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Title: Prostate cancer susceptibility polymorphism rs2660753 is not associated with invasive ovarian cancer.
Authors: Amankwah EK,  Kelemen LE,  Wang Q,  Song H,  Chenevix-Trench G,  Australian Ovarian Cancer Study Group,  Beesley J,  Webb PM,  Australian Cancer Study (Ovarian Cancer),  Pearce CL,  Wu AH,  Pike MC,  Stram DO,  Chang-Claude J,  Wang-Gohrke S,  Ness RB,  Goode EL,  Cunningham JM,  Fridley BL,  Vierkant RA,  Tworoger SS,  Whittemore AS,  McGuire V,  Sieh W,  Gayther SA,  Gentry-Maharaj A,  Menon U,  Ramus SJ,  Rossing MA,  Doherty JA,  Goodman MT,  Carney ME,  Lurie G,  Wilkens LR,  Kjær SK,  Høgdall E,  Cramer DW,  Terry KL,  Garcia-Closas M,  Yang H,  Lissowska J,  Anton-Culver H,  Ziogas A,  Schildkraut JM,  Berchuck A,  Pharoah PD,  Ovarian Cancer Association Consortium
Journal: Cancer Epidemiol Biomarkers Prev
Date: 2011 May
Branches: MEB, OD, OEEB
PubMed ID: 21415361
PMC ID: PMC3176661
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, P(trend) = 0.01) that showed a stronger association with the serous histological subtype (OR = 1.3, 95% CI = 1.1-1.5, P(trend) = 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, P(trend) = 0.61; serous: OR = 1.0, 95% CI = 0.9-1.1, P(trend) = 0.85) or from the combined analysis of discovery and replication studies (all: OR = 1.0, 95% CI = 1.0-1.1, P(trend) = 0.28; serous: OR = 1.1, 95% CI = 1.0-1.2, P(trend) = 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.