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l arginine/rak dojke
Veza se sprema u međuspremnik
Stranica 1 iz 70 rezultatima
L-arginine/5-fluorouracil combination treatment approaches cells selectively: Rescuing endothelial cells while killing MDA-MB-468 breast cancer cells.
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Reducing the adverse effects of chemotherapy on normal cells such as endothelial cells is a determinant factor of treatment success especially in pregnant women. In this regard, modulatory effect of L-arginine on various cancers is still a controversial topic in cancer therapy. So, this study aimed
Stimulation of human breast cancers by dietary L-arginine.
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1. The amino acid L-arginine has been shown to enhance immune mechanisms and inhibit tumour growth in experimental animals, but although many of the immunological effects of arginine have been reproduced in man there have been few studies of its effects on human tumours. In this study the effects of
The effect of N(G)-monomethyl-L-arginine and tamoxifen on nitric oxide production in breast cancer cells stimulated by oestrogen and progesterone.
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OBJECTIVE
To examine the capacity of oestrogen, or progesterone, or both to elicit the release of nitric oxide (NO) from T47D breast cancer cells in vitro.
METHODS
Prospective, longitudinal, controlled in vitro experiment.
METHODS
University Medical School, United Kingdom. MATERIAL AND
Dietary supplementation with L-arginine in patients with breast cancer (> 4 cm) receiving multimodality treatment: report of a feasibility study.
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L-Arginine has been shown, in human breast cancers, to increase protein synthesis and the number of cells in the growth phase of the cell cycle. L-Arginine, therefore, may potentiate the response of breast cancers to cell cycle-specific cytotoxic agents. This phase II pilot study assessed the
Growth arrest and morphological change of human breast cancer cells by dibutyryl cyclic AMP and L-arginine.
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The growth in vitro of human breast cancer cells, line MCF-7, was inhibited by a daily supplement of L-arginine (1 milligram per milliliter). Arginine acted synergistically with dibutyryl adenosine 3',5'-monophosphate (cyclic AMP) (10(-6) molar) to enhance the growth inhibitory effect: the cell
Metabolic relevance for N-hydroxy L-arginine reduction in estrogen-negative breast cancer cells.
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We had shown Nw-hydroxy-L-arginine (NOHA) as a promising blood-based biomarker for estrogen-receptor-negative (ER-) breast cancer (BC) that differentiates ER- BC based on grade and molecular phenotype. In this in vitro study, we assessed the metabolic relevance for ER- BC-specific NOHA modulation
Assessing N w-hydroxy-L-arginine applicability as a novel ethnic specific estrogen-negative breast cancer marker.
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In our prior study we identified N w-hydroxy-L-arginine (NOHA) as a simple, yet sensitive indicator for estrogen negative (ER-) breast cancer early-prognosis, but not estrogen positive (ER+), and to offer ethnic selectivity for ER- detection. However, the ability of NOHA to assess ER- breast tumor
NG-nitro-L-arginine methyl ester inhibits bone metastasis after modified intracardiac injection of human breast cancer cells in a nude mouse model.
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We investigated the effects of NG-nitro-L-arginine-methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, on bone metastasis of human breast cancer, MDA-231 cells. Tumor cells (2 x 10(5) cells in 0.2 ml of phosphate-buffered saline; PBS) were injected through the diaphragm into the left
N w-hydroxy-L-arginine as a novel ethnic specific indicator of estrogen-negative breast cancer.
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As a heterogeneous disease, breast cancer can be divided into distinct subtypes. Among the two major subsets of estrogen receptor-negative (ER-) and ER-positive (ER+) tumors, the ER- is a more aggressive subtype, more difficult to treat, has greater ethnic disparity concerns, worse prognosis, and
Natural cytotoxicity in breast cancer patients receiving neoadjuvant chemotherapy: effects of L-arginine supplementation.
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Certain cytotoxic drugs have been shown to suppress host anti-cancer defence mechanisms. The amino acid L-arginine can significantly enhance natural killer (NK) and lymphokine-activated killer (LAK) cell cytotoxicity in patients with locally advanced breast cancer. In this study, the effect of
Relaxin activates the L-arginine-nitric oxide pathway in human breast cancer cells.
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Recently, we demonstrated that relaxin (RLX), a peptide hormone of ovarian origin, inhibits growth and promotes differentiation of MCF-7 breast adenocarcinoma cells. We also showed that RLX stimulates the production of nitric oxide (NO) in several cell types. NO has been reported to have antitumor
L-arginine stimulates host defenses in patients with breast cancer.
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BACKGROUND
The amino acid L-arginine is known to have immunostimulatory effects in animals and healthy human volunteers. We have studied the effect of dietary supplementation with L-arginine (30 gm/day for 3 days) on host defenses in patients with breast cancer.
METHODS
Mitogenic responses of
Potentiation of the response to chemotherapy in patients with breast cancer by dietary supplementation with L-arginine: results of a randomised controlled trial.
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Patients with large primary breast cancers are being treated with neo-adjuvant chemotherapy. Studies in animals have shown that responses to chemotherapy can be increased by dietary manipulation of tumour cell metabolism. Also dietary supplementation with the amino acid L-arginine, resulted in an
Nitric oxide, N omega-hydroxy-L-arginine and breast cancer.
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Nitric oxide has varied effects on human breast cancer cells. At low concentration (micromolar range) it increases proliferation by increasing synthesis of some cells cycle protein and in higher concentration (nanomolar range) it leads to cytostasis or apoptosis by decreasing the translation of some
Inhibition of breast tumor growth by N(G)-nitro-l-arginine methyl ester (l-NAME) is accompanied by activation of fibroblasts.
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Nitric Oxide (NO) is involved in many physiological and pathological processes. It is generated by a family of NO synthases (NOS), being the inducible isoform, iNOS, responsible for higher amounts of NO. Here, we report that pharmacological inhibition of NO production by l-NAME reduces both
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