phytosterols and Breast-Neoplasms

While many factors are involved in the etiology of cancer, it has been clearly established that diet significantly impacts one's risk for this disease. More recently, specific food components have been identified which are uniquely beneficial in mitigating the risk of specific cancer subtypes. Plant sterols are well known for their effects on blood cholesterol levels, however research into their potential role in mitigating cancer risk remains in its infancy. As outlined in this review, the cholesterol modulating actions of plant sterols may overlap with their anti-cancer actions. Breast cancer is the most common malignancy affecting women and there remains a need for effective adjuvant therapies for this disease, for which plant sterols may play a distinctive role.

Topics: Anticholesteremic Agents; Antineoplastic Agents; Apoptosis; Breast Neoplasms; Cell Membrane; Cholesterol; Estrogens; Female; Glucose; Humans; Immunity; Inflammation; Liver X Receptors; Orphan Nuclear Receptors; Oxidative Stress; Phytosterols; Receptors, Estrogen; Risk Factors; Signal Transduction; Sitosterols

Substantial attention has been given to primary cancer prevention in daily life. Dietary factors are through to contribute to as much as one-third of the factors influencing the development of cancer. Ones of the components of a plant-based diet are beta-sitosterol and taraxasterol, compounds attracting our specific attention. This review summarizes the biological activities of presented phytosterols (anti-inflammatory, cholesterol-lowering, anti-microbial, anti-bacterial, anti-fungal effects). Our interest has been focussed especially on their anti-tumor and chemopreventive activity. They have been shown experimentally to inhibit colon and breast cancer development. They act at various stages of tumor development, including inhibition of tumorigenesis, inhibition of tumor promotion, and induction of cell differentiation. They effectively inhibit invasion of tumor cells and metastasis. With regard to toxicity, no obvious side effects of phytosterols have been observed in studies to date, with the exception of individuals with phytosterolemia. The exact mechanism by which dietary phytosterols act is not fully understood. However, some mechanisms have been offered. Therefore, they have a bright future in clinical application. Further investigation to explore their potential in tumor treatment may prove to be worthwhile.

Topics: Animals; Anti-Inflammatory Agents; Anticarcinogenic Agents; Antineoplastic Agents; Antioxidants; Breast Neoplasms; Colonic Neoplasms; Diet; Drugs, Chinese Herbal; Female; Humans; Phytosterols; Sitosterols; Sterols; Triterpenes

Researches demonstrated that gut microbiota are associated with breast cancer progression. This study aims to evaluate the anti-breast tumor effects of daucosterol linolenate (DLA), daucosterol linoleate (DL), and daucosterol palmitate (DP) from sweet potato in MCF-7 xenograft nude mice by determining the tumor growth, serum tumor markers, tumor-related proteins, and performing 16S rDNA sequencing. After treatment at 87.8 mg/kg/day for 29 days, DLA, DL and DP delayed tumor growth and decreased levels of tumor marker carcinoembryonic antigen (CEA), cancer antigen 125 (CA125) and cancer antigen 153 (CA153) in vivo. All treatments activated caspase 3, 9, PARP1 cleavage, down-regulated Ki67, VEGF, BCL-2, BCL-XL, up-regulated BAX expression, and inhibited PI3K/AKT/NF-κB activation in tumor tissues. Their anti-breast tumor effects were associated with the regulation on gut microbiota. The three treatments increased Bacteroidetes whereas decreased Firmicutes richness. They also modulated the diversity of gut microbiota at family and genus levels. Furthermore, DL treatment promoted butyric acid secretion, DP promoted acetic acid and butyric acid secretion in the colorectal and feces. Our findings indicate that DLA, DL, and DP inhibit tumor growth in MCF-7 xenograft nude mice by regulating the homeostasis of gut microbiota, producing SCFAs, and then disturbing the expression of cancer-related proteins. The present study suggests three phytosterols as gut microbiota regulator for breast cancer prevention.

Topics: Animals; Breast Neoplasms; Female; Gastrointestinal Microbiome; Heterografts; Homeostasis; Humans; Ipomoea batatas; MCF-7 Cells; Mice; Mice, Nude; Phosphatidylinositol 3-Kinases; Phytosterols; Xenograft Model Antitumor Assays

Topics: Animals; Apoptosis; Breast Neoplasms; Cell Line, Tumor; Doxorubicin; Drug Delivery Systems; Female; Humans; Hyaluronan Receptors; Hyaluronic Acid; Liposomes; Male; MCF-7 Cells; Mice, Inbred BALB C; Mice, Nude; Particle Size; Phytosterols; Polyethylene Glycols; Rats; Rats, Sprague-Dawley; Xenograft Model Antitumor Assays

Low fruit and vegetable consumption and high saturated fat consumption causes elevated circulating cholesterol and are breast cancer risk factors. During cholesterol metabolism, oxysterols form that bind and activate the liver X receptors (LXRs). Oxysterols halt breast cancer cell proliferation but enhance metastatic colonization, indicating tumour suppressing and promoting roles. Phytosterols and phytostanols in plants, like cholesterol in mammals, are essential components of the plasma membrane and biochemical precursors, and in human cells can alter LXR transcriptional activity. Here, a panel of breast cancer cell lines were treated with four dietary plant sterols and a stanol, alone or in combination with oxysterols. LXR activation and repression were measured by gene expression and LXR-luciferase reporter assays. Oxysterols activated LXR in all cell lines, but surprisingly phytosterols failed to modulate LXR activity. However, phytosterols significantly inhibited the ability of oxysterols to drive LXR transcription. These data support a role for phytosterols in modulating cancer cell behaviour via LXR, and therefore suggest merit in accurate dietary recordings of these molecules in cancer patients during treatment and perhaps supplementation to benefit recovery.

Topics: Breast Neoplasms; Cell Line, Tumor; Female; Humans; Liver X Receptors; Oxysterols; Phytosterols; Transcriptional Activation

Topics: Animals; Antineoplastic Agents; Breast Neoplasms; Cell Line, Tumor; Cell Survival; Chromatography, High Pressure Liquid; Gas Chromatography-Mass Spectrometry; Humans; Ipomoea batatas; Limit of Detection; MCF-7 Cells; Mice; Mice, Nude; Phytosterols; Plant Extracts; Regression Analysis; Xenograft Model Antitumor Assays

Previously, we observed that wild yam (Dioscorea villosa) root extract (WYRE) was able to activate GATA3 in human breast cancer cells targeting epigenome. This study aimed to find out if dioscin (DS), a bioactive compound of WYRE, can modulate GATA3 functions and cellular invasion in human breast cancer cells. MCF-7 and MDA-MB-231 cells were treated in the absence/presence of various concentrations of DS and subjected to gene analysis by RT-qPCR, immunoblotting, and immunocytochemistry. We determined the ability of MDA-MB-231 cells to migrate into wound area and examined the effects of DS on cellular invasion using invasion assay. DS reduced cell viability of both cell lines in a concentration and time-dependent manner. GATA3 expression was enhanced by DS (5.76 μM) in MDA-MB-231 cells. DS (5.76 μM)-treated MDA-MB-231 cells exhibited the morphological characteristic of epithelial-like cells; mRNA expression of DNMT3A, TET2, TET3, ZFPM2 and E-cad were increased while TET1, VIM and MMP9 were decreased. Cellular invasion of MDA-MB-231 was reduced by 65 ± 5% in the presence of 5.76 μM DS. Our data suggested that DS-mediated pathway could promote GATA3 expression at transcription and translation levels. We propose that DS has potential to be used as an anti-invasive agent in breast cancer.

Topics: Antineoplastic Agents; Breast Neoplasms; Cell Line, Tumor; Cell Survival; Dioscorea; Diosgenin; Dose-Response Relationship, Drug; Humans; MCF-7 Cells; Neoplasm Invasiveness; Phytosterols; Plant Extracts; Plant Roots; Saponins; Treatment Outcome

Topics: Anticholesteremic Agents; Breast Neoplasms; Cholesterol, LDL; Female; Humans; Phytosterols; Survivors

Phytosterols have been proposed to act as potent anticancer agents. However the mechanism of their action has not been elucidated yet. Thus, the aim of our study was to determine whether plant sterols and their thermal processing products (in physiological concentration range) could influence the viability of cancer cells and thus could be considered as positive diet complements. Additionally we decided to study potential specificity of those natural compounds against cells showing high multidrug resistance. In this study we show that the cytotoxic effect of β-sitosterol was observed in both, estrogen-dependent and estrogen-independent cells. It was also shown that the β-sitosterol was significantly more cytotoxic in cells with basal ABCB1 expression (MCF7) than in multidrug resistant NCI/ADR-RES. Surprisingly, 5a,6a-epoxysitosterol did not decrease the viability of any investigated cells but on the contrary, it provoked their increased proliferation. It was shown that oxyphytosterols blocked the cell cycle of MCF7 cells in G0/G1 phase while did not affect NCI/ADR-RES cell cycle in physiological concentration range. We also show that PgP activity (responsible for Multidrug Resistance phenomena) is inhibited by β-sitosterol. Thus, the phytosterols are supposed to act at various mechanisms but, what is most interesting, can target cells showing high multidrug resistance potential.

Topics: Antineoplastic Agents; ATP Binding Cassette Transporter, Subfamily B, Member 1; Breast Neoplasms; Cell Cycle; Cell Survival; Dose-Response Relationship, Drug; Drug Resistance, Multiple; Drug Resistance, Neoplasm; Humans; Phytosterols; Structure-Activity Relationship; Tumor Cells, Cultured; Verapamil

To perform an evaluation of selected phytochemicals intake and breast cancer (BC) risk in Mexican women.. We conducted hospital-based case-control study.. Mexico City between 1994 and 1996.. A total of 141 histologically confirmed BC cases were age-matched (+/-3 years) to an equal number of hospital controls. The reproductive history of each woman was obtained by direct interview. The dietary consumption of flavonols, flavones, flavan-3-ols, cinnamic acid, lariciresinol, pinoresinol, secoisolariciresinol, matairesinol and coumestrol was obtained by means of a validated FFQ.. Among postmenopausal women, high dietary intake of flavonols and flavones was associated with a significant reduction of BC risk (high v. low tertile: OR = 0.21, 95 % CI 0.07, 0.60, P for trend = 0.004 and OR = 0.29, 95 % CI 0.10, 0.82, P for trend = 0.025, respectively); consumption of lignans (lariciresinol and pinoresinol) showed a similar effect, but only among premenopausal women (high v. low tertile: OR = 0.32, 95 % CI 0.10, 0.99, P for trend = 0.051 and OR = 0.19, 95 % CI 0.06, 0.62, P for trend = 0.006, respectively).. Our results support a protective role of specific dietary phytochemicals in BC risk by menopausal status, independent of other reproductive factors.

Topics: Adult; Aged; Breast Neoplasms; Case-Control Studies; Diet; Diet Surveys; Feeding Behavior; Female; Flavones; Flavonols; Humans; Lignans; Mexico; Middle Aged; Odds Ratio; Phytoestrogens; Phytosterols; Postmenopause; Premenopause; Risk Factors; Surveys and Questionnaires; Young Adult

We hypothesized that the phytosterols beta-sitosterol (BSS), beta-sitosterol glucoside (BSSG), and Moducare (MC; BSS:BSSG = 99:1) could modulate the growth of estrogen-dependent human breast cancer cells in vitro and in vivo. The present study evaluated the estrogenic and antiestrogenic effects of BSS, BSSG, and MC (0.001 to 150 micromol/L) on the proliferation of Michigan Cancer Foundation 7 (MCF-7) cells in vitro. Both BSS (>1 micromol/L) and MC (>50 micromol/L) increased MCF-7 cell proliferation. Treatment with 150 micro mol/L of BSS and MC increased cell growth by 2.4 and 1.5 times, respectively, compared to the negative control (NC) group. However, BSSG had no effect at the concentrations tested. The effects of dietary BSS, BSSG, and MC on the growth of MCF-7 cells implanted in ovariectomized athymic mice were also evaluated. Estrogenic effects of the phytosterols were evaluated in the NC, BSS, BSSG, and MC treatment groups, and antiestrogenic effects were evaluated in the 17 beta-estradiol (E(2)), E(2) + BSS, E(2) + BSSG, and E(2) + MC treatment groups. Mice were treated with dietary BSS (9.8 g/kg AIN93G diet), BSSG (0.2 g/kg diet), or MC (10.0 g/kg diet) for 11 wk. Dietary BSS, BSSG, and MC did not stimulate MCF-7 tumor growth. However, dietary BSS, BSSG, and MC reduced E(2)-induced MCF-7 tumor growth by 38.9% (P < 0.05), 31.6% (P = 0.08), and 42.13% (P < 0.05), respectively. The dietary phytosterols lowered serum E(2) levels by 35.1, 30.2, and 36.5% in the E(2) + BSS, E(2) + BSSG, and E(2) + MC groups, respectively (P < 0.05), compared to that of the E(2) treatment group. Estrogen-responsive pS2 mRNA expression in tumors did not differ among groups, but expression of the antiapoptotic marker B-cell lymphoma/leukemia-2 (bcl-2) in tumors from the E(2) + MC group was downregulated, compared to that of the E(2) treatment group. In summary, BSS and MC stimulated MCF-7 cell growth in vitro. Although BSSG comprises only 1% of MC, BSSG made MC less estrogenic than BSS alone in vitro. However, dietary BSS and MC protected against E(2)-stimulated MCF-7 tumor growth and lowered circulating E(2) levels.

Topics: Animals; Breast Neoplasms; Cell Division; Cell Line, Tumor; Drug Combinations; Drug Implants; Estradiol; Estrogen Antagonists; Female; Humans; Mammary Neoplasms, Experimental; Membrane Proteins; Mice; Mice, Nude; Neoplasm Transplantation; Organ Size; Ovariectomy; Phytosterols; Presenilin-2; Proto-Oncogene Proteins c-bcl-2; Sitosterols; Uterus

Epidemiological studies suggest that dietary phytosterols may offer protection form some types of cancer including breast cancer. In an attempt to investigate the mechanism by which phytosterols offer this protection, we investigated the effect of the two most common dietary phytosterols, beta-sitosterol and campesterol, on the mevalonate and MAP Kinase (MAPK) pathways in MDA-MB-231 cells. These pathways play a role in cell growth and apoptosis. MDA-MB-231 cell line was used in this study since it is a hormone-insensitive tumor cell line which represents the majority of advanced breast cancer cases. Cells grown in the presence of 16 microM beta-sitosterol or campesterol for 3 days exhibited a 70% and 6% reduction in cell growth, respectively, while cholesterol treatment had no effect on growth as compared to the control. Studies investigating the effect of sterol supplementation on the relative and total sterol composition of cells, showed that cells supplemented with cholesterol contained 23% more cholesterol than the control. Cells supplemented with campesterol had almost one-half the cholesterol of controls but accumulated campesterol to account for 40% of the total sterols. In the case of cells supplemented with beta-sitosterol, cells had only 25% of their sterols as cholesterol and the rest was in the form of beta-sitosterol. All sterols tested equally inhibited de novo cholesterol synthesis using 14C-acetate as substrate. beta-Sitosterol supplemented cells had reduced cholesterol synthesis when using 3H-mevalonolactone as substrate, which suggests that the inhibition in this pathway is downstream of mevalonate where processes such as isoprenylation of proteins may take place. Mevalonate supplementation to cells treated with beta-sitosterol did not completely correct the observed growth inhibition by beta-sitosterol. There was no effect of sterols on the concentrations of both low (21-26 kDa) or high (44-74 kDa) molecular weight isoprenylated proteins in these cells. On the other hand, both the quantity and activity of MAPK was elevated in the cells supplemented with beta-sitosterol. These data suggest that the down regulation of cholesterol synthesis from mevalonate and stimulation of the MAPK pathway may play roles in the inhibition of MDA-MB-231 cell growth by beta-sitosterol.

Topics: Breast Neoplasms; Cell Division; Cholesterol; Humans; Mevalonic Acid; Mitogen-Activated Protein Kinases; Phytosterols; Protein Prenylation; Sitosterols; Tumor Cells, Cultured

Metastasis plays a major role in morbidity and mortality from breast cancer. Differences in the incidence and mortality of breast cancer between societies suggest that environmental factors such as diet may play a role in the disease. Previous work from this laboratory suggests that dietary phytosterols (PS) may offer protection from breast cancer by inhibiting growth of the tumor and its metastasis in severe combined immunodeficient mice. Because metastasis is a multistep process, the aim of the present study was to investigate the effect of PS on some steps of the metastatic process: tumor cell invasion, adhesion, and migration. In addition, cell growth and cell cycle progression were evaluated. MDA-MB-231 cells were supplemented with cholesterol, beta-sitosterol, and campesterol. Cells were treated for 3 days with 16 microM sterol that was loaded on 5 mM cyclodextrin. beta-Sitosterol inhibited tumor cell invasion through Matrigel and adhesion of cells to plates coated with collagen I, collagen IV, fibronectin, and laminin compared with cholesterol treatments and controls. Cholesterol treatment resulted in increased adhesion to laminin and collagen IV, two basement membrane (BM) components that are implicated in signaling tumor cell invasion in this cell line. Only cholesterol treatment increased cellular migration. beta-Sitosterol inhibited cell growth by 70% compared with controls and induced cell cycle arrest at the G2/M phase. It is concluded that, among PS, beta-sitosterol may offer protection from breast cancer metastasis by inhibiting cell invasion of the BM, which may be mediated by its ability to limit the adhesive interaction of the tumor cell and the BM.

Topics: Breast Neoplasms; Cell Adhesion; Cell Division; Cell Movement; Collagen; Collagen Type I; Collagen Type IV; Drug Combinations; Fibronectins; G2 Phase; Humans; Laminin; Mitosis; Neoplasm Invasiveness; Neoplasm Metastasis; Phytosterols; Proteoglycans; Sitosterols; Sterols; Tumor Cells, Cultured

Epidemiological and experimental studies have suggested a protective role of phytosterols (PS) in the development of some types of cancer such as colon and prostate cancer. No work has been reported on the role of PS in the development of breast cancer, the second leading cancer in woman. The present study was designed to examine the effect of the two most common dietary PS, beta-sitosterol (SIT) and campesterol, as compared to cholesterol, the main sterol in the Western diet, on growth, apoptosis and cytotoxicity of MDA-MB-231 human breast cancer cells in culture. In addition, we investigated the possible role of protein phosphatase 2A (PP2A), an enzyme that has been shown to regulate growth and apoptosis in tumor parameters studied. Breast cancer cell growth was found to be inhibited by 66% after 3 days and 80% after 5 days with 16 microM SIT. Both campesterol and cholesterol sustained tumor growth at levels comparable to that of the vehicle control. None of the sterols tested at this level (16 microM) induced cytotoxicity as measured by lactic dehydrogenase release. SIT supplementation for 3 days at 16 microM resulted in a 6-fold increase in apoptosis in cells when compared to cholesterol treated cells. SIT treatment was found to have no effect on the level and content of tumor cell PP2A. It is concluded that SIT, by a still unknown mechanism, may offer protection from breast cancer by inhibiting growth and stimulating apoptosis.

Topics: Apoptosis; Breast Neoplasms; Cell Division; Cholesterol; Dose-Response Relationship, Drug; Female; Humans; L-Lactate Dehydrogenase; Phosphoprotein Phosphatases; Phytosterols; Protein Phosphatase 2; Sitosterols; Tumor Cells, Cultured

Work from our laboratory, as well as others, suggests a protective role of phytosterols (PS), especially beta-sitosterol, from colon, prostate, and breast cancer. Asians and vegetarians consume higher amounts of PS than Western societies. The latter societies have a higher incidence of these cancers than Asians and vegetarians. The aim of this study was to evaluate peanuts and its products as sources of PS in the American diet. Roasted peanuts contain 61-114 mg PS/100 g depending on the peanut variety, 78-83% of which is in the form of beta-sitosterol. Unrefined peanut oil contains 207 mg PS/100 g, which is similar to that of the US Department of Agriculture Nutrient Database. This value is higher than that of unrefined olive oil. Refining these oils results in reduction in PS concentration in the oil. This loss is greater in the case of olive oil than peanut oil. Further refining, such as deodorization, results in significant loss in PS, but hydrogenation after refining has a minimal effect on PS loss. Peanut butter, which represents 50% of the peanuts consumed in the United States, contains 144-157 mg PS/100 g. Peanut flour, which results from partial removal of oil from peanuts, contains 55-60 mg PS/100 g. The data suggest that peanuts and its products, such as peanut oil, peanut butter, and peanut flour, are good sources of PS.

Topics: Antineoplastic Agents; Arachis; Breast Neoplasms; Colonic Neoplasms; Female; Humans; In Vitro Techniques; Male; Phytosterols; Phytotherapy; Prostatic Neoplasms; Sitosterols

To evaluate whether the protective effect associated with vegetables and fruits in breast cancer could be explained by nutrients and bioactive substances present in these plant foods, we carried out a case-control study in Uruguay including 400 cases and 405 controls. The intake of vegetables, fruits, and related nutrients was estimated with a food frequency questionnaire on 64 food items. This questionnaire allowed the calculation of total energy intake, and nutrients were calorie adjusted by the residuals method. Odds ratios for study variables were estimated by unconditional multiple logistic regression. Total vegetable, total fruit, dietary fiber, vitamin C, vitamin E, lycopene, folate, and total phytosterol intakes were inversely associated with breast cancer risk [4th quartile odds ratio for total vegetable intake = 0.41, 95% confidence interval = 0.26-0.65, p (for trend) = 0.004]. The association with total vegetable intake was not independent of lycopene intake. The results related to vegetable and nutrient intakes are consistent with antioxidant and antiestrogenic effects. This could be mediated, among other nutrients, by dietary fiber and lycopene intake. The role of other unmeasured phytochemicals, correlated with dietary fiber and lycopene intakes, cannot be ruled out.

Topics: Ascorbic Acid; Breast Neoplasms; Carotenoids; Case-Control Studies; Diet Records; Dietary Fiber; Energy Intake; Female; Folic Acid; Fruit; Humans; Lycopene; Phytosterols; Risk Factors; Surveys and Questionnaires; Uruguay; Vegetables; Vitamin E

The wood-derived compound, beta-sitosterol (purity > 90%), was shown to be estrogenic in fish. It induced the expression of the vitellogenin gene in the liver of juvenile and methyltestosterone-treated rainbow trout. Structural similarities to beta-sitosterol notwithstanding, cholesterol, citrostadienol, beta-sitostanol, and 5-androstene-3 beta,17 beta-diol, an estrogenic member of the androstenic steroid group, were inactive. An abietic acid mixture (37% abietic acid, 6% dehydroabietic acid, and a remainder of unknown compounds) showed slight hormonal activity in feed, but it was completely inactive when given intraperitoneally in implants. The estrogenic component of the abietic acid preparation was not identified. In addition, to beta-sitosterol and abietic acid, several other wood-derived compounds including betulin, isorhapontigenin, isorhapontin, and pinosylvin were estrogenic in breast cancer cells (MCF-7 or T-47D). However, betulin and pinosylvin, available in sufficient amounts for in vivo testing, did not induce the expression of the vitellogenin gene. Differences in the primary sequences of human and fish estrogen receptors (hormone as well as DNA-binding regions) or uptake and metabolism of the compounds may explain the discrepancy between the two estrogen bioassays. Wood-derived compounds such as beta-sitosterol, present in pulp and paper mill effluents, may account for the weak estrogenicity of debarking effluent seen at the vitellogenin expression bioassay.

Topics: Animals; Blotting, Northern; Breast Neoplasms; Cell Division; Estrogens; Gene Expression; Humans; Oncorhynchus mykiss; Phytosterols; RNA; Tumor Cells, Cultured; Vitellogenins; Water Pollutants, Chemical; Wood

Tissue phytosterol and cholesterol levels in 10 benign and 8 malignant breast tumors were quantitated to reexamine the hypothesis that malignant tumors had distinctive phytosterol content. Phytosterols were present in 9 of 10 benign and 7 of 8 malignant breast tumors. Mean (+/- S.E.) cholesterol, campesterol, stigmasterol, and beta-sitosterol in malignant and benign tumors (microgram/g wet weight) did not significantly differ (p greater than 0.1): (formula: see text) In the malignant tumors, tissue cholesterol correlated with campesterol (r = 0.97) and beta-sitosterol (r = 0.97) (p less than 0.01), but not stigmasterol (r = -0.06). In benign tumors, tissue cholesterol correlated with campesterol (r = 0.43), stigmasterol (r = 0.64), and beta-sitosterol (r = 0.94), with p less than 0.01 for the latter two. Phytosterols were present in four samples of normal breast tissue with mean (+/- S.E.) campesterol, stigmasterol, and beta-sitosterol (2 +/- 0.8, 15 +/- 9, 7 +/- 5 microgram/g wet weight) slightly but not significantly lower than in benign and malignant breast tumors, p greater than 0.1. The comparability of tissue phytosterols in benign and malignant breast tumors and in normal breast tissue appears to render unlikely and putative etiological relationship between phytosterols and breast carcinoma.

Topics: Adenofibroma; Aorta; Breast Neoplasms; Carcinoma; Cholesterol; Female; Humans; Phytosterols; Sitosterols; Stigmasterol

Topics: Acetates; Adenofibroma; Breast Diseases; Breast Neoplasms; Chromatography, Gas; Female; Humans; Male; Methods; Phytosterols