Skip Navigation


American Journal of Epidemiology Advance Access originally published online on October 21, 2009
American Journal of Epidemiology 2009 170(10):1241-1249; doi:10.1093/aje/kwp298
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Web Table 1
Right arrow All Versions of this Article:
170/10/1241    most recent
kwp298v1
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
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Reding, K. W.
Right arrow Articles by Malone, K. E.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reding, K. W.
Right arrow Articles by Malone, K. E.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

American Journal of Epidemiology © The Author 2009. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

ORIGINAL CONTRIBUTIONS

Genetic Variation in the Progesterone Receptor and Metabolism Pathways and Hormone Therapy in Relation to Breast Cancer Risk

Kerryn W. Reding*, Christopher I. Li, Noel S. Weiss, Chu Chen, Christopher S. Carlson, David Duggan, Kenneth E. Thummel, Janet R. Daling and Kathleen E. Malone

* Correspondence to Dr. Kerryn W. Reding, Department of Epidemiology, School of Public Health, University of Washington, 1100 Fairview Avenue North, Mailstop M4-B874, Seattle, WA 98109 (e-mail: kreding{at}u.washington.edu).

Received for publication April 27, 2009. Accepted for publication August 17, 2009.

The relevance of progesterone to breast carcinogenesis is highlighted by evidence indicating that use of combined estrogen-progesterone therapy (EPT) is more strongly related to breast cancer risk than is use of unopposed estrogen therapy. However, few investigators have assessed how genetic variation in progesterone-related genes modifies the effect of EPT on risk. In an analysis combining data from 2 population-based case-control studies of postmenopausal breast cancer (1,296 cases and 1,055 controls) conducted in Washington State in 1997–1999 and 2000–2004, the authors evaluated how 51 single nucleotide polymorphisms in 7 progesterone-related genes (AKR1C1, AKR1C2, AKR1C3, CYP3A4, SRD5A1, SRD5A2, and PGR) influenced breast cancer risk. There was no appreciable association with breast cancer risk overall for any single nucleotide polymorphism. For rs2854482 in AKR1C2, carrying 1 or 2 A alleles was associated with a 2.0-fold increased breast cancer risk in EPT users (95% confidence interval: 1.0, 4.0) but not in never users (Pheterogeneity = 0.03). For rs12387 in AKR1C3, the presence of 1 or 2 G alleles was associated with a 1.5-fold increased risk among EPT users (95% confidence interval: 1.1, 2.2) but not in never users (Pheterogeneity = 0.02). Interpretation of these subgroup associations must await the results of similar studies conducted in other populations.

breast neoplasms; hormone replacement therapy; progesterone; receptors, progesterone


Abbreviations: CI, confidence interval; EPT, estrogen-progesterone therapy; OR, odds ratio; PACE, Puget Sound Area Breast Cancer Evaluation; PGR, progesterone receptor; SHARE, Seattle Area Hormone and Reproductive Epidemiology; SNP, single nucleotide polymorphism


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.