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17 alpha-Estradiol is a biologically active estrogen in human breast cancer cells in tissue culture.

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The biological effects of 17 alpha-estradiol (17 alpha-E) and its interaction with estrogen receptors were studied in the MCF-7 human breast cancer cell line. Competition for [3H]17 beta-estradiol ([3H]17 beta-E) binding shows that 17 alpha-E binds to receptor with high affinity and has a

On the role of 17 alpha-estradiol and 17 beta-estradiol in the proliferation of MCF7 and T47D-A11 human breast tumor cells.

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A comparative study of the proliferative effect of 17 beta-estradiol and 17 alpha-estradiol on human estrogen-sensitive cell lines was performed. When using charcoal-dextran stripped human female sera-supplemented media the administration of the hormones, 17 alpha-estradiol at 3 X 10(-10)M, and 17

Enhancement of 2- and 16 alpha-estradiol hydroxylation in MCF-7 human breast cancer cells by 2,3,7,8-tetrachlorodibenzo-P-dioxin.

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2,3,7,8-Tetrachlorodibenzo-p-dioxin exhibits antiestrogenic activity and induces cytochromes P-450 in estrogen-dependent MCF-7 human breast-cancer cells. To determine whether induction of 2- or 16 alpha-hydroxylation of 17 beta-estradiol has a role in this antiestrogenic activity, MCF-7 cells which

Effects of pharmacological concentrations of estrogens on proliferation and cell cycle kinetics of human breast cancer cell lines in vitro.

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High dose estrogen therapy has been used effectively in the treatment of human breast cancer. To understand the mechanisms involved, the effects of high concentrations (5-100 microM) of estrogens were studied in estrogen receptor (ER) positive (T-47D and MCF-7) and ER negative (MDA-MB-330) human

Estrogenic effect of tamoxifen and its derivatives on the proliferation of MCF7 human breast tumor cells.

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Cloned human MCF-7 breast tumor cells were prevented from proliferating when grown in charcoal-dextran stripped human female serum (CDFHS)-supplemented media (40% and 10%); this inhibition was maximally cancelled by estradiol-17, cisTamoxifen, and Metabolite E, whereas Tamoxifen,

Control of cell proliferation: evidence for negative control on estrogen-sensitive T47D human breast cancer cells.

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The human breast tumor cloned cell lines T47D-A8 and All are estrogen dependent for cell proliferation in the nude mouse model. In contrast, these cells multiplied at similar rates when grown in serum-free cultures, regardless of the presence of 17 beta-estradiol (3 X 10(-11) to 3 X 10(-8) M

Relation between steroid receptor content and the response to hormone addition in isolated human breast cancer cells in short-term culture.

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The hormone dependence of human breast tumors has been investigated in two ways: (a) estradiol and progesterone receptor determination in tumor tissue; and (b) measurement of the growth-stimulating effect of hormones on cells in short-term culture. Preliminary results from 15 tumors suggest that

Possible role of the aromatase-independent steroid metabolism pathways in hormone responsive primary breast cancers.

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Aromatase inhibitors (AIs) exert antiproliferative effects by reducing local estrogen production from androgens in postmenopausal women with hormone-responsive breast cancer. Previous reports have shown that androgen metabolites generated by the aromatase-independent enzymes, 5α-androstane-3β,

Interleukin 1 alpha blocks estradiol-stimulated growth and down-regulates the estrogen receptor in MCF-7 breast cancer cells in vitro.

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We studied the effect of interleukin 1 alpha (IL-1 alpha) on estradiol stimulation of cell growth and estrogen receptor (ER) content in MCF-7 human breast cancer cells in vitro to determine if IL-1 alpha altered cellular estradiol responsiveness. We found that IL-1 alpha blocked estradiol-stimulated

A gene transcription signature of obesity in breast cancer.

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Obesity is thought to contribute to worse disease outcome in breast cancer as a result of increased levels of adipocyte-secreted endocrine factors, insulin, and insulin-like growth factors (IGFs) that accelerate tumor cell proliferation and impair treatment response. We examined the effects of

Growth factors and hormones which affect survival, growth, and differentiation of the MCF-7 stem cells and their descendants.

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The human breast tumor cell line was separated by Percoll density gradient centrifugation into six different subpopulations, A to F, one of which (E) appears to contain the stem cells on the basis of several criteria (M. Resnicoff et al. 1987, Proc. Natl. Acad. Sci. USA 84, 7295. We now analyzed the

Formation and turnover of long-chain fatty acid esters of 5-androstene-3 beta, 17 beta -diol in estrogen receptor positive and negative human mammary cancer cell lines in culture.

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Microsomal preparations derived from bovine placenta cotyledons, previously investigated as a convenient source of fatty acyl coenzyme A: estradiol-17 beta-acyl transferase, have been shown to acylate other steroids bearing 3 beta- or 17 beta-hydroxyl groups. In the presence of 0.1 mM oleoyl CoA,

Ultrasonographic observation of the breast in early postmenopausal women during therapy with Cimicifuga foetida extract and sequential therapy with estrogen and progestin.

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BACKGROUND It is now recognized that Cimicifuga foetida (C. foetida) extract is effective in alleviating menopausal symptoms. But the durations reported were usually short. The aim of this study was to investigate the effects of C. foetida extract therapy and different estrogen and progesterone

Lack of selective killing by steroids in normal and malignant cells.

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Using a colony formation assay, the cytotoxic effects of steroids and an anti-steroid on an established human breast tumor line and two human diploid fibroblast strains were studied. Experiments involving 17 a-estradiol, 17 beta-estradiol, dexamethasone, cortisone, dihydrotestosterone, and the

Endogenous peroxidase: specific marker enzyme for tissues displaying growth dependency on estrogen.

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Data derived from a correlated morphological and biochemical study suggest the following: (a) estradiol-17beta, diethylstilbestrol, the estrogen antagonists nafoxidine (Upjohn 11,000), and Parke Davis C1628 induce synthesis of an endogenous peroxidase in the epithelium of target tissues like the

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