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@ARTICLE{Viarisio:130723,
      author       = {D. Viarisio$^*$ and K. Müller-Decker$^*$ and P. Zanna and
                      U. Kloz$^*$ and B. Aengeneyndt$^*$ and R. Accardi and C.
                      Flechtenmacher and L. Gissmann$^*$ and M. Tommasino},
      title        = {{N}ovel ß-{HPV}49 {T}ransgenic {M}ouse {M}odel of {U}pper
                      {D}igestive {T}ract {C}ancer.},
      journal      = {Cancer research},
      volume       = {76},
      number       = {14},
      issn         = {1538-7445},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2017-05801},
      pages        = {4216 - 4225},
      year         = {2016},
      abstract     = {The beta genus of human papillomaviruses (ß-HPV) includes
                      approximately 50 different viral types that are subdivided
                      into five species (ß-1 through ß-5). Nonmelanoma cancers
                      may involve some ß-1 and ß-2 HPV types, but the biology of
                      most ß-HPV types and their possible connections to human
                      disease are still little characterized. In this study, we
                      studied the effects of ß-3 type HPV49 in a novel transgenic
                      (Tg) mouse model, using a cytokeratin K14 promoter to drive
                      expression of the E6 and E7 genes from this virus in the
                      basal skin epidermis and the mucosal epithelia of the
                      digestive tract (K14 HPV49 E6/E7-Tg mice). Viral oncogene
                      expression only marginally increased cellular proliferation
                      in the epidermis of Tg animals, compared with wild-type
                      littermates, and we observed no spontaneous tumor formation
                      during their entire lifespan. However, we found that K14
                      HPV49 E6/E7-Tg mice were highly susceptible to upper
                      digestive tract carcinogenesis upon initiation with
                      4-nitroquinoline 1-oxide (4NQO). This was a selective
                      effect, as the same mice did not exhibit any skin lesions
                      after chronic UV irradiation. Opposite results were observed
                      in an analogous Tg model expressing the ß-2 HPV38 E6 and E7
                      oncogenes at the same anatomic sites. While these mice were
                      highly susceptible to UV-induced skin carcinogenesis, as
                      previously shown, they were little affected by 4NQO
                      treatment. Overall, our findings highlight important
                      differences in the biologic properties of certain ß-type
                      HPV that affect their impact on carcinogenesis in an
                      anatomic site-specific manner. Cancer Res; 76(14); 4216-25.
                      ©2016 AACR.},
      keywords     = {Oncogene Proteins, Viral (NLM Chemicals) / Papillomavirus
                      E7 Proteins (NLM Chemicals)},
      cin          = {F020 / W450 / W420},
      ddc          = {610},
      cid          = {I:(DE-He78)F020-20160331 / I:(DE-He78)W450-20160331 /
                      I:(DE-He78)W420-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27216183},
      doi          = {10.1158/0008-5472.CAN-16-0370},
      url          = {https://inrepo02.dkfz.de/record/130723},
}