0000000000191332

AUTHOR

Anna Marfia

showing 5 related works from this author

miR-155 regulative network in FLT3 mutated acute myeloid leukemia

2015

Abstract Background Acute myeloid leukemia (AML) represents a heterogeneous disorder with recurrent chromosomal alterations and molecular abnormalities. Among AML with normal karyotype (NK-AML) FLT3 activating mutation, internal tandem duplication (FLT3-ITD), is present in about 30% of patients, conferring unfavorable outcome. Our previous data demonstrated specific up-regulation of miR-155 in FLT3-ITD+ AML. miR-155 is known to be directly implicated in normal hematopoiesis and in some pathologies such as myeloid hyperplasia and acute lymphoblastic leukemia. Methods and results To investigate about the potential influence of miR-155 de-regulation in FLT3-mutated AML we generated a transcrip…

AdultMaleCancer ResearchMyeloidJUNBNetworkBiologyYoung Adultchemistry.chemical_compoundAMLhemic and lymphatic diseasesmicroRNACEBPBmedicineHumansGene silencingGene Regulatory NetworksAML; MicroRNA; NetworkAgedAged 80 and overGene Expression Regulation LeukemicGene Expression ProfilingMyeloid leukemiaMicroRNAHematologyMiddle AgedLeukemia Myeloid AcuteMicroRNAsmedicine.anatomical_structurefms-Like Tyrosine Kinase 3OncologyRUNX1chemistryMutationCancer researchFemaleMyelopoiesisK562 Cells
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Carboxyamidotriazole inhibits cell growth of imatinib-resistant chronic myeloid leukaemia cells including T315I Bcr-Abl mutant by a redox-mediated me…

2010

Mutation of the Bcr–Abl oncoprotein is one of most frequent mechanisms by which chronic myelogenous leukemia (CML) cells become resistant to imatinib. Here, we show that treat- ment of cell lines harbouring wild type or mutant BCR–ABL with carboxyamidotriazole (CAI), a calcium influx and signal transduction inhibitor, inhibits cell growth, the expres- sion of Bcr–Abl and its downstream signalling, and induces apoptosis. Moreover, we show that CAI acts by increasing intracellular ROS. Clinically significant, CAI has also inhibitory effects on T315I Bcr–Abl mutant, a mutation that causes CML cells to become insensitive to imatinib and second generation abl kinase inhibitors.

Cancer Researchbcr-abl Carboxyamidotriazole chronic myeloid leukemia cells imatinibBlotting WesternFusion Proteins bcr-ablAntineoplastic AgentsApoptosisSignal transduction inhibitorBiologyPiperazineschemistry.chemical_compoundMicehemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineAnimalsHumansneoplasmsCell ProliferationSettore MED/04 - Patologia GeneraleABLCarboxyamidotriazoleCell growthWild typeImatinibTriazolesmedicine.diseaseImatinib mesylatePyrimidinesOncologychemistryDrug Resistance NeoplasmBenzamidesMutationCancer researchImatinib MesylateReactive Oxygen SpeciesOxidation-ReductionChronic myelogenous leukemiamedicine.drug
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Differential expression of specific microRNA and their targets in acute myeloid leukemia

2010

Acute myeloid leukemia (AML) the most common acute leukemia in adults is characterized by various cytogenetic and molecular abnormalities. However, the genetic etiology of the disease is not yet fully understood. MicroRNAs (miRNA) are small noncoding RNAs which regulate the expression of target mRNAs both at transcriptional and translational level. In recent years, miRNAs have been identified as a novel mechanism in gene regulation, which show variable expression during myeloid differentiation. We studied miRNA expression of leukemic blasts of 29 cases of newly diagnosed and genetically defined AML using quantitative reverse transcription polymerase chain reaction (RT-PCR) for 365 human miR…

AdultMaleNPM1Down-RegulationBiologySettore MED/15 - Malattie Del SangueYoung Adulthemic and lymphatic diseasesmicroRNAmedicineGene silencingHumansLeukemia microarray data microRNAGranulocyte Precursor CellsAgedCell ProliferationGeneticsRegulation of gene expressionAged 80 and overAcute leukemiaReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCore Binding FactorsMyeloid leukemiaNuclear ProteinsCell DifferentiationHematologyMiddle Agedmedicine.diseaseUp-RegulationGene expression profilingGene Expression Regulation NeoplasticLeukemiaLeukemia Myeloid AcuteMicroRNAsfms-Like Tyrosine Kinase 3Case-Control StudiesMutationFemaleSettore SECS-S/01 - StatisticaNucleophosmin
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Granulocyte–Colony Stimulating Factor plus Plerixafor in Patients with β-thalassemia Major Results in the Effective Mobilization of Primitive CD34+ C…

2017

Successful gene therapy for β-thalassemia requires optimal numbers of autologous gene-transduced hematopoietic stem and progenitor cells (HSPCs) with high repopulating capacity. Previous studies suggested superior mobilization in these patients by the combination of granulocyte–colony stimulating factor (G-CSF) plus plerixafor over single agents. We mobilized four adult patients using G-CSF+plerixafor to assess the intra-individual variation of the circulating CD34+ cells number and subtypes preand post-plerixafor administration. The procedure was well-tolerated and the target cell dose of ≥8×10 6 CD34+ cells/kg was achieved in three of them with one apheresis procedure. The addition of ple…

Mobilizationbusiness.industryCD34+ cells expression profilingCd34 cellsPlerixaforGenetic enhancementβ-thalassemia; CD34 cells expression profiling; G-CSF plerixafor mobilization; gene therapygene therapySettore MED/15 - Malattie Del SangueGranulocyte colony-stimulating factorSettore BIO/18 - Geneticagene therapy.β-thalassemiaGene expressionImmunologyCancer researchG-CSF+plerixafor mobilizationMedicineDiseases of the blood and blood-forming organsIn patientβ-thalassemia; CD34+ cells expression profiling; G-CSF+plerixafor mobilization; gene therapyRC633-647.5businessβ thalassemia majormedicine.drugThalassemia Reports
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Gene Expression Profile of Chronic Myeloid Leukemia Innately Resistant to Imatinib

2007

Background. Most chronic myeloid leukemia patients who receive imatinib as first line-terapy will obtain, after 12 months treatment, complete cytogenetic and molecular response . However several cases will not achieve molecular response, but their innate mechanism(s) of resistance remain poorly understood. We tried to explore the molecular events involved in innate resistance in CML. Study design. Five patients who were molecular “non responder” and seven “major” responder were investigated by using the expression profile of a set of 380 genes. Multiple testing procedure (MTP), Significance Analysis of Microarrays (SAM), Empirical Bayes Analysis of Microarrays (EBAM), False Discovery Rate (…

business.industryMyeloid leukemiaImatinibGeneral MedicineCell cycleMolecular ResponseImmunologySignificance analysis of microarraysCancer researchmedicineEpigeneticsDNA microarraybusinessGenemedicine.drugClinical Leukemia
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