Search results for " Targeted therapy"

showing 10 items of 198 documents

The potential of neurotrophic tyrosine kinase (NTRK) inhibitors for treating lung cancer

2016

Abstract: Introduction: Molecular alterations in neurotrophic tyrosine kinase (NTRK) genes have been identified in several solid tumors including lung cancer. Pre-clinical and clinical evidence suggested their potential role as oncogenic drivers and predictive biomarkers for targeted inhibition, leading to the clinical development of a new class of compounds blocking the NTRK molecular pathway, which are currently undner early clinical investigation. Area covered: This review describes the biology of the NTRK pathway and its molecular alterations in lung cancer. It focuses on the pre-clinical and clinical development of emerging NTRK inhibitors, which have shown very promising activity in e…

0301 basic medicineLung NeoplasmsNTRKinhibitorsNTRK1/2/3Settore MED/06 - Oncologia Medicamedicine.medical_treatmentReceptor Protein-Tyrosine KinasesEntrectinibPharmacologyTargeted therapy03 medical and health sciences0302 clinical medicineMedicineAnimalsHumansPharmacology (medical)In patientNTRKinhibitorLung cancerProtein Kinase InhibitorsTrkA/B/CPharmacologyNTRK1/2/3; TrkA/B/C; NTRKinhibitors; targeted therapy; lung cancerbiologybusiness.industryPharmacology. TherapyReceptor Protein-Tyrosine KinasesGeneral Medicinemedicine.diseasetargeted therapySettore CHIM/08 - Chimica Farmaceuticalung cancer030104 developmental biology030220 oncology & carcinogenesisbiology.proteinCancer researchbusinessEarly phaseTyrosine kinaseNeurotrophin
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RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1 and TP53 pathways and regulatory miRs as therapeutic targets in hepatocellular carcinoma

2019

Introduction: Hepatocellular carcinoma (HCC) is a significant problem globally because of viral infections and the increasing incidence of obesity and fatty liver disease. However, it is difficult to treat because its inherent genetic heterogeneity results in activation of numerous signaling pathways. Kinases have been targeted for decades with varying results, but the development of therapeutic resistance is a major challenge. Areas covered: The key roles of the RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1, TP53 microRNAs (miRs) as therapeutic targets are discussed and we suggests novel approaches for targeting miRs or their downstream targets to combat HCC. We performed literature searches using…

0301 basic medicineMAPK/ERK pathwayCarcinoma HepatocellularHepatocellular carcinmamedicine.medical_treatmentClinical BiochemistryAntineoplastic AgentsmTORC1signal transduction inhibitorsTargeted therapy03 medical and health sciences0302 clinical medicineDrug DiscoverymicroRNAmedicinePTENAnimalsHumanscancerMolecular Targeted TherapyTP53HCCRAS/RAF/MEK/ERKProtein kinase BPI3K/AKT/mTOR pathwaymiRNAPharmacologybiologybusiness.industryKinaseLiver NeoplasmsMirhepatocellular carcinomatargeted therapyGene Expression Regulation NeoplasticMicroRNAssignal transduction inhibitor030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbiology.proteinCancer researchMolecular MedicinePI3K/PTEN/AKTbusinessSignal Transduction
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Effects of mutations in Wnt/β-catenin, hedgehog, Notch and PI3K pathways on GSK-3 activity—Diverse effects on cell growth, metabolism and cancer

2016

Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase that participates in an array of critical cellular processes. GSK-3 was first characterized as an enzyme that phosphorylated and inactivated glycogen synthase. However, subsequent studies have revealed that this moon-lighting protein is involved in numerous signaling pathways that regulate not only metabolism but also have roles in: apoptosis, cell cycle progression, cell renewal, differentiation, embryogenesis, migration, regulation of gene transcription, stem cell biology and survival. In this review, we will discuss the roles that GSK-3 plays in various diseases as well as how this pivotal kinase interacts with multiple sign…

0301 basic medicineMAPK/ERK pathwaySettore MED/06 - Oncologia MedicaCellular differentiationPI3KTargeted therapyGlycogen Synthase Kinase 3Phosphatidylinositol 3-Kinases0302 clinical medicineGSK-3Neoplasmsbeta CateninGSK-3biologyReceptors NotchKinaseWnt signaling pathwayWnt/beta-cateninCell DifferentiationCell biologyGene Expression Regulation Neoplastic030220 oncology & carcinogenesismTORAkt; GSK-3; Hedgehog; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; mTORSignal TransductionBeta-cateninNotchAkt GSK-3 Hedgehog mTOR Notch PI3K Targeted therapy Therapy resistance Wnt/beta-cateninCell Survivalmacromolecular substancesNO03 medical and health sciencesAkt; GSK-3 Hedgehog Notch PI3K Targeted therapy Therapy resistance Wnt/beta-catenin mTORAnimalsHumansHedgehog ProteinsProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationAktTherapy resistanceAkt; GSK-3; Hedgehog; mTOR; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; Molecular Biology; Cell BiologyCell BiologyWnt ProteinsMicroRNAs030104 developmental biologyMutationCancer researchbiology.proteinTumor Suppressor Protein p53Hedgehog
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Targeting Angiogenesis in Biliary Tract Cancers: An Open Option

2017

Abstract: Biliary tract cancers (BTCs) are characterized by a bad prognosis and the armamentarium of drugs for their treatment is very poor. Although the inflammatory status of biliary tract represents the first step in the cancerogenesis, the microenvironment also plays a key role in the pathogenesis of BTCs, promoting tumor angiogenesis, invasion and metastasis. Several molecules, such as vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF), are involved in the angiogenesis process and their expression on tumor samples has been explored as prognostic marker in both cholangiocarcinoma and gallbladder cancer. Recent studies evaluated the genomic landscape of BTCs and…

0301 basic medicineMAPK/ERK pathwayVascular Endothelial Growth Factor AAngiogenesisDrug Evaluation PreclinicalTyrosine kinase inhibitorAngiogenesis InhibitorsReviewFibroblast growth factorCatalysiMetastasisAntineoplastic Agentlcsh:Chemistrychemistry.chemical_compoundangiogenesis0302 clinical medicinetyrosine kinase inhibitorsMolecular Targeted Therapylcsh:QH301-705.5SpectroscopyClinical Trials as TopicMonoclonal antibodieNeovascularization Pathologicvascular endothelial growth factorComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineComputer Science ApplicationsVascular endothelial growth factorGene Expression Regulation NeoplasticAngiogenesiChemistryBiliary Tract NeoplasmsTreatment OutcomeBiliary Tract Neoplasm030220 oncology & carcinogenesismonoclonal antibodiesTyrosine kinaseAngiogenesis InhibitorHumanSignal TransductionProtein Kinase InhibitorAntineoplastic Agentsbiliary tract cancersBiologyModels BiologicalAngiogenesis; Biliary tract cancers; Monoclonal antibodies; Tyrosine kinase inhibitors; Vascular endothelial growth factor; Angiogenesis Inhibitors; Animals; Antineoplastic Agents; Biliary Tract Neoplasms; Clinical Trials as Topic; Drug Evaluation Preclinical; Gene Expression Regulation Neoplastic; Genetic Variation; Humans; Models Biological; Neovascularization Pathologic; Protein Kinase Inhibitors; Signal Transduction; Treatment Outcome; Vascular Endothelial Growth Factor A; Molecular Targeted Therapy; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisInorganic Chemistry03 medical and health sciencesIn vivomedicineAnimalsHumansPhysical and Theoretical ChemistryGallbladder cancerMolecular BiologyProtein Kinase InhibitorsBiologyAnimalOrganic ChemistryGenetic Variationmedicine.disease030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999Immunologyangiogenesis; biliary tract cancers; monoclonal antibodies; tyrosine kinase inhibitors; vascular endothelial growth factorCancer researchBiliary tract cancerInternational Journal of Molecular Sciences
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Phase 2 study of the bispecific T-cell engager (BiTE) antibody blinatumomab in relapsed/refractory diffuse large B-cell lymphoma.

2015

Few patients with relapsed/refractory diffuse large B-cell lymphoma (DLBCL) achieve prolonged disease-free survival. Blinatumomab, a bispecific T-cell engaging antibody construct, transiently links CD3-positive T cells to CD19-positive B cells. This phase 2 study evaluated stepwise (9-28-112 μg/d with weekly dose increases; n = 23) or flat (112 μg/d; n = 2) dosing of blinatumomab by continuous infusion, with dexamethasone prophylaxis, in patients with relapsed/refractory DLBCL. Patients received a median of 3 prior lines of therapy. Median time since last regimen was 1.5 months. Seventeen patients ended treatment in cycle 1 (induction), 7 in cycle 2 (consolidation), and 1 in retreatment. Am…

0301 basic medicineMaleCD3 ComplexClinical Trials and ObservationsSalvage therapyPhases of clinical researchKaplan-Meier EstimateBiochemistryGastroenterologyDexamethasone0302 clinical medicineRecurrenceAntibodies BispecificMedicineMolecular Targeted TherapyFatigueRemission InductionHematologyMiddle AgedTumor Burden030220 oncology & carcinogenesisBlinatumomabFemaleImmunotherapyLymphoma Large B-Cell Diffusemedicine.drugAdultmedicine.medical_specialtyFeverImmunologyAntigens CD19Antineoplastic AgentsDisease-Free SurvivalDrug Administration Schedule03 medical and health sciencesAntigens NeoplasmInternal medicineHumansDosingAdverse effectAgedSalvage TherapyDose-Response Relationship Drugbusiness.industryCell Biologymedicine.diseaseLymphomaSurgeryRegimen030104 developmental biologyNervous System DiseasesbusinessDiffuse large B-cell lymphomaBlood
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Treatment patterns for metastatic colorectal cancer in Spain

2020

Abstract Purpose The primary aim of this retrospective study was to describe the treatment patterns according to the type of treatment received by patients with metastatic colorectal cancer (mCRC) in Spain. Methods This was a retrospective, observational, multicenter study performed by 33 sites throughout Spain that included consecutive patients aged 18 years or older who had received or were receiving treatment for mCRC. Results At the time of inclusion, of the 873 evaluable patients, 507 (58%) had received two lines, 235 (27%) had received three lines, 106 (12%) had received four lines, and the remaining patients had received up to ten lines. The most frequent chemotherapy schemes were th…

0301 basic medicineMaleCancer ResearchColorectal cancermedicine.medical_treatmentmedicine.disease_causeTargeted therapy0302 clinical medicineFOLFOXAntineoplastic Combined Chemotherapy ProtocolsKRAS/BRAF mutation statusMolecular Targeted TherapyNeoplasm MetastasisCàncerTreatment patternsGeneral MedicineMiddle AgedTreatment OutcomeOncology030220 oncology & carcinogenesisFOLFIRIMetastaticFemaleKRASGuideline AdherenceColorectal NeoplasmsCàncer Pacientsmedicine.drugResearch ArticleProto-Oncogene Proteins B-rafmedicine.medical_specialtyProto-Oncogene Proteins p21(ras)03 medical and health sciencesInternal medicinemedicineHumansAgedRetrospective StudiesClinical practice guidelineChemotherapybusiness.industryRetrospective cohort studymedicine.diseaseColorectal cancerdigestive system diseases030104 developmental biologySpainMutationObservational studybusiness
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NUPR1, a new target in liver cancer: implication in controlling cell growth, migration, invasion and sorafenib resistance

2016

AbstractSorafenib, an oral multikinase inhibitor, is the only approved agent for the treatment of advanced hepatocellular carcinoma (HCC). However, its benefits are modest, and as its mechanisms of action remain elusive, a better understanding of its anticancer effects is needed. Based on our previous study results, we investigated here the implication of the nuclear protein 1 (NUPR1) in HCC and its role in sorafenib treatment. NUPR1 is a stress-inducible protein that is overexpressed in various malignancies, but its role in HCC is not yet fully understood. We found that NUPR1 expression was significantly higher in primary human HCC samples than in the normal liver. Knockdown of NUPR1 signi…

0301 basic medicineMaleCancer ResearchHepatocellular carcinomaCore Binding Factor Alpha 1 Subunit0302 clinical medicineCell MovementBasic Helix-Loop-Helix Transcription FactorsMolecular Targeted TherapyRNA Small InterferingRegulation of gene expressionAged 80 and overGene knockdownRELBLiver NeoplasmsMiddle AgedSorafenib3. Good healthNeoplasm ProteinsSorafenib.Gene Expression Regulation Neoplastic030220 oncology & carcinogenesisGene Knockdown TechniquesOriginal ArticleFemalemedicine.drugSorafenibNiacinamideCarcinoma HepatocellularRUNX2 GeneCell SurvivalIER3ImmunologyDown-RegulationBiology03 medical and health sciencesCellular and Molecular NeuroscienceYoung AdultmedicineGene silencingHumansNeoplasm InvasivenessGene SilencingneoplasmsAgedCell ProliferationCell growthGene Expression ProfilingPhenylurea CompoundsTranscription Factor RelBComputational BiologyMembrane ProteinsCell BiologyNuclear protein-1digestive system diseases030104 developmental biologyDrug Resistance NeoplasmCancer researchApoptosis Regulatory ProteinsTranscriptomeCell Death & Disease
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Moving Towards Precision Urologic Oncology: Targeting Enzalutamide-resistant Prostate Cancer and Mutated Forms of the Androgen Receptor Using the Nov…

2017

Abstract Darolutamide (ODM-201) is a novel androgen receptor (AR) antagonist with a chemical structure distinctly different from currently approved AR antagonists that targets both wild-type and mutated ligand binding domain variants to inhibit AR nuclear translocation. Here, we evaluate the activity of darolutamide in enzalutamide-resistant castration resistant prostate cancer (CRPC) as well as in AR mutants detected in patients after treatment with enzalutamide, abiraterone, or bicalutamide. Darolutamide significantly inhibited cell growth and AR transcriptional activity in enzalutamide-resistant MR49F cells in vitro, and led to decreased tumor volume and serum prostate-specific antigen l…

0301 basic medicineMaleModels MolecularTime FactorsTranscription GeneticProtein ConformationProstate cancerchemistry.chemical_compoundMice0302 clinical medicineMolecular Targeted TherapyTumor BurdenDarolutamideReceptors Androgen030220 oncology & carcinogenesisBenzamidesmedicine.drugSignal Transductionmedicine.medical_specialtyBicalutamideUrologyPartial agonist03 medical and health sciencesStructure-Activity RelationshipIn vivoInternal medicineCell Line TumorNitrilesPhenylthiohydantoinmedicineAndrogen Receptor AntagonistsEnzalutamideAnimalsHumansCell ProliferationDose-Response Relationship DrugCell growthbusiness.industryProstatic Neoplasmsmedicine.diseaseXenograft Model Antitumor AssaysAndrogen receptor030104 developmental biologyEndocrinologychemistryDrug Resistance NeoplasmMutationCancer researchPyrazolesbusinessEuropean urology
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IL-34–Dependent Intrarenal and Systemic Mechanisms Promote Lupus Nephritis in MRL-Faslpr Mice

2019

Background In people with SLE and in the MRL- Fas lpr lupus mouse model, macrophages and autoantibodies are central to lupus nephritis. IL-34 mediates macrophage survival and proliferation, is expressed by tubular epithelial cells (TECs), and binds to the cFMS receptor on macrophages and to a newly identified second receptor, PTPRZ. Methods To investigate whether IL-34–dependent intrarenal and systemic mechanisms promote lupus nephritis, we compared lupus nephritis and systemic illness in MRL- Fas lpr mice expressing IL-34 and IL-34 knockout (KO) MRL- Fas lpr mice. We also assessed expression of IL-34 and the cFMS and PTPRZ receptors in patients with lupus nephritis. Results Intrarenal IL-3…

0301 basic medicineMice Inbred MRL lprChemokineCell SurvivalLupus nephritisRisk AssessmentMonocytesMice03 medical and health sciences0302 clinical medicineSpecies Specificityimmune system diseasesmedicineAnimalsMacrophageMolecular Targeted Therapyskin and connective tissue diseasesCells CulturedCell ProliferationMice KnockoutSystemic lupus erythematosusCell Deathbiologybusiness.industryInterleukinsMacrophagesGeneral MedicineMonocyte proliferationmedicine.diseaseLupus NephritisMice Inbred C57BLDisease Models AnimalBasic ResearchKidney Tubules030104 developmental biologyGene Expression RegulationNephrology030220 oncology & carcinogenesisImmunologyKnockout mouseDisease Progressionbiology.proteinChemokinesbusinessMacrophage proliferationNephritisJournal of the American Society of Nephrology
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Ribosome-Targeting Antibiotics Impair T Cell Effector Function and Ameliorate Autoimmunity by Blocking Mitochondrial Protein Synthesis

2019

Summary While antibiotics are intended to specifically target bacteria, most are known to affect host cell physiology. In addition, some antibiotic classes are reported as immunosuppressive for reasons that remain unclear. Here, we show that Linezolid, a ribosomal-targeting antibiotic (RAbo), effectively blocked the course of a T cell-mediated autoimmune disease. Linezolid and other RAbos were strong inhibitors of T helper-17 cell effector function in vitro, showing that this effect was independent of their antibiotic activity. Perturbing mitochondrial translation in differentiating T cells, either with RAbos or through the inhibition of mitochondrial elongation factor G1 (mEF-G1) progressi…

0301 basic medicineMitochondrial translationmedicine.medical_treatmentT-LymphocytesCellMitochondrionmedicine.disease_causeRibosomemitochondrial translationOxidative PhosphorylationantibioticsAutoimmunityACTIVATIONMice0302 clinical medicineribosome-targetingMedicine and Health SciencesImmunology and AllergyTRANSCRIPTION FACTORMolecular Targeted TherapyMice Knockout0303 health sciencesEffectorExperimental autoimmune encephalomyelitisautoimmunityCell DifferentiationPeptide Elongation Factor GAnti-Bacterial Agents3. Good healthCell biologymitochondriaInfectious DiseasesCytokinemedicine.anatomical_structureRESPIRATION030220 oncology & carcinogenesisEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisT cellImmunologyINHIBITIONT cellsBiologyOXAZOLIDINONEPeptides CyclicArticleMitochondrial Proteins03 medical and health sciencesNAD+medicineAnimalsHumanselongation factor G1030304 developmental biologyAutoimmune diseaseBacteriaLinezolidBiology and Life SciencesPATHWAYSDNANADmedicine.diseaseIn vitroMice Inbred C57BL030104 developmental biologyTh17 CellsArgyrinCHLORAMPHENICOLMEMBRANERibosomesImmunity
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