alpha linolenic acid/cancro

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0/w-emulsion of alpha-linolenic acid stabilized with hydrophobized polysaccharide. Its effect on the growth of human colon cancer cells.

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To pursue a systemic administration of alpha-linolenic acid (ALA), which is a selective cytotoxic agent, we formulated an ALA o/w-emulsion stabilized by cholesterol-bearing pullulan (CHP-55-2.1) and trioctanoylglyceride (TriC8). This emulsion was stable even in the presence of bovine serum albumin

Colon cancer prevention with a small amount of dietary perilla oil high in alpha-linolenic acid in an animal model.

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BACKGROUND Epidemiologic and experimental studies suggest that dietary fish oil and vegetable oil high in omega-3 polyunsaturated fatty acids (PUFAs) suppress the risk of colon cancer. The optimal amount to prevent colon carcinogenesis with perilla oil high in omega-3 PUFA alpha-linolenic acid in a

Alpha-linolenic acid-enriched diacylglycerol oil does not promote tumor development in tongue and gastrointestinal tract tissues in a medium-term multi-organ carcinogenesis bioassay using male F344 rat.

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Alpha-linolenic acid (ALA)-enriched diacylglycerol (DAG) oil is an edible oil enriched with DAG (>80%) and ALA (>50%). The present study investigated whether ALA-DAG oil promotes tumorigenesis in the tongue and gastrointestinal tract, using a rat medium-term multi-organ carcinogenesis bioassay

Does alpha-linolenic acid in combination with linoleic acid influence liver metastasis and hepatic lipid peroxidation in BOP-induced pancreatic cancer in Syrian hamsters?

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Some fatty acids are reported to inhibit tumor growth of pancreatic carcinoma. However, it is still unknown if alpha-linolenic acid (ALA) and linoleic acid (LA) inhibit liver metastasis of ductal pancreatic adenocarcinoma. Therefore we studied the effect of these fatty acids on liver metastasis in

[Antitumor effects of alpha-linolenic acid on the human tumor transplanted in nude mice and on the metastasis of Vx-7 tumor in rabbit].

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Many epidemiological studies and laboratory experimentations have shown that dietary omega-6 fatty acids stimulate and omega-3 fatty acids suppress tumorigenesis. On the other hand, some reports presented that parenteral administrations of unsaturated free fatty acids such as oleic, linoleic and

Alpha-linolenic acid regulates Cox2/VEGF/MAP kinase pathway and decreases the expression of HPV oncoproteins E6/E7 through restoration of p53 and Rb expression in human cervical cancer cell lines.

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Cervical cancer represents the largest cause of mortality in women worldwide. In our previous report, we have shown how alpha-linolenic acid (ALA), an omega-3 fatty acid, regulated the growth of cervical cancer cells. The present study aimed to explore mechanistic details for the anticancer activity

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,

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

Down-regulation of malignant potential by alpha linolenic acid in human and mouse colon cancer cells.

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Omega-3 fatty acids (also called ω-3 fatty acis or n-3 fatty acid) are polyunsaturated fatty acids (PUFAs) with a double bond (C=C) at the third carbon atom from the end of the carbon chain. Numerous test tube and animal studies have shown that omega-3 fatty acids may prevent or inhibit the growth

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

Alpha linolenic acid and oleic acid additively down-regulate malignant potential and positively cross-regulate AMPK/S6 axis in OE19 and OE33 esophageal cancer cells.

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OBJECTIVE Both oleic acid (OA) and alpha-linolenic acid (ALA) have been proposed to down-regulate cell proliferation of prostate, breast, and bladder cancer cells. However, direct evidence that OA and/or ALA suppresses to the development of esophageal cancer has not been studied. Also, no previous

Dietary alpha-linolenic acid is associated with reduced risk of fatal coronary heart disease, but increased prostate cancer risk: a meta-analysis.

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The objective of this meta-analysis was to estimate quantitatively the associations between intake of alpha-linolenic acid [ALA, the (n-3) fatty acid in vegetable oils], mortality from heart disease, and the occurrence of prostate cancer in observational studies. We identified 5 prospective cohort

In vivo anti-tumor activity of a new doxorubicin conjugate via α-linolenic acid.

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The conventional chemotherapy agent, doxorubicin, is of limited clinical use because of its systemic toxicity toward normal healthy tissue. A new doxorubicin conjugate with α-linolenic acid showed good anti-tumor activity with lower toxicity than free doxorubicin and exhibited an active

Effect of an alpha-linolenic acid-rich diet on rat mammary tumor growth depends on the dietary oxidative status.

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To investigate whether the oxidative status of an 18:3(n-3) polyunsaturated fatty acid (PUFA)-enriched diet could modulate the growth of chemically induced rat mammary tumors, three independent experiments were performed. Experiments I and II examined the variation of tumor growth by addition of

Tumor growth suppression by alpha-eleostearic acid, a linolenic acid isomer with a conjugated triene system, via lipid peroxidation.

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We have previously shown that conjugated linolenic acids (CLnA) prepared by alkaline isomerization have a stronger antitumor effect than conjugated linoleic acids (CLA). In this study we have compared the suppressive effect on tumor growth of alpha-eleostearic acid (alpha-ESA, 9Z11E13E-18:3) with

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