Skip Navigation


Japanese Journal of Clinical Oncology Advance Access originally published online on June 9, 2006
Japanese Journal of Clinical Oncology 2006 36(6):357-363; doi:10.1093/jjco/hyl038
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
36/6/357    most recent
hyl038v1
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 arrow Request Permissions
Google Scholar
Right arrow Articles by Toyama, T.
Right arrow Articles by Iwata, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Toyama, T.
Right arrow Articles by Iwata, H.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© 2006 Foundation for Promotion of Cancer Research

Low Expression of the Snail Gene is a Good Prognostic Factor in Node-Negative Invasive Ductal Carcinomas

Tatsuya Toyama1,2, Zhenhuan Zhang2, Hirotaka Iwase2, Hiroko Yamashita2, Yoshiaki Ando2, Maho Hamaguchi2, Mitsuhiro Mizutani1, Naoto Kondo1, Takashi Fujita1, Yoshitaka Fujii2 and Hiroji Iwata1

1 Department of Breast Oncology, Aichi Cancer Center Hospital, Nagoya and 2 Department of Oncology, Immunology and Surgery, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

For reprints and all correspondence: Tatsuya Toyama, Department of Oncology, Immunology and Surgery, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan. E-mail: toyamat-ncu{at}umin.ac.jp

Received September 4, 2005; accepted March 22, 2006

Background: While Snail is a zinc-finger transcription factor that triggers the epithelial-mesenchymal transition, it has also been reported to be indirectly regulated by estrogen receptor {alpha} (ER{alpha}) and to be involved in the transcriptional repression of the aromatase gene. The aim of the present study was to examine the role of Snail expression in node-negative invasive ductal carcinomas.

Methods: We analyzed Snail mRNA expression levels in 86 node-negative invasive ductal carcinomas by real-time quantitative RT–PCR and studied whether Snail mRNA expression correlates with clinicopathological factors.

Results: No correlation was found between Snail mRNA expression and ER{alpha} protein expression levels. However, we observed that none of the 34 patients showing low Snail mRNA expression developed distant metastasis while 6 of 52 (12%) showing high expression of Snail mRNA did. The level of Snail mRNA expression was not found to be significantly correlated with clinicopathological factors. No inverse correlation was found between the Snail and aromatase mRNA expression levels in our series.

Conclusion: Our data show that low expression of Snail mRNA is a good prognostic factor in node-negative invasive ductal carcinomas. Snail expression is suggested to be involved in distant metastasis in node-negative invasive ductal carcinomas.

Key Words: Snail • estrogen receptor • E-cadherin • breast cancer • aromatase


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


This article has been cited by other articles:


Home page
Cancer Res.Home page
S. Baritaki, K. Yeung, M. Palladino, J. Berenson, and B. Bonavida
Pivotal Roles of Snail Inhibition and RKIP Induction by the Proteasome Inhibitor NPI-0052 in Tumor Cell Chemoimmunosensitization
Cancer Res., November 1, 2009; 69(21): 8376 - 8385.
[Abstract] [Full Text] [PDF]



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.