Androgens are differentially associated with ovarian cancer subtypes in the Ovarian Cancer Cohort Consortium

Jennifer Ose, Elizabeth M. Poole, Helena Schock, Matti Lehtinen, Alan A. Arslan, Anne Zeleniuch-Jacquotte, Kala Visvanathan, Kathy Helzlsouer, Julie E. Buring, I. Min Lee, Anne Tjønneland, Laure Dossus, Antonia Trichopoulou, Giovanna Masala, N. Charlotte Onland-Moret, Elisabete Weiderpass, Eric J. Duell, Annika Idahl, Ruth C. Travis, Sabina RinaldiMelissa A. Merritt, Britton Trabert, Nicolas Wentzensen, Shelley S. Tworoger, Rudolf Kaaks, Renée T. Fortner

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


Invasive epithelial ovarian cancer (EOC) is the most lethal gynecologic malignancy. The etiology of EOC remains elusive; however, experimental and epidemiologic data suggest a role for hormone-related exposures in ovarian carcinogenesis and risk factor differences by histologic phenotypes and developmental pathways. Research on prediagnosis androgen concentrations and EOC risk has yielded inconclusive results, and analyses incorporating EOC subtypes are sparse. We conducted a pooled analysis of 7 nested case-control studies in the Ovarian Cancer Cohort Consortium to investigate the association between prediagnosis circulating androgens [testosterone, free testosterone, androstenedione, dehydroepiandrosterone sulfate (DHEAS)], sex hormone binding globulin (SHBG), and EOC risk by tumor characteristics (i.e., histology, grade, and stage). The final study population included 1,331 EOC cases and 3,017 matched controls. Multivariable conditional logistic regression was used to assess risk associations in pooled individual data. Testosterone was positively associated with EOC risk (all subtypes combined, ORlog2 = 1.12; 95% confidence interval 1.02-1.24); other endogenous androgens and SHBG were not associated with overall risk. Higher concentrations of testosterone and androstenedione associated with an increased risk in endometrioid andmucinous tumors [e.g., testosterone, endometrioid tumors, ORlog2 = 1.40 (1.03-1.91)], but not serous or clear cell. An inverse association was observed between androstenedione and high grade serous tumors [ORlog2 = 0.76 (0.60-0.96)]. Our analyses provide further evidence for a role of hormonerelated pathways in EOC risk, with differences in associations between androgens and histologic subtypes of EOC.

Original languageEnglish (US)
Pages (from-to)3951-3960
Number of pages10
JournalCancer Research
Issue number14
StatePublished - Jul 15 2017

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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