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Carcinogenesis Advance Access published online on March 30, 2006
Carcinogenesis, doi:10.1093/carcin/bgl014
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received November 2, 2005
Revised March 3, 2006
Accepted March 7, 2006

CARCINOGENESIS

Single nucleotide polymorphisms of follicle stimulating hormone receptor are associated with ovarian cancer susceptibility

C. Q. Yang 1 {dagger}, K. Y. K. Chan 2 {dagger}, H. Y. S. Ngan 3, U. S. Khoo 1, P. M. Chiu 1, Q. K. Y. Chan 1, W. C. Xue 1, and A. N. Y. Cheung 1 *

1 Department of Pathology, Hong Kong Jockey Club Clinical Research Centre, The University of Hong Kong, Hong Kong, China
2 Department of Pathology, Hong Kong Jockey Club Clinical Research Centre, The University of Hong Kong, Hong Kong, China; Department of Obstetrics and Gynecology, Hong Kong Jockey Club Clinical Research Centre, The University of Hong Kong, Hong Kong, China
3 Department of Obstetrics and Gynecology, Hong Kong Jockey Club Clinical Research Centre, The University of Hong Kong, Hong Kong, China

* To whom correspondence should be addressed.
A. N. Y. Cheung, E-mail: anycheun{at}hkucc.hku.hk


  Abstract

Epidemiological studies suggested that ovulation was associated with ovarian carcinogenesis. Follicle-stimulating hormone (FSH) played an important role in follicular development and was recently found to affect growth of ovarian epithelial cells. Single nucleotide polymorphisms (SNPs) Thr307Ala and Asn680Ser were two nonsynonymous variations in the coding region of the FSH receptor (FSHR) gene. This hitherto first case-control study investigating the association between these two FSHR SNPs and the risk of ovarian cancer involved 202 histopathologically confirmed ovarian-cancer patients and 266 age-matched cancer free control subjects using restriction fragment length polymorphism assay and direct sequencing. Our results demonstrated that the 307Ala and 680Ser carriers were associated with significantly increased risk of developing serous and mucinous types of ovarian cancers [p<0.0005, OR=2.60, 95%CI=1.56-4.34, and p<0.0005, OR=2.89, 95%CI=1.73-4.84, adjusted for age, respectively] but not endometrioid and clear cell types. The two SNPs were found to be in modest linkage disequilibrium, D'=0.804 and 0.701, r2=.581 and 0.406 for the cancer and control groups respectively. The major haplotype of 307Ala-680Ser was also associated with higher cancer risk (p=0.033, OR=1.39, 95%CI=1.03-1.88), especially for the serous and mucinous carcinomas (p=0.001, OR=1.82, 95%CI=1.27-2.60). Our results suggested that the two FSHR SNPs might affect the susceptibility of women to specific subtypes of ovarian cancer. Different types of ovarian cancer might adopt distinct carcinogenetic pathways. Such understanding may be important in selecting patients for ovulation induction therapy.

{dagger}Authors contributed equally to this work
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