Skip Navigation



Annals of Oncology Advance Access published online on September 13, 2006
Annals of Oncology, doi:10.1093/annonc/mdl310
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
17/12/1797    most recent
mdl310v1
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
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 Bamias, A.
Right arrow Articles by Psyrri, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bamias, A.
Right arrow Articles by Psyrri, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2006 European Society for Medical Oncology
Received April 16, 2006
Revised July 18, 2006
Accepted July 18, 2006

original article

Automated quantitative analysis of DCC tumor suppressor protein in ovarian cancer tissue microarray shows association with {beta}-catenin levels and outcome in patients with epithelial ovarian cancer

A. Bamias 1 *, Z. Yu 2, P. M. Weinberger 2, S. Markakis 3, D. Kowalski 4, R. L. Camp 4, D. L. Rimm 4, M. A. Dimopoulos 1, and A. Psyrri 2

1 Department of Clinical Therapeutics, University of Athens, School of Medicine, Athens, Greece
2 Department of Medical Oncology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
3 Histopathology Department, Alexandra Hospital, Athens, Greece
4 Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06520, USA

* To whom correspondence should be addressed.
A. Bamias, E-mail: abamias{at}med.uoa.gr


  Abstract

Background: The deleted in colorectal cancer (DCC) protein, the product of DCC tumor suppressor gene, is frequently altered in cancer. Preclinical data demonstrate that DCC regulates {beta}-catenin levels. Here, we sought to determine the association of DCC with {beta}-catenin protein levels, clinicopathological parameters and patient outcome in ovarian cancer using a method of in situ compartmentalized protein analysis.

Methods: A tissue array composed of 150 advanced-stage ovarian cancers, treated with surgical debulking and platinum-paclitaxel (Taxol) combination chemotherapy, was constructed. For evaluation of protein expression, we used an immunofluorescence-based method of automated in situ quantitative measurement of protein analysis (AQUA).

Results: One hundred and twelve patients (74%) had sufficient tissue for AQUA. The median follow-up time for the entire cohort was 33 months. Patients with low nuclear DCC expression had a 3-year progression-free survival (PFS) rate of 0% compared with 33% of those with high DCC expression (P = 0.0067). In multivariate analysis, low nuclear DCC expression level retained its prognostic significance for PFS. Between DCC and {beta}-catenin, a significant relationship was found, where tumors with low DCC had low {beta}-catenin and vice versa (P = 0.003).

Conclusions: Low nuclear DCC levels predict for poor patient outcome in epithelial ovarian cancer. DCC may exert its antitumor function, in part, through regulation of {beta}-catenin levels.

Keywords: {beta}-catenin; DCC; ovarian cancer; prognosis.
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.