% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Martins:127903,
      author       = {V. C. Martins$^*$ and K. Busch$^*$ and D. Juraeva$^*$ and
                      C. Blum and C. Ludwig and V. Rasche and F. Lasitschka and S.
                      E. Mastitsky$^*$ and B. Brors$^*$ and T. Hielscher$^*$ and
                      H. J. Fehling$^*$ and H.-R. Rodewald$^*$},
      title        = {{C}ell competition is a tumour suppressor mechanism in the
                      thymus.},
      journal      = {Nature},
      volume       = {509},
      number       = {7501},
      issn         = {1476-4687},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2017-03925},
      pages        = {465 - 470},
      year         = {2014},
      abstract     = {Cell competition is an emerging principle underlying
                      selection for cellular fitness during development and
                      disease. Competition may be relevant for cancer, but an
                      experimental link between defects in competition and
                      tumorigenesis is elusive. In the thymus, T lymphocytes
                      develop from precursors that are constantly replaced by
                      bone-marrow-derived progenitors. Here we show that in mice
                      this turnover is regulated by natural cell competition
                      between young bone-marrow-derived and old thymus-resident
                      progenitors that, although genetically identical, execute
                      differential gene expression programs. Disruption of cell
                      competition leads to progenitor self-renewal, upregulation
                      of Hmga1, transformation, and T-cell acute lymphoblastic
                      leukaemia (T-ALL) resembling the human disease in pathology,
                      genomic lesions, leukaemia-associated transcripts, and
                      activating mutations in Notch1. Hence, cell competition is a
                      tumour suppressor mechanism in the thymus. Failure to select
                      fit progenitors through cell competition may explain
                      leukaemia in X-linked severe combined immune deficiency
                      patients who showed thymus-autonomous T-cell development
                      after therapy with gene-corrected autologous progenitors.},
      keywords     = {HMGA Proteins (NLM Chemicals) / Notch1 protein, mouse (NLM
                      Chemicals) / Receptor, Notch1 (NLM Chemicals)},
      cin          = {D110 / B080 / C060 / G200},
      ddc          = {070},
      cid          = {I:(DE-He78)D110-20160331 / I:(DE-He78)B080-20160331 /
                      I:(DE-He78)C060-20160331 / I:(DE-He78)G200-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24828041},
      doi          = {10.1038/nature13317},
      url          = {https://inrepo02.dkfz.de/record/127903},
}