@misc{AichertStaigerSchulteMaeteretal.2010,
  author    = {Aichert, Ingrid and Staiger, Anja and Schulte-M{\"a}ter, Anne and Becker-Redding, Ulrike and Stahn, Corinna and Peschke, Claudia and Heide, Judith and Ott, Susan and Herrmann, Heike and V{\"o}lsch, Juliane and Mayer, J{\"o}rg and Rohnke, Lucie and Frank, Ulrike and Stadie, Nicole and Jentsch, Nadine and Blech, Anke and Kurtenbach, Stephanie and Thieke, Johanna and Schr{\"o}der, Astrid and Stahn, Corinna and H{\"o}rnig, Robin and Burchert, Frank and De Bleser, Ria and Heister, Julian and Bartels, Luise and W{\"u}rzner, Kay-Michael and B{\"o}hme, Romy and Burmester, Juliane and Krajewski, Melanie and Nager, Wido and Jungeh{\"u}lsing, Gerhard Jan and Wartenburger, Isabell and J{\"o}bges, Michael and Schwilling, Eleonore and Lidzba, Karen and Winkler, Susanne and Konietzko, Andreas and Kr{\"a}geloh-Mann, Ingeborg and Rilling, Eva and Wilken, Rainer and Wismann, Kathrin and Glandorf, Birte and Hoffmann, Hannah and Hinnenkamp, Christiane and Rohlmann, Insa and Ludewigt, Jacqueline and Bittner, Christian and Orlov, Tatjana and Claus, Katrin and Ehemann, Christine and Winnecken, Andreas and Hummel, Katja and Breitenstein, Sarah},
  title     = {Spektrum Patholinguistik = Schwerpunktthema: Von der Programmierung zur Artikulation : Sprechapraxie bei Kindern und Erwachsenen},
  number    = {3},
  editor    = {Wahl, Michael and Stahn, Corinna and Hanne, Sandra and Fritzsche, Tom},
  publisher = {Universit{\"a}tsverlag Potsdam},
  address   = {Potsdam},
  organization    = {Verband f{\"u}r Patholinguistik e. V. (vpl)},
  isbn      = {978-3-86956-079-3},
  issn      = {1869-3822},
  doi       = {10.25932/publishup-4578},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-45470},
  year      = {2010},
  abstract  = {Das 3. Herbsttreffen Patholinguistik fand am 21. November 2009 an der Universit{\"a}t Potsdam statt. Der vorliegende Tagungsband enth{\"a}lt die drei Hauptvortr{\"a}ge zum Schwerpunktthema „Von der Programmierung zu Artikulation: Sprechapraxie bei Kindern und Erwachsenen". Dar{\"u}ber hinaus enth{\"a}lt der Band die Beitr{\"a}ge aus dem Spektrum Patholinguistik, sowie die Abstracts der Posterpr{\"a}sentationen.},
  language  = {de}
}
@article{BriestGrassSeddingetal.2017,
  author    = {Briest, Franziska and Grass, Irina and Sedding, Dagmar and Moebs, Markus and Christen, Friederike and Benecke, Joana and Fuchs, Karolin and Mende, Stefanie and Kaemmerer, Daniel and S{\"a}nger, J{\"o}rg and Kunze, Almut and Geisler, Christina and Freitag, Helma and Lewens, Florentine and Worpenberg, Lina and Iwaszkiewicz, Sara and Siegmund, Britta and Walther, Wolfgang and Hummel, Michael and Grabowski, Patricia},
  title     = {Mechanisms of Targeting the MDM2-p53-FOXM1 Axis in Well-Differentiated Intestinal Neuroendocrine Tumors},
  series = {Neuroendocrinology : international journal for basic and clinical studies on neuroendocrine relationships},
  volume    = {107},
  journal   = {Neuroendocrinology : international journal for basic and clinical studies on neuroendocrine relationships},
  number    = {1},
  publisher = {Karger},
  address   = {Basel},
  issn      = {0028-3835},
  doi       = {10.1159/000481506},
  pages     = {1 -- 23},
  year      = {2017},
  abstract  = {Background/Aims: The tumor suppressor p53 is rarely mutated in gastroenteropancreatic neuroendocrine neoplasms (GEP-NEN) but they frequently show a strong expression of negative regulators of p53, rendering these tumors excellent targets for a p53 recovery therapy. Therefore, we analyzed the mechanisms of a p53 recovery therapy on intestinal neuroendocrine tumors in vitro and in vivo. Methods: By Western blot and immunohistochemistry, we found that in GEP-NEN biopsy material overexpression of MDM2 was present in intestinal NEN. Therefore, we analyzed the effect of a small-molecule inhibitor, nutlin-3a, in p53 wild-type and mutant GEP-NEN cell lines by proliferation assay, flow cytometry, immunofluorescence, Western blot, and by multiplex gene expression analysis. Finally, we analyzed the antitumor effect of nutlin-3a in a xenograft mouse model in vivo. During the study, the tumor volume was determined. Results: The midgut wild-type cell line KRJ-I responded to the treatment with cell cycle arrest and apoptosis. By gene expression analysis, we could demonstrate that nutlins reactivated an antiproliferative p53 response. KRJ-I-derived xenograft tumors showed a significantly decreased tumor growth upon treatment with nutlin-3a in vivo. Furthermore, our data suggest that MDM2 also influences the expression of the oncogene FOXM1 in a p53-independent manner. Subsequently, a combined treatment of nutlin-3a and cisplatin (as chemoresistance model) resulted in synergistically enhanced antiproliferative effects. Conclusion: In summary, MDM2 overexpression is a frequent event in p53 wild-type intestinal neuroendocrine neoplasms and therefore recovery of a p53 response might be a novel personalized treatment approach in these tumors. (c) 2017 S. Karger AG, Basel},
  language  = {en}
}