Endocrine treatment of breast cancer in women
Abstract
Hormonal therapy for breast carcinoma began with the observation by George Beatson (1) in 1898 that bilateral oophorectomy caused tumor regression in selected premenopausal patients. Huggins and Bergenstal (2) later introduced surgical adrenalectomy as a form of hormone ablative treatment for postmenopausal women. To these methods were added surgical hypophysectomy and hormonal additive therapies such as the use of androgens, estrogens, progestins, and glucocorticoids (3). Since only one-third of patients experienced objective tumor regression with any of these hormonal therapies, clinicians began to favor use of cytotoxic chemotherapies in the 1960s and 1970s. During this time multiple chemotherapeutic regimens were developed which gained wide acceptance and enthusiastic support (3). However, when hormone receptor measurements were introduced in the mid-1970s, better selection of patients with hormonally responsive tumors became possible, and new impetus was provided for optimizing hormonal therapies. These developments led to the accumulation of a large body of clinical data regarding hormonal agents and provided clinicians with a broad armamentarium for the treatment of patients at the present time. We will summarize this information with the goals of highlighting specific endocrinological aspects of breast cancer treatment and providing practical perspective for choosing among various agents. Where recent comprehensive reviews are readily available, only pertinent concepts are highlighted.
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Aromatase catalyzes the rate-limiting final step in estrogen production, the hydroxylation of androstenedione to estrone and of T to E2.
“It catalyzes the rate-limiting final step in estrogen (E) production, the hydroxylation of androstenedione to estrone and of T to E 2 (Fig. 1).”
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Lazennec, G., Thomas, J. A., & Katzenellenbogen, B. S. (2001) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/s0960-0760(01)00060-7 · Cited by 77 · see citing works
“4 cancers, only in two-third of the cases is antiestrogen treatment effective [26-28].”
BackgroundSucrose as a risk factor for cancer of the colon and rectum: A case-control study in Uruguay
Stéfani, E. D., Mendilaharsu, M., & Deneo‐Pellegrini, H. (1998) · International Journal of Cancer · doi:10.1002/(sici)1097-0215(19980105)75:1 · Cited by 20 · see citing works
Adaptive Hypersensitivity to Estrogen
Santen, R. J., Song, R. X.-D., Zhang, Z., et al. (2004) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-031207 · Cited by 75 · see citing works
Self-citationKatzenellenbogen, B. S., Bhardwaj, B., Fang, H., Ince, B. A., Pakdel, F., Reese, J. C., Schodin, D. J., & Wrenn, C. K. (1993) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/0960-0760(93)90055-2 · Cited by 74 · see citing works
Aromatase inhibitors ? mechanisms of steroidal inhibitors
Brueggemeier, R. W. (1994) · Breast Cancer Research and Treatment · doi:10.1007/bf00682739 · Cited by 75 · see citing works
“Research summaries of aromatase inhibitors have been presented at the three international aromatase conferences [1-3], and several reviews have also been published [6-13].”
BackgroundPreston, S. R., Lf, W., Jones-Blackett, S., et al. (1995) · British Journal of Cancer · doi:10.1038/bjc.1995.210 · Cited by 74 · see citing works
Estrogen Stimulation of Cell Migration Involves Multiple Signaling Pathway Interactions
Li, Y., Wang, J.-P., Santen, R. J., et al. (2010) · Endocrinology · doi:10.1210/en.2009-1506 · Cited by 73 · see citing works
Self-citationEffect of the High-Affinity Estrogen Receptor Ligand ICI 182,780 on the Rat Tibia
Sibonga, J. D., Dobnig, H., Harden, R., & Turner, R. T. (1998) · Endocrinology · doi:10.1210/endo.139.9.6172 · Cited by 74 · see citing works
5α-Reductases in Human Breast Carcinoma: Possible Modulator ofin SituAndrogenic Actions1
Suzuki, T., Darnel, A. D., Akahira, J., Ariga, N., Ogawa, S. A., Kaneko, C., Takeyama, J., Moriya, T., & Sasano, H. (2001) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.86.5.7444 · Cited by 72 · see citing works
“Administration of androgens has been reported to result in the regression of some cases of breast carcinoma, but also to cause androgenic side-effects (5).”
BackgroundKoshizuka, K., Koike, M., Asou, H., et al. (1999) · Breast Cancer Research and Treatment · doi:10.1023/a:1006123819675 · Cited by 72 · see citing works
“and they have a significantly worse prognosis than those with estrogen receptors [24].”
BackgroundMcDougal, A. J., Wilson, C., & Safe, S. H. (1997) · Cancer Letters · doi:10.1016/s0304-3835(97)00299-1 · Cited by 72 · see citing works
“A high percentage of initial mammary tumors are estrogen receptor (ER)-positive and respond to endocrine therapy [2–5].”
Background
- Authors
- SANTEN, R. J., MANNI, A., HARVEY, H., & REDMOND, C.
- Affiliations
- Pennsylvania State University (US)
- Corresponding author
- SANTEN, RICHARD J.
- ORCID
- SANTEN, RICHARD J.
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 1990-05
- Volume
- 11
- Issue
- 2
- Pages
- 221-265
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- OpenAlex
- W2114712559
- Cited by
- 399
- References
- 0
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 1 · 2020: 5 · 2018: 4 · 2017: 3 · 2016: 3 · 2015: 7 · 2014: 5 · 2013: 11 · 2012: 4
- FWCI
- 11.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrine Reviews (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Advanced Breast Cancer Therapies
- Keywords
- breast cancer, endocrine therapy, hormone therapy, oophorectomy, adrenalectomy, hypophysectomy, androgens, estrogen, progestins, glucocorticoids, tumor regression, treatment selection
- MeSH terms
- Androgens, Breast Neoplasms, Estrogen Antagonists, Estrogens, Female, Glucocorticoids, Humans, Progestins
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