Search results for "TYROSINE KINASE"

showing 10 items of 362 documents

Mechanisms underlying the inhibitory effects induced by pituitary adenylate cyclase-activating peptide in mouse ileum

2005

Abstract The aim of this study was to investigate the signal transduction mechanisms underlying the inhibitory effect induced by pituitary adenylate cyclase activating peptide (PACAP-27) on the spontaneous contractile activity of longitudinal muscle of mouse ileum. Mechanical activity of ileal segments was recorded isometrically in vitro. PACAP-27 produced apamin-sensitive reduction of the amplitude of the spontaneous contractions. 9-(Tetrahydro-2-furanyl)-9H-purin-6-amine (SQ 22,536), adenylate cyclase inhibitor, or genistein and tyrphostin 25, tyrosine kinase inhibitors, had negligible effects on PACAP-27-induced inhibition. PACAP-27 effects were significantly inhibited by U-73122, phopho…

MaleIndolesPhosphodiesterase InhibitorsVasodilator AgentsMouse ileumStimulationSettore BIO/09 - FisiologiaMicechemistry.chemical_compoundInositolEnzyme InhibitorsEstrenesRyanodineRyanodine receptorProtein-Tyrosine KinasesTyrphostinsGenisteinPyrrolidinonesCell biologyPituitary adenylate cyclase-activating peptideNG-Nitroarginine Methyl EsterPituitary Adenylate Cyclase-Activating PolypeptideThapsigarginSignal transductionCyclopiazonic acidhormones hormone substitutes and hormone antagonistsMuscle ContractionBoron Compoundsendocrine systemmedicine.medical_specialtyThapsigarginMuscular inhibitionCalcium-Transporting ATPasesIn Vitro TechniquesInositol 145-triphosphateBiologyPACAP-27 (pituitary adenylate cyclase activating peptide)IleumPhospholipase CInternal medicinemedicineAnimalsPharmacologyDose-Response Relationship DrugPhospholipase CAdenineMuscle SmoothMice Inbred C57BLEndocrinologyApaminchemistryAdenylyl Cyclase InhibitorsCalciumNitric Oxide SynthaseEuropean Journal of Pharmacology
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Sorafenib in combination with intensive chemotherapy in elderly patients with acute myeloid leukemia : results from a randomized, placebo-controlled …

2013

Purpose The prognosis of elderly patients with acute myeloid leukemia (AML) is still dismal even with intensive chemotherapy. In this trial, we compared the antileukemic activity of standard induction and consolidation therapy with or without the addition of the kinase inhibitor sorafenib in elderly patients with AML. Patients and Methods All patients received standard cytarabine and daunorubicin induction (7+3 regimen) and up to two cycles of intermediate-dose cytarabine consolidation. Two hundred one patients were equally randomly assigned to receive either sorafenib or placebo between the chemotherapy cycles and subsequently for up to 1 year after the beginning of therapy. The primary ob…

MaleNiacinamideSorafenibOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentPlacebo-controlled studyMedizinPlaceboDouble-Blind MethodInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansProtein Kinase InhibitorsAgedAged 80 and overChemotherapybusiness.industryPhenylurea CompoundsConsolidation ChemotherapyMiddle AgedSorafenibSurgeryLeukemia Myeloid AcuteRegimenfms-Like Tyrosine Kinase 3OncologyTolerabilityMutationCytarabineFemalebusinessmedicine.drug
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Influence of molecular subgroups on outcome of acute myeloid leukemia with normal karyotype in 141 patients undergoing salvage allogeneic stem cell t…

2012

Based on molecular aberrations, in particular the NPM1 mutation (NPM1(mut)) and the FLT3 internal tandem duplication (Flt3-ITD), prognostic subgroups have been defined among patients with acute myeloid leukemia with normal karyotype. Whereas these subgroups are known to play an important role in outcome in first complete remission, and also in the indication for allogeneic stem cell transplantation, data are limited on their role after transplantation in advanced disease. To evaluate the role of molecular subgroups of acute myeloid leukemia with normal karyotype after allogeneic stem cell transplantation beyond first complete remission, we analyzed the data from 141 consecutive adults (medi…

MaleOncologyTransplantation Conditioningmedicine.medical_treatmentHematopoietic stem cell transplantation0302 clinical medicineRecurrenceAntineoplastic Combined Chemotherapy ProtocolsHematopoietic Stem Cell TransplantationNuclear ProteinsMyeloid leukemiaInduction ChemotherapyHematologyMiddle Aged3. Good healthFludarabineTreatment OutcomeLeukemia Myeloid030220 oncology & carcinogenesisAcute DiseaseFemaleNucleophosminmedicine.drugAdultmedicine.medical_specialtyAllogeneic transplantationAdolescentPrimary Induction FailureKaryotypeDisease-Free SurvivalYoung Adult03 medical and health sciencesInternal medicinemedicineHumansTransplantation HomologousAgedSalvage Therapybusiness.industryMinimal residual diseaseSurgeryTransplantationfms-Like Tyrosine Kinase 3Multivariate AnalysisMutationTransplantation ConditioningOriginal Articles and Brief ReportsbusinessFollow-Up Studies030215 immunology
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Five-Year Follow-up of Patients Receiving Imatinib for Chronic Myeloid Leukemia

2006

The cause of chronic myeloid leukemia (CML) is a constitutively active BCR-ABL tyrosine kinase. Imatinib inhibits this kinase, and in a short-term study was superior to interferon alfa plus cytarabine for newly diagnosed CML in the chronic phase. For 5 years, we followed patients with CML who received imatinib as initial therapy.We randomly assigned 553 patients to receive imatinib and 553 to receive interferon alfa plus cytarabine and then evaluated them for overall and event-free survival; progression to accelerated-phase CML or blast crisis; hematologic, cytogenetic, and molecular responses; and adverse events.The median follow-up was 60 months. Kaplan-Meier estimates of cumulative best …

MaleOncologymedicine.medical_specialtyFusion Proteins bcr-ablAntineoplastic AgentsKaplan-Meier EstimateChronic phase chronic myelogenous leukemiaDisease-Free SurvivalPiperazineschemistry.chemical_compoundLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesInternal medicineAntineoplastic Combined Chemotherapy ProtocolsOmacetaxine mepesuccinatemedicineHumansneoplasmsbusiness.industryPonatinibCytarabineInterferon-alphaMyeloid leukemiaImatinibGeneral MedicineProtein-Tyrosine KinasesSurvival AnalysisSurvival RateDasatinibPyrimidinesTreatment OutcomeImatinib mesylatechemistryNilotinibBenzamidesImmunologyImatinib MesylateFemalebusinessFollow-Up Studiesmedicine.drugNew England Journal of Medicine
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Differences among young adults, adults and elderly chronic myeloid leukemia patients

2014

Abstract BACKGROUND: The incidence of chronic myeloid leukemia (CML) increases with age, but it is unclear how the characteristics of the disease vary with age. In children, where CML is very rare, it presents with more aggressive features, including huge splenomegaly, higher cell count and higher blast cell percentage. PATIENTS AND METHODS: To investigate if after childhood the disease maintains or loses these characteristics of aggressiveness, we analyzed 2784 adult patients, at least 18 years old, registered by GIMEMA CML WP over a 40-year period. RESULTS: Young adults (YAs: 18-29 years old) significantly differed from adults (30-59 years old) and elderly patients (at least 60 years old)…

MalePediatricsHost responseBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Oncology; HematologyTyrosine kinase inhibitorDiseaseAntineoplastic AgentTyrosin kinase inhibitorProtein-Tyrosine Kinasehemic and lymphatic diseases80 and overAge FactorProspective StudiesYoung adultChronicBCR-ABLAged 80 and overLeukemiaIncidence (epidemiology)Chronic myeloid leukemiaAge FactorsMyeloid leukemiaHematologyMiddle AgedProtein-Tyrosine KinasesPrognosisLeukemiaOncologybcr-abl1FemaleBCR-ABL; chronic myeloid leukemia; prognosis; tyrosine kinase inhibitors; young adultsHumanAdultyoung adultsmedicine.medical_specialtyPrognosiProtein Kinase InhibitorAntineoplastic Agentschronic myeloid leukemia; bcr-abl1; Tyrosin kinase inhibitor; prognosis; young adultsNOYoung Adultchronic myeloid leukemiaLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young AdultProtein Kinase InhibitorsAgedTyrosine kinase inhibitorsAdult patientsbusiness.industrymedicine.diseaseClinical trialBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Hematology; OncologyProspective StudieBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Medicine (all); Hematology; OncologyImmunologySplenomegalyBCR-ABL PositiveBCR-ABL chronic myeloid leukemia prognosis tyrosine kinase inhibitors young adultsprognosisbusinessSpleenYoung adultsMyelogenous
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Intrinsically determined cell death of developing cortical interneurons.

2009

The cell death of inhibitory neurons, which originate far from the cortical areas to which they migrate during embryonic development, is determined autonomously rather than by competition for trophic signals from other cell types. It has long been known that apoptosis, a form of programmed cell death, eliminates young cells from developing tissues. In the field of neurobiology, it is widely believed that developmental neuronal-cell death results from cellular competition for environmentally derived survival signals that selects for an optimally sized and properly wired population of neurons. This study of developmental cell death in the mouse cortex in vivo, in vitro and after transplantati…

MaleProgrammed cell deathInterneurongenetic structuresCell SurvivalPopulationApoptosisCell CountNeocortexBiologyArticle03 medical and health sciencesMice0302 clinical medicineNeural Stem CellsInterneuronsmedicineAnimalseducationCellular Senescence030304 developmental biologybcl-2-Associated X Protein0303 health scienceseducation.field_of_studyMultidisciplinaryNeocortexMembrane GlycoproteinsCaspase 3musculoskeletal neural and ocular physiologyPyramidal CellsfungiProtein-Tyrosine KinasesCell biologyTransplantationMice Inbred C57BLmedicine.anatomical_structurenervous systemAnimals NewbornInhibitory Postsynaptic PotentialsCerebral cortexbiology.proteinFemaleCell aging030217 neurology & neurosurgeryNeurotrophinNature
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Phenotypic expression of the fibroblast growth factor receptor 3 (FGFR3) mutation P250R in a large craniosynostosis family.

1997

The craniosynostosis syndromes are a heterogeneous group of sporadic, autosomal dominant disorders with significant clinical overlap. Recently, we described a large family with autosomal dominant craniosynostosis suggestive of Saethre-Chotzen syndrome, in which linkage to the Saethre-Chotzen syndrome loci on 7p had been excluded. We now report the presence of a mutation in the fibroblast growth factor receptor 3 (FGFR3) in this family. The mutation, P250R, had been previously reported in 10 patients with non-syndromic craniosynostosis. Variable expression of this mutation is evident especially in two additional members of this family, one of whom is severely affected with pancraniosynostosi…

MaleTurkish populationGenetic LinkageBiologyMuenke syndromeCraniosynostosisVariable ExpressionCraniosynostosesGenetic linkageGeneticsmedicineHumansReceptor Fibroblast Growth Factor Type 3Genetics (clinical)GeneticsGenetic heterogeneityInfant NewbornInfantProtein-Tyrosine KinasesFibroblast growth factor receptor 3medicine.diseaseReceptors Fibroblast Growth FactorPedigreePhenotypeMutationMutation (genetic algorithm)FemaleResearch ArticleJournal of Medical Genetics
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Engineered microenvironments for synergistic VEGF - Integrin signalling during vascularization

2017

We have engineered polymer-based microenvironments that promote vasculogenesis both in vitro and in vivo through synergistic integrin-growth factor receptor signalling. Poly(ethyl acrylate) (PEA) triggers spontaneous organization of fibronectin (FN) into nanonetworks which provide availability of critical binding domains. Importantly, the growth factor binding (FNIII12-14) and integrin binding (FNIII9-10) regions are simultaneously available on FN fibrils assembled on PEA. This material platform promotes synergistic integrin/VEGF signalling which is highly effective for vascularization events in vitro with low concentrations of VEGF. VEGF specifically binds to FN fibrils on PEA compared to …

MaleVascular Endothelial Growth Factor AIntegrinsBiophysicsNeovascularization PhysiologicBioengineeringpoly(ethyl acrylate)ArticleBiomaterialsHuman Umbilical Vein Endothelial CellsImage Processing Computer-AssistedAnimalsHumansPhosphorylationExtracellular Signal-Regulated MAP KinasesFibronectinTissue EngineeringPhospholipase C gammaProtein assemblyVascularizationVEGFFibronectinsMice Inbred C57BLCellular MicroenvironmentMechanics of MaterialsFocal Adhesion Protein-Tyrosine KinasesFISICA APLICADAMutationCeramics and CompositesINGENIERIA ELECTRICAGrowth factorsProtein BindingSignal Transduction
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Perlecan-Induced Suppression of Smooth Muscle Cell Proliferation Is Mediated Through Increased Activity of the Tumor Suppressor PTEN

2004

We were interested in the elucidation of the interaction between the heparan sulfate proteoglycan, perlecan, and PTEN in the regulation of vascular smooth muscle cell (SMC) growth. We verified serum-stimulated DNA synthesis, and Akt and FAK phosphorylation were significantly reduced in SMCs overexpressing wild-type PTEN. Our previous studies showed perlecan is a potent inhibitor of serum-stimulated SMC growth. We report in the present study, compared with SMCs plated on fibronectin, serum-stimulated SMCs plated on perlecan exhibited increased PTEN activity, decreased FAK and Akt activities, and high levels of p27, consistent with SMC growth arrest. Adenoviral-mediated overexpression of cons…

MaleVascular smooth musclePhysiology:CIENCIAS MÉDICAS ::Farmacodinámica [UNESCO]Aorta ThoracicBasement MembraneCulture Media Serum-FreeMuscle Smooth VascularRats Sprague-DawleyMicePhosphorylationCells CulturedGlycosaminoglycansbiologyProtein-Tyrosine KinasesCell cycle:CIENCIAS MÉDICAS [UNESCO]musculoskeletal systemUNESCO::CIENCIAS MÉDICAS ::FarmacodinámicaUNESCO::CIENCIAS MÉDICAScardiovascular systemPhosphorylationSmooth muscle cell proliferationCardiology and Cardiovascular MedicineCell DivisionDNA ReplicationBasement membraneRecombinant Fusion ProteinsPerlecanProtein Serine-Threonine KinasesVascular injurySmooth muscle cell proliferation ; Restenosis ; Vascular injury ; Vascular development ; Basement membraneCatheterizationProto-Oncogene ProteinsAnimalsPTENProtein kinase BRestenosisCell growthVascular developmentOligonucleotides AntisenseFibronectinsRatsFibronectinFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine Kinasesbiology.proteinCancer researchHeparitin SulfateCarotid Artery InjuriesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktHeparan Sulfate ProteoglycansCirculation Research
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Evidence for the existence of FGFR1-5-HT1A heteroreceptor complexes in the midbrain raphe 5-HT system.

2015

The ascending midbrain 5-HT neurons known to contain 5-HT1A autoreceptors may be dysregulated in depression due to a reduced trophic support. With in situ proximity ligation assay (PLA) and supported by co-location of the FGFR1 and 5-HT1A immunoreactivities in midbrain raphe 5-HT cells, evidence for the existence of FGFR1–5-HT1A heteroreceptor complexes were obtained in the dorsal and median raphe nuclei of the Sprague–Dawley rat. Their existence in the rat medullary raphe RN33B cell cultures was also established. After combined FGF-2 and 8-OH-DPAT treatment, a marked and significant increase in PLA positive clusters was found in the RN33B cells. Similar results were reached upon coactivati…

Malemedicine.medical_specialtySerotoninG-protein-coupled receptorReceptor tyrosine kinaseBiophysicsHeteroreceptor complexProximity ligation assayBiologyHeteroreceptorBiochemistryMidbrainRats Sprague-DawleyG-protein-coupled receptors; Receptor tyrosine kinases; Fibroblast growth factor receptor 1; Serotonin receptors; Heteroreceptor complex; DimerizationInternal medicinemedicineFluorescence Resonance Energy TransferAnimalsHumansReceptor Fibroblast Growth Factor Type 1Serotonin receptorMolecular Biology5-HT receptorNeurons8-Hydroxy-2-(di-n-propylamino)tetralinRapheMidbrain Raphe NucleiCell BiologyFibroblast growth factor receptor 1Cell biologyRatsmedicine.anatomical_structureEndocrinologyHEK293 Cellsnervous systemGene Expression RegulationReceptor Serotonin 5-HT1AAutoreceptorFibroblast Growth Factor 2NeuronRaphe nucleiPeptidesDimerizationProtein BindingBiochemical and biophysical research communications
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