-like and malignant urothelial cells.},
      journal      = {Molecular oncology},
      volume       = {nn},
      issn         = {1574-7891},
      address      = {Hoboken, NJ},
      publisher    = {John Wiley $\&$ Sons, Inc.},
      reportid     = {DKFZ-2025-00680},
      pages        = {nn},
      year         = {2025},
      note         = {epub},
      abstract     = {Epigenetic regulators, such as the SWI/SNF complex, with
                      important roles in tissue development and homeostasis, are
                      frequently mutated in cancer. ARID1A, a subunit of the
                      SWI/SNF complex, is mutated in approximately $20\%$ of all
                      bladder tumors; however, the consequences of this remain
                      poorly understood. Finding truncations to be the most common
                      mutation, we generated loss- and gain-of-function models to
                      conduct RNA-Seq, interactome analyses, Omni-ATAC-Seq, and
                      functional studies to characterize ARID1A-affected pathways
                      potentially suitable for the treatment of ARID1A-deficient
                      bladder cancers. We observed decreased cell proliferation
                      and deregulation of stress-regulated pathways, including DNA
                      repair, in ARID1A-deficient cells. Furthermore, ARID1A was
                      linked to alternative splicing and translational regulation
                      on RNA and interactome levels. ARID1A deficiency drastically
                      reduced the accessibility of chromatin, especially around
                      introns and distal enhancers, in a functional enrichment
                      analysis. Less accessible chromatin areas were mapped to
                      pathways such as cell proliferation and DNA damage response.
                      Indeed, the G2/M checkpoint appeared impaired after DNA
                      damage in ARID1A-deficient cells. Together, our data
                      highlight the broad impact of ARID1A loss and the
                      possibility of targeting proliferative and DNA repair
                      pathways for treatment.},
      keywords     = {ARID1A (Other) / ATAC‐Seq (Other) / DNA‐damage
                      checkpoints (Other) / RNA‐Seq (Other) / SWI/SNF (Other) /
                      bladder cancer (Other)},
      cin          = {FR01},
      ddc          = {610},
      cid          = {I:(DE-He78)FR01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40170512},
      doi          = {10.1002/1878-0261.70019},
      url          = {https://inrepo02.dkfz.de/record/300218},
}