Estrogens and breast cancer: Mechanisms involved in obesity-related development, growth and progression
Open accessAbstract
Obesity is a risk factor for estrogen receptor-positive (ER+) breast cancer after menopause. The pro-proliferative effects of estrogens are well characterized and there is a growing body of evidence to also suggest an important role in tumorigenesis. Importantly, obesity not only increases the risk of breast cancer, but it also increases the risk of recurrence and cancer-associated death. Aromatase is the rate-limiting enzyme in estrogen biosynthesis and its expression in breast adipose stromal cells is hypothesized to drive the growth of breast tumors and confer resistance to endocrine therapy in obese postmenopausal women. The molecular regulation of aromatase has been characterized in response to many obesity-related molecules, including inflammatory mediators and adipokines. This review is aimed at providing an overview of our current knowledge in relation to the regulation of estrogens in adipose tissue and their role in driving breast tumor development, growth and progression.
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Obesity is associated with higher circulating and white-adipose-tissue-derived E1 levels.
“obesity is associated with higher circulating and WAT-derived E1 levels (64, 135–138)”
From Metabolic impact of endogenously produced estrogens by adipose tissue in females and males across the lifespan (2025) · cites this paper as [135]
The Aromatase regulation in obesity section (page unavailable) says estrogen production in adipose tissue rises with obesity, particularly after menopause; the Aromatase section identifies estrone (E1) as an estrogen made through aromatase. The paper also describes circulating estrogens as a possible reflection of adipose-derived production, but it does not specifically establish higher circulating or white-adipose-tissue-derived E1 levels in obesity. (LLM, conf=0.83)
Experimental — accuracy not yet measuredElevated aromatase expression in breast white adipose tissue increases local E2 production, which may contribute to estrogen receptor-positive breast cancer pathogenesis.
“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 [135]
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References 214 · Cited by 233
- Authors
- Bhardwaj, P., Au, C. C., Benito-Martin, A., Ladumor, H., Oshchepkova, S., Moges, R., & Brown, K. A.
- Affiliations
- Weill Cornell Medicine (US)
- Weill Cornell Medical College in Qatar (QA)
- Corresponding author
- Brown, Kristy A.
- Venue
- The Journal of Steroid Biochemistry and Molecular Biology
- Publisher
- Elsevier BV
- Published
- 2019-05
- Volume
- 189
- Pages
- 161-170
- ISSN
- 0960-0760 (ISSN-L)
- PMC
- PMC6502693
- OpenAlex
- W2922056742
- Cited by
- 233
- References
- 214
- Citations by year
- 2026: 26 · 2025: 47 · 2024: 36 · 2023: 51 · 2022: 37 · 2021: 15 · 2020: 13 · 2019: 7
- FWCI
- 2.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- The Journal of Steroid Biochemistry and Molecular Biology (acceptedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Dr. Robert C. and Veronica Atkins Foundation
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Oncology › Cancer Risks and Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- obesity, estrogen receptor-positive breast cancer, estrogen, aromatase, adipose tissue, breast cancer progression, postmenopausal women, endocrine therapy resistance, adipokines, inflammatory mediators, tumor growth
- MeSH terms
- Adipose Tissue, Aromatase, Breast, Breast Neoplasms, Estrogens, Female, Humans, Menopause, Obesity, Receptors, Estrogen, Disease Progression
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