Search results for "protein kinase inhibitors"

showing 10 items of 211 documents

Clinical utility of plasma-based digital next-generation sequencing in oncogene-driven non-small-cell lung cancer patients with tyrosine kinase inhib…

2019

[Objectives] Resistance to tyrosine-kinase inhibitors (TKIs) is a clinical challenge in patients with oncogene-driven non-small-cell lung cancers (NSCLC). We have analyzed the utility of next-generation sequencing (NGS) of cell-free circulating tumor DNA (ctDNA) to impact the clinical care of patients with TKI resistance.

0301 basic medicineOncologyMaleCancer ResearchLung NeoplasmsTyrosine-kinase inhibitorCirculating Tumor DNAchemistry.chemical_compound0302 clinical medicineCarcinoma Non-Small-Cell LungMedicineOsimertinibNeoplasm MetastasisProspective cohort studyAged 80 and overDisease ManagementHigh-Throughput Nucleotide SequencingMiddle AgedOncology030220 oncology & carcinogenesisFemalemedicine.drugPulmonary and Respiratory MedicineAdultmedicine.medical_specialtyCabozantinibmedicine.drug_class03 medical and health sciencesInternal medicineROS1Biomarkers TumorHumansLung cancerProtein Kinase InhibitorsAgedNeoplasm StagingDigital next-generation sequencingTKI resistanceCrizotinibbusiness.industryOncogene-driven NSCLCOncogenesctDNAmedicine.diseaseLorlatinibrespiratory tract diseases030104 developmental biologychemistryDrug Resistance NeoplasmMutationbusinessOsimertinib
researchProduct

Clinical outcome of concomitant vs interrupted BRAF inhibitor therapy during radiotherapy in melanoma patients

2018

Background: Concomitant radiation with BRAF inhibitor (BRAFi) therapy may increase radiation-induced side effects but also potentially improve tumour control in melanoma patients. Methods: A total of 155 patients with BRAF-mutated melanoma from 17 European skin cancer centres were retrospectively analysed. Out of these, 87 patients received concomitant radiotherapy and BRAFi (59 vemurafenib, 28 dabrafenib), while in 68 patients BRAFi therapy was interrupted during radiation (51 vemurafenib, 17 dabrafenib). Overall survival was calculated from the first radiation (OSRT) and from start of BRAFi therapy (OSBRAFi). Results: The median duration of BRAFi treatment interruption prior to radiothera…

0301 basic medicineOncologyMaleCancer ResearchRadiation-Sensitizing AgentsSkin Neoplasmsmedicine.medical_treatmentMedizinCohort Studies0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsOximesVemurafenibProspective cohort studyMelanomaAged 80 and overMelanomaImidazolesMiddle AgedTreatment OutcomeOncology030220 oncology & carcinogenesisFemalemedicine.drugAdultProto-Oncogene Proteins B-rafmedicine.medical_specialtyAdolescentDrug Administration ScheduleBRAF03 medical and health sciencesYoung AdultInternal medicinemedicineHumansddc:610dabrafenibProtein Kinase InhibitorsradiotherapyAgedRetrospective Studiesbusiness.industryDabrafenibRetrospective cohort studymedicine.diseaseRadiation therapyradiation030104 developmental biologyVemurafenibConcomitantClinical StudySkin cancerbusinessBritish Journal of Cancer
researchProduct

Progression patterns under BRAF inhibitor treatment and treatment beyond progression in patients with metastatic melanoma

2017

Despite markedly improved treatment options for metastatic melanoma, resistance to targeted therapies such as BRAF inhibitors (BRAFi) or BRAFi plus MEK inhibitors (MEKi) remains a major problem. Our aim was to characterize progression on BRAFi therapy and outcome of subsequent treatment. One hundred and eighty patients with BRAF-mutant metastatic melanoma who had progressed on treatment with single-agent BRAFi from February 2010 to April 2015 were included in a retrospective data analysis focused on patterns of progression, treatment beyond progression (TBP) and subsequent treatments after BRAFi therapy. Analysis revealed that 51.1% of patients progressed with both new and existing metastas…

0301 basic medicineOncologyMaleCancer ResearchSkin NeoplasmsBRAF inhibitorProgrammed Cell Death 1 ReceptorMedizinKaplan-Meier Estimate0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsVemurafenibMelanomaOriginal ResearchAged 80 and overTreatment optionsMiddle AgedMAP Kinase Kinase KinasesPrognosisProgression-Free SurvivalOncology030220 oncology & carcinogenesisDisease ProgressionvemurafenibFemalemedicine.drugmetastatic melanomaBRAF inhibitorAdultProto-Oncogene Proteins B-rafmedicine.medical_specialtyMetastatic melanomaRetrospective data03 medical and health sciencesYoung AdultInternal medicinetreatment beyond progressionmedicineOverall survivalHumansRadiology Nuclear Medicine and imagingIn patientdabrafenibProtein Kinase InhibitorsResponse Evaluation Criteria in Solid TumorsAgedRetrospective Studiesbusiness.industryClinical Cancer ResearchDabrafenib030104 developmental biologyBRAF mutationDrug Resistance NeoplasmMutationprogressionbusinessFollow-Up StudiesCancer Medicine
researchProduct

Chemoresistance and chemosensitization in cholangiocarcinoma

2017

One of the main difficulties in the management of patients with advanced cholangiocarcinoma (CCA) is their poor response to available chemotherapy. This is the result of powerful mechanisms of chemoresistance (MOC) of quite diverse nature that usually act synergistically. The problem is often worsened by altered MOC gene expression in response to pharmacological treatment. Since CCA includes a heterogeneous group of cancers their genetic signature coding for MOC genes is also diverse; however, several shared traits have been defined. Some of these characteristics are shared with other types of liver cancer, namely hepatocellular carcinoma and hepatoblastoma. An important goal in modern onco…

0301 basic medicinePharmacologybile ductschemotherapydrug delivery systems0302 clinical medicineChemosensitizationantineoplastic agentsmolecular biologyReceptorhumansreceptor protein-tyrosine kinasesmedia_commonapoptosisgene expression regulationbile duct neoplasmsDrug Resistance Multipletargeted therapiesGene Expression Regulation Neoplasticmultiplebiliary cancer; chemotherapy; liver cancer; multidrug resistance; targeted therapies; antineoplastic agents; apoptosis; bile duct neoplasms; bile ducts; cell survival; cholangiocarcinoma; drug delivery systems; drug resistance multiple; drug resistance; neoplasm; epithelial cells; gene expression regulation neoplastic; genetic therapy; humans; protein kinase inhibitors; receptor protein-tyrosine kinases; signal transduction; treatment outcome; molecular medicine; molecular biology030220 oncology & carcinogenesisHepatocellular carcinomabiliary cancerLiver cancercholangiocarcinomaTyrosine kinasesignal transductionDrugHepatoblastomamedia_common.quotation_subjectcell survivalPharmacological treatmentliver cancer03 medical and health sciencesmultidrug resistancemedicinemolecular medicinedrug resistancebusiness.industrymedicine.diseaseepithelial cellsneoplasticprotein kinase inhibitors030104 developmental biologyDrug Resistance NeoplasmCancer researchtreatment outcomebusinessneoplasmgenetic therapy
researchProduct

Cancer stem cell-based models of colorectal cancer reveal molecular determinants of therapy resistance

2016

Abstract Colorectal cancer (CRC) therapy mainly relies on the use of conventional chemotherapeutic drugs combined, in a subset of patients, with epidermal growth factor receptor [EGFR]-targeting agents. Although CRC is considered a prototype of a cancer stem cell (CSC)-driven tumor, the effects of both conventional and targeted therapies on the CSC compartment are largely unknown. We have optimized a protocol for colorectal CSC isolation that allowed us to obtain CSC-enriched cultures from primary tumor specimens, with high efficiency. CSC isolation was followed by in vitro and in vivo validation, genetic characterization, and drug sensitivity analysis, thus generating panels of CSC lines w…

0301 basic medicineProteomicscancer stem cellsColorectal cancerDrug ResistanceMice SCIDAnti-EGFR therapy; Cancer stem cells; Cetuximab; Colorectal cancer; Proteomic arrays; Animals; Cells Cultured; Colorectal Neoplasms; Drug Resistance Neoplasm; Female; Gene Expression Profiling; Humans; Mice Inbred NOD; Mice SCID; Mice Transgenic; Microarray Analysis; Models Biological; Neoplastic Stem Cells; Protein Kinase Inhibitors; Proteomics; Signal Transduction; Developmental Biology; Cell BiologyTransgenicMiceMice Inbred NODModelsproteomic arrayscetuximabcell biologyEpidermal growth factor receptorCells CulturedCulturedCetuximabbiologyGeneral MedicinePrimary tumorNeoplastic Stem CellsFemaleSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioStem cellColorectal Neoplasmsmedicine.drugSignal TransductionCellsMice Transgeniccolorectal cancerSCIDModels Biological03 medical and health sciencesdevelopmental biologyProteomic arrayCancer stem cellIn vivoSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansProtein Kinase InhibitorsSettore MED/06 - ONCOLOGIA MEDICAMicroarray analysis techniquesbusiness.industryCancer stem cellGene Expression Profilingmedicine.diseaseMicroarray AnalysisBiological030104 developmental biologyanti-EGFR therapyDrug Resistance Neoplasmanti-EGFR therapy; cancer stem cells; cetuximab; colorectal cancer; proteomic arrays; cell biology; developmental biologyImmunologyCancer researchbiology.proteinNeoplasmInbred NODbusiness
researchProduct

Recent advances on CDK inhibitors: An insight by means of in silico methods

2017

The cyclin dependent kinases (CDKs) are a small family of serine/threonine protein kinases that can act as a potential therapeutic target in several proliferative diseases, including cancer. This short review is a survey on the more recent research progresses in the field achieved by using in silico methods. All the "armamentarium" available to the medicinal chemists (docking protocols and molecular dynamics, fragment-based, de novo design, virtual screening, and QSAR) has been employed to the discovery of new, potent, and selective inhibitors of cyclin dependent kinases. The results cited herein can be useful to understand the nature of the inhibitor-target interactions, and furnish an ins…

0301 basic medicineQuantitative structure–activity relationshipMolecular dynamicIn silicoCDKQuantitative Structure-Activity RelationshipAntineoplastic AgentsComputational biologyMolecular Dynamics SimulationBioinformatics01 natural sciencesSerine03 medical and health sciencesCyclin-dependent kinaseNeoplasmsDrug DiscoveryAnimalsHumansProtein Kinase InhibitorsPharmacologyVirtual screeningHVTSbiologyChemistryKinaseQSARDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryGeneral MedicineCyclin-Dependent Kinases0104 chemical sciencesMolecular Docking Simulation010404 medicinal & biomolecular chemistry030104 developmental biologyDocking (molecular)Drug Designbiology.proteinComputer-Aided DesignIn silico methodMolecular modelling
researchProduct

Developmental effects of the protein kinase inhibitor kenpaullone on the sea urchin embryo

2017

The selection and validation of bioactive compounds require multiple approaches, including in-depth analyses of their biological activity in a whole-animal context. We exploited the sea urchin embryo in a rapid, medium-scale range screening to test the effects of the small synthetic kinase inhibitor kenpaullone. We show that sea urchin embryos specifically respond to this molecule depending on both dose and timing of administration. Phenotypic effects of kenpaullone are not immediately visible, since this molecule affects neither the fertilization nor the spatial arrangement of blastomeres at early developmental stages. Nevertheless, kenpaullone exposure from the beginning of embryogenesis …

0301 basic medicineSea urchinEmbryo NonmammalianIndolesPhysiologymedicine.drug_classHealth Toxicology and MutagenesisMesenchymeSettore BIO/11 - Biologia MolecolareContext (language use)ToxicologyBiochemistry03 medical and health sciencesbiology.animalBotanymedicineAnimalsEpithelial–mesenchymal transitionProtein Kinase InhibitorsSea urchinKinase inhibitorMolecular StructurebiologyEmbryogenesisGene Expression Regulation DevelopmentalCell BiologyGeneral MedicineBlastomereBenzazepinesProtein kinase inhibitorEmbryonic stem cellKenpaulloneCell biology030104 developmental biologymedicine.anatomical_structureEmbryonic developmentembryonic structuresParacentrotusGene expressionComparative Biochemistry and Physiology Part C: Toxicology & Pharmacology
researchProduct

Sorafenib plus topotecan versus placebo plus topotecan for platinum-resistant ovarian cancer (TRIAS): a multicentre, randomised, double-blind, placeb…

2018

Summary Background Antiangiogenic therapy has known activity in ovarian cancer. The investigator-initiated randomised phase 2 TRIAS trial assessed the multi-kinase inhibitor sorafenib combined with topotecan and continued as maintenance therapy for platinum-resistant or platinum-refractory ovarian cancer. Methods We did a multicentre, double-blind, placebo-controlled, randomised, phase 2 trial at 20 sites in Germany. Patients (≥18 years) with platinum-resistant ovarian cancer previously treated with two or fewer chemotherapy lines for recurrent disease were stratified (first vs later relapse) in block sizes of four and randomly assigned (1:1) using a web-generated response system to topotec…

0301 basic medicineSorafenibAdultmedicine.medical_specialtyTime FactorsPerforation (oil well)Angiogenesis InhibitorsPlatinum CompoundsNeutropeniaPlaceboGastroenterologyDrug Administration Schedule03 medical and health sciences0302 clinical medicineMaintenance therapyDouble-Blind MethodInternal medicineGermanyAntineoplastic Combined Chemotherapy ProtocolsmedicineClinical endpointHumansProgression-free survivalProtein Kinase InhibitorsAgedOvarian Neoplasmsbusiness.industryMiddle AgedSorafenibmedicine.diseaseProgression-Free Survival030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisDisease ProgressionTopotecanFemaleTopoisomerase I InhibitorsbusinessTopotecanmedicine.drugThe Lancet. Oncology
researchProduct

Trial Design and Endpoints in Hepatocellular Carcinoma: AASLD Consensus Conference

2020

Proper trial design is critical for the success of clinical investigations. Hepatocellular carcinoma (HCC) is a complex disease that has several unique properties. In 2008, after the approval of sorafenib, a panel of experts proposed guidelines for trial design and endpoints in HCC that have been instrumental during the last decade and provided a framework to allow an homogeneous analysis of reported investigations. Since then, several phase III studies have been reported and novel challenges have emerged. A panel of experts conveyed by AASLD organized a Special Topic Conference on trial design and endpoints to address those emerging challenges. This review summarizes the analysis and concl…

0301 basic medicineSorafenibmedicine.medical_specialtyCarcinoma HepatocellularConsensusEndpoint DeterminationMEDLINEDisease03 medical and health sciences0302 clinical medicinemedicineHumansProgression-free survivalChemoembolization TherapeuticLiquid biopsyIntensive care medicineAdverse effectImmune Checkpoint InhibitorsProtein Kinase InhibitorsClinical Trials as TopicHepatologybusiness.industryLiver NeoplasmsLiquid Biopsymedicine.diseaseLiver TransplantationClinical trial030104 developmental biologyResearch DesignHepatocellular carcinoma030211 gastroenterology & hepatologybusinessmedicine.drugHepatology
researchProduct

Biological Effect of a Hybrid Anticancer Agent Based on Kinase and Histone Deacetylase Inhibitors on Triple-Negative (MDA-MB231) Breast Cancer Cells

2016

We examined the effects of the histone deacetylase inhibitor (HDACi) suberoylanilide\ud hydroxamic acid (SAHA) combined with the vascular endothelial growth factor receptor-1/2 inhibitor\ud (3Z)-5-hydroxy-3-(1H-pyrrol-2-ylmethylidene)-2,3-dihydro-1H-indol-2-one on MDA-MB-231 breast\ud cancer cells (triple-negative) in the form of both a cocktail of the separate compounds and a chemically\ud synthesized hybrid (N-hydroxy-N'-[(3Z)-2-oxo-3-(1H-pyrrol-2-ylmethylidene)-2,3-dihydro-1H-indol-\ud 5-yl]octanediamide). Comparative flow cytometric and Western blot analyses were performed on\ud cocktail- and hybrid-treated cells to evaluate cell cycle distribution, autophagy/apoptosis modulation,\ud an…

0301 basic medicineVascular Endothelial Growth Factor AIndolesCytotoxicityTriple Negative Breast Neoplasmsbreast cancer; MDA-MB231 cells; histone deacetylase inhibitor; vascular endothelial growth factor receptor-2 inhibitor; cytotoxicity; cell cycle; apoptosis; autophagy; mitochondrial metabolismHydroxamic AcidsCatalysi0302 clinical medicineBreast cancerTumor Cells CulturedCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaSpectroscopyVorinostatVascular endothelial growth factor receptor-2 inhibitorApoptosis; Autophagy; Breast cancer; Cell cycle; Cytotoxicity; Histone deacetylase inhibitor; MDA-MB231 cells; Mitochondrial metabolism; Vascular endothelial growth factor receptor-2 inhibitor; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryKinaseHistone deacetylase inhibitorapoptosisComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineCell cycleFlow CytometryComputer Science ApplicationsCell biologyMDA-MB231 cell030220 oncology & carcinogenesisFemaleQD0241Programmed cell deathmedicine.drug_classCell SurvivalBlotting WesternAntineoplastic AgentsBiologyCell cycleCatalysisArticleInorganic Chemistry03 medical and health sciencesmedicineAutophagyHumansPhysical and Theoretical ChemistryProtein Kinase InhibitorsMolecular BiologyQD0415Histone deacetylase inhibitorAutophagyOrganic ChemistryApoptosiHistone Deacetylase Inhibitors030104 developmental biologyApoptosisMitochondrial metabolismMDA-MB231 cellsHistone deacetylaseInternational Journal of Molecular Sciences; Volume 17; Issue 8; Pages: 1235
researchProduct