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Effects of estrogen on breast cancer development: Role of estrogen receptor independent mechanisms
Open accessAbstract
Development of breast cancer involves genetic factors as well as lifetime exposure to estrogen. The precise molecular mechanisms whereby estrogens influence breast tumor formation are poorly understood. While estrogen receptor α (ERα) is certainly involved, nonreceptor mediated effects of estradiol (E2) may also play an important role in facilitating breast tumor development. A “reductionist” strategy allowed us to examine the role of ERα independent effects of E2 on mammary tumor development in ERα knockout (ERKO) mice bearing the Wnt‐1 oncogene. Exogenous E2 “clamped” at early follicular and midluteal phase levels (i.e., 80 and 240 pg/ml) accelerated tumor formation in a dose‐related fashion in ERKO/Wnt‐1 animals (p = 0.0002). Reduction of endogenous E2 by oophorectomy (p < 0.001) or an aromatase inhibitor (AI) (p = 0.055) in intact ERKO/Wnt‐1 animals delayed tumorigenesis as further evidence for an ER‐independent effect. The effects of residual ERα or β were not involved since enhancement of tumor formation could not be blocked by the antiestrogen fulvestrant. 17α‐OH‐E2, a metabolizable but ER‐impeded analogue of E2 stimulated tumor development without measurable uterine stimulatory effects. Taken together, our results suggest that ER‐independent actions of E2 can influence breast tumor development in concert with ER dependent effects. These observations suggest 1 mechanism whereby AIs, which block E2 synthesis, would be more effective for breast cancer prevention than use of antiestrogens, which only block ER‐mediated effects.
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“E2 in breast tissue is not associated with protective metabolic effects, but rather has been linked to proliferative tumor growth (195).”
From Metabolic impact of endogenously produced estrogens by adipose tissue in females and males across the lifespan (2025) · cites this paper as [195]
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“Elevated aromatase expression in breast WAT increases local E2 production, which may contribute to estrogen receptor-positive (ER+) breast cancer pathogenesis (135, 195, 196).”
From Metabolic impact of endogenously produced estrogens by adipose tissue in females and males across the lifespan (2025) · cites this paper as [195]
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Background
Metadata
- Authors
- Yue, W., Wang, J., Li, Y., Fan, P., Liu, G., Zhang, N., Conaway, M., Wang, H., Korach, K. S., Bocchinfuso, W., & Santen, R.
- Affiliations
- University of Virginia Health System (US)
- National Institutes of Health (US)
- Corresponding author
- Yue, Wei
- ORCID
- Venue
- International Journal of Cancer
- Publisher
- Wiley
- Published
- 2010-08-20
- Volume
- 127
- Issue
- 8
- Pages
- 1748-1757
- ISSN
- 0020-7136 (ISSN-L)
- 1097-0215
- PMC
- PMC4775086
- OpenAlex
- W2035185970
- Cited by
- 196
- References
- 73
- Citations by year
- 2026: 2 · 2025: 26 · 2024: 16 · 2023: 30 · 2022: 19 · 2021: 23 · 2020: 21 · 2019: 10 · 2018: 10 · 2017: 7 · 2016: 3 · 2015: 5 · 2014: 6 · 2013: 7 · 2012: 9
- FWCI
- 3.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Cancer (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Environmental Health Sciences (Z01ES070065)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Keywords
- breast cancer, estrogen receptor alpha, estrogen receptor beta, estradiol, ER knockout mice, aromatase inhibitors, oophorectomy, fulvestrant, breast cancer prevention, antiestrogens
- MeSH terms
- Fulvestrant, Letrozole, Animals, Antineoplastic Agents, Dose-Response Relationship, Drug, Estradiol, Estrogen Antagonists, Female, Humans, Mammary Neoplasms, Experimental, Mice, Transgenic, Nitriles, Ovariectomy, Triazoles, Mice, Knockout, Estrogen Receptor alpha, Cell Proliferation, Wnt1 Protein, Mice
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