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Pommier RF, Woltering EA, Keenan EJ, et al. The mechanism of hormone-sensitive breast cancer progression on antiestrogen therapy. Implications for treatment and protocol planning. Arch Surg. 1987;122(11):1311-6doi: 10.1001/archsurg.1987.01400230097017.
Pommier, R. F., Woltering, E. A., Keenan, E. J., & Fletcher, W. S. (1987). The mechanism of hormone-sensitive breast cancer progression on antiestrogen therapy. Implications for treatment and protocol planning. Archives of surgery (Chicago, Ill. : 1960), 122(11), 1311-6. https://doi.org/10.1001/archsurg.1987.01400230097017
Pommier, R F, et al. "The mechanism of hormone-sensitive breast cancer progression on antiestrogen therapy. Implications for treatment and protocol planning." Archives of surgery (Chicago, Ill. : 1960) vol. 122,11 (1987): 1311-6. doi: https://doi.org/10.1001/archsurg.1987.01400230097017
Pommier RF, Woltering EA, Keenan EJ, Fletcher WS. The mechanism of hormone-sensitive breast cancer progression on antiestrogen therapy. Implications for treatment and protocol planning. Arch Surg. 1987 Nov;122(11):1311-6. doi: 10.1001/archsurg.1987.01400230097017. PMID: 2960297.
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Arch Surg. 1987 Nov;122(11):1311-6. doi: 10.1001/archsurg.1987.01400230097017.

The mechanism of hormone-sensitive breast cancer progression on antiestrogen therapy. Implications for treatment and protocol planning.

Archives of surgery (Chicago, Ill. : 1960)

R F Pommier, E A Woltering, E J Keenan, W S Fletcher

Affiliations

  1. Department of Surgery, Oregon Health Sciences University, Portland 97201.

PMID: 2960297 DOI: 10.1001/archsurg.1987.01400230097017

Abstract

Fifteen patients whose tumors progressed while they received tamoxifen citrate therapy were studied by serial determinations of serum levels of estrone (E1), estradiol (E2), and dehydroepiandrosterone (DHEA) obtained during progression after withdrawal from tamoxifen therapy and total endocrine ablation or suppression. Discontinuation of tamoxifen therapy resulted in reductions of DHEA, E1, and E2 levels by 44%, 49%, and 42%, respectively. Ablation or suppression reduced sex steroids to minimal levels and produced responses in all patients. Elevations of DHEA, E1, and E2 could be provoked by readministering tamoxifen to hypophysectomized and oophorectomized, but not adrenalectomized, patients, indicating that the adrenal gland is the source of these sex steroids. We conclude that tamoxifen stimulates adrenal production of DHEA, which is aromatized to E1 and E2. Buildup of E1 and E2 overwhelms the competitive binding of tamoxifen to the estrogen receptor, resulting in tumor progression.

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