melatonin/karcinom prsu

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Biotransformation of melatonin in human breast cancer cell lines: role of sulfotransferase 1A1.

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The biologically active melatonin metabolite, 6-hydroxymelatonin (6-OHMel), is conjugated to form 6-hydroxymelatonin sulfate (6-OHMelS). To elucidate the role of the sulfotransferase (SULT) enzyme 1A1, considerably expressed in normal and malignant human breast cells, we measured the formation of

Breast cancer cells: Modulation by melatonin and the ubiquitin-proteasome system--a review.

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Melatonin inhibits human breast cancer cells stimulated with estrogen. This antiproliferative action depends on the presence of the estrogen receptor alpha (ERα) in the human MCF-7 cell line and is strictly dose-dependent. Since researchers concerned with melatonin and breast cancer have not

Immunohistochemical expression of melatonin receptor MT1 and glucose transporter GLUT1 in human breast cancer.

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BACKGROUND Breast cancer is a heterogeneous disease and is the leading cause of cancer-related deaths among women. Even after diagnosis, the prognosis cannot be concluded since patients can develop resistance to therapy, which favors tumor growth, invasion and metastasis. In e recent years, research

Circadian rhythms of basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), cortisol, and melatonin in women with breast cancer.

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BACKGROUND Circadian rhythms in plasma concentrations of many hormones and cytokines determine their effects on target cells. METHODS Circadian variations were studied in cortisol, melatonin, cytokines (basic fibroblast growth factor IbFGF], EGF, insulin-like growth factor-1 [IGF-1]), and a cytokine

Hypotheses: melatonin/steroid combination contraceptives will prevent breast cancer.

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The use of the conventional combination oral contraceptives (containing ethinyl-estradiol and a progestin) is associated with reduced risk of ovarian and endometrial cancer. However, prolonged use of these pills before first term pregnancy apparently increases the risk of pre menopausal breast

Melatonin modulation of estrogen-receptor expression in mcf-7 human breast-cancer cells.

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MCF-7 human breast cancer cells, which are estrogen receptor (ER)-positive and responsive to the mitogenic actions of estrogen, were used to examine the possible association between the growth-inhibitory activity of melatonin and its ability to modulate the estrogen-response pathway. Melatonin at

Does the negative correlation found in breast cancer patients between plasma melatonin and insulin-like growth factor-I concentrations imply the existence of an additional mechanism of oncostatic melatonin influence involved in defense?

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BACKGROUND Insulin-like growth factor-I (IGF-I) is probably involved in promoting both normal and neoplastic cell growth, neoplastic transformation processes, angiogenesis, and neoplasma progression. On the other hand, one possible mechanism of the oncostatic action of melatonin is its influence on

Seasonal changes in serum melatonin in women with previous breast cancer.

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A seasonal variation in the month of initial detection of breast cancer has been previously observed in pre-menopausal women, and it has been proposed that this may be due to cyclic changes in tumour growth mediated by the effects of melatonin on ovarian function. To investigate this possibility

Membrane-bound melatonin receptor MT1 down-regulates estrogen responsive genes in breast cancer cells.

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Melatonin possesses anti-estrogenic effects on estrogen receptor expressing (ER+) breast cancer cells in culture by reducing cell cycle progression and cell proliferation. There is increasing agreement that on a cellular level the effects of melatonin are primarily induced by the membrane-bound

Melatonin, experimental basis for a possible application in breast cancer prevention and treatment.

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The role of the pineal as an oncostatic gland has been studied in animal models of tumorigenesis, especially on those concerning the mammary gland. The general conclusion is that experimental manipulations activating pineal gland, or the administration of melatonin, reduce the incidence and growth

5-Fluorouracil attenuates an oncostatic effect of melatonin on estrogen-sensitive human breast cancer cells (MCF7).

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The pineal hormone, melatonin, has been reported to have an inhibitory effect on the cell growth of human breast cancer. We have now assessed the interaction of melatonin with 5-fluorouracil (5-FU) on estrogen-sensitive MCF7 and estrogen-insensitive HBC4 cell lines. Melatonin inhibited MCF7 cell

Melatonin circadian-stage-dependently delays breast tumor development in mice injected daily for several months.

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Breast tumor incidence is compared in C3CF1 mice, receiving at one of 6 different circadian stages, daily injections of melatonin or of a vehicle or no treatment, the latter in a slightly cooler environment. Results are summarized when approximately 33% of all animals have a breast tumor. Vehicle

Depression of serum melatonin in patients with primary breast cancer is not due to an increased peripheral metabolism.

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Serum melatonin and its main metabolic product 6-sulfatoxymelatonin were determined in 17 patients with breast cancer (BC) with either a fresh primary tumor (nine) or a secondary tumor (eight) as well as in four patients with untreated benign breast disease (controls). Circadian rhythms were

Growth-inhibitory action of melatonin and thiazolidinedione derivative CGP 52608 on murine 16/C breast cancer cells.

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OBJECTIVE Melatonin may influence directly tumor cells through the specific binding sites. The best known melatonin binding sites are membrane receptors. Recently, the participation of nuclear signalling via estrogen as well as RZR/ROR receptors in oncostatic action of melatonin on the breast cancer

Evaluation of Melatonin Effect on Human Breast Cancer Stem Cells Using a Threedimensional Growth Method of Mammospheres.

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BACKGROUND The high rates of women's death from breast cancer occur due to acquired resistance by patients to certain treatments, enabling the recurrence and/or tumor growth, invasion and metastasis. It has been demonstrated that the presence of cancer stem cells in human tumors, as

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