@article{3118074,
    title = "Sequence variants of estrogen receptor beta and risk of prostate cancer
in the national cancer institute breast and prostate cancer cohort
consortium",
    author = "Chen, Yen-Ching and Kraft, Peter and Bretsky, Philip and Ketkar, Shamika and and Hunter, David J. and Albanes, Demetrius and Altshuler, David and and Andriole, Gerald and Berg, Christine D. and Boeing, Heiner and Burtt, and Noel and Bueno-de-Mesquita, Bas and Cann, Howard and Canzian, Federico and and Chanock, Stephen and Dunning, Alison and Feigelson, Heather S. and and Freedman, Matthew and Gaziano, J. Michael and Giovannucci, Edward and and Sanchez, Maria-Jose and Haiman, Christopher A. and Hallmans, Goran and and Hayes, Richard B. and Henderson, Brian E. and Hirschhorn, Joel and and Kaaks, Rudolf and Key, Timothy J. and Kolonel, Laurence N. and and LeMarchand, Loic and Ma, Jing and Overvad, Kim and Palli, Domenico and and Pharaoh, Paul and Pike, Malcolm and Riboli, Eliot and Rodriguez, Carmen and and Setiawan, V. Wendy and Stampfer, Meir and Stram, Daniel O. and and Thomas, Gilles and Thun, Michael J. and Travis, Ruth C. and Virtamo, and Jarmo and Trichopouiou, Antonia and Wacholder, Sholom and Weinstein, and Stephanie J.",
    journal = "Cancer Epidemiology, Biomarkers & Prevention",
    year = "2007",
    volume = "16",
    number = "10",
    pages = "1973-1981",
    publisher = "AMER ASSOC CANCER RESEARCH",
    issn = "1055-9965, 1538-7755",
    doi = "10.1158/1055-9965.EPI-07-0431",
    abstract = "Background: Estrogen receptor beta (ESR2) may play a role in modulating
prostate carcirtogenesis through the regulation of genes related to cell
proliferation and apoptosis.
Methods: We conducted nested case-control studies in the Breast and
Prostate Cancer Cohort Consortium (BPC3) that pooled 8,323 prostate
cancer cases and 9,412 controls from seven cohorts. Whites were the
predominant ethnic group. We characterized genetic variation in ESR2 by
resequencing exons in 190 breast and prostate cancer cases and
genotyping a dense set of single nucleotide polymorphisms (SNP) spanning
the locus in a multiethnic panel of 349 cancer-free subjects. We
selected four haplotype-tagging SNPs (htSNP) to capture common ESR2
variation in Whites; these htSNPs were then genotyped in all cohorts.
Conditional logistic regression models were used to assess the
association between sequence variants of ESR2 and the risk of prostate
cancer. We also investigated the effect modification by age, body mass
index, and family history, as well as the association between sequence
variants of ESR2 and advanced-stage (>= T3b, N-1, or M-1) and high-grade
(Gleason sum >= 8) prostate cancer, respectively.
Results: The four tag SNPs in ESR2 were not significantly associated
with prostate cancer risk, individually. The global test for the
influence of any haplotype on the risk of prostate cancer was not
significant (P = 0.31). However, we observed that men carrying two
copies of one of the variant haplotypes (TACC) had a 1.46-fold increased
risk of prostate cancer (99% confidence interval, 1.06-2.01) compared
with men carrying zero copies of this variant haplotype. No SNPs or
haplotypes were associated with advanced stage or high grade of prostate
cancer.
Conclusion: In our analysis focused on genetic variation common in
Whites, we observed little evidence for any substantial association of
inherited variation in ESR2 with risk of prostate cancer. A nominally
significant (P < 0.01) association between the TACC haplotype and
prostate cancer risk under the recessive model could be a chance finding
and, in any event, would seem to contribute only slightly to the overall
burden of prostate cancer."
}