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@ARTICLE{Ishaque:141414,
      author       = {N. Ishaque$^*$ and M. L. Abba and C. Hauser and N. Patil
                      and N. Paramasivam$^*$ and D. Huebschmann$^*$ and J. H.
                      Leupold and G. P. Balasubramanian$^*$ and K. Kleinheinz$^*$
                      and U. Toprak$^*$ and B. Hutter$^*$ and A. Benner$^*$ and A.
                      Shavinskaya and C. Zhou and Z. Gu$^*$ and J.
                      Kerssemakers$^*$ and A. Marx and M. Moniuszko and M.
                      Kozlowski and J. Reszec and J. Niklinski and J. Eils$^*$ and
                      M. Schlesner$^*$ and R. Eils$^*$ and B. Brors$^*$ and H.
                      Allgayer},
      title        = {{W}hole genome sequencing puts forward hypotheses on
                      metastasis evolution and therapy in colorectal cancer.},
      journal      = {Nature Communications},
      volume       = {9},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2018-01920},
      pages        = {4782},
      year         = {2018},
      abstract     = {Incomplete understanding of the metastatic process hinders
                      personalized therapy. Here we report the most comprehensive
                      whole-genome study of colorectal metastases vs. matched
                      primary tumors. $65\%$ of somatic mutations originate from a
                      common progenitor, with $15\%$ being tumor- and $19\%$
                      metastasis-specific, implicating a higher mutation rate in
                      metastases. Tumor- and metastasis-specific mutations harbor
                      elevated levels of BRCAness. We confirm multistage
                      progression with new components ARHGEF7/ARHGEF33.
                      Recurrently mutated non-coding elements include ncRNAs
                      RP11-594N15.3, AC010091, SNHG14, 3 UTRs of FOXP2, DACH2,
                      TRPM3, XKR4, ANO5, CBL, CBLB, the latter four potentially
                      dual protagonists in metastasis and efferocytosis-/PD-L1
                      mediated immunosuppression. Actionable metastasis-specific
                      lesions include FAT1, FGF1, BRCA2, KDR, and AKT2-, AKT3-,
                      and PDGFRA-3 UTRs. Metastasis specific mutations are
                      enriched in PI3K-Akt signaling, cell adhesion, ECM and
                      hepatic stellate activation genes, suggesting genetic
                      programs for site-specific colonization. Our results put
                      forward hypotheses on tumor and metastasis evolution, and
                      evidence for metastasis-specific events relevant for
                      personalized therapy.},
      cin          = {B330 / B080 / C060 / W610 / L101 / G200},
      ddc          = {500},
      cid          = {I:(DE-He78)B330-20160331 / I:(DE-He78)B080-20160331 /
                      I:(DE-He78)C060-20160331 / I:(DE-He78)W610-20160331 /
                      I:(DE-He78)L101-20160331 / I:(DE-He78)G200-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30429477},
      pmc          = {pmc:PMC6235880},
      doi          = {10.1038/s41467-018-07041-z},
      url          = {https://inrepo02.dkfz.de/record/141414},
}