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@ARTICLE{Ng:295835,
      author       = {A. W. T. Ng and D. P. McClurg and B. Wesley and S. A.
                      Zamani and E. Black and A. Miremadi and O. Giger and R. T.
                      Hoopen and G. Devonshire and A. M. Redmond and N. Grehan and
                      S. Jammula and A. Blasko and X. Li and S. Aparicio and S.
                      Tavaré and O. C. Clinical and K. Nowicki-Osuch and R. C.
                      Fitzgerald},
      collaboration = {M. Stratification},
      othercontributors = {P. A. W. Edwards and N. Grehan and B. Nutzinger and C.
                          Loreno and S. Abbas and A. Freeman and E. C. Smyth and M.
                          O'Donovan and A. Miremadi and S. Malhotra and M. Tripathi
                          and C. Cheah and H. Coles and C. Millington and M. Eldridge
                          and M. Secrier and S. Jammula and J. Davies and C. Crichton
                          and N. Carroll and R. H. Hardwick and P. Safranek and A.
                          Hindmarsh and V. Sujendran and S. J. Hayes and Y. Ang and A.
                          Sharrocks and S. R. Preston and I. Bagwan and V. Save and R.
                          J. E. Skipworth and T. R. Hupp and J. R. O'Neill and O.
                          Tucker and A. Beggs and P. Taniere and S. Puig and G.
                          Contino and T. J. Underwood and R. C. Walker and B. L. Grace
                          and J. Lagergren and J. Gossage and A. Davies and F. Chang
                          and U. Mahadeva and V. Goh and F. D. Ciccarelli and G.
                          Sanders and R. Berrisford and D. Chan and E. Cheong and B.
                          Kumar and L. Sreedharan and S. L. Parsons and I. Soomro and
                          P. Kaye and J. Saunders and L. Lovat and R. Haidry and M.
                          Scott and S. Sothi and S. Lishman and G. B. Hanna and C. J.
                          Peters and K. Moorthy and A. Grabowska and R. Turkington and
                          D. McManus and H. Coleman and R. D. Petty and F. Bartlet},
      title        = {{D}isentangling oncogenic amplicons in esophageal
                      adenocarcinoma.},
      journal      = {Nature Communications},
      volume       = {15},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2024-02655},
      pages        = {4074},
      year         = {2024},
      abstract     = {Esophageal adenocarcinoma is a prominent example of cancer
                      characterized by frequent amplifications in oncogenes.
                      However, the mechanisms leading to amplicons that involve
                      breakage-fusion-bridge cycles and extrachromosomal DNA are
                      poorly understood. Here, we use 710 esophageal
                      adenocarcinoma cases with matched samples and
                      patient-derived organoids to disentangle complex amplicons
                      and their associated mechanisms. Short-read sequencing
                      identifies ERBB2, MYC, MDM2, and HMGA2 as the most frequent
                      oncogenes amplified in extrachromosomal DNAs. We resolve
                      complex extrachromosomal DNA and breakage-fusion-bridge
                      cycles amplicons by integrating of de-novo assemblies and
                      DNA methylation in nine long-read sequenced cases. Complex
                      amplicons shared between precancerous biopsy and late-stage
                      tumor, an enrichment of putative enhancer elements and
                      mobile element insertions are potential drivers of complex
                      amplicons' origin. We find that patient-derived organoids
                      recapitulate extrachromosomal DNA observed in the primary
                      tumors and single-cell DNA sequencing capture
                      extrachromosomal DNA-driven clonal dynamics across passages.
                      Prospectively, long-read and single-cell DNA sequencing
                      technologies can lead to better prediction of clonal
                      evolution in esophageal adenocarcinoma.},
      keywords     = {Humans / Esophageal Neoplasms: genetics / Esophageal
                      Neoplasms: pathology / Adenocarcinoma: genetics /
                      Adenocarcinoma: pathology / Organoids: pathology / Gene
                      Amplification / DNA Methylation / Oncogenes: genetics / Male
                      / Sequence Analysis, DNA: methods / Clonal Evolution:
                      genetics / Female},
      cin          = {C150},
      ddc          = {500},
      cid          = {I:(DE-He78)C150-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38744814},
      pmc          = {pmc:PMC11094127},
      doi          = {10.1038/s41467-024-47619-4},
      url          = {https://inrepo02.dkfz.de/record/295835},
}