Ovarian ablation for premenopausal breast cancer: A review of treatment considerations and the impact of premature menopause

Nourmoussavi, Melica; Pansegrau, Gary; Popesku, Jason T.; Hammond, Geoffrey L.; Kwon, Janice S.; Carey, Mark

doi:10.1016/j.ctrv.2017.02.005

Cited by 27 publications

(22 citation statements)

References 119 publications

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“…In premenopausal women, where >90% of circulating oestradiol comes from the ovaries, irreversible suppression of ovarian function is achieved by surgical bilateral oophorectomy or radiation to the ovaries. Alternatively, reversible ovarian function suppression (OFS) can be achieved chemically with the use of GnRH analogues that suppress pituitary gonadotropin secretion, thereby decreasing ovarian oestradiol production (Nourmoussavi et al 2017). In postmenopausal women, the low concentrations of circulating oestrogens are still sufficient to exert biological effects on ER-expressing breast cancer cells.…”

Section: Mechanisms Of Adjuvant Endocrine Therapymentioning

confidence: 99%

The effects of adjuvant endocrine therapy on bone health in women with breast cancer

Ramchand

Cheung

Yeo

et al. 2019

Journal of Endocrinology

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In women with oestrogen receptor (ER)-positive early breast cancer, oestradiol is important for breast cancer development and progression. Endocrine therapy prevents the deleterious effects of oestradiol in breast tissue by systemically depleting oestradiol concentration (aromatase inhibitors) or preventing its local action in breast tissue (selective oestrogen receptor modulators i.e. tamoxifen), thereby improving oncological outcomes. Use of aromatase inhibitors in postmenopausal women and ovarian function suppression with either tamoxifen or aromatase inhibition in premenopausal women, consequent to systemic oestradiol depletion, exerts detrimental effects on skeletal health. The oestradiol-deficient state causes increased bone remodelling and a negative bone balance. This results in bone loss, microstructural deterioration and bone fragility predisposing to fractures. Similar effects are also seen with tamoxifen in premenopausal women. In contrast, use of tamoxifen in postmenopausal women appears to exert protective effects on bone but studies on fracture risk are inconclusive. The longevity of women with ER-positive breast cancer treated with adjuvant endocrine therapy emphasises the need to mitigate the adverse skeletal effects of these therapies in order to maximise benefit. In general, fractures are associated with increased morbidity, mortality and are a high socioeconomic burden. Whilst the efficacy of antiresorptive therapy in preventing bone mineral density loss in postmenopausal women has been established, further clinical trial evidence is required to provide guidance regarding fracture risk reduction, when to initiate and stop treatment, choice of agent and optimal management of bone health in premenopausal women receiving endocrine therapy. In addition, potential oncological benefits of antiresorptive therapies will also need to be considered.

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Section: Mechanisms Of Adjuvant Endocrine Therapymentioning

confidence: 99%

The effects of adjuvant endocrine therapy on bone health in women with breast cancer

Ramchand

Cheung

Yeo

et al. 2019

Journal of Endocrinology

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“…Therefore, oophorectomy has been recognized as one of the effective treatments for premenopausal patients with metastatic ER + breast cancers. Besides oophorectomy, medical treatments with LHRH analogs have also been used clinically to ablate ovary function for over 30 years [27]. Through desensitizing gonadotropin-releasing hormone (GnRH) receptors, LHRH analogs suppress the secretion of gonadotropin, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), resulting in reduced estrogen levels in the body (Figure 1).…”

Section: Luteinizing Hormone-releasing Hormone (Lhrh) Analogsmentioning

confidence: 99%

Challenges in Treating Estrogen Receptor-Positive Breast Cancer

Chen¹,

Cheung²

2019

Estrogen

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Despite hormone therapy is widely used (as both adjuvant and neoadjuvant therapy) for the treatment of estrogen receptor-positive (ER +) breast cancer and patients receiving hormone therapy often show satisfactory initial response, resistance to selective estrogen modulators and aromatase inhibitors is frequently found in patients after prolonged treatment. In this chapter, we will discuss the molecular mechanisms of action of various hormone therapy agents and the biology behind the induction of hormone therapy resistance in ER + breast cancer cells. Recent development of novel agents that can be used to treat ER + hormone therapyresistant breast cancer will also be discussed in this chapter.

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“…Besides nuclear receptor antagonists, LHRH agonists are standard therapies in breast and prostate cancer, mostly concomitantly integrated in therapy schedules (Graham and Schweizer, 2016 ; Nourmoussavi et al, 2017 ; Table VIII ).…”

Section: Master Modulators the Backbone Of Anakoinosis Inducing Thermentioning

confidence: 99%

Clinical Efficacy of a Novel Therapeutic Principle, Anakoinosis

et al. 2018

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Classic tumor therapy, consisting of cytotoxic agents and/or targeted therapy, has not overcome therapeutic limitations like poor risk genetic parameters, genetic heterogeneity at different metastatic sites or the problem of undruggable targets. Here we summarize data and trials principally following a completely different treatment concept tackling systems biologic processes: the principle of communicative reprogramming of tumor tissues, i.e., anakoinosis (ancient greek for communication), aims at establishing novel communicative behavior of tumor tissue, the hosting organ and organism via re-modeling gene expression, thus recovering differentiation, and apoptosis competence leading to cancer control – in contrast to an immediate, “poisoning” with maximal tolerable doses of targeted or cytotoxic therapies. Therefore, we introduce the term “Master modulators” for drugs or drug combinations promoting evolutionary processes or regulating homeostatic pathways. These “master modulators” comprise a broad diversity of drugs, characterized by the capacity for reprogramming tumor tissues, i.e., transcriptional modulators, metronomic low-dose chemotherapy, epigenetically modifying agents, protein binding pro-anakoinotic drugs, such as COX-2 inhibitors, IMiDs etc., or for example differentiation inducing therapies. Data on 97 anakoinosis inducing schedules indicate a favorable toxicity profile: The combined administration of master modulators, frequently (with poor or no monoactivity) may even induce continuous complete remission in refractory metastatic neoplasia, irrespectively of the tumor type. That means recessive components of the tumor, successively developing during tumor ontogenesis, are accessible by regulatory active drug combinations in a therapeutically meaningful way. Drug selection is now dependent on situative systems characteristics, to less extent histology dependent. To sum up, anakoinosis represents a new substantive therapy principle besides novel targeted therapies.

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Ovarian ablation for premenopausal breast cancer: A review of treatment considerations and the impact of premature menopause

Cited by 27 publications

References 119 publications

The effects of adjuvant endocrine therapy on bone health in women with breast cancer

The effects of adjuvant endocrine therapy on bone health in women with breast cancer

Challenges in Treating Estrogen Receptor-Positive Breast Cancer

Clinical Efficacy of a Novel Therapeutic Principle, Anakoinosis

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