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@ARTICLE{Blume:126160,
      author       = {C. J. Blume$^*$ and A. Hotz-Wagenblatt$^*$ and J.
                      Hüllein$^*$ and L. Sellner$^*$ and A. Jethwa$^*$ and T.
                      Stolz$^*$ and M. Slabicki$^*$ and K. Lee$^*$ and A.
                      Sharathchandra and A. Benner$^*$ and S. Dietrich$^*$ and C.
                      C. Oakes$^*$ and P. Dreger and D. te Raa and A. P. Kater and
                      A. Jauch and O. Merkel$^*$ and M. Oren and T. Hielscher$^*$
                      and T. Zenz$^*$},
      title        = {p53-dependent non-coding {RNA} networks in chronic
                      lymphocytic leukemia.},
      journal      = {Leukemia},
      volume       = {29},
      number       = {10},
      issn         = {1476-5551},
      address      = {Basingstoke},
      publisher    = {Nature Publ. Group},
      reportid     = {DKFZ-2017-02275},
      pages        = {2015 - 2023},
      year         = {2015},
      abstract     = {Mutations of the tumor suppressor p53 lead to chemotherapy
                      resistance and a dismal prognosis in chronic lymphocytic
                      leukemia (CLL). Whereas p53 targets are used to identify
                      patient subgroups with impaired p53 function, a
                      comprehensive assessment of non-coding RNA targets of p53 in
                      CLL is missing. We exploited the impaired transcriptional
                      activity of mutant p53 to map out p53 targets in CLL by
                      small RNA sequencing. We describe the landscape of
                      p53-dependent microRNA/non-coding RNA induced in response to
                      DNA damage in CLL. Besides the key p53 target miR-34a, we
                      identify a set of p53-dependent microRNAs (miRNAs;
                      miR-182-5p, miR-7-5p and miR-320c/d). In addition to miRNAs,
                      the long non-coding RNAs (lncRNAs) nuclear enriched abundant
                      transcript 1 (NEAT1) and long intergenic non-coding RNA p21
                      (lincRNA-p21) are induced in response to DNA damage in the
                      presence of functional p53 but not in CLL with p53 mutation.
                      Induction of NEAT1 and lincRNA-p21 are closely correlated to
                      the induction of cell death after DNA damage. We used
                      isogenic lymphoma cell line models to prove p53 dependence
                      of NEAT1 and lincRNA-p21. The current work describes the
                      p53-dependent miRNome and identifies lncRNAs NEAT1 and
                      lincRNA-p21 as novel elements of the p53-dependent DNA
                      damage response machinery in CLL and lymphoma.},
      keywords     = {MicroRNAs (NLM Chemicals) / NEAT1 long non-coding RNA,
                      human (NLM Chemicals) / RNA, Long Noncoding (NLM Chemicals)
                      / RNA, Messenger (NLM Chemicals) / TP53 protein, human (NLM
                      Chemicals) / Tumor Suppressor Protein p53 (NLM Chemicals)},
      cin          = {G100 / W180 / C060},
      ddc          = {610},
      cid          = {I:(DE-He78)G100-20160331 / I:(DE-He78)W180-20160331 /
                      I:(DE-He78)C060-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25971364},
      doi          = {10.1038/leu.2015.119},
      url          = {https://inrepo02.dkfz.de/record/126160},
}