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alpha linolenic acid/рак молочной железы

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α-linolenic acid and docosahexaenoic acid, alone and combined with trastuzumab, reduce HER2-overexpressing breast cancer cell growth but differentially regulate HER2 signaling pathways.

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BACKGROUND Diets rich in the n-3 fatty acid alpha-linolenic acid (ALA) have been shown to reduce breast tumor growth, enhance the effectiveness of the HER2-targeted drug trastuzumab (TRAS) and reduce HER2 signaling in mouse models. It is unclear whether this is due to direct effects of ALA or due to

Comparison of stearidonic acid and alpha-linolenic acid on PGE2 production and COX-2 protein levels in MDA-MB-231 breast cancer cell cultures.

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The bioactivity of stearidonic acid (SDA, 18:4n-3) and alpha-linolenic acid (LNA, 18:3n-3) on cyclooxygenase-2 (COX-2) enzyme expression and prostaglandin E2 (PGE2) production has not been evaluated. This investigation examined the effects of SDA and LNA on PGE2 biosynthesis and COX-2 protein and

Low alpha-linolenic acid content of adipose breast tissue is associated with an increased risk of breast cancer.

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Data derived from experimental studies suggest that alpha-linolenic acid may have a protective effect in breast cancer. Observations obtained from epidemiological studies have not allowed conclusions to be drawn about a potential protective effect of dietary alpha-linolenic acid on breast cancer,

alpha-Linolenic acid content of adipose breast tissue: a host determinant of the risk of early metastasis in breast cancer.

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The association between the levels of various fatty acids in adipose breast tissue and the emergence of visceral metastases was prospectively studied in a cohort of 121 patients with an initially localised breast cancer. Adipose breast tissue was obtained at the time of initial surgery, and its

α-Linolenic Acid Reduces Growth of Both Triple Negative and Luminal Breast Cancer Cells in High and Low Estrogen Environments.

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Flaxseed, rich in α-linolenic acid (ALA), is a complementary breast cancer (BC) therapy; however ALA effectiveness and mechanism are unclear. Variation in cellular expression of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), and estrogen (E2)

Growth-inhibitory and proapoptotic effects of alpha-linolenic acid on estrogen-positive breast cancer cells.

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We tested the anticarcinogenic effect of alpha-linolenic acid (ALA) as a single compound. To test the role of ALA in breast cancer cells (MCF-7), we analyzed the antiproliferative pathway and the proapoptotic pathway. ALA exhibited growth inhibition on MCF-7 cells dose-dependently of ALA in 24, 48,

Growth and gene expression differ over time in alpha-linolenic acid treated breast cancer cells.

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METHODS Heterogeneity of breast cancer (BC) subtypes makes BC treatment difficult. α-linolenic acid (ALA), rich in flaxseed oil, has been shown to reduce growth and increase apoptosis in several BC cell lines, but the mechanism of action needs further understanding. RESULTS Four BC cell lines

Oxidized Products of α-Linolenic Acid Negatively Regulate Cellular Survival and Motility of Breast Cancer Cells.

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Despite recent advances in our understanding of the biological processes leading to the development and progression of cancer, there is still a need for new and effective agents to treat this disease. Phytoprostanes (PhytoPs) and phytofurans (PhytoFs) are non-enzymatically oxidized products of

α-Linolenic acid inhibits the migration of human triple-negative breast cancer cells by attenuating twist1 expression and suppressing twist1-mediated epithelial-mesenchymal transition

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α-Linolenic acid (ALA), an essential fatty acid, has anticancer activity in breast cancer, but the mechanism of its effects in triple-negative breast cancer (TNBC) remains unclear. We investigated the effect of ALA on Twist1, which is required to initiate epithelial-mesenchymal transition (EMT) and

HER2 (erbB-2)-targeted effects of the omega-3 polyunsaturated fatty acid, alpha-linolenic acid (ALA; 18:3n-3), in breast cancer cells: the "fat features" of the "Mediterranean diet" as an "anti-HER2 cocktail".

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BACKGROUND Data derived from epidemiological and experimental studies suggest that alphalinolenic acid (ALA; 18:3n-3), the main omega-3 polyunsaturated fatty acid (PUFA) present in the Western diet, may have protective effects in breast cancer risk and metastatic progression. A recent pilot clinical

Dietary beta-carotene inhibits mammary carcinogenesis in rats depending on dietary alpha-linolenic acid content.

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To investigate whether dietary alpha-linolenic acid (ALA) content alters the effect of beta-carotene on mammary carcinogenesis, we conducted a chemically induced mammary tumorigenesis experiment in rats randomly assigned to four nutritional groups (15 rats per group) varying in beta-carotene

Essential fatty acids and breast cancer: a case-control study in Uruguay.

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The relationship between frequency of intake of different types of fat and breast cancer was investigated in a case-control study conducted in Montevideo, Uruguay, during the time period 1994-1996. Our study comprised 365 cases and 397 controls. A moderate and non-significant increase in risk of

The role of n-3 polyunsaturated fatty acids in the prevention and treatment of breast cancer.

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Breast cancer (BC) is the most common cancer among women worldwide. Dietary fatty acids, especially n-3 polyunsaturated fatty acids (PUFA), are believed to play a role in reducing BC risk. Evidence has shown that fish consumption or intake of long-chain n-3 PUFA, such as eicosapentaenoic acid (EPA)
Activity and expression of fatty acid synthase (FAS), a critical enzyme in the de novo biosynthesis of fatty acids in mammals, is exquisitely sensitive to nutritional regulation of lipogenesis in liver or adipose tissue. Surprisingly, a number of studies have demonstrated hyperactivity and

Studies on the chemopreventive potentials of vegetable oils and unsaturated fatty acids against breast cancer carcinogenesis at initiation.

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The effect of dietary fat on breast cancer is a longstanding and an unresolved issue. We found that 17beta-estradiol (E2) could be activated by the epoxide-forming oxidant dimethyldioxirane (DMDO) to bind DNA-forming DNA adducts both in vitro and in vivo, and to inhibit nuclear RNA synthesis. We
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