Search results for "B-CELL"

showing 10 items of 279 documents

ABCL-346: Overall Survival with Tafasitamab + Lenalidomide (LEN) vs Routinely Administered Therapies for ASCT-Ineligible Relapsed or Refractory (R/R)…

2021

Context Tafasitamab+LEN, a chemotherapy-free, novel treatment for R/R DLBCL, demonstrated efficacy in ASCT-ineligible patients in the single-arm Phase II L-MIND study (NCT02399085). Objective To compare outcomes in patients treated with tafasitamab+LEN in the L-MIND study with matched patient populations treated with commonly administered NCCN-/ESMO-recommended therapies for non-transplant-eligible patients with R/R DLBCL in routine clinical practice. Design RE-MIND2 (NCT04150328) is an observational, retrospective cohort study. The L-MIND tafasitamab+LEN cohort was matched with RE-MIND2 patients using estimated propensity score-based 1:1 nearest neighbor matching balanced for nine patient …

BendamustineOncologyCancer Researchmedicine.medical_specialtybusiness.industryContext (language use)Retrospective cohort studyHematologymedicine.diseaseOncologyInternal medicineCohortmedicineClinical endpointRituximabbusinessDiffuse large B-cell lymphomamedicine.drugLenalidomideClinical Lymphoma Myeloma and Leukemia
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Splenic marginal zone lymphoma.

2002

Splenic marginal zone lymphoma (SMZL) is a specific low-grade small B-cell lymphoma that is incorporated in the World Health Organization classification. Characteristic features are splenomegaly, moderate lymphocytosis with villous morphology, intrasinusoidal pattern of involvement of various organs, especially bone marrow, and relative indolent course. Tumor progression with increase of blastic forms and aggressive behavior are observed in a minority of patients. Molecular and cytogenetic studies have shown heterogeneous results probably because of the lack of standardized diagnostic criteria. To date, no definitive therapy has been established. Therapeutic options include treatment absten…

BendamustinePathologymedicine.medical_specialtyLymphoma B-CellLymphocytosismedicine.medical_treatmentImmunologySplenectomyBiochemistryImmunophenotypingDiagnosis DifferentialImmunophenotypingMedicineAnimalsHumansSplenic marginal zone lymphomabusiness.industryLymphoma Non-HodgkinSplenic NeoplasmsCell BiologyHematologymedicine.diseaseLymphomaTumor progressionCytogenetic AnalysisRituximabmedicine.symptombusinessmedicine.drugBlood
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Successful Treatment of Catastrophic Antiphospholipid Antibody Syndrome (CAPS) Associated With Splenic Marginal-zone Lymphoma With Low-molecular Weig…

2008

ABSTRACT Case report A 69-year-old woman with splenic marginal-zone lymphoma was admitted with progressive abdominal pain and splenomegaly as the suspected cause of pain. Rituximab treatment (375 mg/m 2 ) had been initiated on the day of admission. Abdominal computerized tomography revealed splenic infarction. Laboratory tests showed elevation of liver enzymes and creatinine, low platelet count, prolonged partial thromboplastin time, and lupus anticoagulant positivity. The diagnosis of catastrophic antiphospholipid antibody syndrome was made. Weight-adjusted low-molecular weight heparin therapy was initiated. Freedom from symptoms and normalization of liver enzymes and creatinine occurred w…

Bendamustinemedicine.medical_specialtyLymphoma B-Cellmedicine.drug_classLow molecular weight heparinAntineoplastic AgentsGastroenterologyAntibodies Monoclonal Murine-Derivedimmune system diseaseshemic and lymphatic diseasesInternal medicineBendamustine HydrochlorideHumansMedicineSplenic marginal zone lymphomaAgedLupus anticoagulantbusiness.industrySplenic NeoplasmsAnticoagulantAntibodies MonoclonalAnticoagulantsGeneral MedicineHeparinHeparin Low-Molecular-WeightAntiphospholipid Syndromemedicine.diseaseSurgerySplenic infarctionNitrogen Mustard CompoundsFemaleRituximabRituximabbusinessmedicine.drugThe American Journal of the Medical Sciences
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Homozygous deletions localize novel tumor suppressor genes in B-cell lymphomas

2007

AbstractIntegrative genomic and gene-expression analyses have identified amplified oncogenes in B-cell non-Hodgkin lymphoma (B-NHL), but the capability of such technologies to localize tumor suppressor genes within homozygous deletions remains unexplored. Array-based comparative genomic hybridization (CGH) and gene-expression microarray analysis of 48 cell lines derived from patients with different B-NHLs delineated 20 homozygous deletions at 7 chromosome areas, all of which contained tumor suppressor gene targets. Further investigation revealed that only a fraction of primary biopsies presented inactivation of these genes by point mutation or intragenic deletion, but instead some of them w…

BiopsyDNA Mutational AnalysisGene DosageVesicular Transport ProteinsApoptosisBiochemistryEpigenesis Geneticimmune system diseaseshemic and lymphatic diseasesChromosomes HumanGenes Tumor SuppressorPromoter Regions GeneticSorting NexinsOligonucleotide Array Sequence AnalysisSequence DeletionBcl-2-Like Protein 11HomozygoteChromosome MappingNuclear ProteinsNucleic Acid HybridizationRNA-Binding ProteinsHematologyDNA NeoplasmBCL10Gene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2DNA methylationLymphoma B-CellTumor suppressor geneImmunologyBiologyGene dosageCell Line TumorProto-Oncogene ProteinsmedicineCyclin-Dependent Kinase Inhibitor p18HumansPoint MutationGene SilencingB cellAdaptor Proteins Signal TransducingHomeodomain ProteinsMembrane ProteinsCell BiologyDNA Methylationmedicine.diseaseMolecular biologyLymphomaCancer researchMantle cell lymphomaApoptosis Regulatory ProteinsCarrier ProteinsDiffuse large B-cell lymphomaTranscription Factors
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The down-regulation of miR-125b in chronic lymphocytic leukemias leads to metabolic adaptation of cells to a transformed state

2012

AbstractMiR-125b-1 maps at 11q24, a chromosomal region close to the epicenter of 11q23 deletions in chronic lymphocytic leukemias (CLLs). Our results establish that both aggressive and indolent CLL patients show reduced expression of miR-125b. Overexpression of miR-125b in CLL-derived cell lines resulted in the repression of many transcripts encoding enzymes implicated in cell metabolism. Metabolomics analyses showed that miR-125b overexpression modulated glucose, glutathione, lipid, and glycerolipid metabolism. Changes on the same metabolic pathways also were observed in CLLs. We furthermore analyzed the expression of some of miR-125b–target transcripts that are potentially involved in the…

Blotting WesternImmunologyBiologyReal-Time Polymerase Chain ReactionBiochemistryNODownregulation and upregulationmicroRNABiomarkers TumorHumansMetabolomicsRNA MessengerPsychological repressionCells CulturedCell ProliferationOligonucleotide Array Sequence AnalysisRegulation of gene expressionB-LymphocytesLymphoid NeoplasiaReverse Transcriptase Polymerase Chain ReactionCell growthGene Expression ProfilingCell BiologyHematologyLeukemia Lymphocytic Chronic B-CellMolecular biologyGene Expression Regulation NeoplasticGene expression profilingMicroRNAsMetabolic pathwayCell Transformation NeoplasticChromosomal regionCancer researchBlood
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Direct Cellular Interaction with Activated CD4+T Cells Overcomes Hyporesponsiveness of B-Cell Chronic Lymphocytic Leukemiain Vitro

1998

The proliferative response of clonal B cells from patients with chronic lymphocytic leukemia (B-CLL) is drastically reduced compared to normal B lymphocytes stimulated via the B cell antigen receptor complex or by CD40 ligation. In the present study we demonstrate that hyporesponsiveness of CLL-B cells can be overcome by stimulatory pathways mediated by activated CD4(+) T cells. In contrast to CD40 ligation, costimulation with activated T cells promotes a proliferative response in CLL-B cells identical to that in normal B cells. Furthermore, coculture with activated T cells improved survival of CLL-B cells in vitro. Differentiation of CLL-B cells into IgM producing cells was promoted, as we…

CD4-Positive T-LymphocytesImmunologyB-cell receptorLymphocyte ActivationInterleukin 21Antigens CDhemic and lymphatic diseasesHumansCytotoxic T cellIL-2 receptorCD40 AntigensAntigen-presenting cellCells CulturedB-LymphocytesCD40biologyZAP70Cell DifferentiationLeukemia Lymphocytic Chronic B-CellCell biologyB-1 cellImmunoglobulin MAntigens Surfacebiology.proteinInterleukin-2Cell DivisionCellular Immunology
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Cytomegalovirus‐specific T‐cell immunity and DNAemia in patients with chronic lymphocytic leukaemia undergoing treatment with ibrutinib

2021

CD4-Positive T-LymphocytesMaleCongenital cytomegalovirus infectionCytomegalovirusT-Cell Antigen Receptor SpecificityCD8-Positive T-LymphocytesViral Matrix Proteinschemistry.chemical_compoundPiperidinesT-Lymphocyte SubsetsT cell immunitymedicineHumansIn patientViremiaProtein Kinase InhibitorsAgedAged 80 and overLymphocytic leukaemiabusiness.industryAdenineHematologyCmv dnaemiaMiddle Agedmedicine.diseaseLeukemia Lymphocytic Chronic B-CellchemistryIbrutinibCytomegalovirus InfectionsDNA ViralImmunologyFemalebusinessInterferon-gamma Release TestsBritish Journal of Haematology
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Autocrine transforming growth factor- from chronic lymphocytic leukemia-β cells interferes with proliferative T cell signals

1999

Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of noncycling B cells in lymphatic and extralymphatic tissues. In the present study we investigated the possible contribution of TGF-beta, as secreted by CLL-B cells, on this low proliferative state. CLL-B cells were shown to express TGF-beta RNA and to release bioactive TGF-beta into culture supernatants. Antibody neutralization of endogenously secreted TGF-beta increased the proliferation of CLL-B cells as cultured in the presence of IL-2 or IL-4 or in direct contact with activated CD4+ T cells. In these culture systems, addition of exogenous TGF-beta downregulated basal and cytokineinduced proliferation of CLL-B cell…

CD4-Positive T-LymphocytesT cellPalatine TonsilImmunologyAntineoplastic AgentsCell CommunicationLymphocyte ActivationInterleukin 21Antigens CDTransforming Growth Factor betahemic and lymphatic diseasesmedicineHumansImmunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellCells CulturedInterleukin 3B-LymphocytesCD40biologyT-Lymphocytes Helper-InducerHematologyLeukemia Lymphocytic Chronic B-CellCoculture TechniquesCell biologyAutocrine Communicationmedicine.anatomical_structurebiology.proteinInterleukin 12Immunobiology
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Evaluation of humoral and cellular response to four vaccines against COVID-19 in different age groups: A longitudinal study

2022

To date there has been limited head-to-head evaluation of immune responses to different types of COVID-19 vaccines. A real-world population-based longitudinal study was designed with the aim to define the magnitude and duration of immunity induced by each of four different COVID-19 vaccines available in Italy at the time of this study. Overall, 2497 individuals were enrolled at time of their first vaccination (T0). Vaccine-specific antibody responses induced over time by Comirnaty, Spikevax, Vaxzevria, Janssen Ad26.COV2.S and heterologous vaccination were compared up to six months after immunization. On a subset of Comirnaty vaccinees, serology data were correlated with the ability to neutr…

COVID-19 VaccinesAd26COVS1vaccines.SARS-CoV-2ImmunologyCOVID-19serologyViral VaccinesvaccinesHumansB-cell memory; COVID-19; cell-mediated immunity; serology; vaccinescell-mediated immunityImmunology and AllergyB-CELL MEMORY COVID-19 CELL-MEDIATED IMMUNITY SEROLOGY VACCINESB-cell memoryLongitudinal StudiesB-cell memory; COVID-19; cell-mediated immunity; serology; vaccines; Humans; Aged; COVID-19 Vaccines; Longitudinal Studies; Ad26COVS1; SARS-CoV-2; COVID-19; Viral VaccinesAgedFrontiers in Immunology
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CD38/CD31, the CCL3 and CCL4 chemokines, and CD49d/vascular cell adhesion molecule-1 are interchained by sequential events sustaining chronic lymphoc…

2009

AbstractCD38 and CD49d are associated negative prognosticators in chronic lymphocytic leukemia (CLL). Despite evidence that both molecules are involved in interactions occurring between CLL and normal cells in the context of CLL-involved tissues, a functional link is still missing. Using gene expression profiles comparing CD38+CD49d+ versus CD38−CD49d− CLL cells, we showed overexpression of the CCL3 and CCL4 chemokines in cells from the former group. These chemokines were also up-regulated by CD38 signals in CLL; moreover, CCL3 was expressed by CLL cells from bone marrow biopsies (BMB) of CD38+CD49d+ but not CD38−CD49d− cases. High levels of CCR1 and, to a lesser extent, CCR5, the receptors…

Cancer ResearchChemokineChronic lymphocytic leukemiaIntegrin alpha4ApoptosisCD38immune system diseaseshemic and lymphatic diseasesReceptorsChronicMacrophages; Apoptosis; Membrane Glycoproteins; Humans; Integrin alpha4; Antigens CD38; Vascular Cell Adhesion Molecule-1; Endothelial Cells; Receptors Chemokine; Antigens CD31; Cell Survival; Bone Marrow Cells; Leukemia Lymphocytic Chronic B-Cell; Antigens CD; Up-Regulation; Chemokine CCL4; Chemokine CCL3; Cell LineChemokine CCL4Chemokine CCL3Membrane GlycoproteinsLeukemiaCell adhesion moleculehemic and immune systemsLymphocyticCDUp-RegulationPlatelet Endothelial Cell Adhesion Molecule-1Leukemiamedicine.anatomical_structureOncologyChemokineReceptors ChemokineTumor necrosis factor alphaStromal cellCell SurvivalVascular Cell Adhesion Molecule-1Bone Marrow CellsBiologyCell LineAntigens CDmedicineHumansAntigensMonocyteMacrophagesB-CellEndothelial Cellsmedicine.diseaseADP-ribosyl Cyclase 1Leukemia Lymphocytic Chronic B-CellCLL integrins chemokines CD49d CD38 prognosis.Cancer researchbiology.proteinCD31Settore MED/15 - Malattie del SangueCD38
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