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Antiandrogen therapy in metastatic male breast cancer: results from an updated analysis in an expanded case series.

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Male breast cancer is a rare disease treated as hormone receptor-positive female breast cancer. The characterization of breast cancer at the molecular level has lately revealed gender-related differences. As the androgen receptor is emerging as a potential oncogenic driver in male breast cancer, we

The effects of androgens and antiandrogens on hormone-responsive human breast cancer in long-term tissue culture.

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We have examined five human breast cancer cell lines in continuous tissue culture for androgen responsiveness. One of these cell lines shows a 2- to 4-fold stimulation of thymidine incorporation into DNA, apparent as early as 10 hr following androgen addition to cells incubated in serum-free medium.

Manipulation of the growth rate of human breast cancer cells by antiandrogen followed by chemotherapy.

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The effects induced by the antiandrogen Cyproterone Acetate (CPA) on the proliferation of EVSA-T human breast cancer cells endowed with androgen receptors were studied. Kinetic analyses were carried out by two autoradiographic techniques measuring the percentage of cells in S-phase and the growth

The antiandrogen flutamide inhibits growth of mcf-7 human breast-cancer cell-line.

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The antiandrogen flutamide (FLU) has been reported to exert antiproliferative action on both male and postmenopausal breast cancer and to inhibit growth of chemically induced rat breast cancer. We studied the effects of various concentrations of FLU on the growth of the ER+, AR+ and PR+ MCF-7 and

Will the experience with tamoxifen in breast cancer help define the role of antiandrogens in prostate cancer?

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Breast and prostate cancers are the two predominant hormone-responsive tumours. The use of the antioestrogen tamoxifen in the treatment of breast cancer has evolved over the past 30 y from treatment for advanced breast cancer to prevention. Tamoxifen is currently the endocrine treatment of choice

Advanced male breast cancer treatment with the LH-RH analogue buserelin alone or in combination with the antiandrogen flutamide.

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Ten men with advanced breast cancer were evaluated for response to treatment with the luteinizing hormone-releasing hormone (LH-RH) analogue, buserelin, alone or in combination with the antiandrogen, flutamide. One of five patients receiving buserelin as a single agent had a partial remission

Hormonal changes induced by the pure antiandrogen flutamide in postmenopausal women with advanced breast cancer.

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Hormonal changes induced by the pure antiandrogen flutamide were studied in three postmenopausal metastatic breast cancer patients. The drug was administered at a dose of 250 mg, three times a day for 3-6 months. In each patient a sharp decrease of about 50% was observed in the circulating levels of

Androgen receptor and antiandrogen therapy in male breast cancer.

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Cancers arising in the male breast are uncommon. Male breast cancer is a hormone-driven disease that often expresses the estrogen receptor, and antiestrogen therapy represents the mainstay of treatment. Paradoxically, the advent of a wave of antiestrogens eclipsed the therapeutic potential of

Androgen receptor mediated growth control of breast cancer and endometrial cancer modulated by antiandrogen- and androgen-like steroids.

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Androgens are involved in many regulatory processes in mammary and endometrial epithelium, but their role in the development and progression of breast and endometrial carcinoma is poorly understood. Androgen receptors (AR) are found in normal epithelium as well as in more than 50% of specimen from

Tibolone and 5alpha-dihydrotestosterone alone or in combination with an antiandrogen in a rat breast tumour model.

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Tibolone was combined with the antiandrogen flutamide to determine whether the inhibition of tumour growth in the prophylactic 7,12-dimethylbenz(a)anthracene (DMBA) rat model could be attributed to androgenic properties of one of its metabolites. The mean tumour load after tibolone (0.25 or 1.0

The anti-androgen drug dutasteride renders triple negative breast cancer cells more sensitive to chemotherapy via inhibition of HIF-1α-/VEGF-signaling.

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BACKGROUND Triple negative breast cancer (TNBC) is characterized by lack of expression of both estrogen and progesterone receptor as well as lack of amplification of HER2. Patients with TNBC carry an unfavorable prognosis compared to other breast cancer subtypes given that endocrine or HER2 targeted

Anti-androgen therapy in triple-negative breast cancer.

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Assessing the efficacy of androgen receptor and Sox10 as independent markers of the triple-negative breast cancer subtype by transcriptome profiling.

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The Androgen Receptor (AR) has recently garnered a lot of attention as a potential biomarker and therapeutic target in hormone-dependent cancers, including breast cancer. However, several inconsistencies exist within the literature as to which subtypes of breast cancer express AR or whether it can

Effects of androgens on proliferation and progesterone receptor levels in T47D human breast cancer cells.

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The effects of estradiol (E2), dihydrotestosterone (DHT) and dehydro-3-epiandrosterone (DHEA) on proliferation and progesterone receptor induction were studied in a breast cancer cell line (T47D) expressing estrogen, androgen, and progesterone receptors. A significant enhancement of growth and

[Androgen receptors in breast cancer: Expression, value and therapeutic prospects].

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Triple-negative (TN) breast cancer are characterized by lack of estrogen receptor (OR) and progesterone receptor (PR) expression, and the absence of overexpression of human epidermal growth factor receptor 2 (HER2). It is a heterogeneous group of tumors with a more pejorative prognosis than other

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