Search results for "Tyro"

showing 10 items of 816 documents

A phase III study (APROMISS) of AL3818 (Catequentinib, Anlotinib) hydrochloride monotherapy in subjects with metastatic or advanced synovial sarcoma.

2021

11505 Background: AL3818 (Catequentinib, Anlotinib) is a novel, orally administered, small molecule tyrosine kinase inhibitor. The primary objective of this Phase 3 study is to evaluate the efficacy of AL3818 monotherapy in patients (pts) with synovial sarcoma (SS) comparing with dacarbazine in randomization setting. Methods: Patients with a diagnosis of synovial sarcoma requiring second line or further line treatment were eligible for enrollment. The regimen was a 21-day cycle with oral AL3818 administered on 14 days on and 7 days off. This phase 3 trial is randomized in 2:1 ratio of AL3818 comparing to dacarbazine with option of crossover after PD of dacarbazine treatment. Progression fr…

Cancer Researchbusiness.industrymedicine.drug_classPhases of clinical researchmedicine.diseaseSmall moleculeSynovial sarcomaTyrosine-kinase inhibitorOncologyPhase (matter)Cancer researchMedicineAnlotinib HydrochloridebusinessJournal of Clinical Oncology
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Intratumoral Heterogeneity in EGFR-Mutant NSCLC Results in Divergent Resistance Mechanisms in Response to EGFR Tyrosine Kinase Inhibition

2015

Abstract Non–small cell lung cancers (NSCLC) that have developed resistance to EGF receptor (EGFR) tyrosine kinase inhibitor (TKI), including gefitinib and erlotinib, are clinically linked to an epithelial-to-mesenchymal transition (EMT) phenotype. Here, we examined whether modulating EMT maintains the responsiveness of EGFR-mutated NSCLCs to EGFR TKI therapy. Using human NSCLC cell lines harboring mutated EGFR and a transgenic mouse model of lung cancer driven by mutant EGFR (EGFR-Del19-T790M), we demonstrate that EGFR inhibition induces TGFβ secretion followed by SMAD pathway activation, an event that promotes EMT. Chronic exposure of EGFR-mutated NSCLC cells to TGFβ was sufficient to ind…

Cancer Researchmedicine.drug_classCellBiologymedicine.diseaseArticleTyrosine-kinase inhibitorrespiratory tract diseasesmedicine.anatomical_structureGefitinibOncologyProtein kinase domainImmunologymedicineCancer researchEpithelial–mesenchymal transitionErlotinibSignal transductionLung cancerneoplasmsmedicine.drugCancer Research
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Shikonin and its derivatives inhibit the epidermal growth factor receptor signaling and synergistically kill glioblastoma cells in combination with e…

2015

Overexpression and mutation of the epidermal growth factor receptor (EGFR) gene play a causal role in tumorigenesis and resistance to treatment of glioblastoma (GBM). EGFR inhibitors such as erlotinib are currently used for the treatment of GBM; however, their efficacy has been limited due to drug resistance. New treatment strategies are therefore urgently needed. Shikonin, a natural naphthoquinone, induces both apoptosis and necroptosis in human glioma cells, but the effectiveness of erlotinib-shikonin combination treatment as well as the underlying molecular mechanisms is unknown yet. In this study, we investigated erlotinib in combination with shikonin and 14 shikonin derivatives in pare…

Cancer Researchmedicine.drug_classNecroptosisBiologyPharmacologyTyrosine-kinase inhibitorrespiratory tract diseasesOncologyCell culturemedicineCancer researchbiology.proteinErlotinibEpidermal growth factor receptorCytotoxicityneoplasmsProtein kinase Bmedicine.drugEGFR inhibitorsInternational Journal of Cancer
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The role of second-line tyrosine kinase inhibitor monotherapy in EGFR wild-type advanced non-small-cell lung cancer patients: Findings from a retrosp…

2015

e19030 Background: Second-line treatment for advanced non-small-cell lung cancer (aNSCLC) patients includes monotherapy with a third generation cytotoxic drug (CT) or with the tyrosine kinase inhib...

Cancer Researchmedicine.drug_classbusiness.industryWild typePharmacologymedicine.diseaseTyrosine-kinase inhibitorThird generationSecond lineOncologymedicineCancer researchRetrospective analysisNon small cellLung cancerbusinessTyrosine kinaseJournal of Clinical Oncology
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Next-Generation Genomic Profiling of Hepatocellular Adenomas: A New Era of Individualized Patient Care

2014

Hepatocellular adenomas (HCAs) are clinically relevant benign liver lesions that commonly occur in women on hormonal contraceptives. In this issue of Cancer Cell, Pilati and colleagues present an integrative multi-“omics”-based analysis of HCA and identify recurrent genetic alterations associated with adenoma-carcinoma transition and new drugable targets.

Cancer Researchmedicine.medical_specialtyCarcinoma HepatocellularGenomic profilingAdenomaMEDLINEBiologyBioinformaticsPatient careAdenoma Liver CellText miningInternal medicinemedicineCarcinomaAnimalsHumansbusiness.industryLiver NeoplasmsCell BiologyProtein-Tyrosine Kinasesmedicine.diseaseOmicsdigestive system diseasesNeoplasm ProteinsCell Transformation NeoplasticEndocrinologyOncologyCancer cellbusinessCancer Cell
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Autocrine production of interleukin-4 and interleukin-10 is required for survival and growth of thyroid cancer cells.

2006

AbstractAlthough CD95 and its ligand are expressed in thyroid cancer, the tumor cell mass does not seem to be affected by such expression. We have recently shown that thyroid carcinomas produce interleukin (IL)-4 and IL-10, which promote resistance to chemotherapy through the up-regulation of Bcl-xL. Here, we show that freshly purified thyroid cancer cells were completely refractory to CD95-induced apoptosis despite the consistent expression of Fas-associated death domain and caspase-8. The analysis of potential molecules able to prevent caspase-8 activation in thyroid cancer cells revealed a remarkable up-regulation of cellular FLIPL (cFLIPL) and PED/PEA-15, two antiapoptotic proteins whos…

Cancer Researchmedicine.medical_treatmentNF-KAPPA-BOligonucleotidesC-FLIPCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisSuppressor of Cytokine Signaling ProteinsSIGNALING COMPLEXThyroid cancerTumorCARCINOMA CELLSANDROGEN RECEPTORIntracellular Signaling Peptides and ProteinsInterleukinHASHIMOTOS-THYROIDITISMiddle AgedProtein-Tyrosine KinasesInterleukin-10Up-RegulationMALIGNANT GLIOMA-CELLSInterleukin 10CytokineOncologyAged; Antibodies; Apoptosis; CASP8 and FADD-Like Apoptosis Regulating Protein; Cell Growth Processes; Cell Line Tumor; Humans; Interleukin-10; Interleukin-4; Intracellular Signaling Peptides and Proteins; Janus Kinase 1; Middle Aged; Oligonucleotides Antisense; Phosphoproteins; Protein-Tyrosine Kinases; Repressor Proteins; STAT6 Transcription Factor; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Up-Regulation; fas Receptor; Oncology; Cancer Researchmedicine.medical_specialtyANTIAPOPTOTIC PROTEINSCell Growth ProcessesAntibodiesCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinSettore MED/04 - PATOLOGIA GENERALEInternal medicineCell Line TumormedicineHumansThyroid Neoplasmsfas ReceptorAntisenseAutocrine signallingInterleukin 4AgedAPOPTOSIS-INDUCING LIGANDbusiness.industryJanus Kinase 1Oligonucleotides Antisensemedicine.diseasePhosphoproteinsRepressor ProteinsEndocrinologyCancer cellCancer researchInterleukin-4businessApoptosis Regulatory ProteinsSTAT6 Transcription FactorCancer research
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Parthenolide induces superoxide anion production by stimulating EGF receptor in MDA-MB-231 breast cancer cells

2013

The sesquiterpene lactone parthenolide (PN) has recently attracted considerable attention because of its anti-microbial, anti-inflammatory and anticancer effects. However, the mechanism of its cytotoxic action on tumor cells remains scarcely defined. We recently provided evidence that the effect exerted by PN in MDA-MB-231 breast cancer cells was mediated by the production of reactive oxygen species (ROS). The present study shows that PN promoted the phosphorylation of EGF receptor (phospho-EGFR) at Tyr1173, an event which was observed already at 1  h of incubation with 25  µM PN and reached a peak at 8-16  h. This effect seemed to be a consequence of ROS production, because N-acetylcystein…

Cancer Researchparthenolide epidermal growth factor receptor NADPH oxidase breast cancer cellsBreast NeoplasmsAntioxidantschemistry.chemical_compoundSuperoxidesCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolideEnzyme InhibitorsPhosphorylationchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxideKinaseAnti-Inflammatory Agents Non-SteroidalNF-kappa BAcetophenonesNADPH OxidasesTyrphostinsMolecular biologyAcetylcysteineErbB ReceptorsOncologychemistryApoptosisApocyninQuinazolinesbiology.proteinPhosphorylationFemaleProtein Tyrosine PhosphatasesSesquiterpenesInternational Journal of Oncology
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Peroxodisulfate as a chemical initiator for methacrylate-ester monolithic columns for capillary electrochromatography

2008

Organic monolithic stationary phases for CEC were synthesized in situ in fused-silica capillaries. Polymerization mixtures were composed of butyl methacrylate, ethylene dimethacrylate, and [2-(methacryloyloxy)ethyl]trimethyl ammonium chloride in the presence of a porogenic solvent, using ammonium peroxodisulfate as chemical initiator, and N,N,N',N'-tetramethylethylenediamine to activate the reaction. The influence of the amount of initiator, temperature, and composition of porogenic solvent on the physical and chromatographic properties of monolithic stationary phases has been investigated. A minimum plate height of 14.5 microm was obtained at 18 wt% of 1,4-butanediol in the polymerization …

Capillary electrochromatographyChromatographySilicon dioxideClinical BiochemistryAcrylic ResinsAzobisisobutyronitrileEthylenediaminesSilicon DioxideMethacrylateBiochemistryAnalytical ChemistrySolventchemistry.chemical_compoundchemistryPolymerizationAmmonium SulfateCapillary ElectrochromatographyNitrilesMethacrylatesAmmoniumAmmonium chloridePorosityNuclear chemistryELECTROPHORESIS
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Nitroglycerin-induced cardioprotection is endothelial nitric oxide synthase- dependent

2015

Purpose We sought to evaluate the contribution of the endogenous NO pathway to the cardioprotective action of nitroglycerin (NTG). Methods and Results Anesthetized rabbits were subjected to 30-min myocardial ischemia (isc) and 3-h reperfusion (rep) and randomized into: Control group (no further intervention); PostC group (application of 8 cycles 30-sec isc/rep) and NTG treated group (2 μg/kg-1/min-1 IV bolus) for 65 min starting 10 min prior to rep. In additional groups, pharmacological inhibitors of NOS, nNOS, iNOS, PI3K, adenosine receptors and PKG were administrated with or without NTG. The infarcted (I) to risk (R) ratio was estimated. In a second experimental series tissue samples were…

Cardioprotectiongenetic structuresbiologybusiness.industryNitrotyrosineEndogenyPharmacologybiology.organism_classificationBiochemistryAdenosine receptoreye diseaseschemistry.chemical_compoundBolus (medicine)chemistryEnosPhysiology (medical)AnesthesiaMedicinebusinessProtein kinase BPI3K/AKT/mTOR pathwayFree Radical Biology and Medicine
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From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview

2019

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…

Cardiovascular toxicityPhysiologymedicine.medical_treatmentAntineoplastic drugClinical BiochemistryAntineoplastic Agents030204 cardiovascular system & hematologyPharmacologyBiochemistryCardiac cellcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factor; Antineoplastic Agents; Cardiotoxicity; Humans; Mitochondria; Oxidation-Reduction03 medical and health scienceschemistry.chemical_compoundErbB2 inhibitors cancer immunotherapy chemotherapy oxidative/nitrosative stress tyrosine kinase inhibitors vascular endothelial growth factor0302 clinical medicinetyrosine kinase inhibitorcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factorChemotherapy; ErbB2 inhibitors; vascular endothelial growth factor; tyrosine kinase inhibitors; oxidative/nitrosative stress; cancer immunotherapyCancer immunotherapytyrosine kinase inhibitorsmedicineHumansChemotherapyMolecular BiologyGeneral Environmental ScienceCardioprotectionComprehensive Invited ReviewsChemotherapyErbB2 inhibitorcancer immunotherapyvascular endothelial growth factorbusiness.industryCell BiologyCardiotoxicityMitochondriaVascular endothelial growth factoroxidative/nitrosative streErbB2 inhibitorschemistry030220 oncology & carcinogenesisGeneral Earth and Planetary SciencesbusinessOxidation-ReductionAfter treatmentoxidative/nitrosative stress
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