Search results for "kinase inhibitor"

showing 10 items of 414 documents

Coexpression of receptor-tyrosine-kinases in gastric adenocarcinoma-a rationale for a molecular targeting strategy?

2007

AIM: To define the (co-)expression pattern of target receptor-tyrosine-kinases (RTK) in human gastric adenocarcinoma. METHODS: The (co-)expression pattern of VEGFR1-3, PDGFRα/β and EGFR1 was analyzed by RT-PCR in 51 human gastric adenocarcinomas. In addition, IHC staining was applied for confirmation of expression and analysis of RTK localisation. RESULTS: The majority of samples revealed a VEGFR1 (98%), VEGFR2 (80%), VEGFR3 (67%), PDGFRα (82%) and PDGFRβ (82%) expression, whereas only 62% exhibited an EGFR1 expression. 78% of cancers expressed at least four out of six RTKs. While VEGFR1-3 and PDGFRα revealed a predominantly cytoplasmatic staining in tumor cells, accompanied by an additiona…

Pathologymedicine.medical_specialtyStromal cellAntineoplastic AgentsAdenocarcinomaReceptor tyrosine kinaseStomach NeoplasmsmedicineGastric mucosaHumansProtein Kinase InhibitorsbiologyReverse Transcriptase Polymerase Chain ReactionfungiGastroenterologyReceptor Protein-Tyrosine KinasesCancerGeneral Medicinemedicine.diseaseImmunohistochemistrydigestive system diseasesStainingmedicine.anatomical_structureGastric MucosaDrug Designbiology.proteinCancer researchAdenocarcinomaImmunohistochemistryDrug Therapy CombinationRapid CommunicationPlatelet-derived growth factor receptorWorld Journal of Gastroenterology
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Cytotoxic and protein kinase inhibiting nakijiquinones and nakijiquinols from the sponge Dactylospongia metachromia.

2014

Chemical investigation of the sponge Dactylospongia metachromia afforded five new sesquiterpene aminoquinones (1-5), two new sesquiterpene benzoxazoles (6 and 7), the known analogue 18-hydroxy-5-epi-hyrtiophenol (8), and a known glycerolipid. The structures of all compounds were unambiguously elucidated by one- and two-dimensional NMR and by MS analyses, as well as by comparison with the literature. Compounds 1-5 showed potent cytotoxicity against the mouse lymphoma cell line L5178Y with IC50 values ranging from 1.1 to 3.7 μM. When tested in vitro for their inhibitory potential against 16 different protein kinases, compounds 5, 6, and 8 exhibited the strongest inhibitory activity against AL…

Pharmaceutical ScienceAntineoplastic AgentsMarine BiologySesquiterpeneAnalytical Chemistrychemistry.chemical_compoundInhibitory Concentration 50MiceDrug DiscoveryAnimalsHumansProtein kinase ACytotoxicityIC50Nuclear Magnetic Resonance BiomolecularProtein Kinase InhibitorsPharmacologyBenzoxazolesMolecular StructureKinaseOrganic ChemistryQuinonesIn vitroPoriferaComplementary and alternative medicineBiochemistrychemistryCell cultureMolecular MedicineDrug Screening Assays AntitumorSesquiterpenesProto-oncogene tyrosine-protein kinase SrcJournal of natural products
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Impact of nutritional status on the pharmacokinetics of erlotinib in rats

2015

Malnourishment is a complex condition in which physiopathological changes take place in multiple systems as a result of energy, protein and nutrient deficiency. The purpose of this study was to evaluate, using an experimental animal model, the impact of nutritional status on the pharmacokinetic profile of erlotinib, a reversible, highly selective, human epidermal growth factor receptor (HER1/EGFR) tyrosine kinase inhibitor. Two groups of rats -WN (well-nourished) and UN (undernourished) - were fed with different diets for 23-26 days. Rats were assigned randomly to one of three erlotinib treatments (n = 42) consisting of a single dose administered intravenously (i.v.), via oral solution or v…

PharmacologyDrugeducation.field_of_studymedicine.drug_classbusiness.industrymedia_common.quotation_subjectPopulationPharmaceutical ScienceCancerNutritional statusGeneral MedicineAbsorption (skin)Pharmacologymedicine.diseaseTyrosine-kinase inhibitorPharmacokineticsmedicinePharmacology (medical)Erlotinibeducationbusinessmedia_commonmedicine.drugBiopharmaceutics & Drug Disposition
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Synthesis of 2H-Imidazo[2',1':2,3] [1,3]thiazolo[4,5-e]isoindol-8-yl-phenylureas with promising therapeutic features for the treatment of acute myelo…

2022

Despite progressive advances in understanding the molecular biology of acute myeloid leukemia (AML), the conventional therapeutic approach has not changed substantially, and the outcome for most patients is poor. Thus, continuous efforts on the discovery of new compounds with improved features are required. Following a multistep sequence, we have identified a new tetracyclic ring system with strong antiproliferative activity towards several haematological cell lines. The new compounds possess structural properties typical of inactive-state-binding kinase inhibitors and are structurally related to quizartinib which is known as type-II tyrosine kinase inhibitor. In particular, the high activi…

PharmacologyFMS-like tyrosine kinase 3 (FLT3)FLT3/ITD3][13]thiazolo[4Organic Chemistry2H-imidazo [2′1':23][13]thiazolo[45-e]isoindol-8-yl-phenylureas2H-imidazo [2′1':23][13]thiazolo[45-e]isoindol-8-yl-phenylureas; Acute myeloid leukemia (AML); FLT3/ITD; FMS-like tyrosine kinase 3 (FLT3); Internal tandem duplication (ITD)ApoptosisGeneral Medicine2H-imidazo [2′Leukemia Myeloid AcuteMiceInternal tandem duplication (ITD)fms-Like Tyrosine Kinase 35-e]isoindol-8-yl-phenylureasCell Line TumorDrug DiscoveryMutationAcute myeloid leukemia (AML)AnimalsHumansProtein Kinase Inhibitors1':2European journal of medicinal chemistry
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The rates of adult neurogenesis and oligodendrogenesis are linked to cell cycle regulation through p27-dependent gene repression of SOX2

2023

Abstract Cell differentiation involves profound changes in global gene expression that often have to occur in coordination with cell cycle exit. Because cyclin-dependent kinase inhibitor p27 reportedly regulates proliferation of neural progenitor cells in the subependymal neurogenic niche of the adult mouse brain, but can also have effects on gene expression, we decided to molecularly analyze its role in adult neurogenesis and oligodendrogenesis. At the cell level, we show that p27 restricts residual cyclin-dependent kinase activity after mitogen withdrawal to antagonize cycling, but it is not essential for cell cycle exit. By integrating genome-wide gene expression and chromatin accessibil…

PharmacologyModel organismsFOS: Clinical medicineStem CellsNeurosciencesATAC-SeqCell BiologyTumour BiologyBiología y Biomedicina / BiologíaNeural DiferentiationCellular and Molecular NeuroscienceCyclin-Dependent Kinase InhibitorAdult Neural ProgenitorsMolecular MedicineRNA-SeqMolecular BiologyGenetics & GenomicsAdult NeuroblastsDevelopmental Biology
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Multi or Single-Kinase Inhibitors to Counteract Drug Resistance in Cancer: What is New?

2023

The concept of protein kinase inhibition starts from the groundbreaking research on the role of these proteins in the regulation of fundamental processes, including proliferation, cell cycle, apoptosis, metabolism, and inflammation. Kinase genetic mutations, as well as overexpression and dysregulation, can contribute to the development of several diseases, including neoplasms, leading to relapses and resistance to standard drug chemotherapy [1-3].

PharmacologySmall molecules kinase inhibitorspolypharmacologycovalent kinase inhibitorsallosteric inhibitorsDrug DiscoveryOrganic ChemistryMolecular Medicineanticancer drug combinationsBiochemistrykinase genetic aberrationSettore CHIM/08 - Chimica Farmaceutica
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Reduction of tumor necrosis factor-alpha (TNF-α) related nuclear factor-kappaB (NF-κB) translocation but not inhibitor kappa-B (Iκ-B)-degradation by …

2002

Degradation of inhibitor kappa-B (Ikappa-B) followed by translocation of nuclear factor-kappaB (NF-kappaB) into the nucleus and activation of gene expression is essential in tumor necrosis factor-alpha (TNF-alpha)-signaling. In order to analyze the role of Rho proteins in TNF-alpha-induced NF-kappaB-activation in human umbilical cord vein endothelial cells (HUVEC) we used Clostridium difficile toxin B-10463 (TcdB-10463) which inactivates RhoA/Rac1/Cdc42 by glucosylation and Clostridium botulinum C3-toxin which inhibits RhoA/B/C by ADP-ribosylation. Exposure of HUVEC to 10 ng/mL TcdB-10463 or 2.5 microg/mL C3-toxin inhibited TNF-alpha (100 ng/mL)-induced expression of a NF-kappaB-dependent r…

PharmacologyTRAF2RHOATumor Necrosis Factor-alphaNF-kappa BClostridium difficile toxin ABiological TransportRAC1Chromosomal translocationDNABiologyBiochemistryMolecular biologyRho kinase inhibitorbiology.proteinHumansI-kappa B ProteinsTumor necrosis factor alphaEndothelium VascularInterleukin 8rhoA GTP-Binding ProteinCells CulturedBiochemical Pharmacology
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Standard versus personalized schedule of regorafenib in metastatic gastrointestinal stromal tumors: a retrospective, multicenter, real-world study

2021

Background Despite its proven activity as third-line treatment in gastrointestinal stromal tumors (GIST), regorafenib can present a poor tolerability profile which often leads to treatment modifications and transient or permanent discontinuation; thus, in clinical practice physicians usually adopt various dosing and interval schedules to counteract regorafenib-related adverse events and avoid treatment interruption. The aim of this real-world study was to investigate the efficacy and safety of personalized schedules of regorafenib in patients with metastatic GIST, in comparison with the standard schedule (160 mg daily, 3-weeks-on, 1-week-off). Patients and methods Institutional registries a…

Phenylurea CompoundOncologyCancer Researchmedicine.medical_specialtyScheduleStromal cellPyridinesGastrointestinal Stromal TumorsPyridinePersonalized treatmentchemical and pharmacologic phenomenaMultikinase inhibitorchemistry.chemical_compoundQuality of lifeRetrospective Studieimmune system diseaseshemic and lymphatic diseasesInternal medicineRegorafenibmedicineHumansOriginal ResearchRetrospective StudiesGiSTbusiness.industryPhenylurea Compoundstoxicityhemic and immune systemspersonalized treatmentdigestive system diseasesquality of lifeOncologychemistryregorafenibGIST; personalized treatment; quality of life; regorafenib; toxicity; Humans; Phenylurea Compounds; Pyridines; Retrospective Studies; Gastrointestinal Stromal TumorsbusinessHumanGISTESMO Open
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Sodium-glucose cotransporter type 2 inhibitors prevent ponatinib-induced endothelial senescence and disfunction: A potential rescue strategy

2021

Background: Ponatinib (PON), a third-generation tyrosine kinase inhibitor (TKI), has proven cardiovascular toxicity, with no known preventing agents usable to limit such side effect. Sodium-glucose cotransporter type 2 (SGLT2) inhibitors are a new class of glucose-lowering agents, featuring favorable cardiac and vascular effects. Aims: We assessed the effects of the SGLT2 inhibitors empagliflozin (EMPA) and dapagliflozin (DAPA) on human aortic endothelial cells (HAECs) and underlying vasculo-protective mechanisms in an in vitro model of PON-induced endothelial toxicity. Methods and results: We exposed HAECs to PON or vehicle (DMSO) in the presence or absence of EMPA (100 and 500 nmol/L) or …

Physiologymedicine.drug_classCellPharmacologyAutophagy; Ponatinib; Sodium-glucose cotransporter type 2 (SGLT2) inhibitors; Tyrosine kinase inhibitors; Vascular toxicityTyrosine-kinase inhibitorFlow cytometrychemistry.chemical_compoundmedicineAutophagyHumansViability assayDapagliflozinCellular SenescencePharmacologyTyrosine kinase inhibitorsMatrigelmedicine.diagnostic_testChemistrySodiumImidazolesEndothelial CellsEndothelial stem cellPyridazinesmedicine.anatomical_structureGlucoseDiabetes Mellitus Type 2Sodium-glucose cotransporter type 2 (SGLT2) inhibitorsToxicityPonatinibMolecular MedicineVascular toxicity
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Met inhibition revokes IFNγ-induction of PD-1 ligands in MET-amplified tumours

2019

BACKGROUND: Interferon-induced expression of programmed cell death ligands (PD-L1/PD-L2) may sustain tumour immuneevasion. Patients featuring MET amplification, a genetic lesion driving transformation, may benefit from anti-MET treatment. We explored if MET-targeted therapy interferes with Interferon-gamma modulation of PD-L1/PD-L2 in MET-amplified tumours.METHODS: PD-L1/PD-L2 expression and signalling pathways downstream of MET or Interferon-gamma were analysed in MET-amplified tumour cell lines and in patient-derived tumour organoids, in basal condition, upon Interferon-gamma stimulation, and after anti-MET therapy.RESULTS: PD-L1 and PD-L2 were upregulated in MET-amplified tumour cells up…

Programmed cell deathCancer ResearchCancer immunotherapyMET-amplified tumoursB7-H1 AntigenArticleInterferon-gammaTargeted therapiesDownregulation and upregulationInterferonCell Line TumorNeoplasmsHumansMedicineMet inhibitionMolecular Targeted TherapySTAT1Kinase activityReceptorProtein Kinase InhibitorsJanus KinasesReceptors InterferonOncogenebiologyPD-1 ligandsbusiness.industryLiver NeoplasmsOncogenesProto-Oncogene Proteins c-metProgrammed Cell Death 1 Ligand 2 ProteinOrganoidsSTAT1 Transcription FactorOncologybiology.proteinCancer researchOncology; Cancer Research; Met inhibition; IFNγ-induction;PD-1 ligands; MET-amplified tumoursTumor EscapeSignal transductionColorectal NeoplasmsbusinessIFNγ-inductionSignal Transductionmedicine.drug
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