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@ARTICLE{Han:305513,
      author       = {R. Han and J. B. Poell and C. Conde-Lopez$^*$ and T. Salo
                      and I. Kurth$^*$ and R. H. Brakenhoff and J. Hess$^*$},
      title        = {{L}oss of the {Y} {C}hromosome in {O}ral {P}otentially
                      {P}remalignant {D}isorders {P}redicts {M}alignant
                      {P}rogression: {A}n {I}ntegrative {C}ross-{S}pecies
                      {M}ulti-{C}ohort {B}ioinformatic {S}tudy.},
      journal      = {Head $\&$ neck},
      volume       = {nn},
      issn         = {1043-3074},
      address      = {New York, NY [u.a.]},
      publisher    = {Wiley Interscience},
      reportid     = {DKFZ-2025-02197},
      pages        = {nn},
      year         = {2025},
      note         = {#LA:E220# / epub},
      abstract     = {The loss of the Y chromosome (LOY) and the extreme
                      down-regulation of Y chromosome gene expression (EDY) are
                      frequently observed in oral squamous cell carcinoma (OSCC).
                      However, their roles in oral potentially malignant disorders
                      (OPMDs) are unclear.A comprehensive bioinformatic analysis
                      was performed using publicly available datasets from
                      chemically induced mouse OSCC models and human cohorts. The
                      analysis included LOY/EDY detection, gene set variation
                      analysis (GSVA), PROGENy pathway profiling, cell-to-cell
                      communication inference, and epigenetic correlation
                      studies.LOY was prevalent among men with OPMD, and EDY was
                      identified in both mouse models and human OPMDs. The
                      presence of LOY/EDY was associated with a higher risk of
                      OPMD progression to OSCC. Single-cell analysis revealed that
                      EDY-positive epithelial cells exhibited elevated oncogenic
                      pathway activity and enhanced IL17-IL17RC signaling,
                      possibly due to the loss of KDM5D in epithelial cells and
                      altered epigenetic regulation.LOY/EDY can be detected in
                      OPMD and promotes malignant progression by altering
                      oncogenic signaling and epithelial cell interactions.
                      LOY/EDY may serve as both a diagnostic biomarker and a
                      therapeutic target, improving clinical management and
                      patient outcomes.},
      keywords     = {extreme down‐regulation of Y chromosome gene expression
                      (EDY) (Other) / loss of the Y chromosome (LOY) (Other) /
                      lysine demethylase 5D (KDM5D) (Other) / oral potentially
                      premalignant disorders (OPMD) (Other) / oral squamous cell
                      carcinoma (OSCC) (Other)},
      cin          = {E220 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)E220-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {315 - Bildgebung und Radioonkologie (POF4-315)},
      pid          = {G:(DE-HGF)POF4-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41122870},
      doi          = {10.1002/hed.70070},
      url          = {https://inrepo02.dkfz.de/record/305513},
}