17 beta estradiol/breast neoplasms

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DNA demethylation by 5-aza-2-deoxycytidine treatment abrogates 17 beta-estradiol-induced cell growth and restores expression of DNA repair genes in human breast cancer cells.

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Prolonged exposure to elevated levels of estrogen is a risk factor for breast cancer. Though increased cell growth and loss of DNA repair capacity is one of the proposed mechanisms for estrogen-induced cancers, the mechanism through which estrogen induces cell growth and decreases DNA repair

2,3,7,8-Tetrachlorodibenzo-p-dioxin causes an extensive alteration of 17 beta-estradiol metabolism in MCF-7 breast tumor cells.

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MCF-7 breast tumor cells form multicellular foci in vitro when supplemented with 17 beta-estradiol (E2). In the presence of E2 and the aryl hydrocarbon-receptor agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), MCF-7 cells grow to confluence but do not form foci. To investigate the role of E2

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on 17 beta-estradiol-induced glucose metabolism in MCF-7 human breast cancer cells: 13C nuclear magnetic resonance spectroscopy studies.

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The effects of 17 beta-estradiol, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and their combination on the metabolism of [1-13C] glucose were determined in cell suspensions of wild-type MCF-7 human breast cancer cells, by 13C NMR spectroscopy. Preliminary studies showed that, during the 7-hr

Reliability of immunoradiometric assays for sex-hormone binding globulin, androstenedione, 17-Beta estradiol and tumor-markers cea and cb15.3 to assess the biological response of megestrol-acetate treatment in patients with advanced breast-cancer.

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This study evaluated the effect of megestrol acetate administration on the serological assessment of some sex steroid hormones in women with advanced hormone-sensitive breast cancer. The serum levels of 17-beta estradiol, androstenedione and sex hormone binding globulin (SHBG) were measured by means

In vitro analysis of the cellular proliferative response to 17-beta-estradiol of human breast cancer.

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In human breast cancer the proliferating cells appear to differ from those containing estrogen receptors (ER) as shown by studies on isolated cellular subpopulations. In this paper the in vitro effect of 17-beta-estradiol on cell proliferation in 30 primary breast tumors was studied. The effect of

17 beta-estradiol-regulated expression of protein tyrosine phosphatase gamma gene in cultured human normal breast and breast cancer cells.

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BACKGROUND Protein tyrosine phosphatase gamma (PTP gamma) has been implicated as a potential tumor suppressor gene in kidney and lung adenocarcinomas. We have previously shown that PTP gamma mRNA expression levels are lower in DES-induced kidney tumors than in normal kidneys of Syrian hamsters. The

Comparative effects of 17 beta-estradiol, progestin R5020, tamoxifen and RU38486 on lactate dehydrogenase activity in MCF-7 human breast cancer cells.

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The effects of 17 beta-estradiol (estradiol), synthetic progestin R5020 and their antagonists, tamoxifen (Tam) and synthetic RU38486 on lactate dehydrogenase (LDH) activity in MCF-7 human breast cancer cells during the growth period were studied. A specially developed quantitative cytochemical assay

Interaction of 2,3,7,8-tetrachlorodibenzo-p-dioxin, 12-O-tetradecanoylphorbol-13-acetate (TPA) and 17 beta-estradiol in MCF-7 human breast cancer cells.

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and 12-O-tetradecanoylphorbol-13-acetate (TPA) are both tumor promoters which act through different mechanisms. In MCF-7 human breast cancer cells, both TCDD and TPA inhibited constitutive and 17 beta-estradiol-induced cell proliferation but showed no

Induction of jun gene family members by transforming growth factor alpha but not 17 beta-estradiol in human breast cancer cells.

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To investigate whether estrogen treatment of hormone-responsive human breast cancer cells was associated with activation of members of the jun family of immediate early response genes, the expression of these oncogenes in human breast cancer cells was examined. 17 beta-Estradiol had little effect on

Effect of 17-beta-estradiol on doxorubicin cytotoxicity in human breast cancer cell culture.

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Pre-treatment with 17-beta-estradiol appeared to improve the cytotoxic efficacy of doxorubicin on MCF-7 but not on ZR-75-1 and EVSA-T human breast cancer cell lines. MCF-7 and ZR-75-1 are both estrogen receptor-positive cell lines: however, only ZR-75-1 showed improved proliferation in the presence

Reduction of the membrane fluidity of human breast cancer cells by tamoxifen and 17 beta-estradiol.

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The intracellular steady-state levels of methotrexate were previously shown to be reduced in estrogen receptor (ER)-negative human breast cancer MDA-MB-436 cells and ER-positive human breast cancer MCF7 cells following treatment with pharmacologically relevant concentrations of 17 beta-estradiol

Genomic data on breast cancer transcript profile modulation by 17beta-hydroxysteroid dehydrogenase type 1 and 17-beta-estradiol.

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The data presented here are related to the research article entitled "Estradiol-independent modulation of breast cancer transcript profile by 17beta-hydroxysteroid dehydrogenase type 1" (J.A. Aka, E.L. Calvo, S.X. Lin, 2016) [1]. We evaluated the effect of the steroidal enzyme 17β-HSD1 and its

Synergistic proliferative action of insulin-like growth factor I and 17 beta-estradiol in MCF-7S breast tumor cells.

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We have analyzed the mechanism by which the combination of insulin-like growth factor I (IGF-I) and 17 beta-estradiol (E2) induces cell cycle progression in MCF-7S cells. This cell line differs from many other breast cancer-derived cell lines in that E2 (1 nM) does not induce cell cycle progression,

17-beta-estradiol increases expression of 52-kDa and 60-kDa SS-A/Ro autoantigens in human keratinocytes and breast cancer cell line MCF-7.

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SS-A/Ro autoantibodies are detected in high frequency in patients with subacute cutaneous lupus, neonatal lupus, systemic lupus erythematosus, and Sjögren syndrome. It has been reported that estrogen was capable of inducing cell surface expression of SS-A/Ro antigens in human keratinocytes, although

17 beta-estradiol inhibits tumor necrosis factor-alpha-induced nuclear factor-kappa B activation by increasing nuclear factor-kappa B p105 level in MCF-7 breast cancer cells.

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Tumor necrosis factor-alpha (TNF-alpha) exerts many cytological effects on a wide range of cells. TNF-alpha can activate nuclear factor-kappa B (NF-kappa B). Activation of NF-kappa B by TNF-alpha mediates many functions of TNF-alpha. The NF-kappa B inhibitor, I kappa B alpha, negatively regulates

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