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The chemoprevention of breast cancer by reducing sex steroid exposure: perspectives from epidemiology.
J Cell Biochem Suppl. 1993; 17G:26-36.JC

Abstract

Mitogenesis is a major driving force in neoplastic development. Blocking the effect of breast cell mitogens by reducing the actual exposure of the breast to these mitogens is an obvious strategy for breast cancer prevention. The ovarian hormones, estrogens and progesterone, are major effective (direct or indirect) breast cell mitogens. A woman's exposure to ovarian estrogens and progesterone is drastically reduced by the use of combination-type oral contraceptives (COCs), but the synthetic estrogen and progestogen in the COCs effectively replace ovarian estrogens and progesterone, so that breast cell exposure to these hormones is not decreased. Doses of estrogen and progestogen in modern COCs are close to the minimum attainable while still retaining both contraceptive efficacy and ovarian suppression (so that endogenous estrogen and progesterone do not add to the dose of estrogen and progestogen from the COC). Considerably lower effective breast cell exposure to estrogen and progestogen can, however, be achieved by using a gonadotropin-releasing hormone agonist (GnRHA) to suppress ovarian function and compensate for the resulting hypoestrogenemia with low-dose hormone replacement therapy. Compared to modern COCs, estrogen exposure can be reduced by approximately 60%, and progestogen dose by more than 80%. Such a contraceptive is predicted to reduce lifetime breast cancer risk by more than 50% if used for 10 years. The possibility that a practical contraceptive could achieve such a major benefit is shown by the dramatic decline in the incidence of both ovarian and endometrial cancer in young women in the U.S. over the last 3 decades--a direct result of COC use.

Authors+Show Affiliations

Department of Preventive Medicine, University of Southern California School of Medicine, Los Angeles 90033.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

8007706

Citation

Pike, M C., and D V. Spicer. "The Chemoprevention of Breast Cancer By Reducing Sex Steroid Exposure: Perspectives From Epidemiology." Journal of Cellular Biochemistry. Supplement, vol. 17G, 1993, pp. 26-36.
Pike MC, Spicer DV. The chemoprevention of breast cancer by reducing sex steroid exposure: perspectives from epidemiology. J Cell Biochem Suppl. 1993;17G:26-36.
Pike, M. C., & Spicer, D. V. (1993). The chemoprevention of breast cancer by reducing sex steroid exposure: perspectives from epidemiology. Journal of Cellular Biochemistry. Supplement, 17G, 26-36.
Pike MC, Spicer DV. The Chemoprevention of Breast Cancer By Reducing Sex Steroid Exposure: Perspectives From Epidemiology. J Cell Biochem Suppl. 1993;17G:26-36. PubMed PMID: 8007706.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The chemoprevention of breast cancer by reducing sex steroid exposure: perspectives from epidemiology. AU - Pike,M C, AU - Spicer,D V, PY - 1993/1/1/pubmed PY - 1993/1/1/medline PY - 1993/1/1/entrez SP - 26 EP - 36 JF - Journal of cellular biochemistry. Supplement JO - J. Cell. Biochem. Suppl. VL - 17G N2 - Mitogenesis is a major driving force in neoplastic development. Blocking the effect of breast cell mitogens by reducing the actual exposure of the breast to these mitogens is an obvious strategy for breast cancer prevention. The ovarian hormones, estrogens and progesterone, are major effective (direct or indirect) breast cell mitogens. A woman's exposure to ovarian estrogens and progesterone is drastically reduced by the use of combination-type oral contraceptives (COCs), but the synthetic estrogen and progestogen in the COCs effectively replace ovarian estrogens and progesterone, so that breast cell exposure to these hormones is not decreased. Doses of estrogen and progestogen in modern COCs are close to the minimum attainable while still retaining both contraceptive efficacy and ovarian suppression (so that endogenous estrogen and progesterone do not add to the dose of estrogen and progestogen from the COC). Considerably lower effective breast cell exposure to estrogen and progestogen can, however, be achieved by using a gonadotropin-releasing hormone agonist (GnRHA) to suppress ovarian function and compensate for the resulting hypoestrogenemia with low-dose hormone replacement therapy. Compared to modern COCs, estrogen exposure can be reduced by approximately 60%, and progestogen dose by more than 80%. Such a contraceptive is predicted to reduce lifetime breast cancer risk by more than 50% if used for 10 years. The possibility that a practical contraceptive could achieve such a major benefit is shown by the dramatic decline in the incidence of both ovarian and endometrial cancer in young women in the U.S. over the last 3 decades--a direct result of COC use. SN - 0733-1959 UR - https://www.unboundmedicine.com/medline/citation/8007706/The_chemoprevention_of_breast_cancer_by_reducing_sex_steroid_exposure:_perspectives_from_epidemiology_ L2 - http://www.diseaseinfosearch.org/result/960 DB - PRIME DP - Unbound Medicine ER -