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@ARTICLE{Bailey:282336,
      author       = {P. Bailey and R. A. Ridgway and P. Cammareri and M.
                      Treanor-Taylor and U.-M. Bailey and C. Schoenherr and M.
                      Bone and D. Schreyer and K. Purdie and J. Thomson and W.
                      Rickaby and R. Jackstadt$^*$ and A. D. Campbell and E.
                      Dimonitsas and A. J. Stratigos and S. T. Arron and J. Wang
                      and K. Blyth and C. M. Proby and C. A. Harwood and O. J.
                      Sansom and I. M. Leigh and G. J. Inman},
      title        = {{D}river gene combinations dictate cutaneous squamous cell
                      carcinoma disease continuum progression.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-01720},
      pages        = {5211},
      year         = {2023},
      abstract     = {The molecular basis of disease progression from UV-induced
                      precancerous actinic keratosis (AK) to malignant invasive
                      cutaneous squamous cell carcinoma (cSCC) and potentially
                      lethal metastatic disease remains unclear. DNA sequencing
                      studies have revealed a massive mutational burden but have
                      yet to illuminate mechanisms of disease progression. Here we
                      perform RNAseq transcriptomic profiling of 110 patient
                      samples representing normal sun-exposed skin, AK, primary
                      and metastatic cSCC and reveal a disease continuum from a
                      differentiated to a progenitor-like state. This is
                      accompanied by the orchestrated suppression of master
                      regulators of epidermal differentiation, dynamic modulation
                      of the epidermal differentiation complex, remodelling of the
                      immune landscape and an increase in the preponderance of
                      tumour specific keratinocytes. Comparative systems analysis
                      of human cSCC coupled with the generation of genetically
                      engineered murine models reveal that combinatorial
                      sequential inactivation of the tumour suppressor genes
                      Tgfbr2, Trp53, and Notch1 coupled with activation of Ras
                      signalling progressively drives cSCC progression along a
                      differentiated to progenitor axis. Taken together we provide
                      a comprehensive map of the cSCC disease continuum and reveal
                      potentially actionable events that promote and accompany
                      disease progression.},
      cin          = {A014},
      ddc          = {500},
      cid          = {I:(DE-He78)A014-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37626054},
      pmc          = {pmc:PMC10457401},
      doi          = {10.1038/s41467-023-40822-9},
      url          = {https://inrepo02.dkfz.de/record/282336},
}