gms | German Medical Science

82nd Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

01.06. - 05.06.2011, Freiburg

The profile of the phosphokinases in nasal polyps

Meeting Abstract

  • corresponding author presenting/speaker Robert Linke - University of Luebeck, Department of Oto-Rhino-Laryngology, Luebeck, Germany
  • Ralph Pries - University of Luebeck, Department of Oto-Rhino-Laryngology, Luebeck, Germany
  • Brigitte Wollmann - University of Luebeck, Department of Oto-Rhino-Laryngology, Luebeck, Germany
  • Barbara Wollenberg - University of Luebeck, Department of Oto-Rhino-Laryngology, Luebeck, Germany

German Society of Oto-Rhino-Laryngology, Head and Neck Surgery. 82nd Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery. Freiburg, 01.-05.06.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. Doc11hno59

doi: 10.3205/11hno59, urn:nbn:de:0183-11hno596

Published: August 3, 2011

© 2011 Linke et al.
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Outline

Text

Introduction: The origin of nasal polyps is ultimately based on a disturbance in the regulation of cell growth. The biosynthetic pathways are often coordinated by the activity of various phosphokinases. To identify possible dysregulation in nasal polyps, we have characterized the expression profiles of a wide range of phosphokinases.

Methods: In 5 patients with chronic sinusitis with nasal polyps tissue samples of the polyps and the inferior turbinate, which served as internal control, were examined using a protein array. This array determines the expression profiles of 44 phosphorylated phosphokinases, thus allowing conclusions on the regulation of different signal transduction cascades.

Results: In the examined tissue samples of nasal polyps significant shifts were identified in comparison to healthy mucosa. For example, the level of phosphorylation of the protein STAT3, Y705 was significantly increased in all samples.

Conclusions: Our investigations form the basis for further analysis to identify the biosynthetic pathways which are responsible for the proliferation in nasal polyps. For example, STAT3 plays a central role in the JAK-STAT Pathway. The pathway is activated for example by the binding of IL-6 on the JAK-receptor, this results in the phosphorylation of STATs. These dimerize and migrate to the nucleus where they activate transcription of various target genes. We will show the progress of our investigations.