Search results for "leukemia"

showing 10 items of 976 documents

Genetic variation in human leukocyte antigen and susceptibility to acute myeloid leukemia.

2015

In this issue of Acta Haematologica, Authors report the association between the Human Major Histocompatibility complex (MHC) HLA-C3 and Acute Myeloid Leukemia (AML) in Korean population, confirming previous studies on association between HLA-C and AML.

Settore MED/04 - Patologia GeneraleMaleDatabases FactualMyeloid leukemiaHematologyGeneral MedicineHuman leukocyte antigenHLA-C AntigensBiologyVirologyLinkage DisequilibriumHLAAssociationLeukemia Myeloid AcuteHaplotypesGenetic LociGenetic variationImmunologyLeukaemiaHumansFemaleLeukaemia; HLA; AssociationActa haematologica
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Italian multicentricepidemiological case control strudy on risk factors for childhood leukemia,non hodgkin limphoma and neuroblastoma:study populatio…

2014

Background Aetiology of childhood leukaemia and childhood neoplasm is poorly understood. Information on the prevalence of risk factors in the childhood population is limited. SETIL is a population based case/control study on childhood leukaemia, conducted with two companion studies on non-Hodgkin Lymphoma (NHL) and neuroblastoma. The study relies on questionnaire interviews and 50 Hz magnetic field (ELF-MF) indoor measurements. This paper discusses the SETIL study design and includes descriptive information. Methods The study was carried out in 14 Italian regions (78.3% of Italian population aged 0?10). It included leukaemia, NHL and neuroblastoma cases incident in 0?10 year olds in 1998-20…

Settore MED/42 - Igiene Generale E Applicatachildhood leukemia childhood neoplasm
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TRAIL-induced apoptosis of hepatocellular carcinoma cells is augmented by targeted therapies

2009

AIM: To analyze the effect of chemotherapeutic drugs and specific kinase inhibitors, in combination with the death receptor ligand tumor necrosis factor-related apoptosis inducing ligand (TRAIL), on overcoming TRAIL resistance in hepatocellular carcinoma (HCC) and to study the efficacy of agonistic TRAIL antibodies, as well as the commitment of antiapoptotic BCL-2 proteins, in TRAIL-induced apoptosis. METHODS: Surface expression of TRAIL receptors (TRAIL-R1-4) and expression levels of the antiapoptotic BCL-2 proteins MCL-1 and BCL-xL were analyzed by flow cytometry and Western blotting, respectively. Knock-down of MCL-1 and BCL-xL was performed by transfecting specific small interfering RNA…

SorafenibCarcinoma Hepatocellularbcl-X ProteinBcl-xLAntineoplastic AgentsApoptosisTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundCell Line TumormedicineAnimalsHumansLY294002Viability assayEnzyme InhibitorsPI3K/AKT/mTOR pathwaybiologyKinaseLiver NeoplasmsGastroenterologyGeneral Medicinedigestive system diseasesReceptors TNF-Related Apoptosis-Inducing LigandchemistryProto-Oncogene Proteins c-bcl-2ApoptosisDoxorubicinCancer researchbiology.proteinMyeloid Cell Leukemia Sequence 1 ProteinTumor necrosis factor alphaOriginal ArticleFluorouracilmedicine.drug
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Sorafenib maintenance after allogeneic hematopoietic stem cell transplantation for acute myeloid leukemia with FLT3-internal tandem duplication mutat…

2020

PURPOSE Despite undergoing allogeneic hematopoietic stem cell transplantation (HCT), patients with acute myeloid leukemia (AML) with internal tandem duplication mutation in the FMS-like tyrosine kinase 3 gene ( FLT3-ITD) have a poor prognosis, frequently relapse, and die as a result of AML. It is currently unknown whether a maintenance therapy using FLT3 inhibitors, such as the multitargeted tyrosine kinase inhibitor sorafenib, improves outcome after HCT. PATIENTS AND METHODS In a randomized, placebo-controlled, double-blind phase II trial (SORMAIN; German Clinical Trials Register: DRKS00000591), 83 adult patients with FLT3-ITD–positive AML in complete hematologic remission after HCT were r…

SorafenibFLT3 Internal Tandem DuplicationCancer ResearchMyeloidbusiness.industrymedicine.medical_treatmentMyeloid leukemiaHematopoietic stem cell transplantationmedicine.diseaseTransplantationLeukemiamedicine.anatomical_structureOncologyhemic and lymphatic diseasesmedicineCancer researchNeoplasmbusinessmedicine.drug
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Cytotoxicity of Artesunic Acid Homo- and Heterodimer Molecules toward Sensitive and Multidrug-Resistant CCRF-CEM Leukemia Cells

2010

A novel approach to circumvent multidrug resistance is hybridization of natural products in dimers. We analyzed homodimers of two artesunic acid molecules and heterohybrids of artesunic acid and betulin in human CCRF-CEM and multidrug-resistant P-glycoprotein-overexpressing CEM/ADR5000 leukemia cells. Multidrug-resistant cells were not cross-resistant to the novel compounds. Collateral sensitivity was observed for artesunic acid homodimer. Artesunic acid and artesunic acid homodimer induced G0/G1 cell cycle arrest, apoptosis, and formation of reactive oxygen species.

Spectrometry Mass Electrospray IonizationMagnetic Resonance SpectroscopyCell SurvivalApoptosischemistry.chemical_compoundCell Line TumorDrug DiscoverymedicineHumansCytotoxicitychemistry.chemical_classificationReactive oxygen speciesFormazansLeukemiaBetulinCell CycleSuccinatesCell cycleFlow Cytometrymedicine.diseaseArtemisininsTriterpenesMultiple drug resistanceLeukemiachemistryBiochemistryDrug Resistance NeoplasmCell cultureApoptosisMolecular MedicineReactive Oxygen SpeciesJournal of Medicinal Chemistry
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Investigating the Molecular Mechanism of H3B-8800: A Splicing Modulator Inducing Preferential Lethality in Spliceosome-Mutant Cancers.

2021

The SF3B1 protein, part of the SF3b complex, recognizes the intron branch point sequence of precursor messenger RNA (pre-mRNA), thus contributing to splicing fidelity. SF3B1 is frequently mutated in cancer and is the target of distinct families of splicing modulators (SMs). Among these, H3B-8800 is of particular interest, as it induces preferential lethality in cancer cells bearing the frequent and highly pathogenic K700E SF3B1 mutation. Despite the potential of H3B-8800 to treat myeloid leukemia and other cancer types hallmarked by SF3B1 mutations, the molecular mechanism underlying its preferential lethality towards spliceosome-mutant cancer cells remains elusive. Here, microsecond-long a…

SpliceosomeQH301-705.5Protein ConformationPyridinesRNA SplicingMutantDruggabilityH3B-8800Molecular Dynamics Simulationmedicine.disease_causeCatalysisPiperazinesArticleInorganic ChemistryNeoplasmsspliceosome-mutant cancermedicineHumansPhysical and Theoretical ChemistryBiology (General)Molecular BiologyQD1-999SpectroscopyMutationsplicing modulatorsChemistryOrganic ChemistryWild typeIntronleukemiaGeneral MedicinePhosphoproteinsH3B‐8800molecular dynamicsComputer Science ApplicationsCell biologyChemistryPhenotypeCancer cellRNA splicingMutationRNA Splicing FactorsSpliceosome‐mutant cancerInternational journal of molecular sciences
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Stochastic dynamics of leukemic cells under an intermittent targeted therapy

2009

The evolutionary dynamics of cancerous cell populations in a model of Chronic Myeloid Leukemia (CML) is investigated in the presence of an intermittent targeted therapy. Cancer development and progression is modeled by simulating the stochastic evolution of initially healthy cells which can experience genetic mutations and modify their reproductive behavior, becoming leukemic clones. Front line therapy for the treatment of patients affected by CML is based on the administration of tyrosine kinase inhibitors, namely imatinib (Gleevec) or, more recently, dasatinib or nilotinib. Despite the fact that they represent the first example of a successful molecular targeted therapy, the development o…

Statistics and ProbabilityComplex systemsmedicine.medical_treatmentModels BiologicalPiperazinesSettore FIS/03 - Fisica Della MateriaCancer evolutionTargeted therapyLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesStochastic dynamics; Cancer evolution; Complex systemsHumansMedicineComputer SimulationStochastic dynamicMolecular Targeted TherapyProtein Kinase InhibitorsEcology Evolution Behavior and SystematicsStochastic Processesbusiness.industryApplied MathematicsMyeloid leukemiaImatinibmedicine.diseaseSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)DasatinibLeukemiaPyrimidinesImatinib mesylateNilotinibStochastic dynamics Monte Carlo simulationBenzamidesImmunologyCancer cellDisease ProgressionImatinib MesylateCancer researchbusinessmedicine.drug
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Tailoring sparse multivariable regression techniques for prognostic single-nucleotide polymorphism signatures.

2011

When seeking prognostic information for patients, modern technologies provide a huge amount of genomic measurements as a starting point. For single-nucleotide polymorphisms (SNPs), there may be more than one million covariates that need to be simultaneously considered with respect to a clinical endpoint. Although the underlying biological problem cannot be solved on the basis of clinical cohorts of only modest size, some important SNPs might still be identified. Sparse multivariable regression techniques have recently become available for automatically identifying prognostic molecular signatures that comprise relatively few covariates and provide reasonable prediction performance. For illus…

Statistics and ProbabilityEpidemiologyComputer scienceFeature selectionBiostatisticscomputer.software_genrePolymorphism Single NucleotideLasso (statistics)Gene FrequencyResamplingCovariateHumansLikelihood FunctionsModels StatisticalMultivariable calculusRegression analysisGenomicsPrognosisRegressionMinor allele frequencyLeukemia Myeloid AcuteMultivariate AnalysisRegression AnalysisData miningcomputerAlgorithmsStatistics in medicine
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Identification of a Terphenyl Derivative that Blocks the Cell Cycle in the G0−G1 Phase and Induces Differentiation in Leukemia Cells

2006

To further explore the SAR of resveratrol-related trans-stilbene derivatives, here we describe the synthesis of (a) a series of 3,5-dimethoxy analogues in which a variety of substituents were introduced at positions 2', 3', 4', and 5' of the stilbene scaffold and (b) a second group of derivatives (2-phenylnaphthalenes and terphenyls) that incorporate a phenyl ring as a bioisosteric replacement of the stilbene alkenyl bridge. We thoroughly characterized all of the new compounds with respect to their apoptosis-inducing activity and their effects on the cell cycle. One of the new derivatives, 13g, behaved differently from the others, as it was able to block the cell cycle in the G(0)-G(1) phas…

StereochemistryCellular differentiationFusion Proteins bcr-ablAntineoplastic AgentsApoptosis.ResveratrolResting Phase Cell CycleChemical synthesisStructure-Activity Relationshipchemistry.chemical_compoundLeukemia Promyelocytic AcuteCell Line TumorTerphenyl CompoundsTerphenylStilbenesDrug DiscoveryHumansStructure–activity relationshipATP Binding Cassette Transporter Subfamily B Member 1G1 PhaseCell DifferentiationCell cycleIn vitrochemistryDrug Resistance NeoplasmResveratrolCell cultureMolecular MedicineDrug Screening Assays AntitumorJournal of Medicinal Chemistry
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Synthesis and in vitro antileukemic activity of new 4-triazenopyrazole derivatives

2003

Several new 4-(3,3-dimethyltriazeno)-5-benzamidopyrazole derivatives were prepared by reacting 4-diazo-5-benzamidopyrazole derivatives with dimethylamine. The compounds were tested at 10 microM for their vitro antileukemic activity against K562 (Human chronic myelogenous leukemia) and Raji (human Burkitt limphoma ) cell lines. Dacarbazine and methotrexate were used for comparative purpose. The 3-methyl-4-(3,3-dimethyltriazeno)-5-(substituted benzamido)pyrazoles, bearing the pyrazole nucleus free at 1 position, resulted more active than the 1-(substituted phenyl)-3-methyl-4-(3,3-dimethyltriazeno)-5-benzamidopyrazoles. Dacarbazine at 10 microM showed no activity in the above tests. The observ…

StereochemistryDacarbazinePharmaceutical ScienceAntineoplastic AgentsPyrazoleSettore BIO/19 - Microbiologia GeneraleInhibitory Concentration 50Structure-Activity Relationshipchemistry.chemical_compoundCytochrome P-450 Enzyme SystemCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositiveDrug DiscoverymedicineHumansDimethylamine4-Triazenopyrazoles Antiproliferative activity In vitro antileukemic acitivityDemethylationTriazinesGeneral MedicineBurkitt LymphomaSettore CHIM/08 - Chimica FarmaceuticaIn vitroRaji cellchemistryMechanism of actionPyrazolesGrowth inhibitionmedicine.symptommedicine.drugIl Farmaco
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