A prospective, population-based study of androstenedione, estrogens, and prostatic cancer

• Published in: Cancer research (Chicago, Ill.) Vol. 50; no. 1; pp. 169 - 173
• Main Authors: BARRETT-CONNOR, E, GARLAND, C, MCPHILLIPS, J. B, KAY-TEE KHAW, WINGARD, D. L
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 1990
• Subjects: Adult; Aged; Androstenedione - blood; Biological and medical sciences; California; Cohort Studies; Estradiol - blood; Estrone - blood; Humans; Male; Medical sciences; Middle Aged; Nephrology. Urinary tract diseases; Prospective Studies; Prostatic Neoplasms - blood; Prostatic Neoplasms - etiology; Reference Values; Risk Factors; Sex Hormone-Binding Globulin - analysis; Surveys and Questionnaires; Testosterone - blood; Tumors of the urinary system; Urinary tract. Prostate gland; California; Human; Hormone; Urinary system disease; Androgen; Estrogen; Sex hormone binding protein; Malignant tumor; Estradiol; Prostatic disease; Ovarian hormone; Testosterone; Risk factor; Estrone; Serum; Tumor; Androstenedione; Sex steroid hormone; Prostate
• ISSN: 0008-5472; 1538-7445

Endogenous androgens have been suggested as determinants of risk of prostatic cancer. To examine this possibility, baseline sex hormone levels were measured in 1008 men ages 40-79 years who had been followed for 14 years. There were 31 incident cases of prostatic cancer and 26 identified from death certificates with unknown dates of diagnosis. In this study, total testosterone, estrone, estradiol, and sex hormone-binding globulin were not related to prostate cancer, but plasma androstenedione showed a positive dose-response gradient. Age-adjusted relative risks of prostatic cancer for low (0-2.2 nM), middle (2.3-3.1 nM), and high (3.2+ nM) tertiles of androstenedione were 1.00, 1.34, and 1.98, respectively (P trend less than 0.05). The linear gradient of risk persisted after adjustment for age and body mass index. If confirmed, these data suggest that androstenedione might increase the occurrence of clinically manifest prostatic cancer.