Search results for "indoles"

showing 10 items of 251 documents

Bis(1H-indol-2-yl)methanones are effective inhibitors of FLT3-ITD tyrosine kinase and partially overcome resistance to PKC412A in vitro.

2009

Inhibition of the mutated fms-like tyrosine kinase 3 (FLT3) receptor tyrosine kinase is a promising therapeutic strategy in acute myeloid leukaemia (AML). However, development of resistance to FLT3 tyrosine kinase inhibitors (TKI), such as PKC412A, has been described recently. This observation may have an increasing impact on the duration of response and relapse rates in upcoming clinical trials employing FLT3-TKI. Herein we investigated two representatives of a novel class of FLT3-TKI: Bis(1H-indol-2-yl)methanones. Both compounds effectively induced apoptosis in FLT3-internal tandem duplicate (ITD)-transfected murine myeloid cells and in primary FLT3-ITD positive blasts. Combination of bot…

MAPK/ERK pathwayIndolesmedicine.drug_classAntineoplastic AgentsApoptosisTransfectionTyrosine-kinase inhibitorReceptor tyrosine kinaseCell Linefluids and secretionshemic and lymphatic diseasesmedicineTumor Cells CulturedHumansProtein kinase Bbiologyhemic and immune systemsHematologyStaurosporineIn vitroLeukemia Myeloid Acutefms-Like Tyrosine Kinase 3Drug Resistance NeoplasmTandem Repeat SequencesTrk receptorembryonic structuresFms-Like Tyrosine Kinase 3Cancer researchbiology.proteinTyrosine kinasepsychological phenomena and processesBritish journal of haematology
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Imatinib dose escalation versus sunitinib as a second line treatment in KIT exon 11 mutated GIST: a retrospective analysis

2015

We retrospectively reviewed data from 123 patients (KIT exon 11 mutated) who received sunitinib or dose-escalated imatinib as second line. All patients progressed on imatinib (400 mg/die) and received a second line treatment with imatinib (800 mg/die) or sunitinib (50 mg/die 4 weeks on/2 off or 37.5 mg/day). Deletion versus other KIT 11 mutation was recorded, correlated with clinical benefits. 64% received imatinib, 36% sunitinib. KIT exon 11 mutation was available in 94 patients. With a median follow-up of 61 months, median time to progression (TTP) in patients receiving sunitinib and imatinib was 10 (95% CI 9.7–10.9) and 5 months (95% CI 3.6–6.7) respectively (P = 0.012). No difference wa…

Male0301 basic medicineIndolesTime FactorsGIST; exon 11; imatinib; second line; sunitinibGastroenterologyExon 11Exon0302 clinical medicineSecond linehemic and lymphatic diseasesSunitinibMedicineAged 80 and overGiSTSunitinibExonsMiddle AgedProto-Oncogene Proteins c-kitOncology030220 oncology & carcinogenesisDisease ProgressionImatinib MesylateFemaleResearch PaperGISTmedicine.drugAdultmedicine.medical_specialtyGastrointestinal Stromal TumorsAntineoplastic AgentsDisease-Free Survival03 medical and health sciencesInternal medicineHumansPyrrolesAgedRetrospective StudiesSecond lineSecond line treatmentDose-Response Relationship Drugbusiness.industryRetrospective cohort studyImatinibSurgery030104 developmental biologyImatinib mesylateMutationImatinibbusinessOncotarget
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Molecular mechanisms mediating the neuroprotective role of the selective estrogen receptor modulator, bazedoxifene, in acute ischemic stroke: A compa…

2017

As the knowledge on the estrogenic system in the brain grows, the possibilities to modulate it in order to afford further neuroprotection in brain damaging disorders so do it. We have previously demonstrated the ability of the selective estrogen receptor modulator, bazedoxifene (BZA), to reduce experimental ischemic brain damage. The present study has been designed to gain insight into the molecular mechanisms involved in such a neuroprotective action by investigating: 1) stroke-induced apoptotic cell death; 2) expression of estrogen receptors (ER) ERα, ERβ and the G-protein coupled estrogen receptor (GPER); and 3) modulation of MAPK/ ERK1/2 and PI3K/Akt signaling pathways. For comparison, …

Male0301 basic medicineMAPK/ERK pathwayIndolesSignaling pathwaysEndocrinology Diabetes and MetabolismClinical BiochemistryEstrogen receptorApoptosisEstrogen receptorsSecond Messenger SystemsBiochemistryBrain IschemiaReceptors G-Protein-Coupled0302 clinical medicineEndocrinologyPhosphatidylinositol PhosphatesCerebral CortexNeuronsEstradiolNeuroprotectionStrokeNeuroprotective AgentsSelective estrogen receptor modulatorReperfusion InjuryMolecular MedicineSelective estrogen receptor modulatorsGPERmedicine.medical_specialtyMAP Kinase Signaling Systemmedicine.drug_classAcute ischemic strokeNerve Tissue ProteinsBazedoxifeneBiologyNeuroprotection03 medical and health sciencesInternal medicinemedicineAnimalsEstrogen Receptor betaRats WistarMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayEstrogen Receptor alphaEstrogensCell BiologyEstrogen030104 developmental biologyEndocrinologyEstrogen030217 neurology & neurosurgeryThe Journal of Steroid Biochemistry and Molecular Biology
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Nintedanib plus docetaxel after progression on immune checkpoint inhibitor therapy: insights from VARGADO, a prospective study in patients with lung …

2019

Aim: To assess outcomes in patients with advanced adenocarcinoma non-small-cell lung cancer who received nintedanib plus docetaxel after progression on prior chemotherapy followed by immune checkpoint inhibitor (ICI) therapy. Patients & methods: VARGADO is a prospective, noninterventional study. We describe initial data from a cohort of 22 patients who received nintedanib plus docetaxel after chemotherapy and ICI therapy. Results: Median progression-free survival with nintedanib plus docetaxel was 5.5 months (95% CI: 1.9–8.7 months). The objective response rate was 7/12 (58%) and the disease control rate was 10/12 (83%). Data for overall survival rate 12 months after the start of treat…

Male0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyIndolesLung Neoplasmsmedicine.medical_treatmentAdenocarcinoma of LungAntineoplastic AgentsDocetaxelDisease-Free Survival03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCarcinoma Non-Small-Cell LungInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineClinical endpointHumansProspective StudiesLung cancerProspective cohort studyAdverse effectAgedChemotherapybusiness.industryGeneral MedicineMiddle Agedmedicine.diseaseDiscontinuationTreatment Outcome030104 developmental biologyOncologyDocetaxelchemistry030220 oncology & carcinogenesisFemaleNintedanibbusinessmedicine.drugFuture Oncology
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Effect of some indole derivatives on xenobiotic metabolism and xenobiotic-induced toxicity in cultured rat liver slices.

1999

In this study the effect of some indole derivatives on xenobiotic metabolizing enzymes and xenobiotic-induced toxicity has been examined in cultured precision-cut liver slices from male Sprague-Dawley rats. While treatment of rat liver slices for 72 hours with 2-200 microM of either indole-3-carbinol (I3C) or indole-3-acetonitrile (3-ICN) had little effect on cytochrome P-450 (CYP)-dependent enzyme activities, enzyme induction was observed after in vivo administration of I3C. The treatment of rat liver slices with 50 microM 3,3'-diindolylmethane (DIM; a dimer derived from I3C under acidic conditions) for 72 hours resulted in a marked induction of CYP-dependent enzyme activities. DIM appears…

Male33'-DiindolylmethaneAflatoxin B1IndolesCarcinogenicity TestsDiindolylmethaneIn Vitro TechniquesToxicologyXenobioticsRats Sprague-Dawleychemistry.chemical_compoundCytochrome P-450 Enzyme SystemAnimalsAnticarcinogenic AgentsDrug InteractionsEnzyme inducerMonocrotalinebiologyCytochrome P450General MedicineGlutathioneRatschemistryBiochemistryLiverToxicitybiology.proteinCarcinogensXenobioticDrug metabolismFood ScienceFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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BCL-XL inhibition induces an FGFR4-mediated rescue response in colorectal cancer

2022

The heterogeneous therapy response observed in colorectal cancer is in part due to cancer stem cells (CSCs) that resist chemotherapeutic insults. The anti-apoptotic protein BCL-XL plays a critical role in protecting CSCs from cell death, where its inhibition with high doses of BH3 mimetics can induce apoptosis. Here, we screen a compound library for synergy with low-dose BCL-XL inhibitor A-1155463 to identify pathways that regulate sensitivity to BCL-XL inhibition and reveal that fibroblast growth factor receptor (FGFR)4 inhibition effectively sensitizes to A-1155463 both in vitro and in vivo. Mechanistically, we identify a rescue response that is activated upon BCL-XL inhibition and leads …

MaleBH3 mimeticsIndolesAxitinibColonDrug Evaluation Preclinicalbcl-X Proteincolorectal cancerMice SCIDGeneral Biochemistry Genetics and Molecular BiologyresistanceMice Inbred NODstem cellsCell Line TumorBCL-XLBCL-XL FGFR4 colorectal cancer apoptosis.AnimalsHumansReceptor Fibroblast Growth Factor Type 4BenzothiazolesAgedCell DeathDrug SynergismMiddle AgedIsoquinolinesOrganoidsNeoplastic Stem CellsFGFR4FemaleMCL-1Colorectal NeoplasmsCell reports
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Involvement of CB1 and CB2 receptors in the modulation of cholinergic neurotransmission in mouse gastric preparations.

2007

Abstract While most of the studies concerning the role of cannabinoids on gastric motility have focused the attention on the gastric emptying in in vivo animal models, there is little information about the cannabinoid peripheral influence in the stomach. In addition, the functional features of CB2 receptors in the gastrointestinal tract have been poorly characterized. The purpose of the present study was to investigate the effects of cannabinoid drugs on the excitatory cholinergic and inhibitory non-adrenergic non-cholinergic (NANC) neurotransmission in mouse isolated gastric preparations. Intraluminal pressure from isolated whole stomach was recorded and mechanical responses induced by ele…

MaleCB1 receptorCannabinoid receptorIndolesmedicine.medical_treatmentGastric motilityReceptors PresynapticSettore BIO/09 - FisiologiaSynaptic TransmissionReceptor Cannabinoid CB2MicePiperidinesReceptor Cannabinoid CB1Cannabinoid receptor type 2StomachCholinergic Fiberslipids (amino acids peptides and proteins)Rimonabantmedicine.drugAgonistmedicine.medical_specialtyCarbacholmedicine.drug_classPolyunsaturated AlkamidesMorpholinesNeuromuscular JunctionArachidonic AcidsBiologyIn Vitro TechniquesNaphthalenesInternal medicineCannabinoid Receptor ModulatorsmedicineAnimalsCannabinoidPharmacologyEnteric neurotransmissionGastric emptyingCannabinoidsExcitatory Postsynaptic PotentialsCB2 receptorElectric StimulationBenzoxazinesMice Inbred C57BLEndocrinologyInhibitory Postsynaptic PotentialsCholinergicPyrazolesCannabinoidGastrointestinal MotilityGastric motilityEndocannabinoidsPharmacological research
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Association of a functional deficit of the BKCa channel, a synaptic regulator of neuronal excitability, with autism and mental retardation

2006

International audience; Objective: Autism is a complex, largely genetic psychiatric disorder. In the majority of cases, the cause of autism is not known, but there is strong evidence for a genetic etiology. To identify candidate genes, the physical mapping of balanced chromosomal aberrations is a powerful strategy, since several genes have been characterized in numerous disorders. In this study, the authors analyzed a balanced reciprocal translocation arising de novo in a subject with autism and mental retardation. Method: The authors performed the physical mapping of the balanced 9q23/ 10q22 translocation by fluorescent in situ hybridization experiments using bacterial artificial chromosom…

MaleCandidate geneChromosomes Artificial BacterialIndolesDNA Mutational AnalysisRegulatorChromosomal translocationautism mental retardation KCNMA1 genelarge conductance Ca(2+)-activated K(+) (BK(Ca)) channel synaptic transmission chromosomal translocationSynaptic TransmissionTranslocation GeneticPair 10CA2+-ACTIVATED K+ CHANNELSCloning MolecularChildLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMUTATIONIn Situ HybridizationIn Situ Hybridization FluorescenceReverse Transcriptase Polymerase Chain ReactionBacterialChromosome MappingETIOLOGYPsychiatry and Mental healthArtificialKCNMA1 Gene[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]HaploinsufficiencyPsychologyChromosomes Human Pair 9POTASSIUM CHANNELSHumanPair 9Autistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes; Artificial; Bacterial; Chromosomes; Human; Pair 10; Chromosomes; Human; Pair 9; Cloning; Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization; Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation; GeneticTranslocationNeurotransmissionChromosomesFluorescenceGeneticIntellectual DisabilitymedicineHumansAutistic DisorderRELEASEChromosome AberrationsCOMPLEXChromosomes Human Pair 10MolecularAutistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes Artificial Bacterial; Chromosomes Human Pair 10; Chromosomes Human Pair 9; Cloning Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation GeneticPERVASIVE DEVELOPMENTAL DISORDERSmedicine.diseaseDevelopmental disorderINDIVIDUALSLARGE-CONDUCTANCEAutismSCREENNeuroscience[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyCloning
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Metachromatic staining and electron dense reaction of glycosaminoglycans by means of Cuprolinic Blue

1987

The cationic phthalocyanin-like dye Cuprolinic Blue, unlike phthalocyanin dyes such as Alcian Blue or Astra Blue, can definitely exhibit a clear metachromatic reaction with appropriate substrates. The application of Cuprolinic Blue to epoxy-embedded semithin sections revealed that mast cell cytoplasmic granules, goblet cell mucin and cartilage matrix stained in violet shades (metachromatic), whereas nuclear chromatin presented a bright blue coloration (orthochromatic). The metachromatic structures showed a high degree of contrast when ultrathin sections treated with Cuprolinic Blue were examined by electron microscopy. Cytophotometric measurements of stained components from the large intest…

MaleCuprolinic blueIndolesBone matrixCytoplasmic Granuleslaw.inventionGlycosaminoglycanMicelawOrganometallic CompoundsmedicineAnimalsMast CellsIntestinal MucosaColoring AgentsGlycosaminoglycansGoblet cellHistocytochemistryChemistryMetachromasiaMucinsCell BiologyAnatomyMast cellRatsStainingmedicine.anatomical_structureSpectrophotometryBiophysicsFemaleAnatomyElectron microscopeThe Histochemical Journal
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Alterations in striatal neuropeptide mRNA produced by repeated administration of L-DOPA, ropinirole or bromocriptine correlate with dyskinesia induct…

2002

Chronic administration of L-DOPA to MPTP-treated common marmosets induces marked dyskinesia while repeated administration of equivalent antiparkisonian doses of ropinirole and bromocriptine produces only mild involuntary movements. The occurrence of dyskinesia has been associated with an altered balance between the direct and indirect striatal output pathways. Using in situ hybridisation histochemistry, we now compare the effects of these drug treatments on striatal preproenkephalin-A (PPE-A) and adenosine A(2a) receptor mRNA expression as markers of the indirect pathway and striatal preprotachykinin (PPT) mRNA and preproenkephalin-B (PPE-B, prodynorphin) mRNA expression as markers of the d…

MaleDyskinesia Drug-Inducedmedicine.medical_specialtyIndolesCaudate nucleusStriatumIndirect pathway of movementAntiparkinson AgentsLevodopachemistry.chemical_compoundDopamine Uptake InhibitorsParkinsonian DisordersTachykininsInternal medicineNeural PathwaysmedicineAnimalsheterocyclic compoundsRNA MessengerProtein PrecursorsBromocriptineGeneral NeuroscienceMPTPPutamenNeuropeptidesReceptors Purinergic P1CallithrixEnkephalinsMazindoldopamine agonists peptide mRNAs L-DOPA 1-methyl-4-phenyl-1236-tetrahydropyridine primates dyskinesiaBromocriptinenervous system diseasesNeostriatumRopiniroleEndocrinologynervous systemchemistryDyskinesiaSettore BIO/14 - FarmacologiaFemalemedicine.symptommedicine.drugNeuroscience
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