Skip Navigation


Glycobiology Advance Access originally published online on October 10, 2008
Glycobiology 2009 19(1):68-75; doi:10.1093/glycob/cwn105
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplementary Data
Right arrow All Versions of this Article:
19/1/68    most recent
cwn105v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Eude-Le Parco, I.
Right arrow Articles by Poirier, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Eude-Le Parco, I.
Right arrow Articles by Poirier, F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Genetic assessment of the importance of galectin-3 in cancer initiation, progression, and dissemination in mice

Isabelle Eude-Le Parco2,3, Gaëlle Gendronneau2,3, Tien Dang3, Delphine Delacour3, Victor L Thijssen4, Winfried Edelmann5, Michel Peuchmaur6 and Françoise Poirier1,3

3 Institut Jacques Monod, UMR CNRS 7592, Univ. P6 and P7, 2 Place Jussieu, 75251 Paris Cedex 5, France
4 Department of Pathology, Angiogenesis Laboratory, School for Oncology and Developmental Biology, University of Maastricht, The Netherlands
5 Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
6 Assistance Publique-Hôpitaux de Paris (AP-HP) Hôpital R. Debré, Service de Chirurgie Pédiatrique, Paris, France

1 To whom correspondence should be addressed: Tel: +33-1-44-27-40-35; Fax: +33-1-44-27-52-65; E-mail: poirier{at}ijm.jussieu.fr

Received on May 2, 2008; revised on September 24, 2008; accepted on October 1, 2008

The galectin family of β-galactoside binding lectins is involved in normal and pathological processes. Altered expression of galectin-3 has been described in many cancers, and studies of cancer cell lines have implicated this lectin in various aspects of the tumorigenic cascade. The goal of this report was to directly assess the importance of galectin-3 in tumor biology by introducing the galectin-3 null mutation (galectin-3–/–) into mouse lines genetically programmed to develop cancers. We used two mouse models of human intestinal cancer, the ApcMin and Apc1638N lines, to study tumor initiation and tumor progression. We also crossed the galectin-3–/– mice with PyMT transgenic animals, a model in which primary mammary gland tumors give rise to lung metastases at high frequency. Unexpectedly, we show that the absence of galectin-3 does not affect the evolution of the disease in any of these three situations.

Key words: Apc mutations / galectin-3 knock-out mice / metastasis / PyMT transgenic / tumor progression

2 Both authors equally contributed to the work.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.