Journal article

Differential gene expression between human schwannoma and control Schwann cells

  • Hanemann, C. O. Clinical Neurobiology, Peninsula Medical School, Peymouth, UK,
  • Bartelt-Kirbach, B. Center for Clinical Research, Department of Heurology, University Ulm, Germany
  • Diebold, R. Center for Clinical Research, Department of Heurology, University Ulm, Germany
  • Kämpchen, K. Center for Clinical Research, Department of Heurology, University Ulm, Germany
  • Langmesser, Sonja Institut de Biochimie, Université de Fribourg, Switzerland
  • Utermark, T. Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, USA
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    06.11.2006
Published in:
  • Neuropathology and Applied Neurobiology. - 2006, vol. 32, no. 6, p. 605–614
English The NF2 gene encodes the tumour suppressor protein merlin. The mutation of a single allele of this gene causes the autosomal dominantly inherited disease neurofibromatosis type 2 (NF2), which is characterized mainly by vestibular schwannoma carrying a second hit mutation. Complete lack of merlin is also found in spontaneous schwannomas and meningiomas. As the events leading to schwannoma development are largely unknown we investigated the differences in gene expression between schwannoma cells from NF2 patients and normal human primary Schwann cells by cDNA array analysis. We identified 41 genes whose expression levels differed by more than factor 2. Most of these clones were corroborated by real-time reverse transcription polymerase chain reaction analysis. By this method a total of seven genes with increased and seven genes with decreased mRNA levels in schwannoma compared with normal Schwann cells could be identified. Regulated clones, some of which not been described in Schwann cells earlier, included matrix metalloproteinase's, growth factors, growth factor receptors and tyrosine kinases.
Faculty
Faculté des sciences et de médecine
Department
Département de Biologie
Language
  • English
Classification
Biology
License
License undefined
Identifiers
Persistent URL
https://folia.unifr.ch/unifr/documents/300306
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