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@ARTICLE{Salomoni:266479,
      author       = {Salomoni, Paolo and Flanagan, Adrienne M. and Cottone,
                      Lucia},
      title        = {({B}){O}n(e)-cohistones and the epigenetic alterations at
                      the root of bone cancer},
      journal      = {Cell death and differentiation},
      volume       = {32},
      number       = {1},
      issn         = {1350-9047},
      address      = {London},
      publisher    = {Macmillan},
      reportid     = {DZNE-2023-01164},
      pages        = {66 - 77},
      year         = {2025},
      abstract     = {Identification of mutations in histones in a number of
                      human neoplasms and developmental syndromes represents the
                      most compelling evidence to date for a causal role of
                      epigenetic perturbations in human disease. In most cases,
                      these mutations have gain of function properties that cause
                      deviation from normal developmental processes leading to
                      embryo defects and/or neoplastic transformation. These
                      exciting discoveries represent a step-change in our
                      understanding of the role of chromatin (dys)regulation in
                      development and disease. However, the mechanisms of action
                      of oncogenic histone mutations (oncohistones) remain only
                      partially understood. Here, we critically assess existing
                      literature on oncohistones focussing mainly on bone
                      neoplasms. We show how it is possible to draw parallels with
                      some of the cell-autonomous mechanisms of action described
                      in paediatric brain cancer, although the functions of
                      oncohistones in bone tumours remain under-investigated. In
                      this respect, it is becoming clear that histone mutations
                      targeting the same residues display, at least in part,
                      tissue-specific oncogenic mechanisms. Furthermore, it is
                      emerging that cancer cells carrying oncohistones can modify
                      the surrounding microenvironment to support growth and/or
                      alter differentiation trajectories. A better understanding
                      of oncohistone function in different neoplasms provide
                      potential for identification of signalling that could be
                      targeted therapeutically. Finally, we discuss some of the
                      main concepts and future directions in this research area,
                      while also drawing possible connections and parallels with
                      other cancer epigenetic mechanisms.},
      subtyp        = {Review Article},
      keywords     = {Humans / Epigenesis, Genetic / Bone Neoplasms: genetics /
                      Bone Neoplasms: metabolism / Bone Neoplasms: pathology /
                      Histones: metabolism / Mutation / Animals},
      cin          = {AG Salomoni},
      ddc          = {610},
      cid          = {I:(DE-2719)1013032},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37828086},
      pmc          = {pmc:PMC11748643},
      doi          = {10.1038/s41418-023-01227-9},
      url          = {https://pub.dzne.de/record/266479},
}