Role of Wnt inhibitory factor-1 and Wnt/wingless signaling in choroid plexus tumors.

Full Abstract

Little is known on pathways involved in the pathogenesis of choroid plexus tumors (CPTs). The finding of overexpression of Wnt inhibitory factor-1 (Wif-1) prompted us to investigate the functional role of Wif-1 as well as nuclear accumulation of beta-catenin in CPT. In Z310 neoplastic choroid plexus epithelial cells, silencing of Wif1 expression increased proliferative activity not associated with increased canonical Wnt signaling. Nuclear beta-catenin accumulation was also lacking in a series of 16 CPT. In conclusion, our data show that Wif-1 inhibits proliferation of neoplastic choroid plexus epithelial cells, but argue against a role of canonical Wnt/wingless signaling in CPT.

Author information

Author/s: Tomm, Manuel (M); Koch, Arend (A); Mertsch, Sonja (S); Wrede, Brigitte (B); Jeibmann, Astrid (A); Wolff, Johannes (J); Paulus, Werner (W); Hasselblatt, Martin (M);

Affiliation: Institute of Neuropathology, University Hospital Münster, Münster, Germany.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Pediatric blood & cancer (Pediatr Blood Cancer), published in United States. (Language: eng)

Reference: 2009-Dec; vol 53 (issue 6) : pp 1152-5

Dates: Created 2009/09/16; Completed 2009/10/13;

PMID: 19621428, status: MEDLINE (last retrieval date: 10/13/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

External Links for this article
(including full text providers, if available):

Click Electronic Full-text Provider Links to see options for finding the electronic full text links to this article. Note there may be a subscription or fee required for access to the full text. See our FAQ for information on finding FREE full text articles.

This article may also be located in paper journal collections available in many libraries. Use the Journal and Publication Information above to find the full article.