Prostate Cancer Susceptibility Polymorphism rs2660753 Is 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 Krüger 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, on behalf of the Australian Ovarian Cancer Study Group

    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.

    OriginalsprogEngelsk
    TidsskriftCancer Epidemiology, Biomarkers & Prevention
    Vol/bind20
    Udgave nummer5
    Sider (fra-til)1028-1031
    Antal sider4
    ISSN1055-9965
    DOI
    StatusUdgivet - 1 maj 2011

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