Search results for " TYR"

showing 10 items of 362 documents

LS104, a Novel Kinase Inhibitor, Induces Apoptosis, Synergizes with Cytostatic Drugs and Is Targeting the Receptor Tyrosine Kinase FLT3.

2005

Abstract Fms-like tyrosine kinase 3 (FLT3), a member of the class III tyrosine kinase receptor family, is expressed in up to 90% of acute myeloid leukemia (AML). Activating mutations like internal tandem duplication (ITD) of the juxtamembrane domain and kinase domain point mutations are found in approximately 35% of AML-cases and are considered to represent an attractive therapeutic target. In this study, we report that the novel hydroxystyryl-acrylonitrile compound LS104 induces potent cytotoxic effects in FLT3 ITD-positive leukemic cells. As a cellular model to investigate FLT3-ITD specific effects we used 32D myeloid cells stably transfected with FLT3-ITD and wt-FLT3, respectively. In MT…

KinaseCell growthImmunologyTyrosine phosphorylationCell BiologyHematologyBiologymedicine.diseaseBiochemistryMolecular biologyReceptor tyrosine kinaseLeukemiachemistry.chemical_compoundchemistryAnnexinhemic and lymphatic diseasesembryonic structuresmedicinebiology.proteinKinase activityTyrosineBlood
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A novel molecular mechanism of primary resistance to FLT3-kinase inhibitors in AML

2009

Abstract Currently, FLT3 tyrosine kinase inhibitors (TKIs) are emerging as the most promising drug therapy to overcome the dismal prognosis of acute myelogenous leukemia (AML) patients harboring internal tandem duplications (ITDs) of FLT3. However, up-front drug resistance occurs in approximately 30% of patients, and molecular mechanisms of resistance are poorly understood. Here, we have uncovered a novel mechanism of primary resistance to FLT3 TKIs in AML: an FLT3 receptor harboring a nonjuxtamembrane ITD atypically integrating into the β-2 sheet of the first kinase domain (FLT3_ITD627E) induces dramatic up-regulation of the anti-apoptotic myeloid cell leukemia 1 protein (MCL-1). Using RNA…

KinaseMitogen-Activated Protein Kinase 3ImmunologySignal transducing adaptor proteinCell BiologyHematologyBiologyBiochemistryProtein kinase domainhemic and lymphatic diseasesTrk receptorFms-Like Tyrosine Kinase 3Cancer researchSignal transductionTyrosine kinaseBlood
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Genome wide identification of new genes and pathways in patients with both autoimmune thyroiditis and type 1 diabetes

2015

Autoimmune thyroid diseases (AITD) and Type 1 diabetes (T1D) frequently occur in the same individual pointing to a strong shared genetic susceptibility. Indeed, the co-occurrence of T1D and AITD in the same individual is classified as a variant of the autoimmune polyglandular syndrome type 3 (designated APS3v). Our aim was to identify new genes and mechanisms causing the co-occurrence of T1D + AITD (APS3v) in the same individual using a genome-wide approach. For our discovery set we analyzed 346 Caucasian APS3v patients and 727 gender and ethnicity matched healthy controls. Genotyping was performed using the Illumina Human660W-Quad.v1. The replication set included 185 APS3v patients and 340…

Linkage disequilibriumT-LymphocytesImmunologyLocus (genetics)Genome-wide association studyHuman leukocyte antigenBiologyArticleLinkage DisequilibriumAutoimmune thyroiditisGenetic predispositionmedicineHumansImmunology and AllergyCTLA-4 AntigenGenetic Predisposition to DiseaseCD40 AntigensPolyendocrinopathies AutoimmuneGenotypingGenetic associationGeneticsB-LymphocytesHistocompatibility Antigens Class IHistocompatibility Antigens Class IIThyroiditis AutoimmuneProtein Tyrosine Phosphatase Non-Receptor Type 22medicine.diseaseDiabetes Mellitus Type 1ImmunologyGenome-Wide Association StudyJournal of Autoimmunity
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Dendritic cells in liver injury and fibrosis: shortcomings and promises.

2013

SummaryThe phenotype and function of liver dendritic cells (LDCs) are poorly understood. This Snapshot summarizes our current knowledge on LDCs in the healthy and injured liver, and their role in fibrosis progression and reversal. It also draws attention to various pitfalls in the current experimental design and conclusions based on available data.

Liver CirrhosisLiver dendritic cellsPlasmacytoid dendritic cellBiologyCCL2MiceFMS-like tyrosine kinase 3 ligandFibrosismedicineAnimalsHumansAntigen-presenting cellLiver injuryHepatologyFlt3LDendritic Cellsmedicine.diseaseCD11c-DTRDisease Models Animalmedicine.anatomical_structurePhenotypeLiverImmunologyHepatic stellate cellDisease ProgressionBone marrowToleranceJournal of hepatology
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MERTK rs4374383 polymorphism affects the severity of fibrosis in non-alcoholic fatty liver disease

2015

Background & Aim Homozygosity for a common non-coding rs4374383 G>A polymorphism in MERTK (myeloid-epithelial-reproductive tyrosine kinase) has been associated with the protection against fibrosis progression in chronic hepatitis C. The main study objective was to assess whether MERTK AA genotype influences liver fibrosis, and secondarily MERTK expression in patients with non-alcoholic fatty liver disease (NAFLD). We also investigated whether MERTK is expressed in human hepatic stellate cells (HSC) and in murine models of fibrogenesis. Methods We considered 533 consecutive patients who underwent liver biopsy for suspected non-alcoholic steatohepatitis (NASH) without severe obesity from two …

Liver CirrhosisMale0301 basic medicineMessengerMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisInbred BALB CCells CulturedMice Inbred BALB CCulturedmedicine.diagnostic_testMedicine (all)Fatty liverNASHMiddle AgedLiver biopsyFemale030211 gastroenterology & hepatologyAdultmedicine.medical_specialtyMERTKCellsBiology03 medical and health sciencesGeneticProto-Oncogene ProteinsInternal medicinemedicineAnimalsHumansFibrosis; MERTK; NASH; Adult; Animals; Cells Cultured; Female; Humans; Liver Cirrhosis; Male; Mice Inbred BALB C; Middle Aged; Non-alcoholic Fatty Liver Disease; Proto-Oncogene Proteins; RNA Messenger; Receptor Protein-Tyrosine Kinases; Polymorphism Genetic; Medicine (all); HepatologyRNA MessengerPolymorphismPolymorphism Geneticc-Mer Tyrosine KinaseHepatologyGAS6Receptor Protein-Tyrosine Kinasesnafld fibrosis mertkMERTKHepatologymedicine.diseaseFibrosis030104 developmental biologyImmunologyHepatic stellate cellRNASteatohepatitisJournal of Hepatology
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Genetic susceptibility of increased intestinal permeability is associated with progressive liver disease and diabetes in patients with non-alcoholic …

2020

Abstract Background and aim Increased intestinal permeability plays a key role in the pathogenesis of fat deposition in the liver. The aim of our study was to assess whether a single nucleotide polymorphism of protein tyrosine phosphatase non-receptor type 2 (PTPN2) (rs2542151 T→G), involved in intestinal permeability, may be associated with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM). Methods and results We recruited a prospective cohort of NAFLD subjects and matched controls. Clinical data, PTPN2 genotype and laboratory data were collected for each patient. Results were stratified according to liver histology and diabetes. We enrolled 566 cases and 377 co…

Liver CirrhosisMaleEndocrinology Diabetes and MetabolismMedicine (miscellaneous)030204 cardiovascular system & hematologySeverity of Illness IndexGastroenterologyLiver disease0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseasePrevalenceProspective StudiesProtein Tyrosine Phosphatase Non-Receptor Type 2Nutrition and Dieteticsmedicine.diagnostic_testFatty liverMiddle AgedPhenotypeItalyLiver biopsyFemaleCardiology and Cardiovascular MedicineAdultmedicine.medical_specialtySettore MED/12 - GASTROENTEROLOGIA030209 endocrinology & metabolismIntestinal permeabilityPolymorphism Single NucleotideRisk AssessmentPermeability03 medical and health sciencesInternal medicineDiabetes mellitusmedicineGenetic susceptibilityHumansNonalcoholic fatty liver diseaseGenetic Predisposition to DiseaseGenetic Association Studiesbusiness.industryType 2 Diabetes Mellitusmedicine.diseaseCross-Sectional StudiesDiabetes Mellitus Type 2Intestinal AbsorptionCase-Control StudiesSteatosisSteatohepatitisbusiness
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Mer Tyrosine Kinase (MERTK) modulates liver fibrosis progression and hepatocellular carcinoma development.

2022

BackgroundMerTK is a tyrosine kinase receptor that belongs to the TAM (Tyro3/Axl/Mer) receptor family. It is involved in different processes including cellular proliferation/survival, cellular adhesion/migration, and release of the inflammatory/anti-inflammatory cytokines. Although it is reported that MERTK polymorphisms affect the severity of viral and metabolic liver diseases, being able to influence fibrosis progression and hepatocellular carcinoma development, the mechanisms remain unknown. Methods: using a microarray approach, we evaluated the liver expression of genes involved in fibrogenesis and hepatocarcinogenesis in patient with chronic hepatitis C (CHC), stratified for MERTK geno…

Liver CirrhosisSettore MED/12 - GastroenterologiaCarcinoma Hepatocellularc-Mer Tyrosine KinaseMer Tyrosine Kinase polymorphism (MERTK polymorphism) WNT gene family pathway (WNT pathway) hepatocellular carcinoma liver fibrosis matrix metallopeptidase Metalloproteases Protein-Tyrosine Kinases Liver CirrhosisImmunologyLiver NeoplasmsProtein-Tyrosine KinasesFibrosisSettore BIO/13 - Biologia ApplicataProto-Oncogene ProteinsMetalloproteasesImmunology and AllergyHumansFrontiers in immunology
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Optimizing systemic therapy for advanced hepatocellular carcinoma: the key role of liver function

2022

The number of effective systemic therapies for the treatment of advanced hepatocellular carcinoma (HCC) is rapidly increasing, and the advent of immunotherapy has changed the treatment paradigm for these patients, leading to significantly improved survival outcomes. However, many patients with HCC will continue to receive tyrosine kinase inhibitors, partly because of contraindications to immune checkpoint inhibitors. Currently, the best sequential first- and second-line systemic treatment remains elusive. Maintenance of optimal liver function is crucial, it is likely to impinge on temporary or permanent treatment discontinuation, and should also be considered when defining the treatment seq…

Liver CirrhosisTyrosine kinase inhibitorsSettore MED/12 - GastroenterologiaCarcinoma HepatocellularHepatologyDecompensation Free Survival; Hepatocellular carcinoma; Immune checkpoint inhibitor; Overall Survival; Progression Free Survival; Systemic therapies; Time to Decompensation; Time to Progression; Tyrosine kinase inhibitorsSystemic therapieHepatocellular carcinomaOverall SurvivalDecompensation Free SurvivalLiver NeoplasmsGastroenterologyTime to DecompensationTyrosine kinase inhibitorSystemic therapiesImmune checkpoint inhibitorTime to ProgressionProgression Free SurvivalHumansImmunotherapy
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Clinical, immunological, and molecular analysis in a large cohort of patients with X-linked agammaglobulinemia: an Italian multicenter study

2002

A questionnaire-based retrospective clinical and immunological survey was conducted in 73 males with a definite diagnosis of X-linked agammaglobulinemia based on BTK sequence analysis. Forty-four were sporadic and 29 familial cases. At December 2000, the patients' ages ranged from 2 to 33 years; mean age at diagnosis and mean duration of follow-up were 3.5 and 10 years respectively. After the mid-1980s all but 2 were on intravenous immunoglobulin (IVIG) substitution therapy, with residual IgG >500 mg/dl in 94% of the patients at the time of enrollment. Respiratory infections were the most frequent manifestation both prior to diagnosis and over follow-up. Chronic lung disease (CLD) was prese…

Lung DiseasesAdultMalePediatricsmedicine.medical_specialtyGenetic Linkage; Agammaglobulinemia; Humans; Infant Newborn; Protein-Tyrosine Kinases; Child; Child Preschool; X Chromosome; Immunoglobulins Intravenous; Lung Diseases; Adult; Cohort Studies; Chronic Disease; Follow-Up Studies; Adolescent; Mutation; Maleclinical featuresX ChromosomeX-linked agammaglobulinemiaAdolescentGenetic LinkageImmunologyX-linked agammaglobulinemiaImmunoglobulinsX-linked agammaglobulinemia; infections; intravenous immunoglobulin; BTK mutationSepsisCohort StudiesAgammaglobulinemiaImmunopathologyintravenous immunoglobulinEpidemiologymedicineAgammaglobulinaemia Tyrosine KinaseImmunology and AllergyHumansinfectionsChildPreschoolSettore MED/38 - Pediatria Generale e SpecialisticaBTK mutationsbusiness.industryChronic sinusitisInfant NewbornMeningoencephalitisImmunoglobulins IntravenousInfantProtein-Tyrosine Kinasesmedicine.diseaseNewbornBTK mutationagammaglobulinemia; clinical features; BTK mutationsChild PreschoolChronic DiseaseMutationbusinessIntravenousMeningitisCohort studyFollow-Up Studies
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The role of cMET in non-small cell lung cancer resistant to EGFR-Inhibitors: Did we really find the target?

2014

Abstract: The advent of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) represented the most important innovation in NSCLC treatment over the last years. However, despite a great initial activity, secondary mutations in the same target, or different alterations in other molecular pathways, inevitably occur, leading to the emergence of acquired resistance, in median within the first year of treatment. In this scenario, the mesenchymal-epidermal transition (cMET) tyrosine kinase receptor and its natural ligand, the hepatocyte growth factor (HGF), seem to play an important role. Indeed either the overexpression or the amplification of cMET, as well as the overexpr…

Lung NeoplasmscMETcMET; cMET-Inhibitors; EGFR-TKIs resistance; HGF; NSCLC; Targeted therapies; Molecular Medicine; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Clinical BiochemistryClinical BiochemistryAntineoplastic AgentsBiologyPharmacologyNSCLCReceptor tyrosine kinaseTargeted therapiesCarcinoma Non-Small-Cell LungDrug DiscoverymedicineHumansEpidermal growth factor receptorHGFLung cancerProtein Kinase InhibitorsEGFR inhibitorsEGFR-TKIs resistancePharmacologyClinical Trials as TopicPharmacology. TherapyDrug Discovery3003 Pharmaceutical ScienceAntibodies MonoclonalProto-Oncogene Proteins c-metmedicine.diseaseMolecular medicinerespiratory tract diseasesErbB ReceptorsDrug Resistance NeoplasmProto-Oncogene Proteins c-metbiology.proteinCancer researchMolecular MedicineDrug Therapy CombinationHepatocyte growth factorcMET-InhibitorTargeted therapiecMET-InhibitorsTyrosine kinasemedicine.drug
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