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@ARTICLE{Leiendecker:186717,
      author       = {L. Leiendecker and T. Neumann and P. S. Jung and S. M.
                      Cronin and T. L. Steinacker and A. Schleiffer and M.
                      Schutzbier and K. Mechtler and T. Kervarrec and E. Laurent
                      and K. Bachiri and E. Coyaud and R. Murali and K. J. Busam
                      and B. Itzinger-Monshi and R. Kirnbauer and L. Cerroni and
                      E. Calonje and A. Rütten and F. Stubenrauch and K. G.
                      Griewank$^*$ and T. Wiesner and A. C. Obenauf},
      title        = {{H}uman {P}apillomavirus 42 {D}rives {D}igital {P}apillary
                      {A}denocarcinoma and {E}licits a {G}erm {C}ell-like
                      {P}rogram {C}onserved in {HPV}-{P}ositive {C}ancers.},
      journal      = {Cancer discovery},
      volume       = {13},
      number       = {1},
      issn         = {2159-8274},
      address      = {Philadelphia, Pa.},
      reportid     = {DKFZ-2023-00074},
      pages        = {70 - 84},
      year         = {2023},
      abstract     = {The skin is exposed to viral pathogens, but whether they
                      contribute to the oncogenesis of skin cancers has not been
                      systematically explored. Here we investigated 19 skin tumor
                      types by analyzing off-target reads from commonly available
                      next-generation sequencing data for viral pathogens. We
                      identified human papillomavirus 42 (HPV42) in $96\%$ (n =
                      45/47) of digital papillary adenocarcinoma (DPA), an
                      aggressive cancer occurring on the fingers and toes. We show
                      that HPV42, so far considered a nononcogenic, 'low-risk'
                      HPV, recapitulates the molecular hallmarks of oncogenic,
                      'high-risk' HPVs. Using machine learning, we find that
                      HPV-driven transformation elicits a germ cell-like
                      transcriptional program conserved throughout all HPV-driven
                      cancers (DPA, cervical carcinoma, and head and neck cancer).
                      We further show that this germ cell-like transcriptional
                      program, even when reduced to the top two genes (CDKN2A and
                      SYCP2), serves as a fingerprint of oncogenic HPVs with
                      implications for early detection, diagnosis, and therapy of
                      all HPV-driven cancers.We identify HPV42 as a uniform driver
                      of DPA and add a new member to the short list of tumorigenic
                      viruses in humans. We discover that all oncogenic HPVs evoke
                      a germ cell-like transcriptional program with important
                      implications for detecting, diagnosing, and treating all
                      HPV-driven cancers. See related commentary by Starrett et
                      al., p. 17. This article is highlighted in the In This Issue
                      feature, p. 1.},
      keywords     = {Female / Humans / Human Papillomavirus Viruses /
                      Papillomavirus Infections: complications / Uterine Cervical
                      Neoplasms / Skin Neoplasms / Bone Neoplasms / Breast
                      Neoplasms / Papillomaviridae: genetics / Adenocarcinoma,
                      Clear Cell / Adenocarcinoma, Papillary / Germ Cells:
                      pathology},
      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:36213965},
      pmc          = {pmc:PMC9827110},
      doi          = {10.1158/2159-8290.CD-22-0489},
      url          = {https://inrepo02.dkfz.de/record/186717},
}