Search results for "Myeloid"

showing 10 items of 538 documents

Role of hematopoietic cells in Mycobacterium tuberculosis infection.

2021

Tuberculosis remains one of the most significant causes of mortality worldwide and the current situation shows a re-emergence of TB due to the emergence of new antibiotic-resistant strains and the widespread of disease caused by immunodeficiencies. For these reasons, a big effort is made to improve the therapeutic strategies against Mycobacterium tuberculosis and to perform new therapeutic and diagnostic strategies. This review analyzes the various hematopoietic populations, their role and the different changes they undergo during Mycobacterium tuberculosis infection or disease. We have examined the population of lymphocytes, monocytes, neutrophils, eosinophils and platelets, in orderto und…

Microbiology (medical)Blood PlateletsMyeloidTuberculosisNeutrophilsImmunologyPopulationDiseaseMicrobiologyMonocytesMycobacterium tuberculosismedicineHumansTuberculosisLymphocytesProgenitor celleducationeducation.field_of_studyHematopoietic cellsbiologybusiness.industryMycobacterium tuberculosismedicine.diseasebiology.organism_classificationHematopoietic Stem CellsEosinophilsInfectious Diseasesmedicine.anatomical_structureImmunologyMyeloid cellsBone marrowStem cellbusinessLymphoid cellsTuberculosis (Edinburgh, Scotland)
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Identification of a novel activating mutation (Y842C) within the activation loop of FLT3 in patients with acute myeloid leukemia (AML).

2004

Fms-like tyrosine kinase 3 (FLT3) receptor mutations as internal tandem duplication (ITD) or within the kinase domain are detected in up to 35% of patients with acute myeloid leukemia (AML). N-benzoyl staurosporine (PKC412), a highly effective inhibitor of mutated FLT3 receptors, has significant antileukemic efficacy in patients with FLT3-mutated AML. Mutation screening of FLT3 exon 20 in AML patients (n = 110) revealed 2 patients with a novel mutation (Y842C) within the highly conserved activation loop of FLT3. FLT3-Y842C-transfected 32D cells showed constitutive FLT3 tyrosine phosphorylation and interleukin 3 (IL-3)-independent growth. Treatment with PKC412 led to inhibition of proliferat…

Models MolecularImmunologyBiologymedicine.disease_causeBiochemistryCell Linechemistry.chemical_compoundMicefluids and secretionshemic and lymphatic diseasesProto-Oncogene ProteinsmedicineSTAT5 Transcription FactorAnimalsHumansTyrosinePhosphotyrosineMutationCell CycleMyeloid leukemiaReceptor Protein-Tyrosine Kinaseshemic and immune systemsTyrosine phosphorylationCell BiologyHematologymedicine.diseaseMilk ProteinsProtein Structure TertiaryDNA-Binding ProteinsEnzyme ActivationLeukemiaLeukemia Myeloid AcutechemistryGene Expression Regulationfms-Like Tyrosine Kinase 3embryonic structuresFms-Like Tyrosine Kinase 3MutationCancer researchTrans-ActivatorsTyrosineSignal transductionTyrosine kinaseSignal TransductionBlood
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Signaling pathways of the TREM-1- and TLR4-mediated neutrophil oxidative burst.

2008

The triggering receptor expressed on myeloid cells 1 (TREM-1) is involved in the innate inflammatory response to microbial infections. Activation and expression of TREM-1 by polymorphonuclear neutrophils (PMN) occurs in concert with Toll-like receptors (TLR) such as TLR4 for bacterial lipopolysaccharide. However, it is currently unclear how this is mediated on a molecular level. Using pharmacological inhibitors and Western blot analysis we demonstrate that phosphatidyl inositide 3-kinase, phospholipase C and the mitogen-activated kinase p38MAPK are essential for the TREM-1- and TLR4-induced oxidative burst of human PMN. The activation of protein kinase B and extracellular signal-related kin…

Models MolecularLipopolysaccharideNeutrophilsBlotting WesternCell Separationp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundPhosphatidylinositol 3-KinasesImmunology and AllergyHumansReceptors ImmunologicReceptorProtein kinase BRespiratory BurstMembrane GlycoproteinsPhospholipase CKinaseFlow CytometryTriggering Receptor Expressed on Myeloid Cells-1Respiratory burstCell biologyEnzyme ActivationToll-Like Receptor 4chemistryTLR4Signal transductionProto-Oncogene Proteins c-aktSignal TransductionJournal of innate immunity
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Evolutionary dynamics of imatinib-treated leukemic cells by stochastic approach

2008

The evolutionary dynamics of a system of cancerous cells in a model of chronic myeloid leukemia (CML) is investigated by a statistical approach. Cancer progression is explored by applying a Monte Carlo method to simulate the stochastic behavior of cell reproduction and death in a population of blood cells which can experience genetic mutations. In CML front line therapy is represented by the tyrosine kinase inhibitor imatinib which strongly affects the reproduction of leukemic cells only. In this work, we analyze the effects of a targeted therapy on the evolutionary dynamics of normal, first-mutant and cancerous cell populations. Several scenarios of the evolutionary dynamics of imatinib-tr…

Monte Carlo simulation stochastic approach Evolutionary dynamicsMutation rate87.23.kgmedicine.drug_classQC1-999medicine.medical_treatmentPopulationGeneral Physics and AstronomyBiologyTyrosine-kinase inhibitorTargeted therapyhemic and lymphatic diseasesmedicine87.10.mncomplex systemsQuantitative Biology - Populations and EvolutioneducationEvolutionary dynamicseducation.field_of_studycancer evolutionPhysicsstochastic dynamics87.19.xjPopulations and Evolution (q-bio.PE)Myeloid leukemiaImatinibSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)FOS: Biological sciencesCancer cellCancer research87.10.rtmedicine.drugOpen Physics
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Cancer growth dynamics: stochastic models and noise induced effects

2009

In the framework of the Michaelis‐Menten (MM) reaction kinetics, we analyze the cancer growth dynamics in the presence of the immune response. We found the coexistence of noise enhanced stability (NES) and resonant activation (RA) phenomena which act in an opposite way with respect to the extinction of the tumor. The role of the stochastic resonance (SR) in the case of weak cancer therapy has been analyzed. The evolutionary dynamics of a system of cancerous cells in a model of chronic myeloid leukemia (CML) is investigated by a Monte Carlo approach. We analyzed the effects of a targeted therapy on the evolutionary dynamics of normal, first‐mutant and cancerous cell populations. We show how …

Mutation rateStochastic modellingmedicine.medical_treatmentMyeloid leukemiaCancerStochastic resonance (sensory neurobiology)BiologyBioinformaticsmedicine.diseaseTargeted therapyCancer cellCancer researchmedicineEvolutionary dynamics
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Identification of a novel type of ITD mutations located in nonjuxtamembrane domains of the FLT3 tyrosine kinase receptor

2009

Abstract In acute myeloid leukemia (AML), internal tandem duplications (ITDs) of the juxtamembrane (JM) of FLT3 have been shown to play a crucial role in driving proliferation and survival of the leukemic clone. Here, we report the identification of FLT3_ITD mutations located in non-JM domains of the FLT3-receptor. This novel type of FLT3_ITD mutation was found in 216 of 753 (28.7%) of unselected FLT3_ITD-positive AML cases. An FLT3 receptor harbouring a prototypic non-JM ITD (FLT3_ITD627E) mediated constitutive phosphorylation of FLT3 and of STAT5, suggesting that non-JM ITDs confer constitutive activation of the receptor. FLT3_ITD627E induced transformation of hematopoietic 32D cells and …

MutationImmunologyClone (cell biology)MedizinMyeloid leukemiaCell BiologyHematologyBiologymedicine.disease_causeBiochemistryMolecular biologyReceptor tyrosine kinasehemic and lymphatic diseasesTrk receptormedicinebiology.proteinPhosphorylationReceptorSTAT5
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DNMT3A mutations Predict for Inferior Outcome in NPM1-Wildtype and Molecular Unfavorable Cytogenetically-Normal Acute Myeloid Leukemia: A Study of th…

2011

Abstract Abstract 415 Background: Alteration of DNA methylation, a hallmark of epigenetic modification, is currently discussed as one important pathomechanism in leukemogenesis. Using a next-generation sequencing approach, a frameshift mutation of the gene encoding the DNA methyltransferase (DNMT3A) in an acute myeloid leukemia (AML) case was identified. DNMT3A catalyses the addition of a methyl group to the cytosine residue of CpG dinucleotides, thereby affecting promoter methylation status and gene expression. Subsequent sequencing analysis in an independent cohort of 288 AML patients (pts) revealed DNMT3A mutations (DNMT3Amut) in 22% of the pts; mutations were associated with intermediat…

MutationNPM1medicine.medical_specialtyImmunologyCytogeneticsMyeloid leukemiaCell BiologyHematologyBiologymedicine.disease_causeBiochemistryIDH2Molecular biologyFrameshift mutationCEBPAmedicineMissense mutationBlood
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Antiproliferative Effects of St. John’s Wort, Its Derivatives, and Other Hypericum Species in Hematologic Malignancies

2021

Hypericumis a widely present plant, and extracts of its leaves, flowers, and aerial elements have been employed for many years as therapeutic cures for depression, skin wounds, and respiratory and inflammatory disorders. Hypericum also displays an ample variety of other biological actions, such as hypotensive, analgesic, anti-infective, anti-oxidant, and spasmolytic abilities. However, recent investigations highlighted that this species could be advantageous for the cure of other pathological situations, such as trigeminal neuralgia, as well as in the treatment of cancer. This review focuses on the in vitro and in vivo antitumor effects of St. John’s Wort (Hypericum perforatum), its derivat…

MyeloidAngiogenesisDrug Evaluation PreclinicalReviewPharmacologylcsh:Chemistrychemistry.chemical_compoundhyperforinDrug InteractionsMyeloid CellsLymphocyteslcsh:QH301-705.5SpectroscopybiologyapoptosisleukemiaHypericum perforatumGeneral MedicineComputer Science ApplicationsHypericinLeukemiamedicine.anatomical_structurephotodynamic therapyHematologic NeoplasmsHypericumHypericumSt. John’s wortlymphomaCatalysisInorganic ChemistryStructure-Activity Relationshipmultidrug resistanceIn vivoCell Line TumormedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyCell ProliferationPlant Extractsbusiness.industryOrganic Chemistry<i>Hypericum</i>biology.organism_classificationmedicine.diseaseAntineoplastic Agents PhytogenicApoptosis; Hyperforin; Hypericin; Hypericum; Leukemia; Lymphoma; Mul-tidrug resistance; Photodynamic therapy; St. John’s wort; Animals; Antineoplastic Agents Phytogenic; Apoptosis; Cell Line Tumor; Cell Proliferation; Drug Evaluation Preclinical; Drug Interactions; Drug Resistance Neoplasm; Hematologic Neoplasms; Humans; Hypericum; Lymphocytes; Myeloid Cells; Plant Extracts; Structure-Activity RelationshipHyperforinchemistrylcsh:Biology (General)lcsh:QD1-999Drug Resistance NeoplasmhypericinbusinessInternational Journal of Molecular Sciences
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The suppressive effects of recombinant human tumor necrosis factor‐alpha on normal and malignant myelopoiesis: Synergism with interferon‐gamma

1988

The modulation of growth of normal and leukemic myeloid progenitor cells in soft agar cultures by recombinant human tumor necrosis factor-alpha (TNF alpha) and recombinant human interferon-gamma (IFN gamma) was investigated. TNF alpha inhibited colony formation of all colony types representing different maturational stages of normal progenitor cells committed to the myeloid lineage with different orders of sensitivity. Blast-type colonies derived from patients with acute myelogenous leukemia were more sensitive to TNF alpha inhibition than progenitor cells purified from normal bone marrow or bone marrow from patients with stable-phase chronic myelogenous leukemia. The response of most colon…

MyeloidBone Marrow CellsBiologyInterferon-gammaBone MarrowmedicineHumansInterferon gammaProgenitor cellTumor Necrosis Factor-alphaAntibodies MonoclonalDrug SynergismCell BiologyHematopoietic Stem Cellsmedicine.diseaseRecombinant ProteinsLeukemia Myeloid AcuteLeukemiamedicine.anatomical_structureLeukemia MyeloidImmunologyCancer researchTumor necrosis factor alphaBone marrowMyelopoiesisChronic myelogenous leukemiamedicine.drugThe International Journal of Cell Cloning
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Bcr-Abl kinase promotes cell cycle entry of primary myeloid CML cells in the absence of growth factors

1998

Cell cycle control of both immature and differentiated primary myeloid normal and chronic-phase chronic myeloid leukaemia (CML) cells to growth factor deprivation was studied. CD34+ cells were cultured in liquid culture. After removal of growth factors for 48 h normal cells were very efficiently arrested with the fraction of cells in S phase reduced by 70.8 +/- 6.5% in CD34+ and 50.5 +/- 4.2% in CD34- cells. In contrast, a significantly higher proportion of leukaemic cells remained in S phase. The fraction of S-phase cells was reduced by only 29.3 +/- 5.7% in CD34+ CML cells and 21.2 +/- 3.8% in CD34- cells. This abnormal negative cell cycle control in leukaemic cells was specific for growt…

MyeloidCell growthGrowth factormedicine.medical_treatmentCD34HematologyBiologyCell cyclemedicine.diseaseLeukemiamedicine.anatomical_structureImatinib mesylateCytokinehemic and lymphatic diseasesmedicineCancer researchBritish Journal of Haematology
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