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JNCI Journal of the National Cancer Institute 2006 98(18):1311-1320; doi:10.1093/jnci/djj360
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© 2006 The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

ARTICLE

Estrogen Sulfation Genes, Hormone Replacement Therapy, and Endometrial Cancer Risk

Timothy R. Rebbeck, Andrea B. Troxel, Yiting Wang, Amy H. Walker, Saarene Panossian, Stephen Gallagher, Ekaterina G. Shatalova, Rebecca Blanchard, Greta Bunin, Angela DeMichele, Stephen C. Rubin, Mona Baumgarten, Michelle Berlin, Rita Schinnar, Jesse A. Berlin, Brian L. Strom

Affiliations of authors: Center for Clinical Epidemiology and Biostatistics and Department of Biostatistics and Epidemiology (TRR, ABT, YW, AHW, SP, SG, GB, ADM, MB, RS, JAB, BLS), Abramson Cancer Center (TRR, ABT, GB, ADM, JAB, BLS), Department of Medicine (ADM, BLS), Department of Obstetrics and Gynecology (SCR, MB), University of Pennsylvania School of Medicine, Philadelphia, PA; Division of Oncology, Children's Hospital of Philadelphia (GB), Fox Chase Cancer Center (EGS, RB), Philadelphia, PA

Correspondence to: Timothy Rebbeck, PhD, Department of Biostatistics and Epidemiology and Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, 904 Blockley Hall, 423 Guardian Dr., Philadelphia, PA 19104-6021 (e-mail: trebbeck{at}cceb.med.upenn.edu).

Background: Unopposed estrogen replacement therapy is associated with increased risk of endometrial cancer. To investigate the mechanism of this association, we evaluated whether risk of endometrial cancer was associated with the genotypes involved in steroid hormone metabolism and the duration of exogenous hormone use. Methods: A population-based case–control study in nine counties of the Philadelphia metropolitan area was undertaken with 502 case patients with endometrial cancer and 1326 age- and race-matched control subjects. Data regarding exogenous hormone use were obtained by interview, and genotypes of the genes COMT, CYP1A1, CYP1A2, CYP1B1, CYP3A4, PGR, SULT1A1, SULT1E1, and UGT1A1 were obtained by polymerase chain reaction techniques. Conditional logistic regression was used to examine the relationship among genotype, hormone use, and endometrial cancer risk. Results: Associations were observed between the risk of endometrial cancer and genotypes of the following steroid hormone metabolism genes: CYP1A1*2C (adjusted odds ratio [OR] = 1.68, 95% confidence interval [CI] = 1.08 to 2.61); SULT1A1*3 (adjusted OR = 0.51, 95% CI = 0.29 to 0.92); and the G -> A variant in the promoter of SULT1E1 at position –64 (adjusted OR = 1.45, 95% CI = 1.06 to 1.99). We observed a statistically significant interaction between estrogen replacement therapy use and SULT1A1*2 genotype: the SULT1A1*2 allele and long-term use of estrogen replacement therapy were associated with statistically significantly higher risk of endometrial cancer (adjusted OR = 3.85, 95% CI = 1.48 to 10.00) than that of the SULT1A1*2 allele and no estrogen replacement therapy use. Conclusions: Among women with long-term use of estrogen replacement therapy or combined hormone replacement therapy, the risk of endometrial cancer may be associated with functionally relevant genotypes that regulate steroid hormone sulfation.


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