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@ARTICLE{Taylor:283156,
      author       = {J. Taylor$^*$ and L. Uhl$^*$ and I. Moll$^*$ and S. S.
                      Hasan$^*$ and L. Wiedmann$^*$ and J. Morgenstern and B. D.
                      Giaimo and T. Friedrich and E. Alsina-Sanchis$^*$ and F. De
                      Angelis Rigotti$^*$ and R. Mülfarth$^*$ and S. Kaltenbach
                      and D. Schenk$^*$ and F. Nickel and T. Fleming and D.
                      Sprinzak and C. Mogler and T. Korff and A. T. Billeter and
                      B. P. Müller-Stich and M. Berriel Diaz and T. Borggrefe and
                      S. Herzig and M. Rohm and J. Rodriguez-Vita$^*$ and A.
                      Fischer$^*$},
      title        = {{E}ndothelial {N}otch1 signaling in white adipose tissue
                      promotes cancer cachexia.},
      journal      = {Nature cancer},
      volume       = {4},
      number       = {11},
      issn         = {2662-1347},
      address      = {London},
      publisher    = {Nature Research},
      reportid     = {DKFZ-2023-01942},
      pages        = {1544-1560},
      year         = {2023},
      note         = {#EA:A270#LA:A270# / 2023 Nov;4(11):1544-1560},
      abstract     = {Cachexia is a major cause of morbidity and mortality in
                      individuals with cancer and is characterized by weight loss
                      due to adipose and muscle tissue wasting. Hallmarks of white
                      adipose tissue (WAT) remodeling, which often precedes weight
                      loss, are impaired lipid storage, inflammation and
                      eventually fibrosis. Tissue wasting occurs in response to
                      tumor-secreted factors. Considering that the continuous
                      endothelium in WAT is the first line of contact with
                      circulating factors, we postulated whether the endothelium
                      itself may orchestrate tissue remodeling. Here, we show
                      using human and mouse cancer models that during precachexia,
                      tumors overactivate Notch1 signaling in distant WAT
                      endothelium. Sustained endothelial Notch1 signaling induces
                      a WAT wasting phenotype in male mice through excessive
                      retinoic acid production. Pharmacological blockade of
                      retinoic acid signaling was sufficient to inhibit WAT
                      wasting in a mouse cancer cachexia model. This demonstrates
                      that cancer manipulates the endothelium at distant sites to
                      mediate WAT wasting by altering angiocrine signals.},
      cin          = {A270},
      ddc          = {610},
      cid          = {I:(DE-He78)A270-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37749321},
      doi          = {10.1038/s43018-023-00622-y},
      url          = {https://inrepo02.dkfz.de/record/283156},
}