@article{HohenauerBerkingSchmidtetal.2013,
  author    = {Hohenauer, Tobias and Berking, Carola and Schmidt, Andreas and Haferkamp, Sebastian and Senft, Daniela and Kammerbauer, Claudia and Fraschka, Sabine and Graf, Saskia Anna and Irmler, Martin and Beckers, Johannes and Flaig, Michael and Aigner, Achim and H{\"o}bel, Sabrina and Hoffmann, Franziska and Hermeking, Heiko and Rothenfusser, Simon and Endres, Stefan and Ruzicka, Thomas and Besch, Robert},
  title     = {The neural crest transcription factor Brn3a is expressed in melanoma and required for cell cycle progression and survival},
  series = {EMBO Molecular Medicine},
  volume    = {5},
  journal   = {EMBO Molecular Medicine},
  issn      = {1757-4676},
  doi       = {10.1002/emmm.201201862},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-122193},
  pages     = {919-934},
  year      = {2013},
  abstract  = {Pigment cells and neuronal cells both are derived from the neural crest. Here, we describe the Pit-Oct-Unc (POU) domain transcription factor Brn3a, normally involved in neuronal development, to be frequently expressed in melanoma, but not in melanocytes and nevi. RNAi-mediated silencing of Brn3a strongly reduced the viability of melanoma cell lines and decreased tumour growth in vivo. In melanoma cell lines, inhibition of Brn3a caused DNA double-strand breaks as evidenced by Mre11/Rad50-containing nuclear foci. Activated DNA damage signalling caused stabilization of the tumour suppressor p53, which resulted in cell cycle arrest and apoptosis. When Brn3a was ectopically expressed in primary melanocytes and fibroblasts, anchorage-independent growth was increased. In tumourigenic melanocytes and fibroblasts, Brn3a accelerated tumour growth in vivo. Furthermore, Brn3a cooperated with proliferation pathways such as oncogenic BRAF, by reducing oncogene-induced senescence in non-malignant melanocytes. Together, these results identify Brn3a as a new factor in melanoma that is essential for melanoma cell survival and that promotes melanocytic transformation and tumourigenesis.},
  language  = {en}
}
@article{MeierGrossKlotzetal.1989,
  author    = {Meier, Friedegund and Gross, Eva and Klotz, Karl-Norbert and Ruzicka, Thomas},
  title     = {Leukotriene B4 receptors on neutrophils in patients with psoriasis and atopic exzema},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-86265},
  year      = {1989},
  abstract  = {Polymorphonuclear leukocyte (PMNL) infiltration is an important characteristic in psoriatic lesions. Elevated concentrations of the chemoattractant eicosanoid leukotriene B4 (L TB4) are present in psoriatic skin. Its chemotactic activity is mediated via high affinity receptors on PMNL. The goal of our work was to ascertain whether PMNL infiltration in psoriasis can be accounted for by functional abnormalities of the circulating PMNL due to alterations in the LTB4 receptor density or affinity (or both). No significant difference was found between patients with psoriasis, healthy controls and patients with another inflammatory dermatosis (atopic eczema) with regard to the binding parameters of LTB4 receptors on PMNL. Our findings suggest that PMNL accumulation in psoriatic skin may be the result of an excess of cutaneous hemoattractant rather than the increased readiness of psoriatic PMNL to migrate towards L TB4 due to altered LTB4 receptor density or affinity.},
  subject      = {Dermatologie},
  language  = {en}
}