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      author       = {J. van Riet and H. J. G. van de Werken and E. Cuppen and F.
                      A. L. M. Eskens and M. Tesselaar and L. M. van Veenendaal
                      and H.-J. Klümpen and M. W. Dercksen and G. D. Valk and M.
                      P. Lolkema and S. Sleijfer and B. Mostert},
      title        = {{T}he genomic landscape of 85 advanced neuroendocrine
                      neoplasms reveals subtype-heterogeneity and potential
                      therapeutic targets},
      journal      = {Nature Communications},
      volume       = {12},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2022-01696},
      pages        = {4612},
      year         = {2021},
      abstract     = {Metastatic and locally-advanced neuroendocrine neoplasms
                      (aNEN) form clinically andgenetically heterogeneous
                      malignancies, characterized by distinct prognoses based
                      uponprimary tumor localization, functionality, grade,
                      proliferation index and diverse outcomes totreatment. Here,
                      we report the mutational landscape of 85 whole-genome
                      sequenced aNEN.This landscape reveals distinct genomic
                      subpopulations of aNEN based on primary localization and
                      differentiation grade; we observe relatively high tumor
                      mutational burdens (TMB)in neuroendocrine carcinoma (average
                      5.45 somatic mutations per megabase) with TP53,KRAS, RB1,
                      CSMD3, APC, CSMD1, LRATD2, TRRAP and MYC as major drivers
                      versus an overalllow TMB in neuroendocrine tumors (1.09).
                      Furthermore, we observe distinct drivers whichare enriched
                      in somatic aberrations in pancreatic (MEN1, ATRX, DAXX, DMD
                      and CREBBP) andmidgut-derived neuroendocrine tumors
                      (CDKN1B). Finally, $49\%$ of aNEN patients revealpotential
                      therapeutic targets based upon actionable (and responsive)
                      somatic aberrationswithin their genome; potentially
                      directing improvements in aNEN treatment strategies.},
      ddc          = {500},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1038/s41467-021-24812-3},
      url          = {https://inrepo02.dkfz.de/record/180971},