Journal of SAFOMS

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2015 | January-June | Volume 3 | Issue 1

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Book Review

Richa Saxena, HP Pattanaik

Tips & Tricks in Operative Obstetrics & Gynecology

[Year:2015] [Month:January-June] [Volume:3] [Number:1] [Pages:1] [Pages No:0 - 0]

   DOI: 10.5005/jsafoms-3-1-i  |  Open Access |  How to cite  | 



Genitourinary Syndrome of Menopause and Its Management

[Year:2015] [Month:January-June] [Volume:3] [Number:1] [Pages:1] [Pages No:0 - 0]

   DOI: 10.5005/jsafoms-3-1-iv  |  Open Access |  How to cite  | 



Postmenopausal Bleeding

[Year:2015] [Month:January-June] [Volume:3] [Number:1] [Pages:1] [Pages No:0 - 0]

   DOI: 10.5005/jsafoms-3-1-v  |  Open Access |  How to cite  | 



Céline Gérard, Mélanie Mestdagt, Ekaterine Tskitishvili, Laudine Communal, Anne Gompel, Elisabete Silva, Jean-François Arnal, Françoise Lenfant, Agnès Noël, Jean-Michel Foidart, Christel Pequeux

Combined Estrogenic and Antiestrogenic Properties of Estetrol on Breast Cancer may provide a Safe Therapeutic Window for the Treatment of Menopausal Symptoms

[Year:2015] [Month:January-June] [Volume:3] [Number:1] [Pages:3] [Pages No:31 - 33]

   DOI: 10.5005/jsafoms-3-1-31  |  Open Access |  How to cite  | 


Increased risk of breast cancer is a critical side-effect associated with the use of a menopausal hormone therapy (MHT). Estetrol (E4) is a natural estrogen produced by the human fetal liver and is a promising compound for clinical use in MHT. However, its impact on breast cancer is controversial and poorly defined. In this preclinical study, we show that E4 acts as a weak estrogen by stimulating the growth of hormone-dependent breast cancer only at concentrations exceeding menopausal therapeutic needs. Estetrol (E4) presents also an antitumor activity by decreasing the strong proliferative effect of estradiol (E2). While estrogen receptor alpha (ERá) is the predominant receptor mediating its effects, the dual weak-estrogenic/antiestrogenic feature of E4 results from differential signaling pathways activation. Both nuclear and rapid extranuclear signaling pathway are necessary for a complete estrogenic effect of E4. However, the antitumor action of E4 is not due to a capacity to antagonize E2-induced nuclear activity. Altogether, our results highlight that E4 has a limited impact on breast cancer and may offer a safe therapeutic window for the treatment of menopausal symptoms.


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