Future Prospects in Breast Cancer Research - Cancer Stem Cells.

Breast cancer is one of the leading causes of cancer deaths among women. Although significant advances in the prevention, diagnosis and management are made, still every year half a million women die of breast cancer. Personalised treatment has the potential to increase treatment efficacy, and hence decrease mortality rates.

Cancer prevalence in osteoporotic women with low serum vitamin D levels.

Objective: The aim of this study was to assess the role of vitamin D in cancer development in postmenopausal osteoporotic women.

Methods: A cross-sectional and in vitro study was carried out, with statistical analysis with odds ratios and 95% CIs presented. Human estrogen receptor-positive breast cancer cells (MCF-7) were studied in vitro.

Viability analysis and apoptosis induction of breast cancer cells in a microfluidic device: effect of cytostatic drugs.

Breast cancer is the leading cause of cancer deaths among non-smoking women worldwide. At the moment the treatment regime is such that patients receive different chemotherapeutic and/or hormonal treatments dependent on the hormone receptor status, the menopausal status and age. However, in vitro sensitivity testing of tumor biopsies could rationalize and improve the choice of chemo- and hormone therapy.

Breast cancer and climacteric complaints: weighing up risks of hormone therapy against quality of life.

Women with severe menopausal symptoms can, at their request, be treated effectively with hormone therapy. Good information about the advantages and disadvantages of hormone therapy should precede this decision. For women with breast cancer or an inherited increased risk of breast cancer and severe, often therapy-related climacteric symptoms, a high degree of reticence is appropriate in relation to hormone therapy.

Treatment of dysfunctional uterine bleeding in the perimenopause: the effects of adding combined estradiol/norethisterone acetate therapy to goserelin acetate treatment--a randomized, placebo-controlled, double-blind trial.

Objective: To assess the effects of adding combined estradiol/norethisterone acetate therapy (CENT) to goserelin acetate treatment (GA) of dysfunctional uterine bleeding (DUB) in perimenopausal women.

Methods: In a randomized, placebo-controlled, double-blind trial followed by an open follow-up study, 31 perimenopausal women with DUB were recruited from gynecological outpatient departments of two Dutch hospitals and randomized for treatment with either GA/placebo or GA/CENT for 6 months followed by 18 months of GA/CENT for all. The main outcome measures were abdominal pain, number of bleeding days, double-layer endometrial thickness (DET), Greene climacteric score (GCS), visual analog scale for well-being, bone mineral density (BMD) and mammographic density (BI-RAD score).

Gonadal protection by a gonadotropin-releasing hormone agonist depot in young women with Hodgkin's disease undergoing chemotherapy.

Objective: To explore the effects of a gonadotropin-releasing hormone (GnRH) agonist depot (goserelin acetate) in women with Hodgkin's disease receiving chemotherapy while taking a continuous combined estrogen-progestin preparation as add-back on the prevention of premature ovarian failure (POF).

Methods: In a prospective pilot study, five premenopausal women with Hodgkin's disease received a GnRH agonist depot plus add-back until polychemotherapy was completed. Every 4 weeks during treatment and thereafter, a hormonal profile (follicle-stimulating hormone (FSH), luteinizing hormone, 17beta-estradiol, progesterone and inhibin B) was measured until resumption of menstruation or the development of a hypergonadotropic state (2 x FSH > 30 U/l).

Differential effects of progestogens on breast cancer cell lines.

Our in vitro results indicate that not all progestogens act equally on breast cancer cells. Some progestogens (medroxyprogesterone acetate (MPA), norethisterone acetate (NETA) and dienogest) alone or combined with estradiol (E2) stimulate proliferation of breast cancer cells, while others (dihydrodydrogesterone (DHD), the active metabolite of dydrogesterone, tibolone and progesterone (Prog)) alone or combined with estradiol induce apoptosis. Further pharmacological and clinical studies should be initiated to evaluate these findings in vivo.

Effects of low-dose oral and transdermal estrogen replacement therapy on hemostatic factors in healthy postmenopausal women: a randomized placebo-controlled study.

Objective: This study was undertaken to investigate the effect of transdermal and oral estrogen replacement therapy in healthy postmenopausal women on markers of coagulation and fibrinolysis associated with coronary artery disease.

Study Design: In a randomized, placebo-controlled, double-blind study, healthy hysterectomized postmenopausal women received daily either placebo (n=49), transdermal 17beta-estradiol (E(2)) 50 microg (tE(2) group, n=33), oral E(2) 1 mg (oE(2) group, n=37), or oral E(2) 1 mg combined with gestodene 25 microg (oE(2)+G group, n=33) for thirteen 28-day treatment cycles. Hemostatic variables were measured in blood samples collected at baseline and in cycles 4 and 13.

Oral, more than transdermal, estrogen therapy improves lipids and lipoprotein(a) in postmenopausal women: a randomized, placebo-controlled study.

Objective: To assess the effects of low-dose oral and transdermal estrogen therapy on the lipid profile and lipoprotein(a) [Lp(a)] levels in healthy, postmenopausal women and to study the additional influence of gestodene administration.

Design: In a multicenter, randomized, double-blind, placebo-controlled study, 152 healthy, hysterectomized, postmenopausal women received daily either placebo (n = 49), 50 microg transdermal 17beta-estradiol (tE2, n = 33), 1 mg oral 17beta-estradiol (oE2, n = 37), or 1 mg oE2 combined with 25 microg gestodene (oE2 + G, n = 33) for 13 cycles of 28 days, followed by 4 cycles of placebo in each group. Fasting serum concentrations of total, high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol, triglycerides, and Lp(a) were measured at baseline and in cycles 4, 13, and 17.