lignans has been researched along with Adenocarcinoma* in 30 studies
30 other study(ies) available for lignans and Adenocarcinoma
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Management of adenocarcinoma with honokiol: progress so far and the way forward.
Topics: Adenocarcinoma; Biphenyl Compounds; Humans; Lignans | 2023 |
A multidimensional biosensor system to guide LUAD individualized treatment.
Lung cancer, mainly non-small cell lung cancer (NSCLC), has been a global health problem, leading to maximum cancer death. Across adenocarcinoma patients, significant genetic and phenotypic heterogeneity was identified as responsible for individual cancer drug resistance, driving an urgent need for individualized treatment. High expectation has been set on individualized treatment for better responses and extended survival. There are pressing needs for and significant advantages of testing dosages and drugs directly on patient-specific cancer cells for preclinical drug testing and personalized drug selection. Monitoring the drug response based on patient-derived cells (PDCs) is a step toward effective drug development and individualized treatment. Despite the dependence on optical labels, optical equipment, and other complex manual operation, we here report a multidimensional biosensor system to guide adenocarcinoma individualized treatment by integrating 2D and 3D PDC models and cellular impedance biosensors. The cellular impedance biosensors were applied to quantitate drug response in 2D and 3D environments. Compared with 2D plate culture, 3D cultured cells were found to show higher resistance to anti-cancer drugs. Cell-cell, cell-ECM, and mechanical interactions in the 3D environment led to stronger drug resistance. The Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Biosensing Techniques; Biphenyl Compounds; Cell Culture Techniques; Cell Movement; Cell Proliferation; Drug Resistance, Neoplasm; Drug Screening Assays, Antitumor; Humans; Lignans; Lung Neoplasms; Male; Mice; Mice, Nude; Piperidines; Precision Medicine; Quinazolines; Tumor Cells, Cultured | 2021 |
Identification of a natural compound, sesamin, as a novel TRPM8 antagonist with inhibitory effects on prostate adenocarcinoma.
Transient receptor potential melastatin 8 (TRPM8) is a calcium ion-permeable cation channel that is used as a prognostic marker and therapeutic target for different tumor types. To identify natural selective TRPM8 antagonists, we tested 158 traditional Chinese medicine (TCM) compounds for the ability to inhibit TRPM8. Calcium mobilization assays were used to evaluate the 158 TCM compound components in HEK293 cells stably expressing TRPM8. An identified putative TRPM8 antagonist, sesamin, was further evaluated. Publicly available cancer OMICS data were used to explore the expression of TRPM8, its gene regulatory network, and the survival of patients with prostate adenocarcinoma (PRAD). The cytotoxicity and specificity of sesamin to TRPM8 were tested in HEK293/TRPM8 cells. The effect of sesamin on cell proliferation in PRAD cell lines was assessed. Sesamin selectively inhibited TRPM8 in HEK293/TRPM8 cells (IC50: 9.78 μM), and a molecular docking study confirmed the binding of sesamin to TRPM8. TRPM8 was highly overexpressed in PRAD, and high TRPM8 expression was associated with poor survival of PRAD patients. Functional network analysis suggested that TRPM8 has key effects on proliferation, survival, and invasion of prostate cancer cells. Cell proliferation assays supported these findings and showed that sesamin inhibited the proliferation of PRAD cell lines DU145 and LNCaP cells. These data revealed that abnormal TRPM8 expression is associated with PRAD and that sesamin is a new anti-PRAD candidate drug, exerting inhibitory effects on TRPM8. Topics: Adenocarcinoma; Cell Line, Tumor; Cell Proliferation; Dioxoles; HEK293 Cells; Humans; Lignans; Male; Molecular Docking Simulation; Molecular Structure; Prostatic Neoplasms; TRPM Cation Channels | 2020 |
Near IR responsive targeted integrated lipid polymer nanoconstruct for enhanced magnolol cytotoxicity in breast cancer.
Advances in cancer nanotechnology aim at improving specificity and effectiveness for tumor treatment. Amalgamation of different treatment modalities is expected to provide better cancer combating. Herein, We developed a long circulating nanocarrier comprising trastuzumab (TZB) surface modified polylactic-co-glycolic acid (PLGA) nanoparticles (NPs) co-encapsulating magnolol (Mag) and gold nanoparticles (GNPs). A modified single step nanoprecipitation method was adopted ensuring particle coating with D-α-tocopheryl polyethylene glycol 1000 succinate (TPGS) while co-encapsulating GNPs. TZB was then anchored on NPs surface using a carbodiimide chemistry. The cytotoxicity of the developed system was evaluated with and without photothermal irradiation. NPs cellular uptake was then followed using confocal microscopical imaging. A hybrid matrix composed of PLGA/TPGS and surface decorated with TZB with a conjugation efficiency of ˃65%, was confirmed via FTIR, Topics: Adenocarcinoma; Antineoplastic Agents, Phytogenic; Biphenyl Compounds; Breast Neoplasms; Cell Line, Tumor; Drug Carriers; Drug Compounding; Drug Liberation; Female; Gold; Humans; Lignans; Metal Nanoparticles; Microscopy, Confocal; Oxazines; Particle Size; Photothermal Therapy; Polylactic Acid-Polyglycolic Acid Copolymer; Proton Magnetic Resonance Spectroscopy; Spectroscopy, Fourier Transform Infrared; Surface Properties; Trastuzumab; Vitamin E | 2020 |
Inhibition of programmed death ligand 1 (PD-L1) expression in breast cancer cells by sesamin.
Programmed death ligand 1 (PD-L1) is overexpressed in some metastatic breast cancer subtypes, specifically triple-negative breast cancer (TNBC). This feature can assist in the eradication of anti-tumor immunity, thereby enhancing the survival of the tumor. This study aims to explore how sesamin affects PD-L1 expression in breast cancer cells and its related molecular mechanisms. We found high levels of expression of PD-L1 in both mRNA and protein levels in the TNBC cell line, MDA-MB231, but not in the luminal type-breast cancer cell line, MCF-7. We then demonstrated the tumor suppressive effect of sesamin, which induced the inhibition of cell proliferation in MDA-MB231 cells. Additionally, sesamin triggered PD-L1 downregulation (both mRNA and protein) through the inhibition of AKT, NF-κB and JAK/Stat signaling in MDA-MB231 cells. Moreover, the migration ability of MDA-MB231 cells was effectively diminished by sesamin via inhibition of the activation of MMP-9 and MMP-2. In summary, this study demonstrated that sesamin suppresses MDA-MB231 breast cancer cells' proliferation and migration; and decreases the expression of PD-L1 via the downregulation of AKT, NF-κB, and JAK/Stat signaling. Therefore, sesamin may be an effective alternative and novel therapeutic option for immunotherapy in breast cancer cells with high PD-L1 expression. Topics: Adenocarcinoma; B7-H1 Antigen; Biomarkers, Tumor; Breast Neoplasms; Cell Proliferation; Dioxoles; Female; Humans; Janus Kinases; Lignans; Matrix Metalloproteinase 2; Matrix Metalloproteinase 9; MCF-7 Cells; NF-kappa B; Proto-Oncogene Proteins c-akt; Signal Transduction; STAT Transcription Factors; Triple Negative Breast Neoplasms; Up-Regulation | 2020 |
Evaluation of lignan (-)-cubebin extracted from Piper cubeba on human colon adenocarcinoma cells (HT29).
The dibenzylbutyrolactone lignan (-)-cubebin, which is extracted from the seeds of the pepper Piper cubeba, has shown promise as an anti-inflammatory, analgesic, leishmanicidal, antiproliferative, and trypanocidal compound. Given the therapeutic potential of (-)-cubebin, this study aimed to investigate its safety profile by analyzing cytotoxicity, mutagenicity, cell proliferation kinetics, induction of apoptosis, and expression of pro-apoptotic genes in human colon adenocarcinoma cells (HT29) exposed to (-)-cubebin. MTT cytotoxicity assays demonstrated that (-)-cubebin was cytotoxic only at 280 µM, whereas it was not cytotoxic at 2.8, 14, or 28 µM. Data demonstrated that (-)-cubebin was not mutagenic as evidenced by a micronucleus (MN) assay, did not alter cell-growth kinetics over 4 d, and showed absence of induced apoptosis after 24 h. Further, CASP8 and CASP9 gene expression was not markedly changed in HT29 cells exposed to 28 µM or 70 µM (-)-cubebin for 12 h. Based on our observations, (-)-cubebin was cytotoxic at a concentration of 280 µM, suggesting that the use of this concentration should be avoided. However, lower concentrations exerted no apparent damaging effects, indicating that this lignan is safe to use for pharmacological purposes at certain concentrations. Topics: Adenocarcinoma; Antineoplastic Agents, Phytogenic; Apoptosis; Caspase 8; Caspase 9; Cell Proliferation; Cell Survival; Colonic Neoplasms; DNA; HT29 Cells; Humans; Lignans; Micronucleus Tests; Piper | 2016 |
Endogenous enzyme-hydrolyzed fruit of Cirsium brachycephalum: optimal source of the antiproliferative lignan trachelogenin regulating the Wnt/β-catenin signaling pathway in the SW480 colon adenocarcinoma cell line.
The molecular constituents of Cirsium brachycephalum fruits were identified, quantified and isolated for the first time. The lignan glycoside tracheloside was the main compound, which was transformed quantitatively into its aglycone trachelogenin by endogenous enzymatic treatment of the fruit. Following this transformation by high performance liquid chromatography (HPLC) hyphenated with UV and mass spectrometry (MS) detections on a quantitative basis, the enzyme-hydrolyzed fruit was found to be the richest raw material containing trachelogenin (17.2mg/g) reported to date. Thus, the enzyme-hydrolyzed fruit was used to isolate trachelogenin using preparative HPLC in order to (1) unambiguously confirm its identity by gas chromatography-MS, nuclear magnetic resonance spectroscopy and optical rotation, and (2) investigate its in vitro antiproliferative activities against the SW480 colon adenocarcinoma cell line. Trachelogenin significantly affected the phosphorylation of key proteins such as β-Catenin, c-Myc and GSK3 in the β-Catenin signaling pathway in a concentration-dependent manner. These changes account for the antiproliferative effects of trachelogenin. Topics: 4-Butyrolactone; Adenocarcinoma; Antineoplastic Agents, Phytogenic; beta Catenin; Cell Line, Tumor; Cirsium; Colonic Neoplasms; Fruit; Glycogen Synthase Kinase 3; Humans; Lignans; Molecular Structure; Proto-Oncogene Proteins c-myc; Wnt Signaling Pathway | 2015 |
A dietary pattern rich in lignans, quercetin and resveratrol decreases the risk of oesophageal cancer.
Dietary lignans, quercetin and resveratrol have oestrogenic properties, and animal studies suggest that they synergistically decrease cancer risk. A protective effect of lignans on the development of oesophageal cancer in humans has recently been demonstrated, and the present study aimed to test whether these three phytochemicals synergistically decrease the risk of oesophageal cancer. Data from a Swedish nationwide population-based case-control study that recruited 181 cases of oesophageal adenocarcinoma (OAC), 158 cases of oesophageal squamous-cell carcinoma (OSCC), 255 cases of gastro-oesophageal junctional adenocarcinoma (JAC) and 806 controls were analysed. Exposure data were collected through face-to-face interviews and questionnaires. The intake of lignans, quercetin and resveratrol was assessed using a sixty-three-item FFQ. Reduced-rank regression was used to assess a dietary pattern, and a simplified dietary pattern score was categorised into quintiles on the basis of the distribution among the control subjects. Unconditional multivariable logistic regression provided OR with 95% CI, adjusted for all the potential risk factors. A dietary pattern rich in lignans, quercetin and resveratrol was mainly characterised by a high intake of tea, wine, lettuce, mixed vegetables, tomatoes, and whole-grain bread and a low intake of milk. There were dose-dependent associations between simplified dietary pattern scores and all types of oesophageal cancer (all P for trend < 0.05). On comparing the highest quintiles with the lowest, the adjusted OR were found to be 0.24 (95% CI 0.12, 0.49) for OAC, 0.31 (95% CI 0.15, 0.65) for OSCC, and 0.49 (95% CI 0.28, 0.84) for JAC. The results of the present study indicate that a dietary pattern characterised by the intake of lignans, quercetin and resveratrol may play a protective role in the development of oesophageal cancer in the Swedish population. Topics: Adenocarcinoma; Aged; Anticarcinogenic Agents; Antineoplastic Agents, Phytogenic; Carcinoma, Squamous Cell; Case-Control Studies; Diet; Esophageal Neoplasms; Esophagus; Feeding Behavior; Female; Humans; Lignans; Logistic Models; Male; Middle Aged; Odds Ratio; Plant Extracts; Quercetin; Resveratrol; Stilbenes | 2014 |
Update on phase I studies in advanced pancreatic adenocarcinoma. Hunting in darkness?
Over the last twenty years, there is a limited number of effective cytotoxic or biological agents that managed to get approval in advanced pancreatic ductal adenocarcinoma. Despite numerous trials, investments in translational research and generally in health care, the survival of pancreatic cancer patients has improved by a few only months. This disappointing reality necessitates a better understanding of the pathogenesis of this disease and the identification of targetable alterations which might lead to development of more effective drugs or better combinations. At the 2013 Annual Meeting of the American Society of Clinical Oncology, few novel agents and new therapeutic concepts, tested in phase I studies in advanced pancreatic ductal adenocarcinoma, were presented. The first notable phase I study referred to the combination of chemotherapy with local delivery of silencing RNA against the K-ras mutation G12D, in advanced pancreatic ductal adenocarcinoma, which was well tolerated and promising (Abstract #4037). The second one referred to a combination of gemcitabine with pegylated recombinant human hyaluronidase (PEGPH20), an inhibitor of hyaluronan which as a matrix glycosaminoglycan is believed to play role in the reduced drug delivery to cancer (Abstract #4010). The other notable abstract was related to an early phase study which tested the safety and toxicity of arctigenin, a traditional herbal agent found in Arctium lappa Linné, administered as an oral formulation (GMS-01) in pancreatic ductal adenocarcinoma patient resistant to standard chemotherapy (Abstract #2559). The aforementioned early phase studies open new therapeutic approaches which deserve further testing in advanced pancreatic cancer. Topics: Adenocarcinoma; Antineoplastic Combined Chemotherapy Protocols; Clinical Trials, Phase I as Topic; Deoxycytidine; Furans; Gemcitabine; Humans; Hyaluronoglucosaminidase; Lignans; Mutation; Pancreatic Neoplasms; Polyethylene Glycols; Proto-Oncogene Proteins; Proto-Oncogene Proteins p21(ras); ras Proteins; Recombinant Proteins; RNA Interference; Treatment Outcome | 2013 |
Mechanism of arctigenin-mediated specific cytotoxicity against human lung adenocarcinoma cell lines.
The lignan arctigenin (ARG) from the herb Arctium lappa L. possesses anti-cancer activity, however the mechanism of action of ARG has been found to vary among tissues and types of cancer cells. The current study aims to gain insight into the ARG mediated mechanism of action involved in inhibiting proliferation and inducing apoptosis in lung adenocarcinoma cells. This study also delineates the cancer cell specificity of ARG by comparison with its effects on various normal cell lines. ARG selectively arrested the proliferation of cancer cells at the G0/G1 phase through the down-regulation of NPAT protein expression. This down-regulation occurred via the suppression of either cyclin E/CDK2 or cyclin H/CDK7, while apoptosis was induced through the modulation of the Akt-1-related signaling pathway. Furthermore, a GSH synthase inhibitor specifically enhanced the cytotoxicity of ARG against cancer cells, suggesting that the intracellular GSH content was another factor influencing the susceptibility of cancer cells to ARG. These findings suggest that specific cytotoxicity of ARG against lung cancer cells was explained by its selective modulation of the expression of NPAT, which is involved in histone biosynthesis. The cytotoxicity of ARG appeared to be dependent on the intracellular GSH level. Topics: Adenocarcinoma; Adenocarcinoma of Lung; Antineoplastic Agents, Phytogenic; Apoptosis; Arctium; Cell Cycle Proteins; Cell Line; Cyclin E; Cyclin-Dependent Kinase 2; Cyclins; Down-Regulation; Furans; Glutathione; Humans; Lignans; Lung Neoplasms; Nuclear Proteins; Oncogene Proteins; Phytotherapy; Plant Extracts; Proto-Oncogene Proteins c-akt; Signal Transduction | 2013 |
Dietary intake of lignans and risk of esophageal and gastric adenocarcinoma: a cohort study in Sweden.
High intake of phytoestrogen lignans has been found to be associated with decreased risk of esophageal adenocarcinoma in our previous population-based case-control study in Sweden. To further evaluate this possible association, we tested the hypothesis of an inverse association between dietary lignan intake and risk of esophageal and gastric adenocarcinoma using a prospective design. In a population-based cohort study in Sweden, 81,670 participants who were cancer-free at baseline were followed up during 1998 to 2009. All participants completed a 96-item food frequency questionnaire (FFQ), which was used to assess dietary exposure to lignans (secoisolariciresinol, matairesinol, lariciresinol, pinoresinol, medioresinol, and syringaresinol). All cases of esophageal, gastroesophageal junctional, and gastric adenocarcinoma were identified through linkage to the Swedish Cancer Register. Cox proportional hazard models were used to estimate HRs and 95% confidence intervals (CI), with adjustment for potential confounding factors. During an average follow-up of 9.9 years, a total of 211 cases were identified, including 83 cases of esophageal or junctional adenocarcinoma, and 128 cases of gastric adenocarcinoma. There was no statistically significant association between dietary intake of lignans and any of the studied adenocarcinomas. Compared with participants in the lowest quartile of lignan intake, the adjusted HR of the highest quartile was 0.96 (95% CI, 0.46-2.00; P(trend) = 0.70) for adenocarcinoma of the esophagus or gastroesophageal junction, and 0.89 (95% CI, 0.52-1.55: P(trend) = 0.78) for gastric adenocarcinoma. No clear support for a protective role of dietary intake of lignans in the development of esophageal or gastric adenocarcinoma was found. Topics: Adenocarcinoma; Aged; Aged, 80 and over; Case-Control Studies; Diet; Esophageal Neoplasms; Female; Follow-Up Studies; Humans; Lignans; Male; Middle Aged; Prognosis; Prospective Studies; Risk Factors; Stomach Neoplasms; Sweden | 2013 |
Magnolol, a natural compound, induces apoptosis of SGC-7901 human gastric adenocarcinoma cells via the mitochondrial and PI3K/Akt signaling pathways.
Gastric cancer is the fourth most commonly diagnosed cancer with the second highest mortality rate worldwide. Surgery, chemotherapy and radiation therapy are generally used for the treatment of stomach cancer but only limited clinical response is shown by these therapies and still no effectual therapy for advanced gastric adenocarcinoma patients is available. Therefore, there is a need to identify other therapeutic agents against this life-threatening disease. Plants are considered as one of the most important sources for the development of anticancer drugs. Magnolol, a natural compound possesses anticancer properties. However, effects of Magnolol on human gastric cancer remain unexplored. The effects of Magnolol on the viability of SGC-7901 cells were determined by the MTT assay. Apoptosis, mitochondrial membrane potential and cell cycle were evaluated by flow cytometry. Protein expression of Bcl-2, Bax, caspase-3 and PI3K/Akt was analysed by Western blotting. Magnolol induced morphological changes in SGC-7901 cells and its cytotoxic effects were linked with DNA damage, apoptosis and S-phase arrest in a dose-dependent manner. Magnolol triggered the mitochondrial-mediated apoptosis pathway as shown by an increased ratio of Bax/Bcl-2, dissipation of mitochondrial membrane potential (ΔΨm), and sequential activation of caspase-3 and inhibition of PI3K/Akt. Additionally, Magnolol induced autophagy in SGC-7901 cells at high concentration but was not involved in cell death. Magnolol-induced apoptosis of SGC-7901 cells involves mitochondria and PI3K/Akt-dependent pathways. These findings provide evidence that Magnolol is a promising natural compound for the treatment of gastric cancer and may represent a candidate for in vivo studies of monotherapies or combination antitumor therapies. Topics: Adenocarcinoma; Apoptosis; bcl-2-Associated X Protein; Biphenyl Compounds; Caspase 3; Cell Growth Processes; Down-Regulation; Enzyme Activation; Humans; Lignans; Mitochondria; Phosphatidylinositol 3-Kinases; Platelet Aggregation Inhibitors; Proto-Oncogene Proteins c-bcl-2; S Phase; Signal Transduction; Stomach Neoplasms | 2012 |
Dietary intake of lignans and risk of adenocarcinoma of the esophagus and gastroesophageal junction.
The strong male predominance in esophageal and gastroesophageal junctional adenocarcinoma remains unexplained. Sex hormonal influence has been suggested, but not proven. A protective role of dietary phytoestrogen lignans was hypothesized.. A Swedish nationwide population-based case-control study was conducted in 1995-1997, including 181 cases of esophageal adenocarcinoma, 255 cases of gastroesophageal junctional adenocarcinoma, 158 cases of esophageal squamous cell carcinoma, and 806 control subjects. Data on various exposures, including dietary data, were collected through personal interviews and questionnaires. Dietary intake of lignans was assessed using a food frequency questionnaire and categorized into quartiles based on the consumption among the control participants. Unconditional logistic regression was used to calculate odds ratios (ORs) with 95 % confidence intervals (CIs), including adjustment for all established risk factors.. Participants in the highest quartile of intake of lignans compared with the lowest quartile were at a decreased risk of esophageal adenocarcinoma (OR, 0.65; 95 % CI, 0.38-1.12; p for trend =0.03), gastroesophageal junctional adenocarcinoma (OR, 0.37; 95 % CI, 0.23-0.58; p for trend <0.0001), and these adenocarcinomas combined (OR, 0.45; 95 % CI, 0.31-0.67; p for trend <0.0001). No clear associations were found between lignan intake and risk of esophageal squamous cell carcinoma.. This population-based study indicates that a high dietary intake of lignans decreases the risk of adenocarcinoma of the esophagus and gastroesophageal junction. Topics: Adenocarcinoma; Aged; Carcinoma, Squamous Cell; Case-Control Studies; Diet; Esophageal Neoplasms; Esophagogastric Junction; Female; Humans; Lignans; Logistic Models; Male; Middle Aged; Odds Ratio; Phytoestrogens; Risk Factors; Stomach Neoplasms; Sweden | 2012 |
Targeting the intrinsic inflammatory pathway: honokiol exerts proapoptotic effects through STAT3 inhibition in transformed Barrett's cells.
One way to link chronic inflammation with cancer is through the intrinsic inflammatory pathway, in which genetic alterations that induce malignant transformation also produce a cancer-promoting, inflammatory microenvironment. Signal transducer and activator of transcription 3 (STAT3) contributes to the intrinsic inflammatory pathway in Barrett's esophagus. In human tumors, honokiol (a polyphenol in herbal teas) has growth-inhibitory and proapoptotic effects associated with suppressed activation of STAT3. We used human Barrett's epithelial and esophageal adenocarcinoma cell lines to determine effects of honokiol on cell number, necrosis, apoptosis, and anchorage-independent growth and to explore STAT3's role in those effects. We determined Ras activity and expression of phosphorylated ERK1/2, phosphorylated Akt, and phosphorylated STAT3 in the presence or absence of honokiol. Cells were infected with constitutively active Stat3-C to assess effects of honokiol-induced STAT3 inhibition on apoptosis. Honokiol decreased cell number and increased necrosis and apoptosis in transformed Barrett's cells, but not in nontransformed cells. In adenocarcinoma cells, honokiol also increased necrosis and apoptosis and decreased anchorage-independent growth. Within 30 min of honokiol treatment, transformed Barrett's cells decreased expression of phosphorylated STAT3; decreases in Ras activity and phosphorylated ERK1/2 expression were detected at 24 h. Infection with Stat3-C significantly reduced apoptosis after honokiol treatment. Honokiol causes necrosis and apoptosis in transformed Barrett's and esophageal adenocarcinoma cells, but not in nontransformed Barrett's cells, and the proapoptotic effects of honokiol are mediated by its inhibition of STAT3 signaling. These findings suggest a potential role for targeting the intrinsic inflammatory pathways as a therapeutic strategy to prevent Barrett's carcinogenesis. Topics: Adenocarcinoma; Antineoplastic Agents, Phytogenic; Apoptosis; Barrett Esophagus; Biphenyl Compounds; Cell Line, Tumor; Cell Transformation, Neoplastic; Esophageal Neoplasms; Humans; Lignans; Signal Transduction; STAT3 Transcription Factor | 2012 |
Dietary flavonoid and lignan intake and gastric adenocarcinoma risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study.
Several experimental studies have suggested potential anticarcinogenic effects of flavonoids, although epidemiologic evidence for the impact of dietary flavonoids on risk of gastric cancer (GC) is limited.. We investigated the association between intake of dietary flavonoids and lignans and incident GC.. The study followed 477,312 subjects (29.8% men) aged 35-70 y from 10 European countries who participated in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Validated dietary questionnaires and lifestyle information were collected at baseline. A food-composition database on flavonoids and lignans was compiled by using data from USDA and Phenol-Explorer databases.. During an average follow-up of 11 y, 683 incident GC cases (57.8% men) were mostly validated by a panel of pathologists and used in this analysis. We observed a significant inverse association between total flavonoid intake and GC risk in women (HR: 0.81; 95% CI: 0.70, 0.94; for the continuous variable after log₂ transformation) but not in men (HR: 0.97; 95% CI: 0.85, 1.09). In women, significant inverse associations with GC risk were also observed for intakes of some flavonoid subgroups (anthocyanidins, flavonols, flavones, and flavanols), particularly with intestinal type tumors for total flavonoid and flavanol intakes (P-heterogeneity < 0.1). After stratification by smoking status and sex, there was no significant heterogeneity in these associations between ever- and never-smokers.. Total dietary flavonoid intake is associated with a significant reduction in the risk of GC in women. Topics: Adenocarcinoma; Adult; Aged; Anticarcinogenic Agents; Cohort Studies; Diet; Europe; Female; Flavonoids; Follow-Up Studies; Humans; Incidence; Life Style; Lignans; Male; Middle Aged; Prospective Studies; Risk; Sex Factors; Stomach Neoplasms | 2012 |
Phenethyl caffeate benzo[kl]xanthene lignan with DNA interacting properties induces DNA damage and apoptosis in colon cancer cells.
Phenethyl caffeate benzoxanthene lignan (PCBL) is a synthetic compound with DNA interacting, antiangiogenic, antiproliferative and tumor cell death inducing abilities. Though PCBL exhibits the qualities of a prospective antitumor agent, the basic mechanism of PCBL induced cell death remains unknown. This study aims to analyze the molecular mechanisms of PCBL induced cell death in tumor cells to further substantiate its antitumor abilities.. MTT assay was used for finding cell proliferation inhibition, flow cytometric analysis for the detection of cell cycle arrest, comet assay for DNA break detection and immunofluorescence for analyzing H2AX phosphorylation. Western blot analysis was used to detect the activation of different proteins related to DNA damage response and apoptosis.. PCBL inhibited proliferation of WiDr cells more efficiently than its analog, MCBL. Comet analysis of PCBL treated WiDr cells and activity of various DNA damage response proteins such as γ-H2AX, BRCA1, ATR and Chk1 in PCBL treated cells demonstrated the DNA damaging property of PCBL. Effector molecules of apoptosis such as caspase-3, caspase-7 and caspase-9 were found activated along with PARP cleavage in PCBL treated cells, suggesting apoptosis as the main mode of cell death. PCBL induced cell death was found associated with the activation of MAPK signaling. Inhibition of ERK, one of the MAPKs, by U0126 improved the apoptosis inducing ability of PCBL.. In vitro findings suggest that PCBL works by initiating DNA damage and inducing apoptosis in cancer cells and thus could be considered for further preclinical studies. Topics: Adenocarcinoma; Antineoplastic Agents; Apoptosis; Blotting, Western; Caspases; Cell Cycle Checkpoints; Cell Death; Cell Line, Tumor; Cell Proliferation; Colonic Neoplasms; Comet Assay; DNA Damage; Flow Cytometry; Fluorescent Antibody Technique; Humans; Lignans; MAP Kinase Signaling System | 2012 |
New diterpenoids and cytotoxic and anti-inflammatory diterpenoids from Amentotaxus formosana.
Two new abietane diterpenoids, ramentoxide (1) and ramentoxidone (2) and a new icetexane diterpenoid, amentonone (3) were isolated from the barks of Amentotaxus formosana. The structures of 1-3 were determined by spectroscopic methods. Known compounds brevitaxin (4), and (+)-ferruginol (5) and ent-kaur-16-en-15-one (6) isolated from this plant revealed potent cytotoxic activity against human breast adenocarcinoma cells, MCF-7 cells with an IC(50) value of 0.08 ± 0.05 μg/mL, and significant anti-inflammatory activities, respectively. Topics: Abietanes; Adenocarcinoma; Anti-Inflammatory Agents; Antineoplastic Agents, Phytogenic; Breast Neoplasms; Cell Line, Tumor; Diterpenes; Female; Humans; Inhibitory Concentration 50; Lignans; Molecular Structure; Phytotherapy; Plant Bark; Plant Extracts; Taxaceae | 2011 |
Effects of diphyllin as a novel V-ATPase inhibitor on gastric adenocarcinoma.
The natural compound diphyllin, a cytostatic lignan isolated from Cleistanthus collinus, can dramatically inhibit the proliferation and induce the apoptosis of human gastric cancer cells, SGC7901. Our study found that diphyllin can inhibit the expression of V-ATPases in a dose-dependent manner, decrease the internal pH (pHi) and reverse the transmembrane pH gradient in SGC7901 cells. Changes of the pH gradient were positively correlated with diphyllin concentration. Further study found that diphyllin treatment caused a decrease in phospho-LRP6, but not in LRP6. β-catenin in Wnt/β-catenin signaling and its target genes, c-myc and cyclin-D1, were also decreased with the inhibition of V-ATPases. Therefore, diphyllin could be characterized as a new V-ATPase inhibitor in treating gastric cancer and inhibiting the phosphorylation of LRP6 in Wnt/β-catenin signaling. Topics: Adenocarcinoma; Animals; Apoptosis; Benzodioxoles; Cell Line, Tumor; Cell Proliferation; Dioxolanes; Enzyme Inhibitors; Extracellular Space; Humans; Hydrogen-Ion Concentration; Intracellular Space; Lignans; Low Density Lipoprotein Receptor-Related Protein-6; Mice; Mice, Inbred BALB C; Neoplasm Invasiveness; Stomach Neoplasms; Vacuolar Proton-Translocating ATPases; Xenograft Model Antitumor Assays | 2011 |
Antitumor-promoting activity of lignans: inhibition of human cytomegalovirus IE gene expression.
Chemoprevention is a promising new approach to cancer prevention. Since the beginning of chemoprevention studies, short-term in vitro models used in the study of carcinogenesis have been applied in the identification of antitumor-promoting agents.. The lignans threo-4,4'-dihydroxy-3-methoxylignan, (-)-dihydroguaiaretic acid, 4'-hydroxy-3,3',4-trimethoxylignan, 3,3',4,4'-tetramethoxylignan, 4,4'-diacetyl-3,3'-dimethoxylignan, talaumidin, heliobuphthalmin, (-)-dihydro-cubebin, and hinokinin were evaluated for their ability to inhibit human cytomegalovirus (HCMV) IE-antigen expression in lung cancer cells (A549).. Most of the evaluated compounds reduced IE-antigen expression of HCMV, the best result being obtained with 4,4'-dihydroxy-3-methoxylignan. However, a dose-dependent significant increase of IE-antigen expression was found for the derivative (-)-dihydrocubebin.. The results of this study suggest that some of these lignans might be valuable as potential cancer chemopreventive agents. Topics: Adenocarcinoma; Antineoplastic Agents; Cell Survival; Cytomegalovirus; Cytomegalovirus Infections; Gene Expression Regulation, Viral; Humans; Immediate-Early Proteins; Immunoenzyme Techniques; Lignans; Lung Neoplasms; Myristicaceae; Plant Extracts; Tumor Cells, Cultured | 2010 |
Lignans from Santalum album and their cytotoxic activities.
A new neolignan, (7R,8R)-5-O-demethylbilagrewin (1), together with four known lignans (2-5), were isolated from the heartwood of Santalum album (Santalaceae). The structure of 1 was determined by analysis of extensive spectroscopic data. The isolated compounds and derivatives were evaluated for their cytotoxic activities against HL-60 human promyelocytic leukemia cells and A549 human lung adenocarcinoma cells. Compounds 1 and 2 exhibited cytotoxicity against HL-60 cells with IC(50) values of 1.5+/-0.02 and 4.3+/-0.13 microM, and against A549 cells with IC(50) values of 13.6+/-0.32 and 19.9+/-1.27 microM, respectively. The aldehyde group of 1 and 2 was revealed to be a structural requirement for the appearance of cytotoxicity in this type of lignans. These tumor cell deaths were shown to be mediated through induction of apoptosis. Topics: Adenocarcinoma; Antineoplastic Agents, Phytogenic; Apoptosis; Cell Line, Tumor; Cytotoxins; DNA Fragmentation; Humans; Leukemia; Lignans; Lung Neoplasms; Molecular Structure; Neoplasms; Santalum | 2010 |
Biodegradable self-assembled PEG-PCL-PEG micelles for hydrophobic honokiol delivery: I. Preparation and characterization.
This study aims to develop self-assembled poly(ethylene glycol)-poly(epsilon-caprolactone)-poly(ethylene glycol) (PEG-PCL-PEG, PECE) micelles to encapsulate hydrophobic honokiol (HK) in order to overcome its poor water solubility and to meet the requirement of intravenous administration. Honokiol loaded micelles (HK-micelles) were prepared by self-assembly of PECE copolymer in aqueous solution, triggered by its amphiphilic characteristic assisted by ultrasonication without any organic solvents, surfactants and vigorous stirring. The particle size of the prepared HK-micelles measured by Malvern laser particle size analyzer were 58 nm, which is small enough to be a candidate for an intravenous drug delivery system. Furthermore, the HK-micelles could be lyophilized into powder without any adjuvant, and the re-dissolved HK-micelles are stable and homogeneous with particle size about 61 nm. Furthermore, the in vitro release profile showed a significant difference between the rapid release of free HK and the much slower and sustained release of HK-micelles. Moreover, the cytotoxicity results of blank micelles and HK-micelles showed that the PECE micelle was a safe carrier and the encapsulated HK retained its potent antitumor effect. In short, the HK-micelles were successfully prepared by an improved method and might be promising carriers for intravenous delivery of HK in cancer chemotherapy, being effective, stable, safe (organic solvent and surfactant free), and easy to produce and scale up. Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Biphenyl Compounds; Cell Growth Processes; Cell Line, Tumor; Colonic Neoplasms; Drug Delivery Systems; Drug Screening Assays, Antitumor; Drug Stability; Drugs, Chinese Herbal; Humans; Lignans; Lung Neoplasms; Mice; Micelles; Microscopy, Electron, Transmission; Particle Size; Polyesters; Polyethylene Glycols; Solubility; Sonication; X-Ray Diffraction | 2010 |
Cytostatic inhibition of cancer cell growth by lignan secoisolariciresinol diglucoside.
Our previous study demonstrated that lignan metabolites enterolactone and enterodiol inhibited colonic cancer cell growth by inducing cell cycle arrest and apoptosis. However, the dietary lignans are naturally present as glycoside precursors, such as secoisolariciresinol diglucoside (SDG), which have not been evaluated yet. This study tested the hypothesis that dietary SDG might have a different effect than its metabolites in human colonic SW480 cancer cells. Treatment with SDG at 0 to 40 μmol/L for up to 48 hours resulted in a dose- and time-dependent decrease in cell numbers, which was comparable to enterolactone. The inhibition of cell growth by SDG did not appear to be mediated by cytotoxicity, but by a cytostatic mechanism associated with an increase of cyclin A expression. Furthermore, high-performance liquid chromatography analysis indicated that SDG in the media was much more stable than enterolactone (95% of SDG survival vs 57% of enterolactone after 48-hour treatment). When the cells were treated with either enterolactone or SDG at 40 μmol/L for 48 hours, the intracellular levels of enterolactone, as measured by high-performance liquid chromatography-mass spectrometry/electron spray ionization, were about 8.3 × 10(-8) nmol per cell; but intracellular SDG or potential metabolites were undetectable. Taken together, SDG demonstrated similar effects on cell growth, cytotoxicity, and cell cycle arrest when compared with its metabolite enterolactone. However, the reliable stability and undetectable intracellular SDG in treated cells may suggest that metabolism of SDG, if exposed directly to the colonic cells, could be different from the known degradation by microorganisms in human gut. Topics: 4-Butyrolactone; Adenocarcinoma; Anticarcinogenic Agents; Butylene Glycols; Cell Cycle; Cell Line, Tumor; Chromatography, High Pressure Liquid; Colonic Neoplasms; Cyclin A; Cytostatic Agents; Dietary Carbohydrates; Dose-Response Relationship, Drug; Glucosides; Glycosides; Humans; Lignans; Mass Spectrometry | 2010 |
Different redox states in malignant and nonmalignant esophageal epithelial cells and differential cytotoxic responses to bile acid and honokiol.
Esophageal adenocarcinoma (EAC) is a highly lethal cancer in western countries. EAC cells are believed to develop from esophageal epithelial cells through complex transformation processes involving inflammation and oxidative stress. The purpose of this study was to compare the redox status of malignant and nonmalignant esophageal epithelial cells and to test their responses to bile acid-induced oxidative stress and to treatment with honokiol (HNK), a natural product with anticancer activity. We demonstrated that esophageal adenocarcinoma cells express significantly higher levels of antioxidant molecules and were resistant to reactive oxygen species (ROS) stress induced by bile acid, but were sensitive to the cytotoxic action of HNK. Mechanistic study showed that HNK caused cancer cell death by disruption of mitochondrial transmembrane potential and was correlated with cyclophilin D (CypD) expression. Inhibition of CypD by cyclosporin A or abrogation of its expression by siRNA significantly suppressed the cytotoxicity of HNK, suggesting that CypD may be a key molecule that mediates the cytotoxicity. Our study suggests that the high antioxidant capacity in EAC cells confers on them the ability to survive the oxidative microenvironment in the reflux esophagus, and that HNK is a promising compound to kill the transformed cells preferentially. Topics: Adenocarcinoma; Base Sequence; Bile Acids and Salts; Biphenyl Compounds; Cell Line, Transformed; Cyclophilins; Epithelial Cells; Esophageal Neoplasms; Esophagus; Humans; Lignans; Oxidation-Reduction; Peptidyl-Prolyl Isomerase F; RNA, Small Interfering | 2009 |
Macelignan: a new modulator of P-glycoprotein in multidrug-resistant cancer cells.
The effect of macelignan, a phytoestrogen, on P-gp function was investigated using multidrug resistant cancer cells overexpressing P-gp (NCI/ADR-RES) and the fluorescent P-gp substrates, daunorubicin and rhodamine 123. Macelignan (40 microM) increased the cellular accumulation of daunorubicin by approximately threefold in NCI/ADR-RES cells, whereas it did not alter the cellular accumulation of daunorubicin in MCF-7/sensitive cells. Similarly, the presence of macelignan also enhanced significantly (P < 0.05) the cellular accumulation of rhodamine 123 in a concentration-dependent manner in NCI/ADR-RES cells. Furthermore, cancer cells were more susceptible to the cytotoxicity of vinblastine, a P-gp substrate, in the presence of macelignan. Those results suggest that macelignan has inhibitory effects on P-gp mediated cellular efflux. However, P-gp activity did not affect the cellular accumulation of macelignan itself. Taken all together, macelignan was identified as a novel inhibitor of P-gp activity and may be a promising lead compound for the rational design of more efficacious drugs to reverse multidrug resistance in cancer. Topics: Adenocarcinoma; Analysis of Variance; Antineoplastic Agents, Phytogenic; ATP Binding Cassette Transporter, Subfamily B; Biological Transport, Active; Breast Neoplasms; Cell Line, Tumor; Cell Survival; Daunorubicin; Dose-Response Relationship, Drug; Drug Design; Drug Resistance, Multiple; Drug Resistance, Neoplasm; Drug Synergism; Female; Fluorescent Dyes; Growth Inhibitors; Humans; Lignans; Phytoestrogens; Phytotherapy; Rhodamine 123; Vinblastine | 2009 |
Inhibitory effect of nordihydroguaiaretic acid, a plant lignan, on Helicobacter pylori-associated gastric carcinogenesis in Mongolian gerbils.
Recent epidemiological studies have demonstrated that consumption of certain natural products can lower cancer risk in humans. For example, plant-derived lignans have been shown to exert chemopreventive effects against cancer in vitro and in vivo. In the present study, the effects of three such lignans, termed arctiin, arctigenin, and nordihydroguaiaretic acid (NDGA), on the proliferation of Helicobacter pylori and the prevention of H. pylori-associated gastric cancer were investigated in Mongolian gerbils. To examine the effects of arctigenin and NDGA on stomach carcinogenesis, specific pathogen-free male, 5-week-old gerbils were infected with H. pylori, administered 10 p.p.m. N-methyl-N-nitrosourea in their drinking water and fed diets containing various concentrations of lignans until they were killed after 52 weeks. At a dietary level of 0.25%, NDGA significantly decreased the incidence of gastric adenocarcinomas. Arctigenin, in contrast, failed to attenuate neoplasia at a level of 0.1%. Both NDGA and arctigenin significantly reduced serum 8-hydroxy-2'-deoxyguanosine levels at doses of 0.25 and 0.05% (NDGA), and 0.1% (arctigenin). Administration of 0.25% NDGA significantly suppressed the formation of intestinal metaplasia both in the antrum and the corpus. Although all three lignans dose-dependently inhibited the in vitro proliferation of H. pylori, there were no differences in the titers of anti-H. pylori antibodies or the amount of the H. pylori-specific urease A gene among all H. pylori-infected groups. These results suggest that NDGA might be effective for prevention of gastric carcinogenesis. The possible mechanisms appear to be related to inhibitory effects on progression of gastritis and antioxidative activity rather than direct antimicrobial influence. Topics: Adenocarcinoma; Animals; Cell Division; Disease Models, Animal; Furans; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Lignans; Male; Masoprocol; Plants; Polymerase Chain Reaction; Specific Pathogen-Free Organisms; Stomach Neoplasms; Urease | 2007 |
Chemopreventive effects of hydroxymatairesinol on uterine carcinogenesis in Donryu rats.
Hydroxymatairesinol (HMR), obtained from the heartwood of spruce (Picea abies), has been demonstrated to exert chemo-preventive effects on the development of mammary tumors in rats. To examine the influence of HMR on uterine carcinogenesis, adult Donryu rats were initiated with a single intrauterine treatment of N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG) at 11 weeks of age and fed thereafter 0, 200, or 600 ppm HMR mixed in the soy-containing diet until 15 months of age. Incidences of uterine adenocarcinoma in both 200 and 600 ppm HMR-dosed groups were significantly reduced to 11% and 15%, respectively, less than 50% of 0 ppm, at the end of the experiment (P < 0.05). A delay in the start of persistent estrus by HMR was observed at 8 months of age compared with controls given carcinogen alone. From urinalysis, HMR was metabolized mainly to enterolactone and hydroxyenterolactone. These findings suggest that HMR or its metabolites exert chemo-preventive effects in the rat ENNG-uterine carcinogenesis model. Topics: Adenocarcinoma; Animals; Anticarcinogenic Agents; Carcinogens; Dose-Response Relationship, Drug; Estrus; Feeding Behavior; Female; Lignans; Methylnitronitrosoguanidine; Rats; Uterine Neoplasms | 2004 |
Phytoestrogen tissue levels in benign prostatic hyperplasia and prostate cancer and their association with prostatic diseases.
To compare phytoestrogen tissue levels in men with small-volume benign prostatic hyperplasia (BPH), large-volume BPH, and prostate cancer (PCa).. Prostatic tissue samples of men consuming a Western diet who underwent surgery for BPH (n = 63) or PCa (n = 31) were collected and frozen at -40 degrees C. In the tissue samples, the enterolactone and genistein levels were determined in duplicate by monoclonal antibody-based immunoassays. We subsequently compared the tissue levels in patients with BPH and PCa and studied the impact of enterolactone and genistein on prostate volume.. The enterolactone tissue levels were comparable in patients with BPH and PCa and revealed no correlation to prostate volume. The genistein tissue levels tended to be lower in patients with PCa (median 8.4 ng/g dry weight) compared with the entire BPH group (11.0 ng/g dry weight; P = 0.072). In addition, the genistein tissue levels were significantly greater in men with small-volume BPH (median 20.9 ng/g dry weight) compared with those with large-volume BPH (8.8 ng/g dry weight; P = 0.023).. Our data suggest an involvement of genistein in the pathogenesis of BPH and, possibly, of PCa. The impact of enterolactone is currently unknown. Topics: 4-Butyrolactone; Adenocarcinoma; Aged; Aged, 80 and over; Diet; Genistein; Humans; Lignans; Male; Middle Aged; Organ Size; Phytoestrogens; Prostate; Prostatic Hyperplasia; Prostatic Neoplasms | 2004 |
Estrogenic activity of phenylpropanoids from Sarcomelicope megistophylla and structure determination of a new norneolignan.
Bioassay-guided fractionation of the neutral extract of the bark of Sarcomelicope megistophylla resulted in the isolation of the new nor-neolignan sarcomeginal ( 1), together with the known ailanthoidol ( 2) and (+/-)-seco-isolariciresinol ( 3). The structure of 1 was determined by spectroscopic means. Estrogenic activity of the isolated compounds was tested using estrogen receptor-positive MCF7 and estrogen receptor-negative MDA-MB-231 human mammary adenocarcinoma cell lines. Compound 3 displayed significant estrogenic activity. Topics: Adenocarcinoma; Antineoplastic Agents, Hormonal; Benzofurans; Breast Neoplasms; Dose-Response Relationship, Drug; Female; Humans; Inhibitory Concentration 50; Lignans; Lignin; Naphthols; Phytotherapy; Plant Bark; Plant Extracts; Receptors, Estrogen; Rutaceae; Tumor Cells, Cultured | 2003 |
Uptake and metabolism of hydroxymatairesinol in relation to its anticarcinogenicity in DMBA-induced rat mammary carcinoma model.
The chemopreventive effects of hydroxymatairesinol (HMR), a lignan extracted from Norway spruce (Picea abies), on the development of mammary carcinoma induced by 7,12-dimethylbenz[a]anthracene (DMBA) was studied in rats. HMR administered via diet in an average daily dose of 4.7 mg/kg body wt starting before DMBA induction reduced tumor volume and tumor growth, but no significant reduction in tumor multiplicity (number of tumors/rat) was observed. The predominant histological type in the control group was type B (well-differentiated adenocarcinoma, 78%). The proportion of type B tumors decreased to 35% in the HMR group, while the type A (poorly differentiated) and type C (atrophic) tumor proportions increased. Anticarcinogenic effects of dietary HMR (4.7 mg/kg) were also evident when the administration started after DMBA induction and was seen as growth inhibition of established tumors. Dietary HMR supplementation significantly increased serum and urinary enterolactone and HMR concentrations but had no significant effect on the uterine weight, suggesting that HMR or its major metabolite enterolactone did not have an antiestrogenic effect. Further studies are warranted to further clarify and verify HMR action and the associated mechanisms in mammary tumorigenesis. Topics: 4-Butyrolactone; 9,10-Dimethyl-1,2-benzanthracene; Adenocarcinoma; Animals; Anticarcinogenic Agents; Diet; Estrogens, Non-Steroidal; Female; Isoflavones; Lignans; Mammary Neoplasms, Experimental; Organ Size; Phytoestrogens; Plant Preparations; Rats; Rats, Sprague-Dawley; Uterus | 2001 |
Dose effects of flaxseed and its lignan on N-methyl-N-nitrosourea-induced mammary tumorigenesis in rats.
Dietary supplementation with flaxseed or its lignan secoisolariciresinol diglycoside (SDG) has reduced dimethylbenz[a]anthracene-induced mammary tumor size and number in rats. The objective of this study was to determine whether flaxseed has a dose-dependent effect on N-methyl-N-nitrosourea (MNU)-induced mammary tumor promotion and whether this effect can be attributed to its SDG. Two days after injection with MNU (50 mg/kg body wt i.p.), female Sprague-Dawley rats were fed a high-fat (20% soybean oil) AIN-93G basal diet alone (BD) or supplemented with flaxseed (2.5% F and 5% F) or SDG by gavage [SDG in 2.5% F (LSDG) and SDG in 5% F (HSDG)] for 22 weeks. Although tumors tended to be smallest in the 5% F group throughout the experimental period, flaxseed feeding did not significantly affect tumor size, multiplicity, or incidence in comparison to BD. However, there was a dose-dependent effect of SDG on tumor multiplicity. Tumor multiplicity was lowest in the HSDG group and highest in the LSDG group throughout treatment (p < 0.05), indicating that HSDG inhibited, whereas LSDG promoted, MNU-induced mammary tumor development. Tumor invasiveness and grade were decreased in all treatment groups compared with the BD (p < 0.032). Thus, although flaxseed feeding had no significant effect on tumor growth indexes, flaxseed and SDG treatment, regardless of dose, appeared to delay the progression of MNU-induced mammary tumorigenesis. Disparities between this study and previous studies on flaxseed may be related to differences in experimental design, the use and dose of a different carcinogen, and protective effects by the alpha-linolenic acid present in the BD. Topics: Adenocarcinoma; Animals; Butylene Glycols; Carcinogens; Diet; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Flax; Glucosides; Lignans; Mammary Neoplasms, Experimental; Methylnitrosourea; Phytotherapy; Random Allocation; Rats; Rats, Sprague-Dawley | 1999 |