Search results for "Myelogenous Leukemia"

showing 10 items of 58 documents

Exosomal shuttling of miR-126 in endothelial cells modulates adhesive and migratory abilities of chronic myelogenous leukemia cells.

2014

BACKGROUND: Recent findings indicate that exosomes released from cancer cells contain microRNAs (miRNAs) that may be delivered to cells of tumor microenvironment. RESULTS: To elucidate whether miRNAs secreted from chronic myelogenous leukemia cells (CML) are shuttled into endothelial cells thus affecting their phenotype, we first analysed miRNAs content in LAMA84 exosomes. Among the 124 miRNAs identified in LAMA84 exosomes, we focused our attention on miR-126 which was found to be over-overexpressed in exosomes compared with producing parental cells. Transfection of LAMA84 with Cy3-labelled miR-126 and co-culture of leukemia cells with endothelial cells (EC) confirmed that miR-126 is shuttl…

Cancer ResearchEndothelial cellsChronic Myelogenous Leukemia CellsVascular Cell Adhesion Molecule-1Exosomes; Chronic Myelogenous Leukemia; microRNA;BiologyExosomesCell MovementSettore BIO/13 - Biologia ApplicataCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositiveCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineHumansChronic Myelogenous LeukemiamiRNATumor microenvironmentExosomes; Endothelial cells; Chronic Myelogenous Leukemia Cells; miRNAmicroRNAResearchTransfectionmedicine.diseaseChemokine CXCL12MicrovesiclesExosomeMicroRNAsLeukemiamedicine.anatomical_structureOncologyCell cultureCancer cellCancer researchMolecular MedicineBone marrowChronic myelogenous leukemia
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Tyrosine Kinase Inhibitors for the Treatment of Chronic Myeloid Leukemia

2009

Imatinib mesylate (Gleevec) is a drug unique for the treatment of certain forms of cancer. It works by targeting, and turning off, specific tyrosine kinase proteins that cause the uncontrolled cell growth and the inhibition of apoptosis in cancer cells. Imatinib was designed on the basis of the structure of the ATP binding site of the Abl protein kinase with the aim to stabilizes the inactive form of Bcr-Abl, an oncoprotein involved in malignant transformation in chronic myelogenous leukemia (CML). However, imatinib can also target other tyrosine kinase proteins different from Bcr-Abl such as Kit, that is the suspected cause of gastrointestinal stromal tumor (GIST). Despite successful clini…

Cancer ResearchFusion Proteins bcr-ablAntineoplastic AgentsApoptosisPharmacologyhemic and lymphatic diseasesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansProtein kinase AneoplasmsProtein Kinase InhibitorsPharmacologyTyrosine kinase inhibitorsABLbusiness.industryBcr-Abl chronic myelogenous leukemia tyrosine kinase inhibitorsMyeloid leukemiaImatinibProtein-Tyrosine Kinasesmedicine.diseaseBcr-Abl; Chronic myelogenous leukemia; Tyrosine kinase inhibitors;LeukemiaImatinib mesylateCancer researchMolecular MedicinebusinessTyrosine kinaseChronic myelogenous leukemiamedicine.drugChronic myelogenous leukemiaBcr-Abl
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Influence of interferon-alpha on cytokine expression by the bone marrow microenvironment--impact on treatment of myeloproliferative disorders.

1996

Myeloproliferative disorders (MPD) are characterized by several common clinical and biological features, although at the molecular level, each disease entity exhibits distinct abnormalities. IFN-alpha exerts beneficial therapeutic effects in chronic myelogenous leukemia, polycythemia vera and essential thrombocythemia, resulting in control of hematopoietic hyperplasia and, in a minority of patients, in induction of cytogenetic remission. The mechanism of action of IFN-alpha in MPD is poorly defined. Recently published in vitro findings suggest that IFN-alpha interacts with the regulation of hematopoiesis by multiple ways. Its antiproliferative activity is well known for more than a decade, …

Cancer ResearchStromal cellAlpha interferonBiologyPolycythemia veraMyeloproliferative DisordersBone Marrowhemic and lymphatic diseasesmedicineCell AdhesionHumansImmunologic FactorsProgenitor cellMyeloproliferative DisordersEssential thrombocythemiaInterferon-alphaHematologymedicine.diseaseHematopoietic Stem Cellsmedicine.anatomical_structureOncologyAdipose TissueGene Expression RegulationConnective TissueImmunologyCytokinesBone marrowCell DivisionChronic myelogenous leukemiaLeukemialymphoma
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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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Can curcumin induces selective packaging of miRNAs in exosomes? A pilot study in chronic myelogenous leukemia cells.

2015

e13563 Background: Chronic myeloid leukemia is a myeloproliferative disorder that comes from a hematopoietic stem cell or a multipotent progenitor. Exosomes are biological nanovescicles (40-100 nm)...

Cancer Researchbusiness.industryHematopoietic stem cellMyeloid leukemiamedicine.diseaseMicrovesicleschemistry.chemical_compoundmedicine.anatomical_structureOncologychemistryhemic and lymphatic diseasesmicroRNAmedicineCurcuminCancer researchbusinessChronic myelogenous leukemiaProgenitorJournal of Clinical Oncology
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Comparative protEome profiling and functional analysis of chronic myelogenous leucemia cell lines

2008

Chronic Myelogenous Leukemia proteomic analysis
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ROLE OF EXOSOMES RELEASED BY CHRONIC MYELOGENOUS LEUKEMIA CELLS IN THE CROSS-TALK WITH ENDOTHELIAL CELLS

2016

Chronic myelogenous leukemia; exosomes; tumor microenvironment; curcuminexosometumor microenvironmentcurcuminHuman medicineChronic myelogenous leukemia
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Inhibition of activated STAT5 in Bcr/Abl expressing leukemia cells with new pimozide derivatives.

2014

STATs are transcription factors acting as intracellular signaling after stimulation with cytokines, growth factors and hormones. STAT5 is also constitutively active in many forms of cancers, including chronic myelogenous leukemia, acute lymphoblastic leukemia and Hodgkin's lymphoma. Recently, literature reported that the neuroleptic drug pimozide inhibits STAT5 phosphorylation inducing apoptosis in CML cells. We undertook an investigation from pimozide structure, obtaining simple derivatives with cytotoxic and STAT5-inhibitory activity, two of them markedly more potent than pimozide.

Clinical BiochemistryFusion Proteins bcr-ablPharmaceutical ScienceApoptosisBiochemistrySettore MED/15 - Malattie Del SangueCell LineStructure-Activity RelationshipPimozideSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesDrug DiscoverymedicineSTAT5 Transcription FactorCytotoxic T cellHumansPhosphorylationMolecular BiologyTranscription factorSTAT5Cell ProliferationbiologyDose-Response Relationship DrugMolecular StructureChemistrySTAT5 inhibitorsPimozideBCR/ABL expressing leukemia ApoptosisCell growth inhibitionOrganic ChemistryCell CyclePimozidemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaLeukemiaApoptosisCancer researchbiology.proteinSettore BIO/14 - FarmacologiaMolecular MedicinePhosphorylationK562 Cellsmedicine.drugChronic myelogenous leukemia
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2-Cinnamamido, 2-(3-phenylpropiolamido), and 2-(3-phenylpropanamido)benzamides: synthesis, antiproliferative activity, and mechanism of action

2013

Abstract Several new benzamides 4a–q were synthesized by stirring in pyridine the acid chlorides 3a–q with the appropriate anthranilamide derivatives 2a–g. Some of the synthesized compounds were evaluated for their in vitro antiproliferative activity against a panel of 5 human cell lines (K562 human chronic myelogenous leukemia cells, MCF-7 breast cancer cells, HTC-116 and HT26 colon cancer cells and NCI H460 non-small cell lung cancer cells).

Colorectal cancerAntineoplastic AgentsApoptosisPharmacologyArticleStructure-Activity RelationshipDrug DiscoveryTumor Cells CulturedmedicineHumansStructure–activity relationshipCell ProliferationPharmacologyDose-Response Relationship DrugMolecular StructureChemistryCell growthOrganic ChemistryGeneral Medicinemedicine.disease2-cinnamamidobenzamides 2-(3-phenylpropiolamido)benzamides 2-(3-phenylpropanamido)benzamides antiproliferative activity apoptosisSettore CHIM/08 - Chimica FarmaceuticaMechanism of actionApoptosisBenzamidesMCF-7 CellsNon small cellDrug Screening Assays Antitumormedicine.symptomK562 CellsChronic myelogenous leukemiaK562 cells
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Curcumin modulates chronic myelogenous leukemia exosomes composition and affects angiogenic phenotype, via exosomal miR-21.

2016

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Exosomes curcumin chronic myelogenous leukemia angiogenesis
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