Search results for "sulfonamides"

showing 10 items of 160 documents

Elimination of quiescent/slow-proliferating cancer stem cells by Bcl-XL inhibition in non-small cell lung cancer

2014

Lung cancer is the most common cause of cancer-related mortality worldwide, urging the discovery of novel molecular targets and therapeutic strategies. Stem cells have been recently isolated from non-small cell lung cancer (NSCLC), thus allowing the investigation of molecular pathways specifically active in the tumorigenic population. We have found that Bcl-XL is constantly expressed by lung cancer stem cells (LCSCs) and has a prominent role in regulating LCSC survival. Whereas chemotherapeutic agents were scarcely effective against LCSC, the small molecule Bcl-2/Bcl-XL inhibitor ABT-737, but not the selective Bcl-2 inhibitor ABT-199, induced LCSC death at nanomolar concentrations. Differen…

Lung NeoplasmsMice SCIDPharmacologyPiperazinesAntineoplastic AgentNitrophenolsMiceMice Inbred NODCarcinoma Non-Small-Cell LungCytotoxic T cellNon-Small-Cell Lungeducation.field_of_studySulfonamidesTumorAnimals; Antineoplastic Agents; Biphenyl Compounds; Carcinoma Non-Small-Cell Lung; Cell Line Tumor; Cell Proliferation; Cell Survival; Female; Humans; Lung Neoplasms; Mice Inbred NOD; Mice SCID; Neoplastic Stem Cells; Nitrophenols; Piperazines; Sulfonamides; Tumor Burden; Xenograft Model Antitumor Assays; bcl-X Protein; Molecular Biology; Cell BiologyTumor BurdenAnimals; Antineoplastic Agents; Biphenyl Compounds; Carcinoma Non-Small-Cell Lung; Cell Line Tumor; Cell Proliferation; Cell Survival; Female; Humans; Lung Neoplasms; Mice Inbred NOD; Mice SCID; Neoplastic Stem Cells; Nitrophenols; Piperazines; Sulfonamides; Tumor Burden; Xenograft Model Antitumor Assays; bcl-X ProteinNeoplastic Stem CellsFemaleStem cellHumanmedicine.drugXenograft Model Antitumor AssayCell SurvivalPopulationbcl-X ProteinAntineoplastic AgentsBiologySCIDSulfonamideCell LineCancer stem cellCell Line TumormedicineAnimalsHumanseducationLung cancerPiperazineMolecular BiologyCell ProliferationSettore MED/04 - Patologia GeneraleOriginal PaperNitrophenolAnimalCell growthCarcinomaBiphenyl CompoundsCell Biologymedicine.diseaseXenograft Model Antitumor AssaysGemcitabineLung NeoplasmCell cultureBiphenyl CompoundCancer researchInbred NODNeoplastic Stem Cell
researchProduct

The novel dual PI3K/mTOR inhibitor GDC-0941 synergizes with the MEK inhibitor U0126 in non-small cell lung cancer cells.

2011

Lung cancer is a malignant disease with poor outcome, which has led to a search for new therapeutics. The PI3K/Akt/mTOR and Ras/raf/Erk pathways are key regulators of tumor growth and survival. In the present study, their roles were evaluated by MTT assay, flow cytometry and Western blotting in lung cancer cells. We found that a high efficacy of antitumor activity was shown with GDC-0941 treatment in two gefitinib-resistant non-small cell lung cancer (NSCLC) cell lines, A549 and H460. In addition, H460 cells with activating mutations of PIK3CA were relatively more sensitive to GDC-0941 than A549 cells with wild-type PIK3CA. Furthermore, GDC-0941 was highly efficacious in combination with U0…

MAPK/ERK pathwayCancer ResearchIndazolesLung NeoplasmsApoptosisBiologyBiochemistryPhosphatidylinositol 3-KinasesCarcinoma Non-Small-Cell LungCell Line TumorNitrilesGeneticsmedicineButadienesHumansMolecular BiologyProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsSulfonamidesOncogeneCell growthMEK inhibitorTOR Serine-Threonine KinasesCancerDrug SynergismCell cyclemedicine.diseaseG1 Phase Cell Cycle Checkpointsrespiratory tract diseasesEnzyme ActivationOncologyCancer researchMolecular MedicineMitogen-Activated Protein KinasesSignal TransductionMolecular medicine reports
researchProduct

Novel combination of celecoxib and proteasome inhibitor MG132 provides synergistic antiproliferative and proapoptotic effects in human liver tumor ce…

2010

Molecular targeted therapy has shown promise as a treatment for advanced hepatocellular carcinoma (HCC). Celecoxib (Celebrex®) exhibits antitumor effects in human HCC cells, and its mechanism of action is mediated either by its ability to inhibit cyclooxygenase 2 (COX-2) or by a number of various other COX-2 independent effects. Proteasome inhibitors (PIs) can exert cell growth inhibitory and apoptotic effects in different tumor cell types, including HCC cells. The present study examined the interaction between celecoxib and the PI MG132 in two human liver tumor cell lines HepG2 and HA22T/VGH. Our data showed that each inhibitor reduced proliferation and induced apoptosis in a dose-dependen…

MG132TRB3Programmed cell deathLeupeptinsBlotting WesternApoptosisUPRPharmacologyCysteine Proteinase Inhibitorschemistry.chemical_compoundMG132medicineHumansViability assayHCCMolecular BiologyCell ProliferationSettore MED/12 - GastroenterologiaGene knockdownSulfonamidesbiologyCyclooxygenase 2 InhibitorsCell growthReverse Transcriptase Polymerase Chain ReactionDrug SynergismCell BiologyHep G2 CellsCOX-2ER stress responseFlow CytometryapoptosiproteasomechemistryApoptosisCelecoxibSettore BIO/14 - Farmacologiabiology.proteinProteasome inhibitorPyrazolesCyclooxygenaseDevelopmental Biologymedicine.drug
researchProduct

Overall survival in patients with BRAF-mutant melanoma receiving encorafenib plus binimetinib versus vemurafenib or encorafenib (COLUMBUS): a multice…

2018

Summary Background Encorafenib plus binimetinib and encorafenib alone improved progression-free survival compared with vemurafenib in patients with BRAF V600 -mutant melanoma in the COLUMBUS trial. Here, we report the results of the secondary endpoint of overall survival. Methods COLUMBUS was a two-part, randomised, open-label, phase 3 study done at 162 hospitals in 28 countries. Eligible patients were aged at least 18 years with histologically confirmed, locally advanced, unresectable, or metastatic cutaneous melanoma, or unknown primary melanoma, BRAF V600E or BRAF V600K mutation, an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1, and were treatment naive or had pr…

Male0301 basic medicineOncologySkin NeoplasmsTime FactorsMedizinPhases of clinical researchGene mutationchemistry.chemical_compound0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsVemurafenibMelanomaAged 80 and overTrametinibSulfonamides10177 Dermatology ClinicBinimetinibMiddle AgedProgression-Free SurvivalPhenotypeOncologyTolerability030220 oncology & carcinogenesisDisease ProgressionFemale2730 Oncologymedicine.drugAdultProto-Oncogene Proteins B-rafmedicine.medical_specialty610 Medicine & healthYoung Adult03 medical and health sciencesInternal medicineBiomarkers TumormedicineHumansGenetic Predisposition to DiseaseProgression-free survivalProtein Kinase InhibitorsAgedPerformance statusbusiness.industry030104 developmental biologyVemurafenibchemistryMutationBenzimidazolesCarbamatesbusinessThe Lancet Oncology
researchProduct

NPC1L1 and ABCG5/8 induction explain synergistic fecal cholesterol excretion in ob/ob mice co-treated with PPAR-α and LXR agonists

2020

Reverse cholesterol transport (RCT) and transintestinal cholesterol efflux (TICE) are two important pathways for body cholesterol elimination. We studied these pathways in an animal model of diabetes and obesity (ob/ob) where HDL function is compromised as a result of hyperglycemia, low-grade inflammation and oxidative stress. Co-treatment of ob/ob mice with PPAR-α (fenofibrate) and LXR (T0901317) agonists increased fecal cholesterol by 12-fold; PPAR-α and LXR agonists individually showed 2.6- and 4.0-fold fecal cholesterol excretion, respectively. We investigated the mechanism of synergistic efficacy of PPAR-α and LXR agonists in fecal cholesterol excretion. LXR agonist and the combination…

Male0301 basic medicinemedicine.medical_specialtyHydrocarbons FluorinatedHDLLipoproteinsClinical BiochemistryMice ObeseABCA1NPC1L1Cholesterol 7 alpha-hydroxylaseExcretionFecesMiceob/ob03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFenofibrateInternal medicinemedicineAnimalsPPAR alphaTICEATP Binding Cassette Transporter Subfamily G Member 5Liver X receptorMolecular BiologyLiver X ReceptorsSulfonamidesFenofibratebiologyChemistryCholesterolATP Binding Cassette Transporter Subfamily G Member 8Reverse cholesterol transportMembrane Transport ProteinsDrug SynergismCell BiologyGeneral MedicineCholesterol030104 developmental biologyEndocrinology030220 oncology & carcinogenesisABCA1ABCG5/G8biology.proteinIntestinal cholesterol absorptionlipids (amino acids peptides and proteins)medicine.drugMolecular and Cellular Biochemistry
researchProduct

Aspirin and COX-2 Inhibitor Nimesulide Potentiate Adrenergic Contractions of Human Gastroepiploic Artery

2007

Background The aim of the present study was to evaluate the intervention of COX-1- and COX-2-derived prostaglandins in the responses of human gastroepiploic artery to sympathetic stimulation and norepinephrine. Methods Rings of human gastroepiploic artery were obtained from 45 patients (26 men and 19 women) undergoing gastrectomy. The rings were suspended in organ baths for isometric recording of tension. We studied the responses to electrical field stimulation, norepinephrine, and acetylcholine, in the absence and presence of COX-1 or COX-2 inhibition. Results The COX-1 and COX-2 inhibitor aspirin at high concentrations (10 −6 to 10 −5 mol/L) and the COX-2 inhibitor nimesulide (10 −6 mol/L…

MaleAdrenergicStimulationVasodilationGastroepiploic ArteryIn Vitro TechniquesPharmacologyInternal MedicineHumansMedicineCyclooxygenase InhibitorsSulfonamidesAspirinAspirinCyclooxygenase 2 Inhibitorsbiologybusiness.industryMembrane ProteinsAcetylcholineElectric StimulationCyclooxygenase 2Enzyme inhibitorAnesthesiaCyclooxygenase 1Prostaglandinsbiology.proteinPyrazolesFemalebusinessGastroepiploic ArteryAcetylcholinemedicine.drugNimesulideAmerican Journal of Hypertension
researchProduct

Effectiveness and safety of glecaprevir/pibrentasvir in chronic hepatitis C patients: Results of the Italian cohort of a post-marketing observational…

2021

Abstract Background and Aims The MARS post-marketing, observational study evaluates glecaprevir/pibrentasvir in a large population of Italian patients who are infected with HCV. Patients and Methods Achievement of SVR12 was the primary endpoint in the overall population and by subpopulations of interest (treatment-naive and treatment-experienced patients, subjects infected with different HCV genotype/sub-genotype, cirrhotic and non-cirrhotic patients, patients with different severity of fibrosis, patients with an APRI score ≥1, subjects with comorbidities, HIV-coinfected patients, elderly patients and people who use drugs). Safety and quality of life (assessed by SF-36 and Work Productivity…

MaleAdultmedicine.medical_specialtyPyrrolidinesQuinoxalineSustained Virologic ResponseSettore MED/12 - GASTROENTEROLOGIAPopulationAntiviral AgentselderlyBenzimidazoleGLE/PIBQuinoxalinesInternal medicineDrug CombinationClinical endpointmedicineProduct Surveillance PostmarketingHumansProspective StudieseducationAdverse effectAgedAntiviral AgentSulfonamideseducation.field_of_studyHepatologybusiness.industrySettore MED/09 - MEDICINA INTERNAGastroenterologyPWUDGlecaprevirMiddle Agedelderly; GLE/PIB; HCV; PWUDHepatitis C ChronicPibrentasvirDiscontinuationDrug CombinationsGLE/PIB; HCV; PWUD; elderlyItalyCohortHCVQuality of LifeBenzimidazolesFemaleObservational studybusiness
researchProduct

Anti-hypertensive effects of Rosuvastatin are associated with decreased inflammation and oxidative stress markers in hypertensive rats

2009

International audience; Among their pleiotropic effects, statins exert antioxidant and anti-inflammatory properties. The aim of this study was to evaluate in normotensive (WKY) and in spontaneously hypertensive rats (SHR) the effect of rosuvastatin (ROSU) treatment on (1) plasma inflammation markers and endogenous NO synthase inhibitor (ADMA) levels, (2) reactive oxygen species (ROS) generated by circulating leukocytes and (3) vascular oxidative stress and tissue inflammation markers. Plasma cytokines were higher in SHR than in WKY, except for IL-4, which was lower in SHR than in WKY. SHR monocytes exhibited higher production of ROS than did WKY monocytes. In the experimental conditions, RO…

MaleAntioxidantmedicine.medical_treatmentBlood Pressure030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryRats Inbred WKYchemistry.chemical_compound0302 clinical medicineRats Inbred SHR[SDV.IDA]Life Sciences [q-bio]/Food engineeringRosuvastatin CalciumComputingMilieux_MISCELLANEOUSchemistry.chemical_classification0303 health sciencesSulfonamidesGeneral Medicine3. Good healthNAD(P)H oxidasecardiovascular systemmedicine.symptommedicine.drugmedicine.medical_specialtyhypertensionleukocytesInflammationArgininestatins03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineAnimalsRosuvastatin[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process Engineeringcardiovascular diseasesAntihypertensive Agents030304 developmental biologyInflammationReactive oxygen speciesCholesterolNAD(P)H oxidaseNADPH OxidasescytokinesRatsFluorobenzenesOxidative StressEndocrinologyBlood pressurePyrimidineschemistryInterleukin-4Hydroxymethylglutaryl-CoA Reductase InhibitorsReactive Oxygen SpeciesOxidative stress
researchProduct

Effects of K(ATP) channel modulators on acetylcholine release from guinea-pig isolated atria and small intestine.

2002

The effects of K(ATP) channel blockers (glibenclamide, HMR 1883, HMR 1372) and openers (cromakalim, pinacidil, diazoxide) on the electrically-evoked (5 Hz) release of [(3)H]acetylcholine were studied in isolated guinea-pig atria and myenteric plexus-longitudinal muscle preparations which had been preincubated with [(3)H]choline. Atria: Cromakalim (0.3 microM and 1 microM), pinacidil (10 microM) and diazoxide (30 microM) significantly reduced the stimulation-evoked release of [(3)H]acetylcholine. The inhibition produced by cromakalim and pinacidil was prevented by 1 microM of either HMR 1883, HMR 1372 or glibenclamide. The blockers alone significantly increased the release at concentrations …

MaleCromakalimPotassium ChannelsGuinea PigsNeuromuscular JunctionMyenteric PlexusPharmacologyIn Vitro Techniqueschemistry.chemical_compoundGlyburideIntestine SmallmedicineDiazoxidePotassium Channel BlockersAnimalsChannel blockerHeart AtriaPharmacologySulfonamidesPinacidilDiazoxideThioureaPotassium channel blockerMuscle SmoothGeneral Medicinemusculoskeletal systemAtrial FunctionMyocardial ContractionHMR 1883Potassium channelAcetylcholinechemistryAnesthesiaPinacidilcardiovascular systemFemaleCromakalimAcetylcholinemedicine.drugNaunyn-Schmiedeberg's archives of pharmacology
researchProduct

Effect of hypolipidemic treatment on emerging risk factors in mixed dyslipidemia: a randomized pilot trial

2012

Background The effects of different hypolipidemic treatment strategies on emerging atherosclerosis risk factors remain unknown. Materials and methods This is a prespecified analysis of a prospective, randomized, open-label, blinded end point (PROBE) study (ClinicalTrials.gov identifier: NCT01010516). Patients (n = 100) with mixed dyslipidaemia on a standard statin dose who had not achieved lipid targets were randomized to switch to the highest dose of rosuvastatin (40 mg/day) or to add-on-statin extended release nicotinic acid (ER-NA)/laropiprant (LRPT) or to add-on-statin micronized fenofibrate for a total of 3 months. Results Following 3 months of treatment, low-density lipoprotein (LDL) …

MaleIndolesTime FactorsClinical BiochemistryPilot ProjectsPharmacologyBiochemistryGastroenterologychemistry.chemical_compoundFenofibrateRisk FactorsProspective StudiesRosuvastatin CalciumHypolipidemic AgentsSulfonamidesFenofibratebiologyGeneral MedicineMiddle AgedRosuvastatin CalciumC-Reactive ProteinCardiovascular DiseasesDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)Laropiprantmedicine.drugAdultmedicine.medical_specialtyStatinmedicine.drug_classNiacinInternal medicinemedicineHumansRosuvastatinAgedApolipoproteins BDyslipidemiasbusiness.industryCholesterolC-reactive proteinnutritional and metabolic diseasesCholesterol LDLAtherosclerosismedicine.diseaseFluorobenzenesPyrimidineschemistry1-Alkyl-2-acetylglycerophosphocholine Esterasebiology.proteinHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessDyslipidemiaEuropean Journal of Clinical Investigation
researchProduct