Search results for "Androstadienes"

showing 10 items of 32 documents

Adjuvant anastrozole versus exemestane versus letrozole, upfront or after 2 years of tamoxifen, in endocrine-sensitive breast cancer (FATA-GIM3): a r…

2018

Background: Uncertainty exists about the optimal schedule of adjuvant treatment of breast cancer with aromatase inhibitors and, to our knowledge, no trial has directly compared the three aromatase inhibitors anastrozole, exemestane, and letrozole. We investigated the schedule and type of aromatase inhibitors to be used as adjuvant treatment for hormone receptor-positive early breast cancer. Methods: FATA-GIM3 is a multicentre, open-label, randomised, phase 3 trial of six different treatments in postmenopausal women with hormone receptor-positive early breast cancer. Eligible patients had histologically confirmed invasive hormone receptor-positive breast cancer that had been completely remov…

OncologyReceptor ErbB-2Settore MED/06 - Oncologia Medicaletrozolelaw.inventionAdjuvant anastrozolechemistry.chemical_compound0302 clinical medicineRandomized controlled trialExemestanelawAdjuvant anastrozole; exemestane; letrozole; tamoxifen; breast cancerAntineoplastic Combined Chemotherapy Protocols030212 general & internal medicinetamoxifenAromatase InhibitorsLetrozoleHazard ratioMiddle AgedReceptors EstrogenTolerabilityOncologyChemotherapy Adjuvant030220 oncology & carcinogenesisFemaleReceptors ProgesteroneBreast NeoplasmHumanmedicine.drugmedicine.medical_specialtySocio-culturaleAnastrozoleBreast NeoplasmsAnastrozoleDisease-Free SurvivalDrug Administration Schedule03 medical and health sciencesBreast cancerbreast cancerInternal medicinemedicineAromatase InhibitorHumansAgedAntineoplastic Combined Chemotherapy ProtocolAndrostadienebusiness.industrymedicine.diseaseAndrostadieneschemistrybusinessexemestaneTamoxifen
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Inhibition of FcεRI-mediated Activation of Rat Basophilic Leukemia Cells by Clostridium difficile Toxin B (Monoglucosyltransferase)

1996

Abstract Treatment of rat basophilic leukemia (RBL) 2H3-hm1 cells with Clostridium difficile toxin B (2 ng/ml), which reportedly depolymerizes the actin cytoskeleton, blocked [3H]serotonin release induced by 2,4-dinitrophenyl-bovine serum albumin, carbachol, mastoparan, and reduced ionophore A23187-stimulated degranulation by about 55-60%. In lysates of RBL cells, toxin B 14C-glucosylated two major and one minor protein. By using two-dimensional gel electrophoresis and immunoblotting, RhoA and Cdc42 were identified as protein substrates of toxin B. In contrast to toxin B, Clostridium botulinum transferase C3 that selectively inactivates RhoA by ADP-ribosylation did not inhibit degranulation…

SerotoninRHOABacterial ToxinsClostridium difficile toxin AWasp VenomsClostridium difficile toxin BBiologyCytoplasmic GranulesTritiummedicine.disease_causeBiochemistryCell LinePhosphatidylinositol 3-KinasesBacterial ProteinsTumor Cells CulturedmedicineAnimalsEnzyme InhibitorsMolecular BiologyCalcimycinAdenosine Diphosphate RiboseClostridioides difficileReceptors IgEToxinDegranulationSerum Albumin BovineCell BiologyActin cytoskeletonMolecular biologyRatsAndrostadienesKineticsPhosphotransferases (Alcohol Group Acceptor)Leukemia Basophilic AcuteBiochemistryGlucosyltransferasesMastoparanbiology.proteinIntercellular Signaling Peptides and ProteinsClostridium botulinumCarbacholCattle24-DinitrophenolPeptidesWortmanninDinitrophenolsJournal of Biological Chemistry
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Study of the cytolethal distending toxin (CDT)-activated cell cycle checkpoint. Involvement of the CHK2 kinase.

2001

AbstractThe bacterial cytolethal distending toxin (CDT) triggers a G2/M cell cycle arrest in eukaryotic cells by inhibiting the CDC25C phosphatase-dependent CDK1 dephosphorylation and activation. We report that upon CDT treatment CDC25C is fully sequestered in the cytoplasmic compartment, an effect that is reminiscent of DNA damage-dependent checkpoint activation. We show that the checkpoint kinase CHK2, an upstream regulator of CDC25C, is phosphorylated and activated after CDT treatment. In contrast to what is observed with other DNA damaging agents, we demonstrate that the activation of CHK2 can only take place during S-phase. Use of wortmannin and caffeine suggests that this effect is no…

Intracellular FluidCell cycle checkpointCytolethal distending toxinCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiochemistryS PhaseWortmanninchemistry.chemical_compoundStructural BiologyPhosphorylation0303 health sciences030302 biochemistry & molecular biologyCell CycleCell cycleProtein-Tyrosine Kinases3. Good healthCell biologyDNA-Binding Proteinsbiological phenomena cell phenomena and immunityWortmanninG2 PhaseCytolethal distending toxinBacterial ToxinsProto-Oncogene Proteins pp60(c-src)Biophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesCell Line03 medical and health sciencesCaffeineGeneticsHumanscdc25 PhosphatasesCHEK1Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biologyCheckpoint 2 kinaseCyclin-dependent kinase 1Cell growthTumor Suppressor ProteinsCell BiologyG2-M DNA damage checkpointCDC25CAndrostadienesGenes cdcchemistryCancer researchHeLa CellsFEBS letters
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Fluticasone propionate/formoterol: a fixed-combination therapy with flexible dosage.

2014

International guidelines describe asthma control as the main outcome of asthma management. Prevention of symptoms, improved quality of life, and reduction of exacerbations are the main components, consequently decreasing health care costs. However, many of these objectives remain unmet in real life: several surveys show that a large proportion of asthmatic patients are not well controlled despite the efficacy of current available treatment. Several randomized controlled clinical trials indicate that combining inhaled corticosteroids and long-acting β2-agonists, by means of a single inhaler, greatly improves the management of the disease. The results of 9 multicenter phase III clinical studi…

medicine.medical_specialtyCombination therapyAsthma exacerbationSettore MED/10 - Malattie dell'Apparato RespiratorioSettore MED/10 - Malattie Dell'Apparato RespiratorioFluticasone propionateAsthma control; Asthma exacerbations; Fixed-combination therapy; Fluticasone propionate/formoterol; Single-aerosol inhalerAsthma controlFluticasone propionate/formoterolForced Expiratory VolumeFormoterol FumarateInternal MedicineMedicineHumansAnti-Asthmatic AgentsAsthma exacerbationsParticle SizeIntensive care medicineAsthmaFluticasonebusiness.industryInhalerNebulizers and VaporizersFixed-combination therapyAsthma control; Asthma exacerbations; Fixed-combination therapy; Fluticasone propionate/formoterol; Single-aerosol inhaler; Androstadienes; Anti-Asthmatic Agents; Asthma; Bronchodilator Agents; Drug Combinations; Ethanolamines; Fluticasone; Forced Expiratory Volume; Formoterol Fumarate; Humans; Nebulizers and Vaporizers; Particle Size; Quality of Life; Treatment Outcomemedicine.diseaseSingle-aerosol inhalerAsthmaBronchodilator AgentsAndrostadienesDrug CombinationsTreatment OutcomeTolerabilityAsthma control Asthma exacerbations Fixed-combination therapy Fluticasone propionate/formoterol Single-aerosol inhalerEthanolaminesAnesthesiaAsthma exacerbations; Asthma control; Fixed-combination therapy; Fluticasone propionate/formoterol; Single-aerosol inhalerQuality of LifeFluticasoneFormoterol FumarateFormoterolbusinessmedicine.drugEuropean journal of internal medicine
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Activation of c-Jun N-terminal kinase 1 by UV irradiation is inhibited by wortmannin without affecting c-iun expression.

1999

Activation of c-Jun N-terminal kinases (JNKs)/stress-activated protein kinases is an early response of cells upon exposure to DNA-damaging agents. JNK-mediated phosphorylation of c-Jun is currently understood to stimulate the transactivating potency of AP-1 (e.g., c-Jun/c-Fos; c-Jun/ATF-2), thereby increasing the expression of AP-1 target genes. Here we show that stimulation of JNK1 activity is not a general early response of cells exposed to genotoxic agents. Treatment of NIH 3T3 cells with UV light (UV-C) as well as with methyl methanesulfonate (MMS) caused activation of JNK1 and an increase in c-Jun protein and AP-1 binding activity, whereas antineoplastic drugs such as mafosfamide, mito…

Alkylating AgentsProto-Oncogene Proteins c-junUltraviolet RaysStimulationBiologyenvironment and public healthWortmanninTransactivationchemistry.chemical_compoundMiceAnimalsPhosphatidylinositolCollagenasesProtein kinase AMolecular BiologyCell Growth and DevelopmentMitogen-Activated Protein Kinase 1Kinasec-junJNK Mitogen-Activated Protein KinasesCell Biology3T3 CellsMethyl MethanesulfonateMolecular biologyAndrostadienesEnzyme ActivationGene Expression Regulation NeoplasticTranscription Factor AP-1chemistryCalcium-Calmodulin-Dependent Protein KinasesPhosphorylationMitogen-Activated Protein KinasesWortmanninMolecular and cellular biology
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Randomized placebo-controlled trial comparing fluticasone aqueous nasal spray in mono-therapy, fluticasone plus cetirizine, fluticasone plus monteluk…

2004

BACKGROUND: Corticosteroids are considered to be particularly effective in reducing nasal congestion and are therefore recommended as first-line treatment in allergic rhinitis patients with moderate to severe and/or persistent symptoms. OBJECTIVE: We compared the clinical efficacy of fluticasone propionate aqueous nasal spray (FPANS) 200 microg given once daily, administered in mono-therapy or combined therapy with a H1 receptor antagonist (cetirizine, CTZ) or with a leukotriene antagonist (montelukast, MSK), and the combined therapy of CTZ plus MSK in the treatment of patients affected by allergic rhinitis to Parietaria during natural pollen exposure. In addition, we examined the effect of…

CyclopropanesMaleAllergySettore MED/09 - Medicina Internamedicine.medical_treatmentseasonal allergic rhinitisAcetatesGastroenterologyImmunology and AllergyMedicineChildFluticasonepollen seasonRandomized placebo-controlled trialBlood Proteinsrespiratory systemEosinophil Granule ProteinsMiddle AgedCetirizineAnesthesiamontelukastHistamine H1 AntagonistsQuinolineseosinophil cationic proteinDrug Therapy CombinationFemaleeosinophilsmedicine.symptommedicine.drugAdultmedicine.medical_specialtyAdolescentImmunologyNasal congestionSulfidesPlaceboFluticasone propionateDrug Administration ScheduleRibonucleasesDouble-Blind MethodInternal medicineHumansRandomized placebo-controlled trial; fluticasone; cetirizine; montelukast; seasonal allergic rhinitisGlucocorticoidsMontelukastAdministration IntranasalAnalysis of Variancerhinorrheafluticasone propionatebusiness.industrynasal lavageRhinitis Allergic Seasonalmedicine.diseaseCetirizineAndrostadienesParietariaNasal sprayFluticasoneLeukotriene AntagonistsNasal administrationbusinessClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
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Erratum: Phase II study of sequential hormonal therapy with anastrozole/exemestane in advanced and metastatic breast cancer

2005

Hormonal therapy is the preferred systemic treatment for recurrent or metastatic, post-menopausal hormone-receptor-positive breast cancer. Previous studies have shown that there is no cross-resistance between exemestane and reversible aromatase inhibitors. Exposure to hormonal therapy does not hamper later response to chemotherapy. Patients with locally advanced or metastatic, hormonal receptor positive or unknown, breast cancer were treated with oral anastrozole, until disease progression, followed by oral exemestane until new evidence of disease progression. The primary end point of the study was clinical benefit, defined as the sum of complete responses (CR), partial responses (PR) and >…

AdultOncologyCancer Researchmedicine.medical_specialtyNeoplasms Hormone-DependentAntineoplastic Agents Hormonalmedicine.medical_treatmentAdministration OralPhases of clinical researchAnastrozoleBreast NeoplasmsAnastrozoleMetastasischemistry.chemical_compoundbreast cancerBreast cancerExemestaneInternal medicineAntineoplastic Combined Chemotherapy ProtocolsNitrilesClinical StudiesHumansMedicineAgedGynecologybusiness.industrysequential hormonal therapyCancerMiddle AgedTriazolesmedicine.diseaseMetastatic breast cancerAndrostadienesOncologychemistryChemotherapy AdjuvantHormonal therapyFemaleHormone therapyCorrigendumbusinessmedicine.drugBritish Journal of Cancer
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Regulation ofMUC1Expression in Human Mammary Cell Lines by the c-ErbB2 and Ras Signaling Pathways

2001

The MUC1 protein is a highly O-glycosylated transmembrane molecule that is expressed at the luminal surface of most glandular epithelial cells and is upregulated in carcinomas. Here, we report the effect of the activation of the c-ErbB2 --Ras pathway on the expression of the MUC1 gene in the nontumorigenic mammary cell lines MTSV1-7 and HB2 and in the malignant cell lines T47D and ZR75. Endogenous levels of MUC1 mRNA and protein in HB2 clones permanently overexpressing c-ErbB2 or V12-H-Ras were markedly reduced compared with levels in the parental cell lines. Furthermore, in transient transfection assays, the transcription of a CAT reporter construct driven by the MUC1 promoter was inhibite…

Transcription GeneticReceptor ErbB-2Recombinant Fusion ProteinsMutantDown-RegulationBreast NeoplasmsBiologyTransfectionCell LineWortmanninPhosphatidylinositol 3-Kinaseschemistry.chemical_compoundGenes ReporterTranscription (biology)Anti-apoptotic Ras signalling cascadeTumor Cells CulturedGeneticsHumansBreastPromoter Regions Geneticskin and connective tissue diseasesneoplasmsMolecular BiologyMUC1Phosphoinositide-3 Kinase InhibitorsOncogeneMucin-1Cell BiologyGeneral MedicineGenes erbB-2Molecular biologyTransmembrane proteinCell biologyAndrostadienesGenes rasGene Expression Regulationchemistryras ProteinsFemaleSignal transductionWortmanninSignal TransductionDNA and Cell Biology
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Aspidin PB, a phloroglucinol derivative, induces apoptosis in human hepatocarcinoma HepG2 cells by modulating PI3K/Akt/GSK3β pathway.

2012

Aspidin PB, a phloroglucinol derivative isolated from Dryopteris fragrans (L.) Schott, has been previously reported to exert high biological activities. In the present study, we analyzed the apoptotic mechanisms of aspidin PB on human hepatoma cell line, HepG2. Initially, aspidin PB was shown to inhibit the growth of HepG2 cells in a time and dose-dependent manner. After treatment with aspidin PB for 72 h, 48 h and 24 h using MTT assay, the IC(50) values were 10.59 μM, 20.86 μM and 46.59 μM, respectively. Aspidin PB was capable to induce apoptosis, as measured by mitochondrial membrane potential (ΔΨm), acridine orange (AO) staining and propidium iodide (PI)/annexin V-FITC double staining. T…

Carcinoma HepatocellularApoptosisBiologyPhloroglucinolToxicologyWortmanninchemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesAnnexinHumansMTT assayPropidium iodideProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationPhosphoinositide-3 Kinase InhibitorsMembrane Potential MitochondrialGlycogen Synthase Kinase 3 betaMicroscopy ConfocalAcridine orangeLiver NeoplasmsGeneral MedicineHep G2 CellsFlow CytometryMolecular biologyAndrostadieneschemistryApoptosisWortmanninProto-Oncogene Proteins c-aktSignal TransductionChemico-biological interactions
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Leptin and leptin receptor expression in asthma.

2009

Background The adipokine leptin is a potential new mediator for bronchial epithelial homeostasis. Asthma is a chronic inflammatory disease characterized by airway remodeling that might affect disease chronicity and severity. TGF-β is a tissue growth factor the dysregulation of which is associated with airway remodeling. Objective We sought to determine whether a bronchial epithelial dysfunction of the leptin/leptin receptor pathway contributes to asthma pathogenesis and severity. Methods We investigated in vitro the presence of leptin/leptin receptor on human bronchial epithelial cells. Then we studied the effect of TGF-β and fluticasone propionate on leptin receptor expression. Finally, th…

AdultLeptinMalemedicine.medical_specialtyPyridinesMorpholinesImmunologyAdipokineBronchiRespiratory MucosaSettore MED/10 - Malattie Dell'Apparato RespiratorioSettore BIO/09 - FisiologiaCell LinePathogenesisTransforming Growth Factor beta1Leptin leptin receptor severe asthma epithelium TGF-b remodelingInternal medicineImmunology and AllergyMedicineHumansEnzyme InhibitorsReceptorCell ProliferationLeptin receptorbusiness.industryTumor Necrosis Factor-alphaLeptindigestive oral and skin physiologyImidazolesMiddle AgedEpitheliumAsthmaRecombinant Proteinsrespiratory tract diseasesAndrostadienesmedicine.anatomical_structureEndocrinologyChromonesImmunologyFluticasoneReceptors LeptinFemalebusinesshormones hormone substitutes and hormone antagonistsEx vivoTransforming growth factorThe Journal of allergy and clinical immunology
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