Search results for "kinase inhibitors"

showing 10 items of 269 documents

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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Timely recognition of cardiovascular toxicity by anticancer agents: a common objective of the pharmacologist, oncologist and cardiologist.

2011

Both conventional and new anticancer drugs can frequently cause adverse cardiovascular effects, which can span from subclinical abnormalities to serious life-threatening and sometimes fatal events. This review examines the principal basic and clinical elements that may be of profit to identify, prevent and treat such toxicities. Clearly, the accomplishment of such objectives requires the strong commitment and cooperation of different professional figures including, but not limited to, pharmacologists, oncologists and cardiologists. The aspect of anticancer drug cardiotoxicity seems to be somehow underestimated, mainly due to inadequate reporting of adverse reactions from oncology drugs in t…

Cardiovascular toxicityTime FactorsSettore MED/06 - Oncologia MedicaPharmacology toxicologyCardiologyAntineoplastic AgentsPharmacologyToxicologyMedical OncologyCardiotoxinsCardiovascular SystemProfessional RolePharmacovigilanceMedicineAnimalsHumansPhysician's RoleMolecular BiologyPharmacologyCardiotoxicitybusiness.industryCardiovascular toxicity Anthracyclines Tyrosine kinase inhibitors TrastuzumabSettore MED/11 - Malattie Dell'Apparato CardiovascolareAnticancer drugLaboratory PersonnelCardiovascular DiseasesSettore BIO/14 - FarmacologiaCardiology and Cardiovascular MedicinebusinessOncology drugsCardiovascular toxicology
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Kinetic and thermodynamic insights into interaction of erlotinib with epidermal growth factor receptor: Surface plasmon resonance and molecular docki…

2020

Abstract Epidermal growth factor receptor (EGFR) plays an important role in cell proliferation at non-small cell lung cancer (NSCLC). Therefore, targeted therapy of cancer via this kind of receptor is highly interested. Small molecule drugs such as erlotinib and gefitinib inhibit EGFR tyrosine kinase and thus suppress cell proliferation. At this paper, erlotinib interaction with EGFR on the cell surface was studied via surface plasmon resonance (SPR) and molecular docking methods. Kinetic parameters indicated that erlotinib affinity toward EGFR was increased through increment of temperature. The thermodynamic analysis showed that van der Waals and hydrogen binding forces play a major role i…

Cell Culture TechniquesQuantitative Structure-Activity RelationshipAntineoplastic Agents02 engineering and technologyMolecular Dynamics SimulationBiochemistry03 medical and health sciencesErlotinib HydrochlorideGefitinibStructural BiologymedicineHumansheterocyclic compoundsEpidermal growth factor receptorSurface plasmon resonanceReceptorneoplasmsMolecular BiologyProtein Kinase Inhibitors030304 developmental biology0303 health sciencesBinding SitesbiologyChemistryCell growthGeneral MedicineSurface Plasmon Resonance021001 nanoscience & nanotechnologySmall moleculerespiratory tract diseasesErbB ReceptorsMolecular Docking SimulationKineticsDocking (molecular)biology.proteinBiophysicsThermodynamicsErlotinib0210 nano-technologymedicine.drugProtein BindingInternational journal of biological macromolecules
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Recent advances in the development of cyclin-dependent kinase 7 inhibitors.

2019

Abstract Cyclin dependent kinase 7 (CDK7) plays a double role as it activates several other cyclin dependent kinases and participates to the initiation of transcription. This kinase is overexpressed in various types of tumors. Relatively few selective CDK7 inhibitors have been up to now disclosed. Most of these inhibitors belong to two chemical families: pyrazolopyrimidines and pyrazolotriazines on one side and pyrimidines on another side. They also differ by their molecular mechanism of action. Some are acting as competitive inhibitors and some others are covalent inhibitors. With these tools, the understanding of the potential therapeutic interest of CDK7 inhibitors in cancer is rapidly g…

Cell SurvivalAntineoplastic Agents01 natural sciences03 medical and health sciencesDrug DevelopmentCyclin-dependent kinaseTranscription (biology)Cell Line TumorDrug DiscoverymedicineAnimalsHumansIC50Protein Kinase Inhibitors030304 developmental biologyPharmacology0303 health sciencesbiology010405 organic chemistryChemistryKinaseTriazinesOrganic ChemistryGeneral Medicinemedicine.diseaseCyclin-Dependent Kinases0104 chemical sciencesLeukemiaPyrimidinesbiology.proteinCancer researchMolecular mechanismCyclin-dependent kinase 7Cyclin-Dependent Kinase-Activating KinaseEuropean journal of medicinal chemistry
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Computational Evaluation and In Vitro Validation of New Epidermal Growth Factor Receptor Inhibitors

2020

Background:The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein that acts as a receptor of extracellular protein ligands of the epidermal growth factor (EGF/ErbB) family. It has been shown that EGFR is overexpressed by many tumours and correlates with poor prognosis. Therefore, EGFR can be considered as a very interesting therapeutic target for the treatment of a large variety of cancers such as lung, ovarian, endometrial, gastric, bladder and breast cancers, cervical adenocarcinoma, malignant melanoma and glioblastoma.Methods:We have followed a structure-based virtual screening (SBVS) procedure with a library composed of several commercial collections of chemicals (615,46…

Cell SurvivalDrug Evaluation PreclinicalAntineoplastic Agents01 natural sciencesReceptor tyrosine kinaseStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineErbBEpidermal growth factorCell Line TumorDrug DiscoverymedicineHumansEpidermal growth factor receptorPropidium iodideProtein Kinase InhibitorsCell ProliferationEGFR inhibitorsDose-Response Relationship DrugMolecular StructurebiologyCell growthChemistryGeneral Medicine0104 chemical sciencesErbB ReceptorsMolecular Docking Simulation010404 medicinal & biomolecular chemistry030220 oncology & carcinogenesisbiology.proteinCancer researchErlotinibDrug Screening Assays Antitumormedicine.drugCurrent Topics in Medicinal Chemistry
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Synthesis and antiproliferative activity of substituted 3[2-(1H-indol-3-yl)-1,3-thiazol-4-yl]-1H-pyrrolo[3,2-b]pyridines, marine alkaloid nortopsenti…

2014

A large number of indolyl-4-azaindolyl thiazoles, nortopsentin analogues, were conveniently synthesized. The antiproliferative activity of the new derivatives was examined against four human tumor cell lines with different histologic origin. Seven derivatives consistently reduced the growth of the experimental models independently of TP53 gene status and exhibited the highest activity against the malignant peritoneal mesothelioma (STO) cell line. The most active compound of this series acts as a CDK1 inhibitor, and was found to cause cell cycle arrest at G 2 /M phase, to induce apoptosis by preventing the phosphorylation of survivin in Thr 34 and to increase the cytotoxic activity of paclit…

Cell cycle checkpointCDK1 InhibitorsAntiproliferative Activity CDK1 Inhibitors Diffuse Malignant Peritoneal Mesothelioma Nortopsentin Analogues SurvivinPyridinesStereochemistrySurvivinDiffuse Malignant Peritoneal MesotheliomaAntineoplastic AgentsApoptosisAntiproliferative Activity; CDK1 Inhibitors; Diffuse Malignant Peritoneal Mesothelioma; Nortopsentin Analogues; SurvivinBiochemistryCell LineAntiproliferative ActivityStructure-Activity Relationshipchemistry.chemical_compoundDrug DiscoverySurvivinHumansCytotoxic T cellProtein Kinase InhibitorsCell ProliferationPharmacologyCyclin-dependent kinase 1AlkaloidOrganic ChemistrySettore CHIM/08 - Chimica FarmaceuticaPaclitaxelchemistryCell cultureApoptosisNortopsentin AnaloguesMolecular Medicine
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Comparative analysis of virtual screening approaches in the search for novel EphA2 receptor antagonists

2015

The EphA2 receptor and its ephrin-A1 ligand form a key cell communication system, which has been found overexpressed in many cancer types and involved in tumor growth. Recent medicinal chemistry efforts have identified bile acid derivatives as low micromolar binders of the EphA2 receptor. However, these compounds suffer from poor physicochemical properties, hampering their use in vivo. The identification of compounds able to disrupt the EphA2-ephrin-A1 complex lacking the bile acid scaffold may lead to new pharmacological tools suitable for in vivo studies. To identify the most promising virtual screening (VS) protocol aimed at finding novel EphA2 antagonists, we investigated the ability of…

Cell signalingDatabases Pharmaceuticaldrug designPharmaceutical ScienceComputational biologyBiologyCrystallography X-RayMolecular Docking SimulationArticleAnalytical Chemistrylcsh:QD241-441Structure-Activity RelationshipUser-Computer Interfacelcsh:Organic chemistryPPI inhibitorsDrug Discoveryshape screeningStructure–activity relationshipPhysical and Theoretical ChemistryReceptorProtein Kinase InhibitorsVirtual screeningMolecular StructureDrug discoveryReceptor EphA2EphA2 antagonistOrganic ChemistryEphrin-A1virtual screeningEPH receptor A2C700Combinatorial chemistryMolecular Docking SimulationUniPR129Chemistry (miscellaneous)Docking (molecular)dockingMolecular Medicinepharmacophore search
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Endothelial transcriptomic changes induced by oxidized low density lipoprotein disclose an up-regulation of Jak-Stat pathway.

2015

Oxidized low density lipoproteins (oxLDLs) act as an etiological factor in the development of atherosclerosis by modifying the biological properties of endothelial cells through mechanisms of vascular inflammation. To deepen the oxLDL changes at cellular level, a transcriptomic analysis of human umbilical artery endothelial cells (HUAECs) treated with oxLDL was performed to identify the modified signaling pathways. Total RNA was isolated from HUAECs treated with oxLDL (100 μg/ml). Gene expression analysis was carried out using Affymetrix oligonucleotide microarrays. Biological pathway analysis was performed using Ingenuity Pathway Analysis software. Microarray assay demonstrated that oxLDL …

Cell signalingTime FactorsPhysiologyBlotting WesternBiologyReal-Time Polymerase Chain ReactionTransfectionGene Expression Regulation EnzymologicBiological pathwayTranscriptomeRNA interferenceGene expressionHuman Umbilical Vein Endothelial CellsHumansGene Regulatory NetworksProtein Kinase InhibitorsCells CulturedOligonucleotide Array Sequence AnalysisPharmacologyGene Expression ProfilingJAK-STAT signaling pathwaySTAT2 Transcription FactorJanus Kinase 1Janus Kinase 2Cell biologyEndothelial stem cellLipoproteins LDLSTAT1 Transcription FactorMolecular Medicinelipids (amino acids peptides and proteins)RNA InterferenceSignal transductionTranscriptomeSignal TransductionVascular pharmacology
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Single-cell cloning of colon cancer stem cells reveals a multi-lineage differentiation capacity.

2008

Colon carcinoma is one of the leading causes of death from cancer and is characterized by a heterogenic pool of cells with distinct differentiation patterns. Recently, it was reported that a population of undifferentiated cells from a primary tumor, so-called cancer stem cells (CSC), can reconstitute the original tumor on xenotransplantation. Here, we show that spheroid cultures of these colon CSCs contain expression of CD133, CD166, CD44, CD29, CD24, Lgr5, and nuclear β-catenin, which have all been suggested to mark the (cancer) stem cell population. More importantly, by using these spheroid cultures or freshly isolated tumor cells from multiple colon carcinomas, we now provide compelling…

Cellular differentiationPopulationmultilineage differentationCell SeparationAdenocarcinomaTissue Culture TechniquesPhosphatidylinositol 3-KinasesCancer stem cellBiomarkers TumormedicineHumansCell LineageeducationProtein Kinase InhibitorsPhosphoinositide-3 Kinase Inhibitorseducation.field_of_studyMultidisciplinarybiologyCD44LGR5Cell DifferentiationBiological Sciencesmedicine.diseasePrimary tumorCell biologyIsolated Tumor CellsColonic NeoplasmsNeoplastic Stem Cellsbiology.proteinStem cell
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Proliferation state and polo-like kinase1 dependence of tumorigenic colon cancer cells.

2012

Abstract Tumor-initiating cells are responsible for tumor maintenance and relapse in solid and hematologic cancers. Although tumor-initiating cells were initially believed to be mainly quiescent, rapidly proliferating tumorigenic cells were found in breast cancer. In colon cancer, the proliferative activity of the tumorigenic population has not been defined, although it represents an essential parameter for the development of more effective therapeutic strategies. Here, we show that tumorigenic colon cancer cells can be found in a rapidly proliferating state in vitro and in vivo, both in human tumors and mouse xenografts. Inhibitors of polo-like kinase1 (Plk1), a mitotic kinase essential fo…

Colorectal cancerCancer stem cellscolorectal cancercell proliferationcell cycle.Cell Cycle ProteinsMice0302 clinical medicineMice Inbred NODAC133 AntigenRNA Small Interfering0303 health scienceseducation.field_of_studyPteridinesCell CycleCell cycleImmunohistochemistry3. Good healthMitochondriaGene Expression Regulation Neoplastic030220 oncology & carcinogenesisColonic NeoplasmsMolecular MedicineFemaleStem cellPopulationTransplantation HeterologousCell Growth ProcessesBiologyProtein Serine-Threonine KinasesPLK103 medical and health sciencesCancer stem cellAntigens CDCell Line TumorProto-Oncogene ProteinsmedicineAnimalsHumanseducationProtein Kinase Inhibitors030304 developmental biologyGlycoproteinsSettore MED/04 - Patologia GeneraleCell growthCell Biologymedicine.diseaseTumor progressionImmunologyCancer researchPeptidesDevelopmental BiologyStem cells (Dayton, Ohio)
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