Testosterone inhibits estrogen/progestogen-induced breast cell proliferation in postmenopausal women

Hofling, Marie; Hirschberg, Angelica Lindén; Skoog, Lambert; Tani, Edneia; Hägerström, T; Schoultz, Bo von

doi:10.1097/01.gme.0000232033.92411.51

Cited by 102 publications

(73 citation statements)

References 33 publications

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“…However, many of these studies had a relatively short follow-up period (!4 years), which may not be sufficient to observe a change in breast cancer development. Studies at the cellular level show a reduced proliferative index in tissues from women given HRT with added testosterone compared with HRT alone, which suggests a protective effect of androgens in normal breast tissue (Hofling et al 2007). Similarly, a reduced proliferative index was observed in normal human breast tissues cultured ex vivo when exposed to the most potent androgen, DHT (Eigeliene et al 2012, Ochnik et al 2014, further supporting a growth inhibitory effect of androgens.…”

Section: Exogenous Androgensmentioning

confidence: 91%

Complexities of androgen receptor signalling in breast cancer

McNamara¹,

Moore²,

Hickey³

et al. 2014

Endocrine-Related Cancer

123

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While the clinical benefit of androgen-based therapeutics in breast cancer has been known since the 1940s, we have only recently begun to fully understand the mechanisms of androgen action in breast cancer. Androgen signalling pathways can have either beneficial or deleterious effects in breast cancer depending on the breast cancer subtype and intracellular context. This review discusses our current knowledge of androgen signalling in breast cancer, including the relationship between serum androgens and breast cancer risk, the prognostic significance of androgen receptor (AR) expression in different breast cancer subtypes and the downstream molecular pathways mediating androgen action in breast cancer cells. Intracrine androgen metabolism has also been discussed and proposed as a potential mechanism that may explain some of the reported differences regarding dichotomous androgen actions in breast cancers. A better understanding of AR signalling in this disease is critical given the current resurgence in interest in utilising contemporary AR-directed therapies for breast cancer and the need for biomarkers that will accurately predict clinical response.

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Section: Exogenous Androgensmentioning

confidence: 91%

Complexities of androgen receptor signalling in breast cancer

McNamara¹,

Moore²,

Hickey³

et al. 2014

Endocrine-Related Cancer

123

View full text Add to dashboard Cite

show abstract

“…81 However, recent research has shown testosterone's reduction of the typical proliferative effects of postmenopausal estrogen and progesterone therapy. 82 The risk of cardiovascular disease (CVD) from supplementing androgens is unknown. A link between higher androgens and CVD continues to be debated.…”

Section: Systemic Estrogenmentioning

confidence: 99%

Women's sexual function and dysfunction: current uncertainties, future directions

Basson

2008

Int J Impot Res

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There is increasing evidence that women at the outset of sexual activity do not need to have sexual desire, as in 'drive', and that many do not distinguish desire from arousal. Multiple modes of investigation confirm poor correlation between women's subjective arousal and measured genital congestion. Suggested revisions to the DSM-IV definitions of sexual disorder have been published: there is now need to align interview assessments and screening questionnaires with contemporary understanding of women's sexual response. Whereas the psychological factors associated with women's sexual function and resilience to biological insults and external stressors are well documented, the role of biological factors is less clear. Variations in the rate of decline of adrenal and ovarian pro-hormones, activity of converting enzymes in peripheral cells, sensitivity of androgen and estrogen receptors and cerebral production of sex steroids may all be involved. Thus there is great complexity underlying the question of sex hormone supplementation, and in particular, little clarity as to which women have decreased brain and/or peripheral androgen activity. When psychosexual etiological factors appear to be minimal and investigational testosterone supplementation is considered, it would be appropriate to target women with disordered arousal and desire in keeping with the recently recommended revised definitions.

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“…Breast cancer patients appear to have relative sex steroid hormone imbalance, in favour of estrogens (McTiernan et al, 2003). High bio-available testosterone counteracts the proliferative effects of estrogens on the mammary tissues and exerts a protective role to the breast, inhibiting cancer development and/or tumour growth (Hofling et al, 2007). However, preclinical studies have suggested that testosterone serves as a natural, endogenous protector of the breast.…”

Section: Dietary Boron Intake Sex Steroid Hormones and Breast Cancermentioning

confidence: 99%

Boron Compounds in the Breast Cancer Cells Chemoprevention and Chemotherapy

Scorei¹

2011

Breast Cancer - Current and Alternative Therapeutic Modalities

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Testosterone inhibits estrogen/progestogen-induced breast cell proliferation in postmenopausal women

Abstract: Addition of testosterone may counteract breast cell proliferation as induced by estrogen/progestogen therapy in postmenopausal women.

Cited by 102 publications

References 33 publications

Complexities of androgen receptor signalling in breast cancer

Complexities of androgen receptor signalling in breast cancer

Women's sexual function and dysfunction: current uncertainties, future directions

Boron Compounds in the Breast Cancer Cells Chemoprevention and Chemotherapy

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