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Flaxseed, Lignans, And Inhibiting Cancer

Flaxseed, Lignans, And Inhibiting Cancer

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Published by Aviva
Flaxseed's lignans appear to reduce the spread of prostate and breast cancer, according to recent studies (2005-2007) by researchers from Duke University, Mayo Clinic, Karolinska Institute, and other prestigious cancer research centers, ncluding the National Cancer Institute (NCI) of the National Institutes of Health (NIH). More research needs to be done to determine mechanisms and causality, but for now, clinical trials show promising results.
Flaxseed's lignans appear to reduce the spread of prostate and breast cancer, according to recent studies (2005-2007) by researchers from Duke University, Mayo Clinic, Karolinska Institute, and other prestigious cancer research centers, ncluding the National Cancer Institute (NCI) of the National Institutes of Health (NIH). More research needs to be done to determine mechanisms and causality, but for now, clinical trials show promising results.

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Published by: Aviva on Jun 07, 2007
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Pubs Related to Flaxseed AND Cancer 1: Clin Cancer Res. 2007 Feb 1;13(3):1061-7.Related Articles, LinksClick here to readFlaxseed and its lignans inhibit estradiol-induced growth, angiogenesis, and secretion of vascular endothelial growth factor in human breast cancer xenografts in vivo.Bergman Jungeström M, Thompson LU, Dabrosin C.Divison of Oncology, Faculty of Health Sciences, University Hospital, Linköping, Sweden.PURPOSE: Vascular endothelial growth factor (VEGF) is a potent stimulator of angiogenesis,which is crucial in cancer progression. We have previously shown that estradiol (E2) increasesVEGF in breast cancer. Phytoestrogens are potential compounds in breast cancer prevention andtreatment by poorly understood mechanisms. The main phytoestrogens in Western diet arelignans, and flaxseed is a rich source of the mammalian lignans enterodiol and enterolactone.EXPERIMENTAL DESIGN: In the present study, ovariectomized mice were treated withcontinuous release of E2. MCF-7 tumors were established and mice were fed with basal diet or 10% flaxseed, and two groups that were fed basal diet received daily injections with enterodiol or enterolactone (15 mg/kg body weight). RESULTS: We show that flaxseed, enterodiol, andenterolactone counteracted E2-induced growth and angiogenesis in solid tumors. Extracellular VEGF in vivo, sampled using microdialysis, in all intervention groups was significantly decreasedcompared with tumors in the basal diet group. Our in vivo findings were confirmed in vitro. Byadding enterodiol or enterolactone, E2-induced VEGF secretion in MCF-7 cells decreasedsignificantly without agonistic effects. The increased VEGF secretion by E2 in MCF-7 cellsincreased the expression of VEGF receptor-2 in umbilical vein endothelial cells, suggesting aproangiogenic effect by E2 by two different mechanisms, both of which were inhibited by theaddition of lignans. CONCLUSIONS: Our results suggest that flaxseed and its lignans havepotent antiestrogenic effects on estrogen receptor-positive breast cancer and may prove to bebeneficial in breast cancer prevention strategies in the future.Publication Types:* Research Support, Non-U.S. Gov'tPMID: 17289903 [PubMed - indexed for MEDLINE]2: Clin Transl Oncol. 2006 Nov;8(11):812-20.Related Articles, LinksHER2 (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".Menéndez JA, Vázquez-Martín A, Ropero S, Colomer R, Lupu R.Fundació d'Investigació Biomédica de Girona Dr. Josep Trueta (IdIBGi), Girona, Catalonia.Spain. javiermenendez72@yahoo.comBACKGROUND: Data derived from epidemiological and experimental studies suggest thatalphalinolenic acid (ALA; 18:3n-3), the main omega-3 polyunsaturated fatty acid (PUFA) presentin the Western diet, may have protective effects in breast cancer risk and metastatic progression.A recent pilot clinical trial assessing the effects of ALA-rich dietary flaxseed on tumor biologicalmarkers in postmenopausal patients with primary breast cancer demonstrated significantreductions in tumor growth and in HER2 (erbB-2) oncogene expression. HYPOTHESIS: Themolecular mechanism by which ALA inhibits breast cancer cell growth and metastasis formation
 
may involve a direct regulation of HER2, a well-characterized oncogene playing a key role in theetiology, progression and response to some chemo- and endocrine therapies in approximately20% of breast carcinomas. METHODS: Using HER2-specific ELISA, flow cytometry,immunofluorescence microscopy, Western blotting, RT-PCR and HER2 promoter-reporter analyses, we characterized the effects of exogenous supplementation with ALA on the expressionof HER2 oncogene, a master key player in the onset and metastasis formation of breast cancer disease. Metabolic status (MTT) assays were performed to evaluate the nature of the cytotoxicinteraction between ALA and the humanized anti-HER2 monoclonal antibody trastuzumab(Herceptin). To study these issues we used BT-474 and SKBr-3 breast cancer cells, whichnaturally exhibit amplification of the HER2 oncogene. RESULTS: ALA treatment dramaticallysuppressed the expression of HER2-coded p185Her-2/neu oncoprotein as determined by ELISA,flow cytometry, immunofluorescence microscopy and immunoblotting techniques. Interestingly,ALA-induced down-regulation of p185Her-2/neu correlated with a transcriptional response as noHER2 mRNA signal could be detected by RT-PCR upon treatment with optimal concentrations of ALA (up to 20 microM). Consistent with these findings, ALA exposure was found to dramaticallyrepress the activity of a Luciferase reporter gene driven by the HER2 promoter. Moreover, thenature of the cytotoxic interaction between ALA and trastuzumab (Herceptin) revealed asignificant synergism as assessed by MTT-based cell viability assays. CONCLUSIONS: i) Thesefindings reveal that the omega-3 PUFA ALA suppresses overexpression of HER2 oncogene at thetranscriptional level, which, in turn, interacts synergistically with anti-HER2 trastuzumab- basedimmunotherapy. ii) Our results molecularly support a recent randomized double-blind placebo-controlled clinical trial suggesting that ALA may be a potential dietary alternative or adjunct tocurrently used drugs in the management of HER2-positive breast carcinomas. iii) Considering our previous findings demonstrating the <<HER2 upregulatory actions>> of the omega-6 PUFAlinolenic acid (LA; 18:2n-6) and the <<HER2 down-regulatory actions >> of the omega-3 PUFAdocosahexaenoic acid (DHA; 22:6n-3) and of the omega-9 monounsaturated fatty acid oleic acid(OA; 18:1n-9), it is reasonable to suggest that a low omega-6/omega-3 PUFA ratio and elevatedMUFA levels, the two prominent <<fat features>> of the <<Mediterranean diet>>, should beextremely efficient at blocking HER2 expression in breast cancer cells.Publication Types:* Research Support, N.I.H., Extramural* Research Support, Non-U.S. Gov'tPMID: 17134970 [PubMed - indexed for MEDLINE]3: J Nutr. 2006 Apr;136(4):906-12.Related Articles, LinksClick here to readSesamin is one of the major precursors of mammalian lignans in sesame seed (Sesamumindicum) as observed in vitro and in rats.Liu Z, Saarinen NM, Thompson LU.Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON,M5S 3E2, Canada.Plant lignans occur in many foods, with flaxseed presently recognized as the richest source.Some plant lignans can be converted by intestinal microbiota to the mammalian lignans,enterodiol and enterolactone, which may have protective effects against hormone-relateddiseases such as breast cancer. This study determined whether plant lignans in sesame seed,particularly sesamin, could be metabolized to the mammalian lignans. The total plant lignanconcentration in sesame seed (2180 micromol/100 g) was higher than that in flaxseed (820micromol/100 g). In vitro fermentation with human fecal inoculum showed conversion of sesaminto the mammalian lignans, although at a lower rate (1.1%) compared with that of 
 
secoisolariciresinol diglucoside (57.2%). However, when fed to female Sprague-Dawley rats for 10 d, sesamin (15 mg/kg body weight) and a 10% sesame seed diet resulted in greater (P < 0.05)urinary mammalian lignan excretion (3.2 and 11.2 micromol/d, respectively), than the control (<0.05 micromol/d). We conclude that sesame seed is a rich source of mammalian lignanprecursors and sesamin is one of them. From intermediate metabolites of sesamin identified in raturine by GC-MS, a tentative metabolic pathway of sesamin to mammalian lignans is suggested.Publication Types:* Research Support, Non-U.S. Gov'tPMID: 16549449 [PubMed - indexed for MEDLINE]4: Int J Cancer. 2005 Sep 20;116(5):793-8.Related Articles, LinksClick here to readThe inhibitory effect of flaxseed on the growth and metastasis of estrogen receptor negativehuman breast cancer xenograftsis attributed to both its lignan and oil components.Wang L, Chen J, Thompson LU.Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON,Canada.Our previous studies have shown that dietary flaxseed (FS) can reduce the growth andmetastasis of human estrogen receptor negative (ER-) breast cancer in nude mice. The aims of our study were to determine (i) whether the tumor inhibitory effect of FS was due to its oil (FO),lignan secoisolariciresinol diglycoside (SDG), or both components, and (ii) whether the effect ontumor growth was related to increased lipid peroxidation. Athymic nude mice were orthotopicallyinjected with ER- breast cancer cells (MDA-MB-435) and 8 weeks later were fed either the basaldiet (BD) or BD supplemented with 10% FS, SDG, FO, or combined SDG and FO (SDG + FO) for 6 weeks. The SDG and FO levels were equivalent to the amounts in the 10% FS. Compared tothe BD group, the tumor growth rate was significantly lower (p < 0.05) in the FS, FO, and SDG +FO groups, in concordance with decreased cell proliferation and increased apoptosis; however,these did not significantly relate to the lipid peroxidation, indexed as malonaldehyde (MDA), in theprimary tumors. Lung metastasis incidence was reduced (16-70%) by all treatments, significantlyin the FS and SDG + FO groups. The distant lymph node metastasis was significantly decreased(52%) only in the FO group. Although the total metastasis incidence was lowered (42%)significantly only in the SDG + FO group, all treatment groups did not differ significantly. Inconclusion, FS reduced the growth and metastasis of established ER- human breast cancer inpart due to its lignan and FO components, and not to lipid peroxidation. (c) 2005 Wiley-Liss, Inc.PMID: 15849746 [PubMed - indexed for MEDLINE]5: Clin Cancer Res. 2005 May 15;11(10):3828-35.Related Articles, LinksClick here to readDietary flaxseed alters tumor biological markers in postmenopausal breast cancer.Thompson LU, Chen JM, Li T, Strasser-Weippl K, Goss PE.Department of Nutritional Sciences, Princess Margaret Hospital, University of Toronto, Toronto,Ontario, Canada.PURPOSE: Flaxseed, the richest source of mammalian lignan precursors, has previously beenshown to reduce the growth of tumors in rats. This study examined, in a randomized double-blindplacebo-controlled clinical trial, the effects of dietary flaxseed on tumor biological markers and

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