Search results for "Kinase inhibitor"

showing 10 items of 414 documents

Personalization of regorafenib treatment in metastatic gastrointestinal stromal tumours in real-life clinical practice

2017

Background: Regorafenib (REG) has now been approved as the standard third-line therapy in metastatic gastrointestinal stromal tumour (GIST) patients at the recommended dose and schedule of 160 mg once daily for the first 3 weeks of each 4-week cycle. However, it has a relevant toxicity profile that mainly occurs within the first cycles of therapy, and dose and schedule adjustments are often required to reduce the frequency or severity of adverse events and to avoid early treatment discontinuation. To date, large amounts of data on the use of REG in metastatic GIST patients in daily clinical practice are not available, and we lack information about how this treatment personalization really a…

0301 basic medicineOncologymedicine.medical_specialtyScheduleStromal cellSettore MED/06 - Oncologia Medicalcsh:RC254-282PersonalizationNO03 medical and health scienceschemistry.chemical_compound0302 clinical medicinetyrosine kinase inhibitorQuality of lifeInternal medicineRegorafenibtyrosine kinase inhibitorsmedicineOriginal Researchreferral centresGiSTbusiness.industryGIST; personalized treatment; quality of life; referral centres; regorafenib; tyrosine kinase inhibitors; OncologyGastrointestinal stromal tumourslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenspersonalized treatmentClinical PracticeGIST; personalized treatment; quality of life; referral centres; regorafenib; tyrosine kinase inhibitorsreferral centre030104 developmental biologychemistryquality of lifeOncology030220 oncology & carcinogenesisregorafenibbusinessGIST personalized treatment quality of life referral centres regorafenib tyrosine kinase inhibitorsGIST
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A narrative review of MET inhibitors in non-small cell lung cancer with MET exon 14 skipping mutations

2021

Treatment of advanced non-small cell lung cancer (NSCLC) has radically improved in the last years due to development and clinical approval of highly effective agents including immune checkpoint inhibitors (ICIs) and oncogene-directed therapies. Molecular profiling of lung cancer samples for activated oncogenes, including epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), c-ros oncogene 1 (ROS1) and BRAF, is routinely performed to select the most appropriate up-front treatment. However, the identification of new therapeutic targets remains a high priority. Recently, MET exon 14 skipping mutations have emerged as novel actionable oncogenic alterations in NSCLC, sensiti…

0301 basic medicineOncologymedicine.medical_specialtybiologybusiness.industryCancernon-small cell lung cancer (NSCLC)medicine.disease03 medical and health sciencesExon030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesisInternal medicineROS1biology.proteinMET; MET exon 14 skipping mutations; MET-tyrosine kinase inhibitors (TKIs); Non-small cell lung cancer (NSCLC)MedicineAnaplastic lymphoma kinaseEpidermal growth factor receptorbusinessLung cancerTyrosine kinase
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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
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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
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Potential treatment strategy for the rare osimertinib resistant mutation EGFR L718Q

2020

Epidermal growth factor receptor (EGFR) L718Q is a rare resistant mutation which independently leads to third-generation tyrosine kinase inhibitor (TKI) resistance. Although a few studies have examined its resistance mechanisms, no effective treatment strategy has yet been proposed for patients with this mutation. Here, we report an effective treatment strategy for the rare EGFR L718Q mutation for the first time. A 44-year-old Chinese male patient initially presented with the sensitizing EGFR L858R mutation, and the progression-free survival (PFS) time after initial icotinib treatment was 9 months. When the progression of the disease (PD) and the EGFR T790M mutation were identified, he did …

0301 basic medicinePulmonary and Respiratory MedicineOncologyiMDT Cornermedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentnon-small cell lung cancer (NSCLC)Tyrosine-kinase inhibitorTargeted therapy03 medical and health sciencesT790M0302 clinical medicineInternal medicinemedicineOsimertinibEpidermal growth factor receptorbiologybusiness.industrymedicine.disease030104 developmental biology030220 oncology & carcinogenesisMutation (genetic algorithm)Icotinibbiology.proteinbusiness
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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
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PI3K-driven HER2 expression is a potential therapeutic target in colorectal cancer stem cells

2020

ObjectiveCancer stem cells are responsible for tumour spreading and relapse. Human epidermal growth factor receptor 2 (HER2) expression is a negative prognostic factor in colorectal cancer (CRC) and a potential target in tumours carrying the gene amplification. Our aim was to define the expression of HER2 in colorectal cancer stem cells (CR-CSCs) and its possible role as therapeutic target in CRC resistant to anti- epidermal growth factor receptor (EGFR) therapy.DesignA collection of primary sphere cell cultures obtained from 60 CRC specimens was used to generate CR-CSC mouse avatars to preclinically validate therapeutic options. We also made use of the ChIP-seq analysis for transcriptional…

0301 basic medicineReceptor ErbB-2Colorectal cancerCetuximabcolorectal cancermedicine.disease_cause03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineSettore MED/04 - PATOLOGIA GENERALECancer stem cellstem cellsTumor Cells CulturedmedicineAdjuvant therapyAnimalsHumansEpidermal growth factor receptorProtein kinase BPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsMitogen-Activated Protein Kinase Kinasesdrug resistancebiologybusiness.industryGastroenterologyTrastuzumabmedicine.diseaseantibody targeted therapy030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisNeoplastic Stem CellsCancer researchbiology.proteinKRASPhosphatidylinositol 3-KinaseStem cellColorectal Neoplasmsbusiness
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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
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Gut microbiota and cancer: How gut microbiota modulates activity, efficacy and toxicity of antitumoral therapy

2019

Gut microbiota is involved in gastrointestinal carcinogenesis. Also, it modulates the activity, efficacy and toxicity of several chemotherapy agents, such as gemcitabine, cyclophosphamide, irinotecan, cisplatin and 5-Fluorouracil, and target therapy, such as tyrosine kinase inhibitors. More recently, accumulating data suggest that the composition of gut microbiota may also affect efficacy and toxicity of cancer immunotherapy. Therefore, the manipulation of gut microbiota through antibiotics, probiotics, prebiotics or fecal transplantation has been investigating with the aim to improve efficacy and mitigate toxicity of anticancer drugs.

0301 basic medicineSettore MED/06 - Oncologia Medicamedicine.drug_class5-Fluorouracilmedicine.medical_treatmentAntibioticsAntineoplastic AgentsImmune checkpoint inhibitorGut floraPharmacologyIrinotecandigestive systemImmune checkpoint inhibitors03 medical and health sciences0302 clinical medicineCancer immunotherapyNeoplasmsmedicineAnimalsHumansCyclophosphamide5-Fluorouracil; Cisplatin; Cyclophosphamide; Gemcitabine; Immune checkpoint inhibitors; Irinotecan; Microbiota; Tyrosine kinase inhibitorsTyrosine kinase inhibitorsChemotherapybiologybusiness.industryMicrobiotaCancerHematologyFecal Microbiota Transplantationbiology.organism_classificationmedicine.diseaseGemcitabineGemcitabineGastrointestinal MicrobiomeIrinotecan030104 developmental biologyOncology030220 oncology & carcinogenesisToxicityImmunotherapyCisplatinbusinessmedicine.drugCritical Reviews in Oncology/Hematology
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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
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