Search results for " Erythroblastic"

showing 5 items of 5 documents

Antiproliferative and chemomodulatory effects of interferon-γ on doxorubicin-sensitive and -resistant tumor cell lines

1993

Biological agents might offer various therapeutic opportunities in the treatment of cancer, including a direct and/or host-mediated antiproliferative effect and also the possibility to favorably modulate tumor resistance to antineoplastic drugs. We studied the in vitro antiproliferative effects of interferon (IFN)-gamma on the mouse B16 melanoma and Friend erythroleukemia, and the human K562 erythroleukemia, as doxorubicin (DXR)-sensitive and -resistant (multidrug resistant) variants. These effects were marked in B16 melanoma and rather slight in K562 erythroleukemia, without any difference between the DXR-sensitive and -resistant lines. The chemosensitive variant of Friend erythroleukemia …

Antimetabolites AntineoplasticCancer Researchmedicine.medical_treatmentDrug ResistanceMelanoma ExperimentalInterferon-gammaMicechemistry.chemical_compoundInterferonMethionine Sulfoximinehemic and lymphatic diseasesTumor Cells CulturedmedicineAnimalsHumansCytotoxic T cellPharmacology (medical)DoxorubicinButhionine sulfoximineInterferon gammaButhionine SulfoximinePharmacologyGlutathioneFriend murine leukemia virusCytokineOncologychemistryDoxorubicinCell cultureCancer researchLeukemia Erythroblastic AcuteCell Divisionmedicine.drugK562 cellsAnti-Cancer Drugs
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A natural-like synthetic small molecule impairs bcr-abl signaling cascades and induces megakaryocyte differentiation in erythroleukemia cells

2013

Over the past years, we synthesized a series of new molecules that are hybrids of spirocyclic ketones as complexity-bearing cores with bi- and ter-phenyls as privileged fragments. Some of these newly-shaped small molecules showed antiproliferative, pro-apoptotic and differentiating activity in leukemia cell lines. In the present study, to investigate more in depth the mechanisms of action of these molecules, the protein expression profiles of K562 cells treated with or without the compounds IND_S1, MEL_T1, IND_S7 and MEL_S3 were analyzed using two-dimensional gel electrophoresis coupled with mass spectrometry. Proteome comparisons revealed several differentially expressed proteins, mainly r…

Cell signalingProteomeMegakaryocyte differentiationCellular differentiationFusion Proteins bcr-abllcsh:MedicineBiologyProteomicsSmall Molecule Librariesbi- and ter-phenylsantiproliferative pro-apoptotic differentiating activity leukemiaMolecular Cell BiologyChemical BiologyBiomarkers TumorCluster AnalysisHumansnetwork analysiRNA Messengerlcsh:ScienceBiologyCell ShapeMultidisciplinaryGene Expression Regulation LeukemicEffectorSystems Biologylcsh:RleukemiaReproducibility of ResultsHNF4-alphaHematologyMolecular biologyNeoplasm ProteinsChemistrycell differentiationSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationMultivariate AnalysisProteomeMedicineEGR1PROTEOMICSlcsh:QLeukemia Erythroblastic AcuteMedicinal ChemistrySignal transductionK562 CellsMegakaryocytesResearch ArticleSignal TransductionK562 cells
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Essential thrombocythemia terminating in pure erythroleukemia

2004

Transformation into acute leukemia is a rare event in essential thrombocythemia (ET). The blasts are usually of myeloid, rarely of megakaryoblastic differentiation. We present the case of a patient with pure erythroleukemia after a nearly 10-year course of ET, which was treated with hydroxyurea. The patient, a 58-year-old male, presented with an elevated thrombocyte count (926,000/μL) and normal values of hemoglobin and leukocytes. After 10 years of therapy with hydroxyurea, the patient developed acute leukemia of solely erythroid differentiation. Chemotherapy with cytarabine and daunorubicin resulted in incomplete remission. The patient died 2 months after diagnosis of acute erythroleukemi…

Malemedicine.medical_specialtyTime FactorsMyeloidDaunorubicinmedicine.medical_treatmentFatal OutcomeBone Marrowhemic and lymphatic diseasesInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansThrombocytosisChemotherapyAcute leukemiaHematologybusiness.industryEssential thrombocythemiaHematologyMiddle Agedmedicine.diseaseCell Transformation Neoplasticmedicine.anatomical_structureImmunologyCytarabineAcute erythroleukemiaLeukemia Erythroblastic Acutebusinessmedicine.drugAmerican Journal of Hematology
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Identification of residues in the putative 5th helical region of human interleukin-6, important for activation of the IL-6 signal transducer, gp130

1996

AbstractWe have previously shown that L58 in the putative 5th helical region of human interleukin-6 (IL-6) is important for activation of the IL-6 signal transducer gp130 [de Hon et al. (1995) FEBS Lett. 369, 187–191]. To further explore the importance of individual residues in this region for gp130 activation we have now combined Ala substitutions of residues E52, S53, S54, K55, E56, L58 and E60 with other substitutions in IL-6, known to affect gp130 activation (Q160E and T163P). The combination mutant protein with L58A completely lost the capacity to induce the proliferation of XG-1 myeloma cells, and could effectively antagonize wild type IL-6 activity on these cells. Moreover, the data …

Models MolecularBiophysicsHuman Interleukin-6BiochemistryProtein Structure SecondaryStructure-function analysisgp130Signal Transducer gp130Antigens CDStructural BiologyMutant proteinCytokine Receptor gp130Escherichia coliTumor Cells CulturedGeneticsHumansPoint MutationCloning MolecularInterleukin 6Molecular BiologyAlanineMembrane GlycoproteinsbiologyInterleukin-6Wild typeCell BiologyGlycoprotein 130Recombinant ProteinsProtein Structure TertiaryCell biologyKineticsBiochemistryMutagenesis Site-Directedbiology.proteinLeukemia Erythroblastic AcuteMultiple MyelomaCell DivisionSignal TransductionFEBS Letters
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Wild-type JAK2 secondary acute erythroleukemia developing after JAK2-V617F-mutated primary myelofibrosis.

2009

A 54-year-old female patient developed acute erythroleukemia after an 8-year course of primary myelofibrosis. The latter harbors the JAK2-V617F mutation and was treated with hydroxyurea and anagrelide. A bone marrow trephine biopsy disclosed 2 morphologically distinct areas of chronic primary myelofibrosis and acute erythroleukemia. Microdissection and a separate molecular pathological analysis was performed. Although the activating JAK2-V617F mutation was not maintained in blasts of acute erythroleukemia, it was detectable in the chronic phase of primary myelofibrosis, indicating that this mutation did not play a role in the leukemic transformation of erythroid cells.

business.industryWild typeHematologyGeneral MedicineAnagrelideJanus Kinase 2Middle Agedmedicine.diseaseCell Transformation NeoplasticFatal OutcomePrimary Myelofibrosishemic and lymphatic diseasesMutation (genetic algorithm)Female patientCancer researchMedicineAcute erythroleukemiaHumansFemaleLeukemia Erythroblastic AcutebusinessMyelofibrosisJAK2 V617Fmedicine.drugActa haematologica
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