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@ARTICLE{Woodcock:294791,
      author       = {D. J. Woodcock and A. Sahli and R. Teslo and V. Bhandari
                      and A. J. Gruber and A. Ziubroniewicz and G. Gundem and Y.
                      Xu and A. Butler and E. Anokian and B. J. Pope and C.-H.
                      Jung and M. Tarabichi and S. Dentro$^*$ and J. H. R. Farmery
                      and P. Van Loo and A. Y. Warren and V. Gnanapragasam and F.
                      C. Hamdy and G. S. Bova and C. S. Foster and D. E. Neal and
                      Y.-J. Lu and Z. Kote-Jarai and M. Fraser and R. G. Bristow
                      and P. C. Boutros and A. J. Costello and N. M. Corcoran and
                      C. M. Hovens and C. E. Massie and A. G. Lynch and D. S.
                      Brewer and R. A. Eeles and C. S. Cooper and D. C. Wedge},
      title        = {{G}enomic evolution shapes prostate cancer disease type},
      journal      = {Cell genomics},
      volume       = {4},
      number       = {3},
      issn         = {2666-979X},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2024-02503},
      pages        = {100511 -},
      year         = {2024},
      abstract     = {The development of cancer is an evolutionary process
                      involving the sequential acquisition of genetic alterations
                      that disrupt normal biological processes, enabling tumor
                      cells to rapidly proliferate and eventually invade and
                      metastasize to other tissues. We investigated the genomic
                      evolution of prostate cancer through the application of
                      three separate classification methods, each designed to
                      investigate a different aspect of tumor evolution.
                      Integrating the results revealed the existence of two
                      distinct types of prostate cancer that arise from divergent
                      evolutionary trajectories, designated as the Canonical and
                      Alternative evolutionary disease types. We therefore propose
                      the evotype model for prostate cancer evolution wherein
                      Alternative-evotype tumors diverge from those of the
                      Canonical-evotype through the stochastic accumulation of
                      genetic alterations associated with disruptions to androgen
                      receptor DNA binding. Our model unifies many previous
                      molecular observations, providing a powerful new framework
                      to investigate prostate cancer disease progression.Keywords:
                      AR binding; cancer evolution; evotype model; evotypes;
                      ordering; prostate cancer.},
      cin          = {B450},
      ddc          = {610},
      cid          = {I:(DE-He78)B450-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1016/j.xgen.2024.100511},
      url          = {https://inrepo02.dkfz.de/record/294791},
}