Search results for "leukemia"

showing 10 items of 976 documents

Pharmacogenetics of Metabolic Genes of Anthracyclines in Acute Myeloid Leukemia.

2018

Background Anthracyclines in combination with cytarabine have been the standard therapy for acute myeloid leukemia (AML) for decades with high efficacy. However, the majority of patients will show initial resistance or will relapse after initial complete remission. Genetic variability in genes involved in anthracyclines metabolic pathway could be one of the causes of the interindividual differences in clinical outcomes. Methods A systematic review of published studies in AML cohorts was carried out in order to analyze the influence of polymorphisms in genes of anthracycline metabolism on efficacy and toxicity. Results Polymorphisms in the main enzymes of anthracyclines metabolism (CBR, AKR,…

0301 basic medicineAnthracyclinemedicine.medical_treatmentClinical BiochemistryEfficacy03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsMedicineIdarubicinHumansAnthracyclinesPharmacologyCardiotoxicityChemotherapyPolymorphism Geneticbusiness.industryCytarabineMyeloid leukemiaLeukemia Myeloid Acute030104 developmental biologyPharmacogenetics030220 oncology & carcinogenesisCytarabineCancer researchbusinessPharmacogeneticsmedicine.drugCurrent drug metabolism
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Novel iodoacetamido benzoheterocyclic derivatives with potent antileukemic activity are inhibitors of STAT5 phosphorylation

2016

Signal Transducer and Activator of Transcription 5 (STAT5) protein, a component of the STAT family of signaling proteins, is considered to be an attractive therapeutic target because of its involvement in the progression of acute myeloid leukemia. In an effort to discover potent molecules able to inhibit the phosphorylation-activation of STAT5, twenty-two compounds were synthesized and evaluated on the basis of our knowledge of the activity of 2-(3’,4’,5’-trimethoxybenzoyl)-3-iodoacetamido-6-methoxy benzo[b]furan derivative 1 as a potent STAT5 inhibitor. Most of these molecules, structurally related to compound 1, were characterized by the presence of a common 3’,4’,5’-trimethoxybenzoyl moi…

0301 basic medicineApoptosisAntineoplastic Agentchemistry.chemical_compoundBenzophenone0302 clinical medicinehemic and lymphatic diseasesFuranDrug DiscoverySTAT5 Transcription FactorTumor Cells CulturedThiopheneMoietyPhosphorylationSTAT5Molecular StructurebiologyChemistryBiological activityGeneral MedicineApoptosis; BCR/ABL expressing leukemia; In vitro antiproliferative activity; STAT5 inhibitors; Structure-activity relationship; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry; PharmacologyLeukemia Myeloid Acute030220 oncology & carcinogenesisBCR/ABL expressing leukemiaApoptosis; BCR/ABL expressing leukemia; In vitro antiproliferative activity; STAT5 inhibitors; Structure-activity relationship; Antineoplastic Agents; Apoptosis; Benzofurans; Benzophenones; Cell Proliferation; Dose-Response Relationship Drug; Drug Screening Assays Antitumor; Humans; K562 Cells; Leukemia Myeloid Acute; Molecular Structure; Phosphorylation; STAT5 Transcription Factor; Structure-Activity Relationship; Tumor Cells Cultured; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry; PharmacologyHumanStereochemistryAntineoplastic AgentsArticleNOBenzophenones03 medical and health sciencesK562 CellHumansStructure–activity relationshipBenzofuransCell ProliferationPharmacologyIndole testDose-Response Relationship DrugIn vitro antiproliferative activitySTAT5 inhibitorsDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryApoptosiSTAT5 inhibitorStructure-activity relationshipIn vitro030104 developmental biologybiology.proteinBenzofuranDrug Screening Assays AntitumorK562 Cells
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Characterization of a Fetal Liver Cell Population Endowed with Long-Term Multiorgan Endothelial Reconstitution Potential.

2016

et al.

0301 basic medicineBiologyEndothelial progenitor cellProgenitor cellsTissue‐Specific Stem CellsCell Line03 medical and health sciencesMiceFetusAntigens CDmedicineAnimalsNewborn transplantationProgenitor cellT-Cell Acute Lymphocytic Leukemia Protein 1Cell AggregationExtracellular Matrix ProteinsLiver cellEndothelial CellsCell BiologyCadherinsCell aggregation3. Good healthHematopoiesisEndothelial stem cellHaematopoiesisEndothelial reconstitutionFetal liver030104 developmental biologymedicine.anatomical_structureHematopoietic progenitorsLiverFetal liver ; Endothelial reconstitution ; Hematopoietic progenitors ; Progenitor cellsOrgan SpecificityImmunologyCancer researchMolecular MedicineBlood VesselsLeukocyte Common AntigensBone marrowStem cellDevelopmental Biology
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Drug Repurposing of the Anthelmintic Niclosamide to Treat Multidrug-Resistant Leukemia

2017

Multidrug resistance, a major problem that leads to failure of anticancer chemotherapy, requires the development of new drugs. Repurposing of established drugs is a promising approach for overcoming this problem. An example of such drugs is niclosamide, a known anthelmintic that is now known to be cytotoxic and cytostatic against cancer cells. In this study, niclosamide showed varying activity against different cancer cell lines. It revealed better activity against hematological cancer cell lines CCRF-CEM, CEM/ADR5000, and RPMI-8226 compared to the solid tumor cell lines MDA-MB-231, A549, and HT-29. The multidrug resistant CEM/ADR5000 cells were similar sensitive as their sensitive counterp…

0301 basic medicineBiologyPharmacologychemotherapy03 medical and health sciences0302 clinical medicinetranscription factorsmedicineoxidative stressCytotoxic T cellPharmacology (medical)NiclosamideOriginal ResearchpharmacogenomicsPharmacologydrug resistanceNFATmedicine.diseaseGlutathione synthetaseMultiple drug resistanceLeukemia030104 developmental biologyCell culture030220 oncology & carcinogenesisCancer cellmedicine.drugFrontiers in Pharmacology
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HLA-DPB1 mismatch alleles represent powerful leukemia rejection antigens in CD4 T-cell immunotherapy after allogeneic stem-cell transplantation.

2016

Refractory or relapsed acute myeloid leukemia (AML) represents a frequent complication after allogeneic hematopoietic stem-cell transplantation (HSCT). We show herein that primary in vitro stimulation of CD45RA-selected CD4 T cells of stem-cell donors with 10/10 HLA-matched AML blasts results in expansion of cytolytic T-lymphocytes (CTL) that almost all recognize HLA-DPB1 mismatch alleles, which clinically occur in up to 80% of donor-patient pairs. Primary AML blasts were found to strongly express HLA-DPB1, whereas fibroblasts and keratinocytes used as surrogate target cells for graft-versus-host disease did express HLA-DPB1 only upon IFN-γ pre-treatment. Since patients' AML blasts are rare…

0301 basic medicineCD4-Positive T-LymphocytesCytotoxicity ImmunologicCancer ResearchAdoptive cell transferGenotypemedicine.medical_treatmentHematopoietic stem cell transplantationBiologyLymphocyte ActivationImmunotherapy Adoptive03 medical and health sciencesMice0302 clinical medicinehemic and lymphatic diseasesmedicineAnimalsHumansTransplantation HomologousAllelesHLA-DP beta-ChainsLeukemiaHematopoietic Stem Cell TransplantationMyeloid leukemiaHematologyImmunotherapymedicine.diseaseTissue DonorsTransplantationCTL*LeukemiaLeukemia Myeloid Acute030104 developmental biologyOncologyImmunologyFemaleImmunotherapyStem cell030215 immunologyLeukemia
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Patient-individualized CD8+cytolytic T-cell therapy effectively combats minimal residual leukemia in immunodeficient mice

2015

Adoptive transfer of donor-derived cytolytic T-lymphocytes (CTL) has evolved as a promising strategy to improve graft-versus-leukemia (GvL) effects in allogeneic hematopoietic stem-cell transplantation. However, durable clinical responses are often hampered by limited capability of transferred T cells to establish effective and sustained antitumor immunity in vivo. We therefore analyzed GvL responses of acute myeloid leukemia (AML)-reactive CD8(+) CTL with central and effector memory phenotype in a new allogeneic donor-patient specific humanized mouse model. CTL lines and clones obtained upon stimulation of naive CD45RA(+) donor CD8(+) T cells with either single HLA antigen-mismatched or HL…

0301 basic medicineCancer ResearchAdoptive cell transferbusiness.industryT cellMyeloid leukemiamedicine.diseaseMinimal residual disease03 medical and health sciencesCTL*Leukemia030104 developmental biologymedicine.anatomical_structureOncologyhemic and lymphatic diseasesHumanized mouseImmunologyMedicineBone marrowbusinessInternational Journal of Cancer
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Extracellular vesicles as miRNA nano-shuttles : dual role in tumor progression

2018

[EN] Tumor-derived extracellular vesicles (EVs) have a pleiotropic role in cancer, interacting with target cells of the tumor microenvironment, such as fibroblasts, immune and endothelial cells. EVs can modulate tumor progression, angiogenic switch, metastasis, and immune escape. These vesicles are nano-shuttles containing a wide spectrum of miRNAs that contribute to tumor progression. MiRNAs contained in extracellular vesicles (EV-miRNAs) are disseminated in the extracellular space and are able to influence the expression of target genes with either tumor suppressor or oncogenic functions, depending on both parental and target cells. Metastatic cancer cells can balance their oncogenic pote…

0301 basic medicineCancer ResearchAngiogenic SwitchLung-CancerBIOLOGIA CELULARMessenger-RNAsSuppressor-CellsDendritic cellsMetastasisLiquid biopsies03 medical and health sciencesExtracellular VesiclesImmune systemSettore BIO/13 - Biologia ApplicatamicroRNAMedicineHumansNanotechnologyPharmacology (medical)miRNAMyelogenous Leukemia-CellsExtracellular vesicles; miRNA; cancer cellsTumor microenvironmentExosome-Mediated transferbusiness.industryCancerProteinsmedicine.diseaseMicrornasMicroRNAs030104 developmental biologyOncologyTumor progressionCancer cellcancer cellsCancer researchDisease ProgressionHuman medicineExtracellular vesiclebusinessMicrovesiclesTargeted oncology
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Cationic Amino Acid Transporter-1-Mediated Arginine Uptake Is Essential for Chronic Lymphocytic Leukemia Cell Proliferation and Viability

2019

Interfering with tumor metabolism by specifically restricting the availability of extracellular nutrients is a rapidly emerging field of cancer research. A variety of tumor entities depend on the uptake of the amino acid arginine since they have lost the ability to synthesize it endogenously, that is they do not express the rate limiting enzyme for arginine synthesis, argininosuccinate synthase (ASS). Arginine transport through the plasma membrane of mammalian cells is mediated by eight different transporters that belong to two solute carrier (SLC) families. In the present study we found that the proliferation of primary as well as immortalized chronic lymphocytic leukemia (CLL) cells depen…

0301 basic medicineCancer ResearchArginineArgininosuccinate synthaseargininelcsh:RC254-282amino acid transporter03 medical and health sciences0302 clinical medicineDownregulation and upregulationhemic and lymphatic diseasesAmino acid transporterViability assayOriginal Researchchemistry.chemical_classificationnutrient restrictionArginine transportbiologylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAmino acidSolute carrier familyCell biology030104 developmental biologyOncologychemistry030220 oncology & carcinogenesisbiology.proteinchronic lymphocytic leukemiatumor metabolismFrontiers in Oncology
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Bacitracin and Rutin Regulate Tissue Factor Production in Inflammatory Monocytes and Acute Myeloid Leukemia Blasts

2021

Simple Summary Aberrant tissue factor (TF) expression by transformed myeloblasts and inflammatory monocytes contributes to coagulation activation in acute myeloid leukemia (AML). TF procoagulant activity (PCA) is regulated by protein disulfide isomerase (PDI), an oxidoreductase with chaperone activity, but its specific role in AML-associated TF biology is unclear. Here, we provide novel mechanistic insights into this interrelation. We show that bacitracin and rutin, two pan-inhibitors of the PDI family, prevent lipopolysaccharide (LPS)-induced monocyte TF production under inflammatory conditions and constitutive TF expression by THP1 cells and AML blasts, thus exerting promising anticoagula…

0301 basic medicineCancer ResearchMyeloidDaunorubicinacute myeloid leukemia030204 cardiovascular system & hematologyPeripheral blood mononuclear cellArticleFlow cytometry03 medical and health sciencesTissue factor0302 clinical medicineDownregulation and upregulationhemic and lymphatic diseasesmedicinecoagulationProtein disulfide-isomeraseRC254-282medicine.diagnostic_testChemistryrutinNeoplasms. Tumors. Oncology. Including cancer and carcinogensMyeloid leukemiatissue factorprotein disulfide isomeraseMolecular biology030104 developmental biologymedicine.anatomical_structureOncologyinflammationtissue factor; protein disulfide isomerase; acute myeloid leukemia; coagulation; inflammation; rutin; monocytesmonocytesmedicine.drugCancers
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Imiquimod inhibits growth and induces differentiation of myeloid leukemia cell lines

2018

Background: The antitumoral effects of different Toll-like receptor (TLRs) agonists is mediated by activating immune responses to suppress tumors growth, although TLR ligands may also have a direct effect on tumoral cells. Given that TLR signaling induces hematopoietic cell differentiations this may serve as a novel differentiation therapeutic approach for AML. Methods: We investigated the effects of agonists for the ten human TLRs on the proliferation, apoptosis, cell cycle and differentiation of ten different types of myeloid leukemia cell lines (HL-60, U-937, KG-1, KG-1a, K-562, Kasumi-1, EOL-1, NB4, MOLM-13 and HEL). Proliferation was measured using the CellTiter 96 (R) Aqueous One Solu…

0301 basic medicineCancer ResearchMyeloidImiquimodlcsh:RC254-282Flow cytometry03 medical and health sciences0302 clinical medicineToll-like receptorGeneticsmedicineCytotoxic T cellMyeloid leukemia cell lineslcsh:QH573-671Toll-like receptorImiquimodmedicine.diagnostic_testChemistryCell growthlcsh:CytologyMyeloid leukemiaCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchPrimary Researchmedicine.drugCancer Cell International
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