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Endocrine Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Aromatase inhibitors act predominantly by blocking the conversion of androgens to estrogens in the peripheral tissues. Thus, they should not be used in premenopausal women as they do not inhibit ovarian estrogen synthesis. Anastrozole and letrozole are the two most commonly used nonsteroidal aromatase inhibitors, and exemestane is a steroidal aromatase inhibitor frequently prescribed as initial adjuvant therapy in postmenopausal women with ER+ve tumors. Tamoxifen is used if an aromatase inhibitor is not appropriate. Adjuvant hormone-antagonist therapy is generally continued for five years following removal of the tumor. However, in postmenopausal women considered for extended adjuvant therapy, 5 years of tamoxifen is followed by letrozole for a further 2–3 years.
The Fight Against Cancer
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
Some cancers are hormone-dependent. Hormones can serve as a signal for DNA replication, and derangements in this signalling process may lead to cancer. Steroid hormones bind to intracellular receptors to form complexes that act as nuclear transcription factors to control whether transcription takes place. Hormone antagonists can be used to block these receptors, thus impede cell proliferation. Oestrogen is commonly involved in these pathways. Oestrogen drugs are used in the treatment of prostate cancer because they inhibit the production of luteinising hormone and thereby decrease the synthesis of testosterone, which is linked with prostate cancer. In hormone-dependent breast cancer, oestrogen antagonists are used to block oestrogen receptors and prevent hormone binding.
Steroid Hormone Receptors Involved in Reproduction: Mechanism of Action
Published in Robert E. Garfield, Thomas N. Tabb, Control of Uterine Contractility, 2019
Paul Robel, Baulieu Etienne-Emile
Nonsteroidal antiestrogens were the first hormone antagonists in use. They belong to the triphenyl-ethylene series, and are structurally related to diethylstibestrol, although they bear a third phenolic ring (hence their designation), which is responsible for their antagonistic effects. They are characterized by two complex features: They are pure antagonists in birds, whereas they are strongly estrogenic in mice, the situation being intermediary in the human species;Their agonist properties are dissociated: they stimulate the synthesis of proteins in the liver, for example, the human plasma protein SBP (sex hormone binding protein, which binds estradiol and progesterone), or the uterine and mammary gland progesterone receptor, whereas they generally do not stimulate target cell growth and behave as pure estrogen antagonists in this respect, hence their therapeutic use in estrogen-dependent cancers.
Cancer epigenetics and the potential of epigenetic drugs for treating solid tumors
Published in Expert Review of Anticancer Therapy, 2019
Zhenghui Liu, Yingxue Gao, Xiong Li
The progression of many cancers depends on aberrant hormone metabolism or the mutation of hormone receptors, for example the mutation of estrogen/estrogen receptor in breast cancer and androgen/androgen receptor in prostate cancer. Hormone antagonists or inhibitors of hormone receptors have become the first-in-class therapeutics for these cancer types. However, cancer patients inevitably develop drug resistance after treatment and epigenetic changes have been identified as a key element for drug resistance. Epigenetic drugs may, therefore, overcome cancer resistance to hormonal drugs. Vorinostat and Bicalutamide, an androgen receptor antagonist, had a synergistic effect on cell proliferation and apoptosis induction in prostate cancer cell lines. In a phase II clinical trial, the combination of these two drugs followed by radical prostatectomy decreased the tumor size of primary prostate cancer [99,100]. A triple combination of TSA, Bicalutamide and Finasteride (a 5α-reductase inhibitor) targeting the androgen pathway had synergistic effects inducing prostate cancer cell apoptosis [101]. Azacytidine plus TSA and Diarylpropionitrile (DPN, a highly potent ERβ agonist) displayed strong anticancer effects, inducing apoptosis and decreasing proliferation in prostate cancer cells, along with downregulation of Cyclin D1 and VEGF [94].
Disruptions in the reproductive system of female rats after prenatal lipopolysaccharide-induced immunological stress: role of sex steroids
Published in Stress, 2019
V. M. Ignatiuk, M. S. Izvolskaya, V. S. Sharova, S. N. Voronova, L. A. Zakharova
We hypothesized that the development of disorders in the female reproductive system after prenatal LPS-induced immunological stress can be potentiated by sex hormones during the prepubertal period. The aim of this study was to investigate the role of sex steroids and actions of their antagonists in the development of the reproductive system disorders in female offspring prenatally exposed to LPS. Sex hormone antagonists (fulvestrant or flutamide) were injected during the time frames detected in our previous research when the level of sex hormones is elevated in prepubertal offspring after prenatal LPS treatment (Izvolskaia et al., 2016). Parameters of reproductive system function in postnatal females (body weight, time of vaginal opening (VO), quantitative ovary histology and sex steroid concentrations) were studied.
Investigational drugs for the treatment of endometriosis, an update on recent developments
Published in Expert Opinion on Investigational Drugs, 2018
Fabio Barra, Carolina Scala, Valerio Mais, Stefano Guerriero, Simone Ferrero
GnRH is the hypothalamic hormone that induces pituitary secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Gonadotropin-releasing hormone antagonists (GnRH-ant) act by binding to the same pituitary GnRH receptor, and, they suppress gonadotropin production. The induced hypoestrogenic state inhibits proliferation and invasion of ectopic endometrial cell. However, differently form GnRH-as, GnRH-ant maintain sufficient circulating estradiol (E2) levels to avoid vasomotor symptoms or loss of BMD. When starting the therapy, there is a further advantage of GnRH-ant over GnRH-as: they have an immediate onset of action and they rapidly reduce sex hormone levels without the initial estrogen surge [17], not causing flare-up effect. Currently, GnRH-ant are available as injectable formulation and increasingly as oral nonpeptide forms [9,17].