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17 beta estradiol/καρκίνος
Ο σύνδεσμος αποθηκεύεται στο πρόχειρο
Σελίδα 1 από 218 Αποτελέσματα
Induction of progesterone receptor with 17 beta-estradiol in human ovarian cancer.
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Σύνδεση εγγραφή
We utilized a xenograft model of human ovarian cancer to study the ability of estrogen to induce progesterone receptor. Tumor cytosol from 17 beta-estradiol treated oophorectomized animals, but not oophorectomized controls, contained a [3H]ORG 2058 binding moiety of sedimentation coefficient 6-9S.
17 beta-estradiol stimulates a rapid Ca2+ influx in LNCaP human prostate cancer cells.
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Σύνδεση εγγραφή
Prostate growth is known to be controlled by steroids such as androgens and estradiol. For this reason steroids (estradiol, adrenal androgens) or steroid inhibitors are commonly used as palliative treatments for prostate carcinoma. In view of the pivotal role played by Ca2+ ions in cell
Improvement of function and morphology of tumor necrosis factor-alpha treated endothelial cells with 17-beta estradiol: a preliminary study for a feasible simple model for atherosclerosis.
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BACKGROUND
Dysfunction of endothelial cells (EC) to produce endothelial nitric oxide synthase (eNOS) by tumor necrosis factor-alpha (TNF-alpha) causes critical features of vascular inflammation associated with several disease states (eg, atherosclerosis including increased platelet aggregation and
Covalent binding of 17 beta-estradiol and retinoic acid to proteins in the human breast cancer cell line MCF-7.
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Both retinoic acid and 17 beta-estradiol formed covalent bonds with proteins of the human breast cancer cell line MCF-7. Two-dimensional gel patterns of the labeled proteins were unique for each ligand. There were four major retinoylated proteins in MCF-7 consisting of two doublets with molecular
The metabolism of 17 beta-estradiol by lactoperoxidase: a possible source of oxidative stress in breast cancer.
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Electron spin resonance (ESR) spectroscopy and oxygen consumption measurements using a Clark-type oxygen electrode have been used to study the metabolism of the estrogen 17 beta-estradiol by lactoperoxidase. Evidence for a one-electron oxidation of estradiol to its reactive phenoxyl radical
Conversion of estrone to 17-beta-estradiol in human non-small-cell lung cancer cells in vitro.
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It has recently been suggested that, in addition to genetic and environmental factors and tobacco exposure, estrogens also may be an independent risk factor in the development of lung cancer. Therefore, we evaluated the transcript and protein levels of 17-beta-hydroxysteroid-dehydrogenase type 1
17 beta-estradiol-induced increases in glucose-regulated protein 78kD and 94kD protect human breast cancer T47-D cells from thermal injury.
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Heat shock alters the susceptibility of tumor cells to chemotherapeutic agents. We conducted experiments to study the regulation of expression of heat shock proteins (HSP) in 17 beta-estradiol-treated T47-D cells, a human breast cancer cell line. Cells exposed to 17 beta-estradiol for 24-48 h
Baicalein suppresses 17-β-estradiol-induced migration, adhesion and invasion of breast cancer cells via the G protein-coupled receptor 30 signaling pathway.
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Flavonoids are structurally similar to steroid hormones, particularly estrogens, and therefore have been studied for their potential effects on hormone-dependent cancers. Baicalein is the primary flavonoid derived from the root of Scutellaria baicalensis Georgi. In the present study, we investigated
Anticancer effect of genistein on BG-1 ovarian cancer growth induced by 17 β-estradiol or bisphenol A via the suppression of the crosstalk between estrogen receptor α and insulin-like growth factor-1 receptor signaling pathways.
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The interaction between estrogen receptor (ER) and insulin-like growth factor-1 receptor (IGF-1R) signaling pathway plays an important role in proliferation of and resistance to endocrine therapy to estrogen dependent cancers. Estrogen (E2) upregulates the expression of components of IGF-1 system
Zinc oxide nanoparticles enhance expression of maspin in human breast cancer cells
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Toxic and apoptotic impacts of zinc oxide nanoparticle (ZNP) on different cancer cells have been reported. Maspin (a mammary serine protease inhibitor) as a tumor suppressor gene can inhibit tumor growth and metastasis. The expression of maspin is modulated by p53, Bcl-2 family genes, and estrogen
Enhanced tight junction function in human breast cancer cells by antioxidant, selenium and polyunsaturated lipid.
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Paracellular permeability (PCP) is governed by tight junctions (TJs) in epithelial cells, acting as cell-cell adhesion structures, the aberration of which is known to be linked to the dissociation and metastasis of breast cancer cells. This study hypothesized that the function of TJs in human breast
Androgen control of cytosol progesterone receptor levels in the MT-W9B transplantable mammary tumor in the rat.
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The effect of androgen on the levels of the cytosol progesterone receptor was examined in the transplantable rat mammary tumor MT-W9B and in the normal uteri of inbred WF rats. Progesterone receptor levels were barely detectable in tumors grown in male WF rats but were increased after castration or
Progestin inhibition of estrogen-dependent proliferation in ZR-75-1 human breast cancer cells: antagonism by insulin.
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The effect of R5020 [17,21-dimethyl-19-nor-4,9-pregnadiene-3,20-dione], a synthetic progestin, was studied in the hormone-responsive ZR-75-1 human breast cancer cell line. Following a 12-day incubation with increasing concentrations of R5020, the mitogenic effect of 17 beta-estradiol (E2, 1nM) was
Regulation of androgen receptor mRNA and protein level by steroid hormones in human mammary cancer cells.
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The regulation of the human androgen receptor (AR) by steroid hormones in human mammary cancer cells was investigated using immunocytochemical and ligand binding assays for its protein and Northern blot analyses for the corresponding mRNA. MFM-223 cells contain high levels of ARs and are
An antiestrogenic action of androgens in human breast cancer cells.
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We have recently observed that androgens prevent the estrogen-dependent augmentation of cytoplasmic progesterone receptor (PRc) in MCF-7 human breast cancer cells and now report the results of studies that further characterize this new example of sex steroid antagonism. Using a single saturating
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