Search results for "TrkA"

showing 10 items of 10 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
researchProduct

Identification of Differentially Expressed Genes in Papillary Thyroid Carcinomas With and Without Rearrangements of the Tyrosine Kinase Receptors RET…

2005

Background The transforming capacities of RET and/or NTRK1 chimeric oncogenes as well as the molecular background of non-rearranged papillary thyroid carcinomas (PTCs) remain to be elucidated. To assess altered gene expression, we examined PTCs with and without tyrosine kinase receptor rearrangements by mRNA differential display (DD). Materials and methods Six of 13 PTCs examined harbored RET chimeras (3× RET/PTC1, 1× RET/PTC3) and/or NTRK1 chimeras (2× trk, 1× TRK-T3, 2 unknown TRK hybrids). The method of DD analysis was refined by a novel fragment-recovery technique using a high-performance fluorescence scanner. Results Of 500 up- or down-regulated mRNA transcripts, 19 selected fragments …

AdultMaleAdolescentendocrine system diseasesDown-RegulationBiologyReceptor tyrosine kinaseGene expressionHumansThyroid NeoplasmsReceptor trkAGeneAgedCell ProliferationGene RearrangementRegulation of gene expressionGene Expression ProfilingProto-Oncogene Proteins c-retGene rearrangementMiddle AgedCarcinoma PapillaryUp-RegulationGene Expression Regulation NeoplasticGene expression profilingTumor progressionTrk receptorDisease ProgressionCancer researchbiology.proteinFemaleSurgeryJournal of Surgical Research
researchProduct

Heterotopic ossifications and Charcot joints: Congenital insensitivity to pain with anhidrosis (CIPA) and a novel NTRK1 gene mutation

2018

Abstract Congenital insensitivity to pain with anhidrosis (CIPA), also known as hereditary sensory and autonomic neuropathy type IV (HSAN-IV), is a rare and severe autosomal recessive disorder. We report on an adult female patient whose clinical findings during childhood were not recognized as CIPA. There was neither complete anhidrosis nor a recognizable sensitivity to heat. Tumorlike swellings of many joints and skeletal signs of Charcot neuropathy developed in adolescence which, together with a history of self-mutilation, led to a clinical suspicion of CIPA confirmed by identification of a novel homozygous variant c.1795G > T in the NTRK1 gene in blood lymphocytes. Both parents were hete…

AdultPremature Stop Codonmedicine.medical_specialtyPainmedicine.disease_causeYoung AdultCongenital insensitivity to pain with anhidrosisHereditary sensory and autonomic neuropathyGeneticsmedicineHumansGenetic Predisposition to DiseaseReceptor trkAAnhidrosisGenetics (clinical)HypohidrosisMutationAdult femalebusiness.industryOssification HeterotopicGeneral MedicineEuropean populationNTRK1 Genemedicine.diseaseDermatologyFemaleArthropathy Neurogenicmedicine.symptombusinessEuropean Journal of Medical Genetics
researchProduct

Exon-level expression analyses identify MYCN and NTRK1 as major determinants of alternative exon usage and robustly predict primary neuroblastoma out…

2012

BACKGROUND: Using mRNA expression-derived signatures as predictors of individual patient outcome has been a goal ever since the introduction of microarrays. Here, we addressed whether analyses of tumour mRNA at the exon level can improve on the predictive power and classification accuracy of gene-based expression profiles using neuroblastoma as a model. METHODS: In a patient cohort comprising 113 primary neuroblastoma specimens expression profiling using exon-level analyses was performed to define predictive signatures using various machine-learning techniques. Alternative transcript use was calculated from relative exon expression. Validation of alternative transcripts was achieved using q…

Cancer ResearchMedizinComputational biologyBiologyexon arraysBioinformaticsN-Myc Proto-Oncogene ProteinExonNeuroblastomaRisk FactorsNeuroblastomaCell Line TumorGene expressionmedicineHumansRNA MessengerReceptor trkAGeneSurvival analysisOncogene ProteinsN-Myc Proto-Oncogene ProteinGene Expression ProfilingInfantNuclear ProteinsGenetics and GenomicspredictionExonsalternative transcript usemedicine.diseasePrognosisSurvival AnalysisGene expression profilingOncologyChild PreschoolPAMDNA microarray
researchProduct

Compromised Neurotrophic and Angiogenic Regenerative Capability during Tendon Healing in a Rat Model of Type-II Diabetes

2017

Metabolic diseases such as diabetes mellitus type-II (DM-II) may increase the risk of suffering painful connective tissue disorders and tendon ruptures. The pathomechanisms, however, by which diabetes adversely affects connective tissue matrix metabolism and regeneration, still need better definition. Our aim was to study the effect of DM-II on expressional changes of neuro- and angiotrophic mediators and receptors in intact and healing Achilles tendon. The right Achilles tendon was transected in 5 male DM-II Goto-Kakizaki (GK) and 4 age-matched Wistar control rats. The left Achilles tendons were left intact. At week 2 post-injury, NGF, BDNF, TSP, and receptors TrkA, TrkB and Nk1 gene expre…

Male0301 basic medicinePhysiologyGene Expressionlcsh:MedicineSubstance PCardiovascular PhysiologyTendonsEndocrinology0302 clinical medicineNerve Growth FactorMedicine and Health SciencesHomeostasisMedicinelcsh:ScienceMammalsAchilles tendonMultidisciplinarybiologyAnimal ModelsAnatomyReceptors Neurokinin-1musculoskeletal systemTendonmedicine.anatomical_structureExperimental Organism SystemsConnective TissueVertebratesAnatomyResearch ArticleNeurotrophinmedicine.medical_specialtyWistar RatsEndocrine DisordersNeovascularization PhysiologicConnective tissueResearch and Analysis MethodsRodentsAchilles Tendon03 medical and health sciencesModel OrganismsTendon InjuriesInternal medicineTissue RepairDiabetes MellitusGeneticsAnimalsReceptor trkBRats WistarReceptor trkABrain-derived neurotrophic factorWound Healingbusiness.industryBrain-Derived Neurotrophic Factorlcsh:RScleraxisOrganismsBiology and Life SciencesRatsTenomodulinDisease Models AnimalBiological Tissue030104 developmental biologyNerve growth factorEndocrinologyDiabetes Mellitus Type 2Metabolic DisordersAmniotesbiology.proteinlcsh:QAngiogenesisPhysiological Processesbusiness030217 neurology & neurosurgeryDevelopmental BiologyPLOS ONE
researchProduct

Entrectinib: a potent new TRK, ROS1, and ALK inhibitor

2015

Abstract: Introduction: Receptor tyrosine kinases (RTKs) and their signaling pathways, control normal cellular processes; however, their deregulation play important roles in malignant transformation. In advanced non-small cell lung cancer (NSCLC), the recognition of oncogenic activation of specific RTKs, has led to the development of molecularly targeted agents that only benefit roughly 20% of patients. Entrectinib is a pan-TRK, ROS1 and ALK inhibitor that has shown potent anti-neoplastic activity and tolerability in various neoplastic conditions, particularly NSCLC. Areas covered: This review outlines the pharmacokinetics, pharmacodynamics, mechanism of action, safety, tolerability, pre-cl…

Receptor Protein-Tyrosine KinasesEntrectinibNTRK1NTRK2NTRK3Receptor tyrosine kinaseEntrectinibMalignant transformationAntineoplastic AgentNeoplasmsProtein-Tyrosine KinaseALK; colorectal cancer; Entrectinib; non-small cell lung cancer; NTRK1; NTRK2; NTRK3; precision medicine; ROS1; salivary gland cancer; TrkA; TrkB; TrkC; Animals; Antineoplastic Agents; Benzamides; Humans; Indazoles; Neoplasms; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Receptor Protein-Tyrosine Kinases; Receptor; trkA; Receptor; trkB; Receptor; trkC; Pharmacology; Pharmacology (medical)Anaplastic Lymphoma KinasePharmacology (medical)salivary gland cancerProto-Oncogene ProteinbiologyTrkAPharmacology. TherapyTrkCTrkBGeneral MedicineProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinaseBenzamidesmedicine.symptomROS1ReceptorHumanIndazolesmedicine.drug_classprecision medicineAntineoplastic Agentscolorectal cancerBenzamideProto-Oncogene ProteinsmedicineROS1AnimalsHumansReceptor trkBReceptor trkCReceptor trkAnon-small cell lung cancerPharmacologyAnimalReceptor Protein-Tyrosine KinasesALK inhibitorIndazoleMechanism of actionALKTrk receptorbiology.proteinCancer researchNeoplasmALK; colorectal cancer; Entrectinib; non-small cell lung cancer; NTRK1; NTRK2; NTRK3; precision medicine; ROS1; salivary gland cancer; TrkA; TrkB; TrkC; Animals; Antineoplastic Agents; Benzamides; Humans; Indazoles; Neoplasms; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Receptor Protein-Tyrosine Kinases; Receptor trkA; Receptor trkB; Receptor trkC; Pharmacology; Pharmacology (medical)Expert Opinion on Investigational Drugs
researchProduct

Mecanismo de activación del receptor de neurotrofinas TrkA

2022

234 págs, figuras y tablas

UNESCO::CIENCIAS DE LA VIDA::Biología moleculartropomyosin receptor kinase (TrkA):CIENCIAS DE LA VIDA::Neurociencias [UNESCO]UNESCO::CIENCIAS DE LA VIDA::Biología celularCongenital insensitivity to pain with anhidrosis (CIPA):CIENCIAS DE LA VIDA::Biología molecular [UNESCO]nerve growth factor (NGF)Neurotrofinasneurotrofinas:CIENCIAS DE LA VIDA::Biología celular [UNESCO]Nerve growth factor (NGF)UNESCO::CIENCIAS DE LA VIDA::NeurocienciasTropomyosin receptor kinase (TrkA)p75 neurotrophin receptor
researchProduct

Activation of TRK Genes in Ewingʼs Sarcoma Trk A Receptor Expression Linked to Neural Differentiation

1997

Trk receptors have been identified by immunohistochemical methods in primitive neuroectodermal tumor (PNET)/Ewing's sarcoma (ES). However, the presence of different members of the Trk family of receptors in PNET/ES has not been specified. We have examined whether Trk A, B, and C receptors are specifically expressed in ES both with and without features of neural differentiation. Ten ES tumors (five primary tumors of bone and five extraosseous tumors transplanted into nude mice) were investigated for expression of Trk receptors by immunohistochemistry and reverse transcription-polymerase chain reaction. One primary ES and the five grafted ES tumors exhibited signs of neural differentiation; t…

animal structuresReceptor expressionReceptors Nerve Growth FactorSarcoma EwingBiologyPathology and Forensic MedicineMiceProto-Oncogene ProteinsmedicineAnimalsNeuroectodermal Tumors PrimitiveReceptor trkCReceptor trkAReceptorReceptor Ciliary Neurotrophic FactorMolecular BiologyNeuronsMembrane ProteinsReceptor Protein-Tyrosine KinasesEwing's sarcomaCell DifferentiationCell BiologyProtein-Tyrosine Kinasesmedicine.diseaseMolecular biologyGene Expression Regulation Neoplasticenzymes and coenzymes (carbohydrates)nervous systemTrk receptorPrimitive neuroectodermal tumorembryonic structuresImmunohistochemistrySarcomaImmunostainingDiagnostic Molecular Pathology
researchProduct

Expression of neurotrophins, GDNF, and their receptors in rat thyroid tissue

1999

Levels of mRNA for neurotrophins (brain-derived neurotrophic factor, BDNF; neurotrophin 3, NT-3; neurotrophin 4, NT-4) and their receptors (trkA, trkB, trkC) and for glial cell line-derived neurotrophic factor (GDNF) and its receptors (ret, GDNFR-alpha) were measured in rat thyroid tissue by ribonuclease protection assays. In thyroid tissue the NT-3 mRNA level was threefold lower and the NT-4 mRNA level sixfold higher than those detected in adult rat hippocampus, while BDNF mRNA was undetectable. Very low levels of mRNA for truncated trkB and trkC receptors and no catalytic trkA, trkB or trkC were found. In conclusion NT-3 and NT-4, but not the corresponding functional receptors, are expres…

endocrine systemmedicine.medical_specialtyGlial Cell Line-Derived Neurotrophic Factor ReceptorsHistologyendocrine system diseasesThyroid GlandGene ExpressionNerve Tissue ProteinsReceptors Nerve Growth FactorNeurotrophin-3Tropomyosin receptor kinase AFollicular cellPathology and Forensic MedicineNeurotrophin 3Proto-Oncogene ProteinsInternal medicinemedicineGlial cell line-derived neurotrophic factorAnimalsDrosophila ProteinsHumansLow-affinity nerve growth factor receptorReceptor trkCGlial Cell Line-Derived Neurotrophic FactorNerve Growth FactorsRNA MessengerReceptor trkAReceptor Ciliary Neurotrophic FactorbiologyBrain-Derived Neurotrophic FactorProto-Oncogene Proteins c-retReceptor Protein-Tyrosine KinasesCell BiologyRatsCell biologyEndocrinologynervous systemProto-Oncogene Proteins c-retbiology.proteinGDNF family of ligandsNeurotrophinCell and Tissue Research
researchProduct

Tiam1 as a Signaling Mediator of Nerve Growth Factor-Dependent Neurite Outgrowth

2010

Nerve Growth Factor (NGF)-induced neuronal differentiation requires the activation of members of the Rho family of small GTPases. However, the molecular mechanisms through which NGF regulates cytoskeletal changes and neurite outgrowth are not totally understood. In this work, we identify the Rac1-specific guanine exchange factor (GEF) Tiam1 as a novel mediator of NGF/TrkA-dependent neurite elongation. In particular, we report that knockdown of Tiam1 causes a significant reduction in Rac1 activity and neurite outgrowth induced by NGF. Physical interaction between Tiam1 and active Ras (Ras- GTP), but not tyrosine phosphorylation of Tiam1, plays a central role in Rac1 activation by NGF. In add…

rac1 GTP-Binding ProteinTiam1; Nerve growth factor (NGF)GTPaseTropomyosin receptor kinase ABiochemistryPC12 CellsCell Biology/Cell Signalingchemistry.chemical_compoundChlorocebus aethiopsNerve Growth FactorTiam1Guanine Nucleotide Exchange FactorsT-Lymphoma Invasion and Metastasis-inducing Protein 1NGFNeuronsMultidisciplinaryUNESCO::CIENCIAS DE LA VIDA::Biología molecularQOtras Medicina BásicaRCell Differentiation//purl.org/becyt/ford/3.1 [https]Cell biologyNeoplasm ProteinsMedicina BásicaNeuronal differentiationNerve growth factor (NGF)COS CellsMedicine//purl.org/becyt/ford/3 [https]Guanine nucleotide exchange factorSignal transductionResearch ArticleSignal TransductionCIENCIAS MÉDICAS Y DE LA SALUDNeuriteScienceCell Biology/Neuronal Signaling MechanismsRAC1Biology:CIENCIAS DE LA VIDA::Biología molecular [UNESCO]Neuroscience/Neuronal Signaling MechanismsNeuritesAnimalsHumansReceptor trkATyrosine phosphorylationMolecular biologyRatsNerve growth factorchemistrynervous systemras ProteinsRac1 GTPasePLoS ONE
researchProduct