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@ARTICLE{Georgilis:136720,
      author       = {A. Georgilis and S. Klotz and C. J. Hanley and N. Herranz
                      and B. Weirich$^*$ and B. Morancho and A. C. Leote and L.
                      D'Artista and S. Gallage$^*$ and M. Seehawer and T. Carroll
                      and G. Dharmalingam and K. B. Wee and M. Mellone and J.
                      Pombo and D. Heide$^*$ and E. Guccione and J. Arribas and N.
                      L. Barbosa-Morais and M. Heikenwalder$^*$ and G. J. Thomas
                      and L. Zender$^*$ and J. Gil},
      title        = {{PTBP}1-{M}ediated {A}lternative {S}plicing {R}egulates the
                      {I}nflammatory {S}ecretome and the {P}ro-tumorigenic
                      {E}ffects of {S}enescent {C}ells.},
      journal      = {Cancer cell},
      volume       = {34},
      number       = {1},
      issn         = {1535-6108},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2018-01158},
      pages        = {85 - 102.e9},
      year         = {2018},
      abstract     = {Oncogene-induced senescence is a potent tumor-suppressive
                      response. Paradoxically, senescence also induces an
                      inflammatory secretome that promotes carcinogenesis and
                      age-related pathologies. Consequently, the
                      senescence-associated secretory phenotype (SASP) is a
                      potential therapeutic target. Here, we describe an RNAi
                      screen for SASP regulators. We identified 50 druggable
                      targets whose knockdown suppresses the inflammatory
                      secretome and differentially affects other SASP components.
                      Among the screen candidates was PTBP1. PTBP1 regulates the
                      alternative splicing of genes involved in intracellular
                      trafficking, such as EXOC7, to control the SASP. Inhibition
                      of PTBP1 prevents the pro-tumorigenic effects of the SASP
                      and impairs immune surveillance without increasing the risk
                      of tumorigenesis. In conclusion, our study identifies SASP
                      inhibition as a powerful and safe therapy against
                      inflammation-driven cancer.},
      cin          = {F180 / V076 / L801},
      ddc          = {610},
      cid          = {I:(DE-He78)F180-20160331 / I:(DE-He78)V076-20160331 /
                      I:(DE-He78)L801-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29990503},
      pmc          = {pmc:PMC6048363},
      doi          = {10.1016/j.ccell.2018.06.007},
      url          = {https://inrepo02.dkfz.de/record/136720},
}