Prostate cancer susceptibility polymorphism rs2660753 s not associated with invasive ovarian cancer

Ernest K. Amankwah, Linda E. Kelemen, Qinggang Wang, Honglin Song, Georgia Chenevix-Trench, Jonathan Beesley, Penelope M. Webb, Celeste L. Pearce, Anna H. Wu, Malcolm C. Pike, Daniel O. Stram, Jenny Chang-Claude, Shan Wang-Gohrke, Roberta B. Ness, Ellen L. Goode, Julie M. Cunningham, Brooke L. Fridley, Robert A. Vierkant, Shelley S. Tworoger, Alice S. WhittemoreValerie McGuire, Weiva Sieh, Simon A. Gayther, Aleksandra Gentry-Maharaj, Usha Menon, Susan J. Ramus, Mary Anne Rossing, Jennifer A. Doherty, Marc T. Goodman, Michael E. Carney, Galina Lurie, Lynne R. Wilkens, Susanne Kruger Kjær, Estrid Høgdall, Daniel W. Cramer, Kathryn L. Terry, Montserrat Garcia-Closas, Hannah Yang, Jolanta Lissowska, Hoda Anton-Culver, Argyrios Ziogas, Joellen M. Schildkraut, Andrew Berchuck, Paul D.P. Pharoah

Research output: Contribution to journalArticle

Abstract

Background: We previously reported an association between rs2660753, a prostate cancer susceptibility polymorphism, and invasive epithelial ovarian cancer (EOC; OR = 1.2, 95% CI= 1.0-1.4, Ptrend = 0.01) that showed a stronger association with the serous histological subtype (OR = 1.3, 95% CI = 1.1-1.5, Ptrend = 0.003). Methods: We sought to replicate this association in 12 other studies comprising 4,482 cases and 6,894 controls of white non-Hispanic ancestry in the Ovarian Cancer Association Consortium. Results: No evidence for an association with all cancers or serous cancers was observed in a combined analysis of data from the replication studies (all: OR = 1.0, 95% CI = 0.9-1.1, Ptrend = 0.61; serous: OR = 1.0, 95% CI = 0.9-1.1, Ptrend = 0.85) or from the combined analysis of discovery and replication studies (all: OR = 1.0, 95% CI = 1.0-1.1, Ptrend = 0.28; serous: OR = 1.1, 95% CI = 1.0-1.2, Ptrend = 0.11). There was no evidence for statistical heterogeneity in ORs across the studies. Conclusions: Although rs2660753 is a strong prostate cancer susceptibility polymorphism, the association with another hormonally related cancer, invasive EOC, is not supported by this replication study. Impact: Our findings, based on a larger sample size, emphasize the importance of replicating potentially promising genetic risk associations.

Original languageEnglish (US)
Pages (from-to)1028-1031
Number of pages4
JournalCancer Epidemiology Biomarkers and Prevention
Volume20
Issue number5
DOIs
StatePublished - May 2011

ASJC Scopus subject areas

  • Epidemiology
  • Oncology

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    Amankwah, E. K., Kelemen, L. E., Wang, Q., Song, H., Chenevix-Trench, G., Beesley, J., Webb, P. M., Pearce, C. L., Wu, A. H., Pike, M. C., Stram, D. O., Chang-Claude, J., Wang-Gohrke, S., Ness, R. B., Goode, E. L., Cunningham, J. M., Fridley, B. L., Vierkant, R. A., Tworoger, S. S., ... Pharoah, P. D. P. (2011). Prostate cancer susceptibility polymorphism rs2660753 s not associated with invasive ovarian cancer. Cancer Epidemiology Biomarkers and Prevention, 20(5), 1028-1031. https://doi.org/10.1158/1055-9965.EPI-11-0053