Search results for "Tyrosine kinase"

showing 10 items of 362 documents

IFI16 reduced expression is correlated with unfavorable outcome in chronic lymphocytic leukemia.

2017

Chronic lymphocytic leukemia (CLL) is the most common leukemia in adults. Its clinical course is typically indolent; however, based on a series of pathobiological, clinical, genetic, and phenotypic parameters, patient survival varies from less than 5 to more than 20 years. In this paper, we show for the first time that the expression of the interferon-inducible DNA sensor IFI16, a member of the PYHIN protein family involved in proliferation inhibition and apoptosis regulation, is associated with the clinical outcome in CLL. We studied 99 CLLs cases by immunohistochemistry and 10 CLLs cases by gene expression profiling. We found quite variable degrees of IFI16 expression among CLLs cases. No…

0301 basic medicineMaleChronic lymphocytic leukemiaGene Expressionhemic and lymphatic diseasesGene expression80 and overImmunology and AllergyChronicNuclear ProteinCD20Aged 80 and overLeukemiaMembrane GlycoproteinsZAP-70 Protein-Tyrosine KinasebiologyZAP70Nuclear ProteinsGeneral MedicineMiddle AgedPhenotypeImmunohistochemistryLymphocyticchronic lymphocytic leukemia; gene expression; IFI16; immunohistochemistry; prognosis; ZAP70; Adult; Aged; Aged 80 and over; Antigens CD38; Female; Gene Expression Profiling; Humans; Immunohistochemistry; Leukemia Lymphocytic Chronic B-Cell; Male; Membrane Glycoproteins; Middle Aged; Nuclear Proteins; Phosphoproteins; Treatment Outcome; Young Adult; ZAP-70 Protein-Tyrosine Kinase; Gene Expression; Immunology and Allergy; 2734; Microbiology (medical)LeukemiaTreatment OutcomePhosphoproteinimmunohistochemistryImmunohistochemistryZAP70FemaleMembrane GlycoproteinprognosiHumanMicrobiology (medical)Adult2734IFI16; ZAP70; chronic lymphocytic leukemia; gene expression; immunohistochemistry; prognosisNOPathology and Forensic Medicine03 medical and health sciencesYoung AdultmedicineHumansAntigensIFI16Agedbusiness.industryGene Expression ProfilingB-Cellchronic lymphocytic leukemia; gene expression; IFI16; immunohistochemistry; prognosis; ZAP70; ADP-ribosyl Cyclase 1; Adult; Aged; Aged 80 and over; Female; Gene Expression Profiling; Humans; Immunohistochemistry; Leukemia Lymphocytic Chronic B-Cell; Male; Membrane Glycoproteins; Middle Aged; Nuclear Proteins; Phosphoproteins; Treatment Outcome; Young Adult; ZAP-70 Protein-Tyrosine Kinase; Gene Expression; 2734; Immunology and Allergy; Microbiology (medical)medicine.diseasePhosphoproteinsADP-ribosyl Cyclase 1Leukemia Lymphocytic Chronic B-CellGene expression profilingchronic lymphocytic leukemia; gene expression; IFI16; immunohistochemistry; prognosis; ZAP70; Immunology and Allergy; 2734; Microbiology (medical)030104 developmental biologygene expressionCancer researchbiology.proteinchronic lymphocytic leukemiaprognosisbusinessCD38APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
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The TrkB agonist 7,8-dihydroxyflavone changes the structural dynamics of neocortical pyramidal neurons and improves object recognition in mice

2018

This is a pre-print of an article published in Brain Structure and Function. The final authenticated version is available online at: https://doi.org/10.1007/s00429-018-1637-x. BDNF and its receptor TrkB have important roles in neurodevelopment, neural plasticity, learning, and memory. Alterations in TrkB expression have been described in different CNS disorders. Therefore, drugs interacting with TrkB, specially agonists, are promising therapeutic tools. Among them, the recently described 7,8-dihydroxyflavone (DHF), an orally bioactive compound, has been successfully tested in animal models of these diseases. Recent studies have shown the influence of this drug on the structure of pyramidal …

0301 basic medicineMaleDendritic spineTrkB receptorNeocortexTropomyosin receptor kinase B78-Dihydroxyflavoneaxonal dynamicsMice0302 clinical medicineReceptorMembrane GlycoproteinsGeneral NeurosciencePyramidal CellsProtein-Tyrosine Kinases2-Photonbarrel cortexFemaleMicrogliaAnatomyAgonistHistologymedicine.drug_classDendritic SpinesMice TransgenicBiologyspine dynamicsrecognition memory03 medical and health sciencesBacterial ProteinsNeuroplasticitymedicinepyramidal neuronAnimalsMaze LearningParenchymal TissueRecognition memoryAnalysis of VarianceRecognition PsychologyBarrel cortexFlavonesAxonsLuminescent Proteins030104 developmental biologynervous systemAstrocytesen passant boutonsThy-1 AntigensNeuroscience030217 neurology & neurosurgery
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CAMKIIγ suppresses an efferocytosis pathway in macrophages and promotes atherosclerotic plaque necrosis

2017

Atherosclerosis is the underlying etiology of cardiovascular disease, the leading cause of death worldwide. Atherosclerosis is a heterogeneous disease in which only a small fraction of lesions lead to heart attack, stroke, or sudden cardiac death. A distinct type of plaque containing large necrotic cores with thin fibrous caps often precipitates these acute events. Here, we show that Ca2+/calmodulin-dependent protein kinase gamma (CaMKII gamma) in macrophages plays a major role in the development of necrotic, thin-capped plaques. Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation of CaMKII. We…

0301 basic medicineMalePathologymedicine.medical_specialtyPhagocytosisGene ExpressionInflammationApoptosisMice TransgenicBiologyPHAGOCYTOSISLIPID MEDIATORS03 medical and health sciencesNecrosisENDOPLASMIC-RETICULUM STRESSINFLAMMATIONCa2+/calmodulin-dependent protein kinaseC/EBP HOMOLOGOUS PROTEINmedicineMacrophageAnimalsHumansKINASE-IILiver X receptorEfferocytosisCells CulturedLiver X ReceptorsAPOE-DEFICIENT MICEc-Mer Tyrosine KinaseATF6MacrophagesAPOPTOTIC CELL ACCUMULATIONGeneral MedicineMERTKAtherosclerosisPlaque AtheroscleroticActivating Transcription Factor 6Enzyme ActivationMice Inbred C57BL030104 developmental biologyRESOLUTIONmedicine.symptomCalcium-Calmodulin-Dependent Protein Kinase Type 2LIVER-X-RECEPTORResearch ArticleSignal TransductionJournal of Clinical Investigation
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Facial cutaneo-mucosal venous malformations can develop independently of mutation of TEK gene but may be associated with excessive expression of Src…

2017

International audience; We aimed to search for mutations in the germline and somatic DNA of the TEK gene and to analyze the expression level of Src and phospho- Src (p-Src) in tumor and healthy tissues from patients with facial cutaneo-mucosal venous malformations (VMCM). Eligible patients from twelve families and thirty healthy controls were recruited respectively at the Departments of Stomatology and Oral Surgery, and Transfusion Medicine of Tlemcen University Medical Centre. Immunoblot analyses of Src and p-Src were performed after direct DNA sequencing. No somatic or germline mutations were found in all the 23 exons and their 5' and 3' intronic flanking regions, except for one case in w…

0301 basic medicineMaleSomatic cellVascular MalformationsCutaneo-mucosal venous malformationsTyrosine Kinase Tie2Bioinformaticsmedicine.disease_causeGermlineMetastasisp-SrcExonPharmacology Toxicology and Pharmaceutics(all)General Pharmacology Toxicology and PharmaceuticsPhosphorylationCancerMedicine(all)MutationBrief ReportGeneral MedicineReceptor TIE-2[SDV.BDD.MOR] Life Sciences [q-bio]/Development Biology/Morphogenesis3. Good healthsrc-Family Kinases[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]FemaleProto-oncogene tyrosine-protein kinase SrcReceptorSrc[SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]AdolescentDirect sequencingContext (language use)BiologyVegfGeneral Biochemistry Genetics and Molecular BiologyPermeability03 medical and health sciencesGermline mutationTEK gene[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN][ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicine[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumansAmino Acid SequenceGeneMucous MembraneCell-Lines[ SDV ] Life Sciences [q-bio]Base SequenceBiochemistry Genetics and Molecular Biology(all)[SDV.BDD.MOR]Life Sciences [q-bio]/Development Biology/MorphogenesisGermline and somatic DNA030104 developmental biologyFaceMutationCancer researchSkin AbnormalitiesAngiogenesisPathwayJournal of negative results in biomedicine
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The Emerging Therapeutic Landscape of ALK Inhibitors in Non-Small Cell Lung Cancer.

2020

The treatment of metastatic non-small cell lung cancer (NSCLC) has undergone a paradigm shift over the last decade. Better molecular characterization of the disease has led to the rapid improvement of personalized medicine and the prompt delivery of targeted therapies to patients with NSCLC. The discovery of the EML4-ALK fusion gene in a limited subset of patients affected by NSCLC and the subsequent clinical development of crizotinib in 2011 has been an impressive milestone in lung cancer research. Unfortunately, acquired resistances regularly develop, hence disease progression occurs. Afterward, modern tyrosine kinase inhibitors (TKIs), such as ceritinib, alectinib, brigatinib, and lorlat…

0301 basic medicineOncologyAlectinibALK inhibitorsmedicine.medical_specialtybrigatinibBrigatinibmedicine.medical_treatmentPharmaceutical Sciencenon-small cell lung cancer (NSCLC)lcsh:Medicinelcsh:RS1-441ReviewALK inhibitorTargeted therapylcsh:Pharmacy and materia medica03 medical and health sciences0302 clinical medicinelorlatinibInternal medicineDrug DiscoveryMedicineAnaplastic lymphoma kinaseceritinibalectinibensartinibcrizotinibCrizotinibCeritinibbusiness.industrylcsh:Rmedicine.diseaseLorlatinibrespiratory tract diseasesnon-small cell lung cancer (NSCLC)030104 developmental biologytyrosine kinase inhibitors (TKIs)030220 oncology & carcinogenesisMolecular Medicinebusinessmedicine.drugPharmaceuticals (Basel, Switzerland)
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Integrating Liquid Biopsy and Radiomics to Monitor Clonal Heterogeneity of EGFR-Positive Non-Small Cell Lung Cancer

2020

BackgroundEGFR-positive Non-small Cell Lung Cancer (NSCLC) is a dynamic entity and tumor progression and resistance to tyrosine kinase inhibitors (TKIs) arise from the accumulation, over time and across different disease sites, of subclonal genetic mutations. For instance, the occurrence of EGFR T790M is associated with resistance to gefitinib, erlotinib, and afatinib, while EGFR C797S causes osimertinib to lose activity. Sensitive technologies as radiomics and liquid biopsy have great potential to monitor tumor heterogeneity since they are both minimally invasive, easy to perform, and can be repeated over patient’s follow-up, enabling the extraction of valuable information. Yet, to date, t…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyAfatinibEGFRprecision medicinelcsh:RC254-282cell free DNA; EGFR; liquid biopsy; non-small cell lung cancer; precision medicine; radiomics; tyrosine kinase inhibitors03 medical and health sciencesT790M0302 clinical medicineGefitinibInternal medicinetyrosine kinase inhibitorsmedicineOsimertinibLiquid biopsynon-small cell lung cancerOriginal ResearchReceiver operating characteristiccell free DNAliquid biopsybusiness.industrylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologyOncologyTumor progressionradiomics030220 oncology & carcinogenesisErlotinibbusinessmedicine.drug
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BCR-ABL1 Doubling-Times and Halving-Times May Predict CML Response to Tyrosine Kinase Inhibitors

2019

In Chronic Myeloid Leukemia (CML), successful treatment requires accurate molecular monitoring to evaluate disease response and provide timely interventions for patients failing to achieve the desired outcomes. We wanted to determine whether measuring BCR-ABL1 mRNA doubling-times (DTs) could distinguish inconsequential rises in the oncogene’s expression from resistance to tyrosine kinase inhibitors (TKIs). Thus, we retrospectively examined BCR-ABL1 evolution in 305 chronic-phase CML patients receiving imatinib mesylate (IM) as a first line treatment. Patients were subdivided in two groups: those with a confirmed rise in BCR-ABL1 transcripts without MR3.0 loss and those failing IM. We found …

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyDisease ResponseChronic Myeloid LeukemiaBCR-ABL1/ABL1IShalving-timelcsh:RC254-28203 medical and health sciences0302 clinical medicineInternal medicinehemic and lymphatic diseasesBCR-ABL1/ABL1; IS; Chronic Myeloid Leukemia; Doubling-time; Halving-time; Tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineDoubling timeOriginal ResearchBCR-ABL1/ABL1Oncogenebusiness.industryMyeloid leukemialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensDiscontinuationdoubling-time030104 developmental biologyImatinib mesylateOncology030220 oncology & carcinogenesisCohortISBCR-ABL1/ABL1 ISbusinessTyrosine kinaseFrontiers in Oncology
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Focal Adhesion Genes Refine the Intermediate-Risk Cytogenetic Classification of Acute Myeloid Leukemia

2018

© 2018 by the authors.

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyNPM1PTK2acute myeloid leukemialcsh:RC254-282Article03 medical and health sciences0302 clinical medicinePTK2BLYNInternal medicinehemic and lymphatic diseasesmedicineLYNprognostic factorPrognostic factorintermediate-riskPTK2BAcute myeloid leukemiaPTK2business.industryMyeloid leukemialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologyOncology030220 oncology & carcinogenesisCohortIntermediate-riskbusinessTyrosine kinaseProto-oncogene tyrosine-protein kinase SrcCancers
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High BCR-ABL/GUS(IS) levels at diagnosis of chronic phase CML are associated with unfavorable responses to standard-dose imatinib

2017

Abstract Purpose: The approval of second-generation tyrosine kinase inhibitors (TKIs) for the first-line treatment of chronic myeloid leukemia (CML) has generated an unmet need for baseline molecular parameters associated with inadequate imatinib responses. Experimental Design: We correlated BCR–ABL/GUSIS and BCR–ABL/ABL transcripts at diagnosis with the outcome—defined by the 2013 European LeukemiaNet recommendations—of 272 patients newly diagnosed with CML receiving imatinib 400 mg/daily. Applying receiver-operating characteristic curves, we defined BCR–ABL/GUSIS and BCR–ABL/ABL levels associated with lower probabilities of optimal response, failure-free (FFS), event-free (EFS), transform…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyPathologyMyeloidBCR-ABL Diagnosis CMLDrug intolerance03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesInternal medicineDiagnosismedicineBCR-ABLCMLneoplasmsABLbusiness.industryCancerMyeloid leukemiaImatinibOncology cancer researchmedicine.diseaseLeukemia030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisbusinessTyrosine kinasemedicine.drug
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Recent Advances in Desmoid Tumor Therapy

2020

The desmoid tumor is a locally aggressive proliferative disease within the family of soft-tissue sarcomas. Despite its relatively good prognosis, the clinical management of desmoid tumors requires constant multidisciplinary evaluation due to its highly variable clinical behavior. Recently, active surveillance has being regarded as the appropriate strategy at diagnosis, as indolent persistence or spontaneous regressions are not uncommon. Here, we review the most recent advances in desmoid tumor therapy, including low-dose chemotherapy and treatment with tyrosine kinase inhibitors. We also explore the recent improvements in our knowledge of the molecular biology of this disease, which are lea…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentProliferative diseasedesmoid tumorDiseaseReviewchemotherapylcsh:RC254-282aggressive fibromatosis03 medical and health sciences0302 clinical medicineInternal medicinedesmoid tumor; aggressive fibromatosis; active surveillance; chemotherapy; tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineChemotherapybusiness.industryactive surveillanceTumor therapyaggressive fibromatosimedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensClinical trialbody regions030104 developmental biologyOncology030220 oncology & carcinogenesisAggressive fibromatosisGood prognosisbusinessCancers
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