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Testosterone and biological characteristics of breast cancers in postmenopausal women
Cancer Epidemiology, Biomarkers & Prevention, 10/28/09

Secreto G et al. – To further investigate androgens in breast cancer, we examined the relations between serum testosterone and age, body mass index (BMI), tumor size, histologic type, grade, axillary node involvement, estrogen receptor status, progesterone receptor status, and HER2 overexpression. The age-related differences in the association of testosterone with other disease and patient characteristics suggest that breast cancers in older postmenopausal women differ markedly from those in younger postmenopausal women.

Methods

Cross-sectional study of 592 postmenopausal breast cancer patients
Mean testosterone differences according to categories of patient and tumor characteristics were assayed by Fisher's or Kruskall-Wallis test as appropriate; adjusted odds ratios (OR) of having a tumor characteristic by testosterone tertiles estimated by logistic regression

Results

Testosterone concentrations significantly higher in women with BMI ≥ 30 versus BMI < 25
ORs of having a tumor ≥ 2 cm increased significantly with increasing testosterone tertiles, and the association was stronger in women ≥ 65 years
OR of having infiltrating ductal carcinoma significantly higher in highest compared with lowest testosterone tertile
ORs of having estrogen receptor– and progesterone receptor–negative versus estrogen receptor– and progesterone receptor–positive tumors decreased significantly with increasing testosterone tertiles
In women ≥ 70 years, those with high testosterone had significantly greater OR of HER2-negative cancer than those with low testosterone

Exclusive Author Commentary
Giorgio Secreto, 10/30/09

The article confirm a role for androgens in breast cancer, thus supporting the androgen excess theory, that was conceived and developed in our laboratory since the late ‘60s of the past century. According to the theory, androgen excess is the endocrine abnormality that characterizes patients with breast cancer and stimulates the growth of breast epithelium, acting either directly by itself or after conversion into estrogen. Hence, on this basis, estrogen simply makes its own work, that is to stimulate breast epithelium, independently whether the epithelium is normal or cancerous, provided that the last contains the right amount of ER. This view is corroborated by finding in the present report of a significant association between high circulating testosterone and positive ER status. The association between testosterone and ER indicates that testosterone is a marker of hormone-dependent breast cancer, in accordance with the androgen excess theory. We suggest that testosterone levels should be routinary measured in breast cancer patients at the time of the diagnosis, to programme therapies with the double objective to treat cancer and, contemporarily, to correct the basic hormonal abnormality, thus reducing the probability of recurrences. We also suggest to schedule serial measurements of testosterone during the follow-up period, to evaluate the effectiveness of therapies in reducing its circulating levels. The role of androgens in breast cancer development and progression is rather still unexplored. We intend to extend our knowledge in this field also investigating the association of estradiol and dihydrotestosterone (a not aromatizable androgen) with the ER, AR, and PR content of the tumours and with some polymorphisms of AR, and CYP19arom genes. We also plan to confirm the intriguing association of testosterone with the HER-2 status in patients over 70 years of age.

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