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@ARTICLE{Crouchet:304510,
      author       = {E. Crouchet and E. Schaeffer and M. A. Oudot and J. Moehlin
                      and C. Gadenne and F. Jühling and H. El Saghire and N.
                      Fujiwara and S. Zhu and F. Akter Rasha and S. C. Durand and
                      A. Charlot and C. Ponsolles and R. Martin and N. Brignon and
                      F. Del Zompo and L. Meiss Heydmann and M. Parnot and N.
                      Hamdane and D. Heide$^*$ and J. Hetzer$^*$ and M.
                      Heikenwälder$^*$ and E. Felli and P. Pessaux and N. Pochet
                      and J. Zoll and B. Cunniff and Y. Hoshida and L. Mailly and
                      T. F. Baumert and C. Schuster},
      title        = {{T}argeting peroxiredoxin 2 prevents hepatocarcinogenesis
                      in metabolic liver disease models.},
      journal      = {The journal of clinical investigation},
      volume       = {135},
      number       = {21},
      issn         = {0021-9738},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DKFZ-2025-01898},
      pages        = {e169395},
      year         = {2025},
      note         = {2025 Sep 11;135(21):e169395},
      abstract     = {Treatment options for advanced liver disease and
                      hepatocellular carcinoma (HCC) are limited and strategies to
                      prevent HCC development are lacking. Aiming to discover
                      novel therapeutic targets, we combined genome wide
                      transcriptomic analysis of liver tissues from patients with
                      advanced liver disease and HCC and a cell-based system
                      predicting liver disease progression and HCC risk.
                      Computational analysis predicted peroxiredoxin 2 (PRDX2) as
                      a candidate gene mediating hepatocarcinogenesis and HCC
                      risk. Analysis of HCC patient tissues confirmed a perturbed
                      expression of PRDX2 in cancer. In vivo perturbation studies
                      in mouse models for MASH driven hepatocarcinogenesis showed
                      that specific Prdx2 knockout in hepatocytes significantly
                      improved metabolic liver functions, restored AMPK activity
                      and prevented HCC development by suppressing oncogenic
                      signaling. Perturbations studies in HCC cell lines, a CDX
                      mouse model and patient-derived HCC spheroids unraveled that
                      PRDX2 also mediates cancer initiation, cancer cell
                      proliferation and survival through its antioxidant activity.
                      Targeting PRDX2 may therefore be a valuable strategy to
                      prevent HCC development in metabolic liver disease.},
      keywords     = {Carbohydrate metabolism (Other) / Hepatology (Other) /
                      Oncology (Other) / Preventative medicine (Other) /
                      Therapeutics (Other)},
      cin          = {D440},
      ddc          = {610},
      cid          = {I:(DE-He78)D440-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40932790},
      doi          = {10.1172/JCI169395},
      url          = {https://inrepo02.dkfz.de/record/304510},
}