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@ARTICLE{Lei:305515,
      author       = {K. C. Lei$^*$ and N. Kolar Srinivas$^*$ and M. Chandra$^*$
                      and V. Serobyan$^*$ and S. Ugurel and D. Hoffmann and T.
                      Kervarrec and W.-O. Lui and J. Becker$^*$},
      title        = {{H}igh-resolution spatial transcriptomics uncover
                      epidermal-dermal divergences in {M}erkel cell carcinoma:
                      spatial context reshapes the gene expression landscape.},
      journal      = {Oncogene},
      volume       = {nn},
      issn         = {0950-9232},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-02199},
      pages        = {nn},
      year         = {2025},
      note         = {epub},
      abstract     = {Merkel cell carcinoma (MCC) is an aggressive skin cancer
                      with neuroendocrine differentiation marked by high cellular
                      plasticity, often manifesting as rapid therapy resistance.
                      Although the cell-of-origin is presumed to be epithelial,
                      epidermal localization of MCC is rarely observed, largely
                      because in situ MCC is typically an incidental finding.
                      Nevertheless, a subset of MCC tumors exhibits
                      epidermotropism, wherein tumor cells are present in the
                      epidermis. The behavior of cancer cells is profoundly
                      influenced by the tumor microenvironment and interactions
                      with neighboring cells. Notably, the normal counterparts of
                      the cancer's cell-of-origin have been shown to attenuate
                      tumor aggressiveness. Thus, epidermotropic MCC presents a
                      unique opportunity to explore the potential role of
                      epidermal microenvironment in modulating tumor cell
                      behavior. While the epidermotropic tumor nests share
                      histological resemblance with their dermal counterparts,
                      their transcriptomic profiles remain unexplored. Here, we
                      employed high-definition spatial and single-cell
                      transcriptomics to dissect the gene expression profiles of
                      epidermotropic MCC cells, comparing them to MCC cells in the
                      tumor core and those adjacent to blood vessels. Notably,
                      epidermotropic MCC cells exhibit a transcriptomic signature
                      reminiscent of cutaneous squamous cell carcinoma,
                      characterized by upregulation of genes encoding keratins,
                      S100A proteins, as well as calmodulin-like proteins 3 and 5.
                      Mechanistically, this keratinocytic differentiation is
                      associated with enhanced p63 activity, leading to the
                      upregulation of PERP. Collectively, our study demonstrates
                      that MCC cells can adopt a keratinocytic differentiation
                      program in response to microenvironmental cues, underscoring
                      the remarkable phenotypic plasticity of this malignancy and
                      the importance of the microenvironment for tumor cell
                      characteristics.},
      cin          = {ED01},
      ddc          = {610},
      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:41131107},
      doi          = {10.1038/s41388-025-03608-5},
      url          = {https://inrepo02.dkfz.de/record/305515},
}