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Title
Prediagnostic circulating anti-Müllerian hormone concentrations are not associated with prostate cancer risk.
Pubmed ID
25159294 (View this publication on the PubMed website)
Publication
Cancer Epidemiol. Biomarkers Prev. 2014 Nov; Volume 23 (Issue 11): Pages 2597-602
Authors
Sklavos MM, Zhou CK, Pinto LA, Cook MB
Affiliations
  • Human Papillomavirus Immunology Laboratory, Leidos Biomedical Research, Incorporated, Frederick National Laboratory for Cancer Research, Frederick, Maryland.
  • Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland. Department of Epidemiology and Biostatistics, George Washington University, Washington, District of Columbia.
  • Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland. michael.cook@nih.gov.
Abstract

Despite considerable research, the pathogenesis of prostate cancer remains poorly understood. Meanwhile, PSA testing has shifted prostate cancer case populations for study to include a greater proportion of asymptomatic and indolent disease. Thus, efforts to identify prostate cancer biomarkers-particularly for aggressive disease-are required to elucidate pathogenesis and aid screening efficacy. Current evidence suggests that decreased circulating concentrations of the testis-derived, TGFβ family peptide hormone-anti-Müllerian hormone (AMH)-may be associated with prostate cancer pathogenesis. To test this hypothesis, we measured AMH concentrations in prediagnostic (cohort baseline) sera using the Beckman Coulter AMH Gen II ELISA in 1,000 cases and 1,000 controls nested within the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Controls were frequency matched to cases on age at entry, enrollment year, and years of follow-up. Unconditional logistic regression models, adjusted for age at randomization, were used to estimate odds ratios (ORs) and 95% confidence intervals (95% CI). We found that prediagnostic serologic AMH concentrations were not significantly associated with total (ORQ4 vs. Q1 = 1.15; 95% CI, 0.89-1.48; Ptrend = 0.13), aggressive (ORQ4 vs. Q1 = 1.14; 95% CI, 0.80-1.63; Ptrend = 0.51), or nonaggressive (ORQ4 vs. Q1 = 1.22; 95% CI, 0.91-1.63; Ptrend = 0.07) prostate cancer risks. Different definitions of aggressive disease did not meaningfully alter these results. Despite in vitro studies linking AMH to prostate cancer, this first analysis of prediagnostic, circulating AMH concentrations in men provides no evidence for an association with prostate cancer risk.

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