linoleic acid/karcinóm prsníka

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[Conjugated linoleic acid as a potential protective factor in prevention of breast cancer].

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Cancers are the second leading cause of deaths in Poland, among both women and men. Breast cancer is the malignancy most frequently diagnosed in women. In 2008 mammary cancer was diagnosed in up to 14 500 patients. It is also the second most common cause of cancer deaths among women in our country.

Inhibition of stearoyl-CoA desaturase activity by the cis-9,trans-11 isomer and the trans-10,cis-12 isomer of conjugated linoleic acid in MDA-MB-231 and MCF-7 human breast cancer cells.

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Conjugated linoleic acid (CLA) is a collective term for a group of positional and geometric conjugated dienoic isomers of linoleic acid. CLA has been shown to have strong inhibitory effects on mammary carcinogenesis both in vitro and in vivo. In this study, we investigated the regulation of human

Chemometric analysis of the interactions among different parameters describing health conditions, breast cancer risk and fatty acids profile in serum of rats supplemented with conjugated linoleic acids.

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We investigated how different doses of conjugated linoleic acids applied for various periods of time influence breast cancer risk and fatty acids profile in serum of rats treated or not with 7,12-dimethylbenz[a]anthracene (DMBA). We also search for interactions among parameters describing health

Effects of linoleic acid on the growth and metastasis of two human breast cancer cell lines in nude mice and the invasive capacity of these cell lines in vitro.

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The purpose of the study was to compare the effects of dietary linoleic acid (LA) intake on the growth and metastasis of MDA-MB-435 and MDA-MB-231 human breast cancer cells in nude mice, together with their invasive capacity and secretion of type IV collagenase (gelatinase) in vitro. Each tumor cell

The aldehydic metabolites of linoleic acid are cytotoxic against human breast cancer cells.

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The cytotoxic effect of aldehydic metabolites of linoleic acid, 13-oxo-tridecadienoic acids, on MCF-7 human breast cancer cells was investigated. The metabolites inhibited the growth of the cancer cells and the effect was dependent on both time of exposure and concentration of the metabolites; 50%

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

Role of LOXs and COX-2 on FAK activation and cell migration induced by linoleic acid in MDA-MB-231 breast cancer cells.

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BACKGROUND Epidemiological studies and animal models suggest a link between high levels of dietary fat intake and an increased risk of developing breast cancer. Particularly, free fatty acids (FFAs) are involved in several processes, including proliferation, migration and invasion, in breast cancer

Conjugated linoleic acid (CLA) inhibits expression of the Spot 14 (THRSP) and fatty acid synthase genes and impairs the growth of human breast cancer and liposarcoma cells.

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Spot 14 (THRSP, S14) is a nuclear protein involved in the regulation of genes required for fatty acid synthesis in normal and malignant mammary epithelial and adipose cells. Harvatine and Bauman (1) reported that conjugated linoleic acid (CLA) inhibits S14 gene expression in bovine mammary and mouse

Enhanced anticancer effect of conjugated linoleic acid by conjugation with Pluronic F127 on MCF-7 breast cancer cells.

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This study is designed to evaluate whether conjugated linoleic acid-coupled Pluronic F127 (Plu-CLA) enhances anticancer efficacy in MCF-7 breast cancer cells when compared to conjugated linoleic acid (CLA) itself. CLA was simply coupled to Pluronic F127 through ester linkage between carboxyl group

Conjugated linoleic acid induces apoptosis in MDA-MB-231 breast cancer cells through ERK/MAPK signalling and mitochondrial pathway.

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We investigated the molecular mechanisms involved in the anti-proliferative activity exerted by conjugated linoleic acid (CLA) on the estrogen unresponsive MDA-MB-231 human breast cancer cell line. The effects on cell proliferation, cell cycle progression and induction of apoptosis were examined.

A mixture of trans, trans conjugated linoleic acid induces apoptosis in MCF-7 human breast cancer cells with reciprocal expression of Bax and Bcl-2.

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The growth inhibitory effect of a mixture of trans, trans conjugated linoleic acid isomers (t, t CLA) was investigated in a human breast cancer cell line, MCF-7, with references to c9, t11 CLA, t10, c12 CLA, and linoleic acid. The t, t CLA treatment effectively induced a cytotoxic effect in a

Fatty acid binding protein 7 mediates linoleic acid-induced cell death in triple negative breast cancer cells by modulating 13-HODE

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Different fatty acids have distinct effects on the survival of breast cancer cells, which could be mediated by fatty acid binding proteins (FABPs), a family of lipid chaperones. Due to the diverse structures of the members of FABP family, each FABP demonstrates distinct binding affinities to

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

Influence of dietary linoleic acid on experimental human breast cancer cell metastasis in athymic nude mice.

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The effects of linoleic acid (LA), an omega-6 fatty acid precursor for prostaglandin biosynthesis, on the later stages of human breast cancer cell metastasis were studied by the intravenous injection of tumor cells into nude mice (). MDA-MB-435 cells were grown as solid

Effects of linoleic acid and eicosanoid synthesis inhibitors on the growth and c-myc oncogene expression of human breast cancer cells.

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We investigated the effects of linoleic acid and eicosanoid synthesis inhibitors on the growth, DNA synthesis, and c-myc oncogene expression of human breast cancer cell lines. The cell growth of all cell lines examined was stimulated by linoleic acid, although the optimal concentration of linoleic

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