gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

The involvement of Wnt/beta-catenin pathway in pituitary adenomas

Der Einfluss des Wnt/beta-catenin-Weges auf Hypophysenadenome

Meeting Abstract

  • corresponding author N. Kremenevskaya - Neurochirurgische Klinik, Friedrich-Alexander Universität Erlangen-Nürnberg
  • M. N. K. Khattak - Neurochirurgische Klinik, Friedrich-Alexander Universität Erlangen-Nürnberg
  • M. Buchfelder - Neurochirurgische Klinik, Friedrich-Alexander Universität Erlangen-Nürnberg

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocP 099

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dgnc2007/07dgnc354.shtml

Veröffentlicht: 11. April 2007

© 2007 Kremenevskaya et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: The pituitary neoplasm is the third most common tumour developing in the human cranial cavity. Altered Wnt/beta-catenin signalling has recently been recognized to be associated with the development of various human cancers. Wnt stabilizes beta-catenin (free beta-catenin) by preventing its normal phosphorylation which targets beta-catenin for degradation. Free beta-catenin is translocated to the nucleus where it stimulates a number of genes involved in proliferation and differentiation control upon binding to TCF/LEF-1. The aim of the present study was to investigate the role of the Wnt/beta-catenin pathway in a series of pituitary adenomas.

Methods: Samples of 10 growth hormone secreting, 10 hormone inactive adenomas and 4 normal adenohypophyseal glands were studied by Western blot analyses, direct DNA sequencing, single strand conformation polymorphism and RT-PCR.

Results: The beta-catenin expression was high at protein and RNA levels in both GH secreting and hormone inactive pituitary adenomas as compared to normal pituitary tissues. The expression of cyclin D1, a target gene of Wnt/beta-catenin signalling, was found only in GH-secreting and hormone inactive adenomas, but was undetectable in the normal pituitary. Specific mutations in exon 3 of CTNNB1 are rare in the pituitary adenomas according to our study.

Conclusions: We suggest that there is an involvement of the Wnt/beta-catenin pathway in pituitary adenomas, but not through beta-catenin exon 3 mutations. The overexpression of beta-catenin and cyclin D1 underlines the potential importance of beta-catenin deregulation for the pathophysiology of pituitary adenomas.