lipoxygenase/breast neoplasms

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Association of a functional polymorphism (Gln261Arg) in 12-lipoxygenase with breast cancer.

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The overexpression of arachidonyl lipoxygenase-12 (ALOX12) in breast cancer has been reported. Hence, we examined whether a non-synonymous polymorphism of ALOX12 (mRNA, A835G; Gln261Arg) is associated with breast cancer in females. The polymorphism was detected in genomic DNA by PCR-RFLP. The

Aberrant expression of 5-lipoxygenase-activating protein (5-LOXAP) has prognostic and survival significance in patients with breast cancer.

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5-lipoxygenase (5-LOX)-activating protein, 5-LOXAP also known as LOX5AP or FLAP, is a protein that works closely with 5-LOX in regulating the metabolism of arachidonate. Some of the eicosanoid products of 5-LOX/5-LOXAP are known to play active roles in the function of cancer cells, including breast

5-lipoxygenase and 5-lipoxygenase-activating protein gene polymorphisms, dietary linoleic acid, and risk for breast cancer.

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The n-6 polyunsaturated fatty acid 5-lipoxygenase pathway has been shown to play a role in the carcinogenesis of breast cancer. We conducted a population-based case-control study among Latina, African-American, and White women from the San Francisco Bay area to examine the association of the

Attenuation of breast tumor cell growth by conjugated linoleic acid via inhibition of 5-lipoxygenase activating protein.

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Conjugated linoleic acid (CLA) consists of a group of linoleic acid geometric isomers that have been shown to reduce tumor growth and metastasis in animal models of breast, prostate and colon cancer. To delineate a possible mechanism of action for CLA, we have recently shown that the 5-lipoxygenase

Breast cancer cell-derived EMMPRIN stimulates fibroblast MMP2 release through a phospholipase A(2) and 5-lipoxygenase catalyzed pathway.

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Metalloproteinases (MMP) produced by both cancer and normal stromal fibroblast cells play a critical role in the metastatic spread of tumours, however little is known of the regulation of their release. In this report we demonstrate that breast cancer cells in culture release apparently full length

A positive feedback between activated extracellularly regulated kinase and cyclooxygenase/lipoxygenase maintains proliferation and migration of breast cancer cells.

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Metastasis of breast cancer cells is the leading cause of death in breast cancer patients. Why do breast cancer cells with high metastatic potential always keep in high proliferation and migration? The endogenous signaling pathways associated with tumor metastasis remain unclear. In the present

A lipoxygenase inhibitor in breast cancer brain metastases.

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The complication of multiple brain metastases in breast cancer patients is a life threatening condition with limited success following standard therapies. The arachidonate lipoxygenase pathway appears to play a role in brain tumor growth as well as inhibition of apoptosis in in-vitro studies. The

Tetrahydrofurandiol stimulation of phospholipase A2, lipoxygenase, and cyclooxygenase gene expression and MCF-7 human breast cancer cell proliferation.

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BACKGROUND We characterized an endocrine disruptor from ground corncob bedding material that interferes with male and female sexual behavior and ovarian cyclicity in rats and stimulates estrogen receptor (ER)-positive and ER-negative breast cancer cell proliferation. The agents were identified as an

Expression of cyclooxygenase-2 and 12-lipoxygenase in human breast cancer and their relationship with HER-2/neu and hormonal receptors: impact on prognosis and therapy.

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BACKGROUND A number of studies have shown over-expression of cox-2 in breast cancer. Also it has been recorded that human breast cancer expresses high level of cox-2 and 12-lipoxygenase which may be beneficial in future therapy plan for those patients. OBJECTIVE The present study aims to examine the

Cyclooxygenase and lipoxygenase gene expression in the inflammogenesis of breast cancer.

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We examined the expression of major inflammatory genes, cyclooxygenase-1 and 2 (COX1, COX2) and arachidonate 5-lipoxygenase (ALOX5) in 1090 tumor samples of invasive breast cancer from The Cancer Genome Atlas (TCGA). Mean cyclooxygenase expression (COX1 + COX2) ranked in the upper 99th percentile of

Enhanced angiogenesis and growth of 12-lipoxygenase gene-transfected MCF-7 human breast cancer cells in athymic nude mice.

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Transfection of the estrogen-dependent and poorly invasive MCF-7 human breast cancer cell line so that it stably overexpressed 12-lipoxygenase and secreted high levels of 12-hydroxyeicosatetraenoic acid when cultured with arachidonate resulted in rapid growth in athymic nude mice when compared with

The 12-lipoxygenase gene-transfected MCF-7 human breast cancer cell line exhibits estrogen-independent, but estrogen and omega-6 fatty acid-stimulated proliferation in vitro, and enhanced growth in athymic nude mice.

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The estrogen-dependent, linoleic acid (LA)-unresponsive, MCF-7 breast cancer cell line was transfected with 12-lipoxygenase (12-LOX) cDNA (MCF-7/12-LOX cells). The transfectant stably expressed high levels of 12-LOX mRNA and protein, and secreted large quantities of 12-hydroxyeicosatetraenoic acid

Cytotoxicity of arachidonic acid and of its lipoxygenase metabolite 15-hydroperoxyeicosatetraenoic acid on human breast cancer MCF-7 cells in culture.

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Monolayer cultures of MCF-7 human breast cancer cell line were treated with arachidonic acid (AA) and 15-L-(s)-hydroperoxyeicosatetraenoic acid (15-L-(s)-HPETE) in a concentration range of 10(-5)-10(-11) M and their relative cytotoxic potential was determined. Both compounds had a time and

Increased 12-lipoxygenase expression in breast cancer tissues and cells. Regulation by epidermal growth factor.

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The interaction of growth factors, such as epidermal growth factor (EGF) with their receptors, on breast cancer cells can lead to the hydrolysis of phospholipids and release of fatty acids, such as arachidonic acid, which can be further metabolized by the lipoxygenase (LO) pathway. Several LO

Involvement of 15-lipoxygenase-1 in the regulation of breast cancer cell death induced by sodium butyrate.

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15-Lipoxygenase-1 (15-Lox-1) as a member of fatty acid dioxygenases family has received considerable attention as an effector of cancer cell growth. The relevance of sodium butyrate on 15-Lox-1 pathway has not been determined in breast cancer. This study is aimed to investigate the possible

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