Clinical Cancer Research CTRC-AACR San Antonio Breast Cancer Symposium
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ohuchida, K.
Right arrow Articles by Tanaka, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ohuchida, K.
Right arrow Articles by Tanaka, M.
Clinical Cancer Research Vol. 12, 5417-5422, September 15, 2006
© 2006 American Association for Cancer Research


Imaging, Diagnosis, Prognosis

S100A11, A Putative Tumor Suppressor Gene, Is Overexpressed in Pancreatic Carcinogenesis

Kenoki Ohuchida1, Kazuhiro Mizumoto1, Seiji Ohhashi1, Hiroshi Yamaguchi2, Hiroyuki Konomi1, Eishi Nagai1, Koji Yamaguchi1, Masazumi Tsuneyoshi2 and Masao Tanaka1

Authors' Affiliations: Departments of 1 Surgery and Oncology and 2 Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan

Requests for reprints: Kazuhiro Mizumoto, Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Fukuoka 812-8582, Japan. Phone: 81-92-642-5440; Fax: 81-92-642-5458; E-mail: mizumoto{at}med.kyushu-u.ac.jp.

Purpose: Recent microarray analyses revealed that expression of S100A11 is up-regulated in pancreatic cancer. The aim of the present study was to evaluate the association of S100A11 with pancreatic carcinogenesis.

Experimental Design: We measured S100A11 mRNA expression in various clinical samples related to pancreatic cancer and its precursor lesions, intraductal papillary mucinous neoplasm (IPMN) and pancreatic intraepithelial neoplasia, by quantitative reverse transcription-PCR.

Results: Levels of S100A11 were significantly higher in pancreatic cancer (n = 22) and IPMN (n = 18) bulk tissues than in nonneoplastic bulk tissues (n = 22; P < 0.0001 for both). Levels of S100A11 did not differ between pancreatic cancer and IPMN bulk tissues. In microdissection analyses, however, IPMN cells (n = 21) expressed significantly higher levels of S100A11 than did cancer cells (n = 23; P = 0.003). The median level of S100A11 expression was higher in pancreatic intraepithelial neoplasia cells (n = 6) than in cancer cells. In pancreatic juice analyses, cancer-related (n = 24; P = 0.004) and IPMN-related (n = 18; P = 0.001) juice expressed significantly higher levels of S100A11 than did chronic pancreatitis–related juice (n = 23).

Conclusions: The present data suggest that expression of S100A11, a putative tumor suppressor gene, is increased in the early stage of pancreatic carcinogenesis and decreased during subsequent progression to cancer. Analysis of the S100A11 level in pancreatic juice may be an effective tool for screening of patients with high-risk lesions that could progress to pancreatic cancer or detecting early-stage pancreatic cancer.




This article has been cited by other articles:


Home page
Clin. Cancer Res.Home page
T. Egami, K. Ohuchida, K. Mizumoto, M. Onimaru, H. Toma, S. Nishio, E. Nagai, K. Matsumoto, T. Nakamura, and M. Tanaka
Radiation Enhances Adenoviral Gene Therapy in Pancreatic Cancer via Activation of Cytomegalovirus Promoter and Increased Adenovirus Uptake
Clin. Cancer Res., March 15, 2008; 14(6): 1859 - 1867.
[Abstract] [Full Text] [PDF]


Home page
Mol. Biol. CellHome page
M. Sakaguchi, H. Sonegawa, H. Murata, M. Kitazoe, J.-i. Futami, K. Kataoka, H. Yamada, and N.-h. Huh
S100A11, an Dual Mediator for Growth Regulation of Human Keratinocytes
Mol. Biol. Cell, January 1, 2008; 19(1): 78 - 85.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
M. Sakaguchi, H. Murata, H. Sonegawa, Y. Sakaguchi, J.-i. Futami, M. Kitazoe, H. Yamada, and N.-h. Huh
Truncation of Annexin A1 Is a Regulatory Lever for Linking Epidermal Growth Factor Signaling with Cytosolic Phospholipase A2 in Normal and Malignant Squamous Epithelial Cells
J. Biol. Chem., December 7, 2007; 282(49): 35679 - 35686.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 2006 by the American Association for Cancer Research.