Search results for "Fms-Like Tyrosine Kinase 3"

showing 8 items of 28 documents

Differential impact of allelic ratio and insertion site in FLT3-ITD-positive AML with respect to allogeneic transplantation.

2014

The objective was to evaluate the prognostic and predictive impact of allelic ratio and insertion site (IS) of internal tandem duplications (ITDs), as well as concurrent gene mutations, with regard to postremission therapy in 323 patients with FLT3-ITD-positive acute myeloid leukemia (AML). Increasing FLT3-ITD allelic ratio (P = .004) and IS in the tyrosine kinase domain 1 (TKD1, P = .06) were associated with low complete remission (CR) rates. After postremission therapy including intensive chemotherapy (n = 121) or autologous hematopoietic stem cell transplantation (HSCT, n = 17), an allelic ratio ≥ 0.51 was associated with an unfavorable relapse-free (RFS, P = .0008) and overall survival …

OncologyAdultmedicine.medical_specialtyAllogeneic transplantationMyeloidAdolescentmedicine.medical_treatmentImmunologyDNA Mutational AnalysisHematopoietic stem cell transplantationBiologyGene mutationBiochemistryYoung AdultGene FrequencyInternal medicineGene DuplicationGene duplicationmedicineHumansTransplantation HomologousAllelesHematopoietic Stem Cell TransplantationMyeloid leukemiaCell BiologyHematologyMiddle Agedmedicine.diseaseProtein Structure TertiaryTransplantationLeukemiaLeukemia Myeloid AcuteMutagenesis Insertionalmedicine.anatomical_structureTreatment Outcomefms-Like Tyrosine Kinase 3Tandem Repeat SequencesImmunologyBlood
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Impact of NPM1/FLT3-ITD genotypes defined by the 2017 European LeukemiaNet in patients with acute myeloid leukemia

2020

Contains fulltext : 218279.pdf (Publisher’s version ) (Open Access) Patients with acute myeloid leukemia (AML) harboring FLT3 internal tandem duplications (ITDs) have poor outcomes, in particular AML with a high (>/=0.5) mutant/wild-type allelic ratio (AR). The 2017 European LeukemiaNet (ELN) recommendations defined 4 distinct FLT3-ITD genotypes based on the ITD AR and the NPM1 mutational status. In this retrospective exploratory study, we investigated the prognostic and predictive impact of the NPM1/FLT3-ITD genotypes categorized according to the 2017 ELN risk groups in patients randomized within the RATIFY trial, which evaluated the addition of midostaurin to standard chemotherapy. The 4 …

OncologyPROBABILITIESMalePROGNOSISCancer development and immune defence Radboud Institute for Molecular Life Sciences [Radboudumc 2]NPM1 MUTATIONBiochemistryEuropean LeukemiaNetchemistry.chemical_compoundALLELIC RATIOAMLRisk FactorsGene Duplicationhemic and lymphatic diseasesMidostaurinFLT3Myeloid NeoplasiaHematopoietic Stem Cell TransplantationMyeloid leukemiaNuclear ProteinsHematologyCHEMOTHERAPYMiddle AgedPrognosisChemotherapy regimenEuropeLeukemia Myeloid Acutemedicine.anatomical_structureTreatment OutcomeTandem Repeat SequencesFemaleNucleophosminmedicine.medical_specialtyNPM1GenotypeImmunologyYOUNGER ADULTSInternal medicineWhite blood cellmedicineNORMAL CYTOGENETICSHumansGenetic Predisposition to DiseaseProportional Hazards ModelsProportional hazards modelbusiness.industryCell BiologyINTERNAL TANDEM DUPLICATIONTransplantationchemistryfms-Like Tyrosine Kinase 3Multivariate AnalysisbusinessSettore MED/15 - Malattie del Sangue
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High activity of sorafenib in FLT3-ITD-positive acute myeloid leukemia synergizes with allo-immune effects to induce sustained responses.

2012

Preliminary evidence suggests that the multikinase inhibitor sorafenib has clinical activity in FLT3-ITD-positive (FLT3-ITD) acute myeloid leukemia (AML). However, the quality and sustainability of achievable remissions and clinical variables that influence the outcome of sorafenib monotherapy are largely undefined. To address these questions, we evaluated sorafenib monotherapy in 65 FLT3-ITD AML patients treated at 23 centers. All but two patients had relapsed or were chemotherapy-refractory after a median of three prior chemotherapy cycles. Twenty-nine patients (45%) had undergone prior allogeneic stem cell transplantation (allo-SCT). The documented best responses were: hematological remi…

OncologySorafenibMaleNiacinamideCancer Researchmedicine.medical_specialtyMyeloidPyridinesmedicine.medical_treatmentAntineoplastic Agentshemic and lymphatic diseasesInternal medicinemedicineHumansAgedRetrospective StudiesChemotherapyHematologybusiness.industryPhenylurea CompoundsBenzenesulfonatesMyeloid leukemiaHematologyMiddle AgedSorafenibmedicine.diseaseTransplantationLeukemiaLeukemia Myeloid Acutemedicine.anatomical_structureOncologyfms-Like Tyrosine Kinase 3ImmunologyFemaleBone marrowbusinessmedicine.drugLeukemia
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Midostaurin in patients with acute myeloid leukemia and FLT3-TKD mutations: a subanalysis from the RATIFY trial

2020

Abstract The results from the RATIFY trial (ClinicalTrials.gov: NCT00651261; CALGB 10603) showed that midostaurin combined with standard chemotherapy significantly improved outcomes in patients with FMS-like tyrosine kinase 3 (FLT3)–mutated acute myeloid leukemia (AML), compared with placebo. In this post hoc subgroup analysis from the trial, we evaluated the impact of midostaurin in 163 patients with FLT3-tyrosine kinase domain (TKD) mutations. At a median follow-up of 60.7 months (95% CI, 55.0-70.8), the 5-year event-free survival (EFS) rate was significantly higher in patients treated with midostaurin than in those treated with placebo (45.2% vs 30.1%; P = .044). A trend toward improved …

Oncologymedicine.medical_specialtyNPM1Myeloidmedicine.medical_treatmentCancer development and immune defence Radboud Institute for Molecular Life Sciences [Radboudumc 2]Context (language use)03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAll institutes and research themes of the Radboud University Medical CenterInternal medicinehemic and lymphatic diseasesmedicineHumansMidostaurinChemotherapyMyeloid Neoplasiabusiness.industryMyeloid leukemiaHematologyStaurosporineSettore MED/15medicine.diseaseTransplantationLeukemia Myeloid AcuteLeukemiamedicine.anatomical_structurefms-Like Tyrosine Kinase 3chemistry030220 oncology & carcinogenesisMutationbusinessNucleophosmin030215 immunology
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Synthesis of 2H-Imidazo[2',1':2,3] [1,3]thiazolo[4,5-e]isoindol-8-yl-phenylureas with promising therapeutic features for the treatment of acute myelo…

2022

Despite progressive advances in understanding the molecular biology of acute myeloid leukemia (AML), the conventional therapeutic approach has not changed substantially, and the outcome for most patients is poor. Thus, continuous efforts on the discovery of new compounds with improved features are required. Following a multistep sequence, we have identified a new tetracyclic ring system with strong antiproliferative activity towards several haematological cell lines. The new compounds possess structural properties typical of inactive-state-binding kinase inhibitors and are structurally related to quizartinib which is known as type-II tyrosine kinase inhibitor. In particular, the high activi…

PharmacologyFMS-like tyrosine kinase 3 (FLT3)FLT3/ITD3][13]thiazolo[4Organic Chemistry2H-imidazo [2′1':23][13]thiazolo[45-e]isoindol-8-yl-phenylureas2H-imidazo [2′1':23][13]thiazolo[45-e]isoindol-8-yl-phenylureas; Acute myeloid leukemia (AML); FLT3/ITD; FMS-like tyrosine kinase 3 (FLT3); Internal tandem duplication (ITD)ApoptosisGeneral Medicine2H-imidazo [2′Leukemia Myeloid AcuteMiceInternal tandem duplication (ITD)fms-Like Tyrosine Kinase 35-e]isoindol-8-yl-phenylureasCell Line TumorDrug DiscoveryMutationAcute myeloid leukemia (AML)AnimalsHumansProtein Kinase Inhibitors1':2European journal of medicinal chemistry
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The high-performance technology CRISPR/Cas9 improves knowledge and management of acute myeloid leukemia

2021

Knowledge on acute myeloid leukemia pathogenesis and treatment has progressed recently, but not enough to provide ideal management. Improving the prognosis of acute myeloid leukemia patients depends on advances in molecular biology for the detection of new therapeutic targets and the production of effective drugs. The CRISPR/Cas9 technology allows gene insertions and deletions and it is the first step in investigating the function of their encoded proteins. Thus, new experimental models have been developed and progress has been made in understanding protein metabolism, antitumor activity, leukemic cell maintenance, differentiation, growth, apoptosis, and self-renewal, the combined pathogene…

TechnologyCD38acute myeloid leukemiamedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biologycd38bcl2chemistry.chemical_compoundcrispr/cas9flt3 inhibitorshemic and lymphatic diseasesmedicineCRISPRHumansMidostaurinProtein Kinase InhibitorsCell ProliferationMutationCas9business.industryCell growthRMyeloid leukemiamedicine.diseaseidh2LeukemiaLeukemia Myeloid Acutechemistryfms-Like Tyrosine Kinase 3MutationCancer researchMedicineCRISPR-Cas SystemsbusinessBiomedical Papers
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A minireview on NHE1 inhibitors. A rediscovered hope in oncohematology.

2015

Background: Na+/H+ exchanger-1 (NHE-1) is involved in pH regulation and is up-regulated in different malignancies. Activation of NHE-1 is one way for allowing cells to avoid intracellular acidification and protect them against apoptosis. Inhibitors of NHE-1 are able to decrease intracellular pH and induce apoptosis. Some statins can also act by partial inhibition of NHE-1. This review presents progress in understanding the mechanisms of action of these inhibitors, connections with certain genetic mutations and acquired treatment resistance, as well as new patents on them. Methods: A MEDLINE search for original and review articles using key terms, Na+/H+ exchanger, leukemia, cariporide, and …

lovastatinlcsh:MedicineApoptosisPharmacologyGuanidinesAmiloridep-glycoproteinhemic and lymphatic diseasesDrug InteractionsSulfonesCation Transport ProteinsSodium-Hydrogen Exchanger 1leukemiaMyeloid leukemiaHydrogen-Ion ConcentrationSorafenibUp-RegulationLeukemiaLeukemia Myeloid AcuteImatinib MesylateSignal transductionTyrosine kinasemedicine.drugSignal TransductionSorafenibNiacinamideisoprenylationSodium-Hydrogen Exchangersbcr/ablAntineoplastic AgentsGenes ablGeneral Biochemistry Genetics and Molecular BiologystatinsPatents as TopicCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansProtein Kinase Inhibitorscariporidena+/h+ exchangerTumor hypoxiabusiness.industryPhenylurea Compoundslcsh:ROsmolar Concentrationintracellular phmedicine.diseaseImatinib mesylatefms-Like Tyrosine Kinase 3Fms-Like Tyrosine Kinase 3MutationCancer researchTumor Hypoxiaflt3/itdHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessHeme Oxygenase-1DNA DamageBiomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia
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FLT3 as a therapeutic target in AML: still challenging after all these years

2010

Abstract Mutations within the FMS-like tyrosine kinase 3 (FLT3) gene on chromosome 13q12 have been detected in up to 35% of acute myeloid leukemia (AML) patients and represent one of the most frequently identified genetic alterations in AML. Over the last years, FLT3 has emerged as a promising molecular target in therapy of AML. Here, we review results of clinical trials and of correlative laboratory studies using small molecule FLT3 tyrosine kinase inhibitors (TKIs) in AML patients. We also review mechanisms of primary and secondary drug resistance to FLT3-TKI, and from the data currently available we summarize lessons learned from FLT3-TKI monotherapy. Finally, for using FLT3 as a molecul…

medicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentImmunologyBiologyBiochemistryTyrosine-kinase inhibitorTargeted therapychemistry.chemical_compoundfluids and secretionshemic and lymphatic diseasesInternal medicinemedicineHumansProtein Kinase InhibitorsQuizartinibHematologyMyeloid leukemiaCancerhemic and immune systemsCell BiologyHematologymedicine.diseaseLeukemia Myeloid Acutefms-Like Tyrosine Kinase 3chemistryDrug Resistance Neoplasmembryonic structuresCancer researchTyrosine kinaseCrenolanibBlood
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