0000000000363194

AUTHOR

Alessandro Isidori

0000-0002-5723-9229

showing 3 related works from this author

Persistent immune stimulation exacerbates genetically driven myeloproliferative disorders via stromal remodeling

2017

Abstract Systemic immune stimulation has been associated with increased risk of myeloid malignancies, but the pathogenic link is unknown. We demonstrate in animal models that experimental systemic immune activation alters the bone marrow stromal microenvironment, disarranging extracellular matrix (ECM) microarchitecture, with downregulation of secreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation. These changes were accompanied by a decrease in Treg frequency and by an increase in activated effector T cells. Under these conditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal …

0301 basic medicineCancer ResearchStromal cellMyeloidMice TransgenicVascular RemodelingBiologyInbred C57BLTransgenicMice03 medical and health sciencesMyelogenousMyeloproliferative DisordersmedicineAnimalsHumansMyeloproliferative DisorderAnimals; Cell Proliferation; Humans; Mice; Mice Inbred C57BL; Mice Inbred CBA; Mice Transgenic; Myeloproliferative Disorders; Stromal Cells; Vascular Remodeling; Oncology; Cancer ResearchCell ProliferationMyeloproliferative DisordersAnimalStromal CellInbred CBANeutrophil extracellular trapsmedicine.diseaseMice Inbred C57BLHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureOncologyImmunologyMice Inbred CBABone marrowStromal CellsNucleophosminHuman
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Differences among young adults, adults and elderly chronic myeloid leukemia patients

2014

Abstract BACKGROUND: The incidence of chronic myeloid leukemia (CML) increases with age, but it is unclear how the characteristics of the disease vary with age. In children, where CML is very rare, it presents with more aggressive features, including huge splenomegaly, higher cell count and higher blast cell percentage. PATIENTS AND METHODS: To investigate if after childhood the disease maintains or loses these characteristics of aggressiveness, we analyzed 2784 adult patients, at least 18 years old, registered by GIMEMA CML WP over a 40-year period. RESULTS: Young adults (YAs: 18-29 years old) significantly differed from adults (30-59 years old) and elderly patients (at least 60 years old)…

MalePediatricsHost responseBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Oncology; HematologyTyrosine kinase inhibitorDiseaseAntineoplastic AgentTyrosin kinase inhibitorProtein-Tyrosine Kinasehemic and lymphatic diseases80 and overAge FactorProspective StudiesYoung adultChronicBCR-ABLAged 80 and overLeukemiaIncidence (epidemiology)Chronic myeloid leukemiaAge FactorsMyeloid leukemiaHematologyMiddle AgedProtein-Tyrosine KinasesPrognosisLeukemiaOncologybcr-abl1FemaleBCR-ABL; chronic myeloid leukemia; prognosis; tyrosine kinase inhibitors; young adultsHumanAdultyoung adultsmedicine.medical_specialtyPrognosiProtein Kinase InhibitorAntineoplastic Agentschronic myeloid leukemia; bcr-abl1; Tyrosin kinase inhibitor; prognosis; young adultsNOYoung Adultchronic myeloid leukemiaLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young AdultProtein Kinase InhibitorsAgedTyrosine kinase inhibitorsAdult patientsbusiness.industrymedicine.diseaseClinical trialBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Hematology; OncologyProspective StudieBCR-ABL; Chronic myeloid leukemia; Prognosis; Tyrosine kinase inhibitors; Young adults; Adult; Age Factors; Aged; Aged 80 and over; Antineoplastic Agents; Female; Humans; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Prospective Studies; Protein Kinase Inhibitors; Protein-Tyrosine Kinases; Spleen; Splenomegaly; Young Adult; Medicine (all); Hematology; OncologyImmunologySplenomegalyBCR-ABL PositiveBCR-ABL chronic myeloid leukemia prognosis tyrosine kinase inhibitors young adultsprognosisbusinessSpleenYoung adultsMyelogenous
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SNPs array karyotyping reveals a novel recurrent 20p13 amplification in primary myelofibrosis.

2011

The molecular pathogenesis of primary mielofibrosis (PMF) is still largely unknown. Recently, single-nucleotide polymorphism arrays (SNP-A) allowed for genome-wide profiling of copy-number alterations and acquired uniparental disomy (aUPD) at high-resolution. In this study we analyzed 20 PMF patients using the Genome-Wide Human SNP Array 6.0 in order to identify novel recurrent genomic abnormalities. We observed a complex karyotype in all cases, detecting all the previously reported lesions (del(5q), del(20q), del(13q), +8, aUPD at 9p24 and abnormalities on chromosome 1). In addition, we identified several novel cryptic lesions. In particular, we found a recurrent alteration involving cytob…

MaleMicroarraysMIELOFIBROSISChromosomes Human Pair 20Loss of Heterozygositylcsh:MedicineLoss of heterozygosityCohort StudiesHematologic Cancers and Related DisordersGene duplicationTaq Polymeraselcsh:ScienceOligonucleotide Array Sequence AnalysisMultidisciplinaryMYELOFIBROSIS; SNPKaryotypeGenomicsHematologyUniparental disomyMedicineFemaleImmunohistochemical AnalysisSNP arrayResearch ArticleTest Evaluationmedicine.medical_specialtyDNA Copy Number VariationsImmunologySNPLocus (genetics)Single-nucleotide polymorphismReceptors Cell SurfaceBiologyPolymorphism Single NucleotideDiagnostic MedicinemedicineGeneticsHumansBiologyAgedEvolutionary BiologyMyeloproliferative DisordersPopulation Biologylcsh:RCytogeneticsGene AmplificationComputational BiologyDNAUniparental Disomymedicine.diseaseMolecular biologyMYELOFIBROSISPrimary MyelofibrosisKaryotypingGenetic PolymorphismImmunologic TechniquesClinical Immunologylcsh:QPopulation GeneticsPLoS ONE
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