Skip Navigation



Carcinogenesis Advance Access published online on July 22, 2004
Carcinogenesis, doi:10.1093/carcin/bgh244
© 2004 by Oxford University Press
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
25/11/2225    most recent
bgh244v1
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
Google Scholar
Right arrow Articles by Sun, T.
Right arrow Articles by Lin, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sun, T.
Right arrow Articles by Lin, D.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Received June 12, 2004
Revised July 15, 2004
Accepted July 18, 2004

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Functional Phe31Ile polymorphism in Aurora A and risk of breast carcinoma

Tong Sun 1, Xiaoping Miao 1, Jinwei Wang 2, Wen Tan 1, Yifeng Zhou 1, Chunyuan Yu 1, Dongxin Lin 1*

1 Department of Etiology and Carcinogenesis, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China
2 Surgery, Cancer Institute & Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China

* To whom correspondence should be addressed. E-mail: dlin{at}public.bta.net.cn.


  Abstract

Aurora-A/BTAK/STK15 involved in regulating centrosomes and chromosome segregation is overexpressed in human breast carcinoma and other cancers. The Phe31Ile polymorphism in Aurora A alters the kinase function, with the 31Ile variant being preferentially amplified and associated with degree of aneuploidy in human tumors. We previously have shown that the Phe31Ile polymorphism is associated with the occurrence and advanced disease status of esophageal cancer. This case-control study examined the contribution of this polymorphism to susceptibility to development and progression of breast cancer. Aurora A genotypes were determined in 520 patients with breast carcinoma, 191 patients with benign breast diseases (BBD), and 520 controls. It was found that the Aurora A Ile/Ile genotype was significantly associated with increased risk of breast carcinoma occurrence [odds ratio (OR), 1.66; 95% confidence interval (95% CI), 1.29 to 2.12)], compared with the Phe/Phe or Phe/Ile genotype. The increased risk for BBD and breast carcinoma related to the Ile/Ile genotype was more pronounced in younger subjects. Moreover, we found that patients carrying the Ile/Ile genotype tended to have ER-carcinomas (OR, 1.84; 95% CI, 1.27 to 2.67). No significant association was observed between the polymorphism and metastasis and disease stage of the cancer. These findings suggest that the Phe31Ile polymorphism in Aurora A may be a genetic modifier for developing breast carcinoma.

Keywords: Aurora A; genetic polymorphism; breast cancer; molecular epidemiology.
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 Epidemiol. Biomarkers Prev.Home page
F. J. Couch, O. Sinilnikova, R. A. Vierkant, V. S. Pankratz, Z. S. Fredericksen, D. Stoppa-Lyonnet, I. Coupier, D. Hughes, A. Hardouin, P. Berthet, et al.
AURKA F31I Polymorphism and Breast Cancer Risk in BRCA1 and BRCA2 Mutation Carriers: A Consortium of Investigators of Modifiers of BRCA1/2 Study
Cancer Epidemiol. Biomarkers Prev., July 1, 2007; 16(7): 1416 - 1421.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
I. Perez de Castro, G. de Carcer, and M. Malumbres
A census of mitotic cancer genes: new insights into tumor cell biology and cancer therapy
Carcinogenesis, May 1, 2007; 28(5): 899 - 912.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
B. Zhang, T. Sun, L. Xue, X. Han, B. Zhang, N. Lu, Y. Shi, W. Tan, Y. Zhou, D. Zhao, et al.
Functional polymorphisms in FAS and FASL contribute to increased apoptosis of tumor infiltration lymphocytes and risk of breast cancer
Carcinogenesis, May 1, 2007; 28(5): 1067 - 1073.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
J. Gu, Y. Gong, M. Huang, C. Lu, M. R. Spitz, and X. Wu
Polymorphisms of STK15 (Aurora-A) gene and lung cancer risk in Caucasians
Carcinogenesis, February 1, 2007; 28(2): 350 - 355.
[Abstract] [Full Text] [PDF]

Home page
 Hum Mol GenetHome page
P. Briassouli, F. Chan, and S. Linardopoulos
The N-terminal domain of the Aurora-A Phe-31 variant encodes an E3 ubiquitin ligase and mediates ubiquitination of I{kappa}B{alpha}
Hum. Mol. Genet., November 15, 2006; 15(22): 3343 - 3350.
[Abstract] [Full Text] [PDF]

Home page
 JNCI J Natl Cancer InstHome page
O. Fletcher, N. Johnson, C. Palles, I. dos Santos Silva, V. McCormack, J. Whittaker, A. Ashworth, and J. Peto
Inconsistent association between the STK15 F31I genetic polymorphism and breast cancer risk.
J Natl Cancer Inst, July 19, 2006; 98(14): 1014 - 1018.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
T. Sun, Y. Zhou, H. Li, X. Han, Y. Shi, L. Wang, X. Miao, W. Tan, D. Zhao, X. Zhang, et al.
FASL -844C polymorphism is associated with increased activation-induced T cell death and risk of cervical cancer
J. Exp. Med., October 3, 2005; 202(7): 967 - 974.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
A. Ewart-Toland, Q. Dai, Y.-T. Gao, H. Nagase, M. G. Dunlop, S. M. Farrington, R. A. Barnetson, H. Anton-Culver, D. Peel, A. Ziogas, et al.
Aurora-A/STK15 T+91A is a general low penetrance cancer susceptibility gene: a meta-analysis of multiple cancer types
Carcinogenesis, August 1, 2005; 26(8): 1368 - 1373.
[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.