Search results for "protein kinase inhibitors"

showing 10 items of 211 documents

Osimertinib in first-line treatment of advanced EGFR-mutated non-small-cell lung cancer: a cost–effectiveness analysis

2019

Aim: Osimertinib improves progression-free survival in first-line EGFR mutation–positive non-small-cell lung cancer. Materials & methods: A Markov cohort model including costs, utilities and disutilities, was conducted to estimate quality-adjusted life-year (QALY) and incremental cost–effectiveness ratio when treating with osimertinib versus standard first-line tyrosine kinase inhibitors (TKIs). Results: Osimertinib presented higher QALYs (0.61) compared with standard EGFR–TKIs (0.42). Osimertinib costs were €83,258.99, in comparison with €29,209.45 for the standard EGFR–TKIs. An incremental cost–effectiveness ratio of €273,895.36/QALY was obtained for osimertinib. Conclusion: Osimerti…

Oncologymedicine.medical_specialtyLung NeoplasmsCost effectivenessCost-Benefit AnalysisAntineoplastic Agents03 medical and health scienceschemistry.chemical_compoundEgfr tki0302 clinical medicineCarcinoma Non-Small-Cell LungInternal medicinemedicineHumansOsimertinib030212 general & internal medicineLung cancerProtein Kinase Inhibitorshealth care economics and organizationsAcrylamidesAniline Compoundsbusiness.industryHealth PolicyCost-effectiveness analysismedicine.diseaseMarkov ChainsDacomitinibrespiratory tract diseasesErbB ReceptorsFirst line treatmentchemistry030220 oncology & carcinogenesisMutationQuality-Adjusted Life YearsNon small cellbusinessModels EconometricJournal of Comparative Effectiveness Research
researchProduct

Are erlotinib and gefitinib interchangeable, opposite or complementary for non-small cell lung cancer treatment? Biological, pharmacological and clin…

2014

Abstract: Gefitinib and erlotinib are the two anti-epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) approved for treatment of advanced NSCLC patients. These drugs target one of the most important pathways in lung carcinogenesis and are able to exploit the phenomenon of 'oncogene addiction', with different efficacy according to EGFR gene mutational status in tumor samples. Gefitinib has been approved only for EGFR mutation bearing patients regardless the line of treatment, while erlotinib is also indicated in patients without EGFR mutation who undergo second- or third-line treatment. Some studies evaluated the main differences between these drugs both for direct comp…

Oncologymedicine.medical_specialtyLung NeoplasmsEGFR; Erlotinib; Gefitinib; Lung cancer; NSCLC; Tyrosine kinaseSettore MED/06 - Oncologia MedicaEGFRAntineoplastic Agentsmedicine.disease_causeNSCLCErlotinib HydrochlorideGefitinibGrowth factor receptorPharmacokineticsCarcinoma Non-Small-Cell LungInternal medicineHumansMedicineLung cancerLungProtein Kinase InhibitorsneoplasmsTyrosine kinasebusiness.industryGefitinibHematologyOncogene Addictionmedicine.diseaserespiratory tract diseasesErbB ReceptorsOncologyErlotinibQuinazolinesHuman medicineErlotinibLung cancerbusinessCarcinogenesisTyrosine kinasemedicine.drug
researchProduct

Prognostic and predictive biomarkers for targeted therapy in NSCLC: For whom the bell tolls?

2015

Introduction: The discovery of molecular biomarkers and the advent of targeted therapies have led to a radical change in the treatment of several tumors, including NSCLC. In the last few years, the number of molecular biomarkers has rapidly increased, and a growing interest has been recently focused on their potential prognostic and predictive value in clinical settings. Areas covered: This review describes all the molecular biomarkers with prognostic and predictive value in NSCLC, including both clinically approved biomarkers, and emerging biomarkers under investigation in clinical trials. Liquid biopsy and applications of circulating biomarkers are also described. Expert opinion: The onco…

Oncologymedicine.medical_specialtyPathologyLung NeoplasmsOncogene Proteins Fusionmedicine.medical_treatmentClinical BiochemistryNSCLCprognostic biomarkersTargeted therapytissue biopsypredictive biomarkersInternal medicineCarcinoma Non-Small-Cell LungProto-Oncogene ProteinsDrug DiscoveryBiomarkers TumorMedicineHumansBiomarker discoveryLiquid biopsypredictive biomarkerprognostic biomarkerProtein Kinase InhibitorsPredictive biomarkerPharmacologyliquid biopsybusiness.industryDrug Discovery3003 Pharmaceutical Scienceliquid biopsy; NSCLC; predictive biomarkers; prognostic biomarkers; targeted therapy; tissue biopsy; Pharmacology; Clinical Biochemistry; Drug Discovery3003 Pharmaceutical ScienceProtein-Tyrosine KinasesPrognosistargeted therapyMolecular biomarkersPredictive valueClinical trialErbB ReceptorsCirculating biomarkersras Proteinsbusiness
researchProduct

Looking for a new panacea in ALK-rearranged NSCLC: may be Ceritinib?

2014

Abstract: In the past decade, the advent of targeted therapy led to a silent revolution in the war against lung cancer and a significant evolution on the concept of Phase I clinical trials design. Thanks to the specificity of their target, the new drugs have radically changed NSCLC treatment, leading to the development of personalized strategies. The accelerated approval of the first ALK-inhibitor, Crizotinib and more recently Ceritinib, without a Phase III randomized, clinical trial, has been an amazing success story in lung cancer research, marking the beginning of a new decade of targeted drugs development, characterized by modern, biomarker-driven, early clinical trial design and shorte…

Oncologymedicine.medical_specialtyPathologyLung NeoplasmsPyridinesSettore MED/06 - Oncologia Medicamedicine.medical_treatmentClinical BiochemistryEML4-ALKCeritinibNSCLCTargeted therapyPanacea (medicine)CrizotinibCarcinoma Non-Small-Cell LungInternal medicineDrug DiscoveryHumansMedicineAnaplastic Lymphoma KinaseMolecular Targeted TherapySulfonesPrecision MedicineLung cancerDrug ApprovalProtein Kinase InhibitorsGene RearrangementPharmacologyCeritinib; Crizotinib; EML4-ALK; NSCLCClinical Trials Phase I as TopicCrizotinibCeritinibbusiness.industryPharmacology. TherapyClinical study designReceptor Protein-Tyrosine Kinasesmedicine.diseaseCeritinib Crizotinib EML4-ALK NSCLCClinical trialPyrimidinesDrug DesignPyrazolesMolecular MedicineAccelerated approvalbusinessmedicine.drugExpert Opinion on Therapeutic Targets
researchProduct

Early diagnosis, clinical management, and follow-up of cardiovascular events with ponatinib

2020

Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by neoplastic transformation of pluripotent cells due to a typical cytogenetic and molecular mutation known as Philadelphia (Ph) chromosome. In 2001, the introduction of the tyrosine kinasis inhibitor (TKI) imatinib as a therapeutic strategy for CML with PH chromosome mutation represented an important step towards treatment of these patients, and nowadays, this drug represents the gold therapeutic standard in this clinical setting. A second generation of TKIs (dasatinib, nilotinib, and bosutinib) showed an effective action in all patients with mutations resistant to imatinib. Ponatinib is a third-generation TKI an…

Oncologymedicine.medical_specialtyTyrosine kinase inhibitorReview030204 cardiovascular system & hematology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRisk FactorsLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesInternal medicinemedicineHumansNeoplastic transformation030212 general & internal medicineProtein Kinase InhibitorsTyrosine kinase inhibitorsCardiotoxicitybusiness.industryPonatinibChronic myeloid leukemiaImidazolesDisease ManagementMyeloid leukemiaImatinibPyridazinesDasatinibCardio-oncologyEarly DiagnosisNilotinibchemistryCardiovascular DiseasesPonatinibPonatinib . Tyrosine kinase inhibitors . Chronic myeloid leukemia . Cardio-oncology . ReviewCardiology and Cardiovascular MedicinebusinessBosutinibFollow-Up Studiesmedicine.drug
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

Investigation of cancer drug resistance mechanisms by phosphoproteomics

2020

Abstract Cancer cell mutations can be identified by genomic and transcriptomic techniques. However, they are not sufficient to understand the full complexity of cancer heterogeneity. Analyses of proteins expressed in cancers and their modification profiles show how these mutations could be translated at the functional level. Protein phosphorylation is a major post-translational modification critical for regulating several cellular functions. The covalent addition of phosphate groups to serine, threonine, and tyrosine is catalyzed by protein kinases. Over the past years, kinases were strongly associated with cancer, thus inhibition of protein kinases emanated as novel cancer treatment. Howev…

Proteomics0301 basic medicineProteomeAntineoplastic AgentsBiologyProteomics03 medical and health sciences0302 clinical medicineNeoplasmsBiomarkers TumormedicineAnimalsHumansProtein phosphorylationPhosphorylationProtein Kinase InhibitorsPharmacologyKinasePhosphoproteomicsCancermedicine.diseaseNeoplasm Proteins030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellCancer researchPhosphorylationProtein Processing Post-TranslationalTyrosine kinasePharmacological Research
researchProduct