0000000000191330

AUTHOR

Domenico Salemi

0000-0002-2688-4145

showing 3 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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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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UPREGULATION OF MIR-29A AND GENOMIC DNA HYPERMETHYLATION IN NORMAL KARYOTYPE AML SHOWING DNMT3A MUTATION UPREGOLAZIONE DEL MIR-29A E IPERMETILAZIONE …

2015

DNMT3A, a member of DNA methyltransferases, is mutated in approximately 22% of de novo normal karyotype acute myeloid leukemia (NK-AML) patients leading to adverse overall survival. The highly recurrent mutation in DNMT3A is a “gain of function-like” at codon R882. To indagate about miRNA signature in NK-AML R882-DNMT3A mutated we studied by qRT-PCR the expression of 384 known human miRNA in 9 selected de-novo AML DNMT3A mutated. We compared miRNA expression data with our previous results obtained in 31 AML DNMT3A wild type (WT) and we focused on a strong up-regulation of miR155, miR29a, miR196b and miR25. We consolidated this data in additional 24 new DNMT3A mutated AML and we confirmed th…

Settore BIO/18 - GeneticaAcute Myeloid Leukemia miRNA Genomewide DNA Methylation
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