Search results for " B-Cell"

showing 10 items of 207 documents

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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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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Chemokine stromal cell-derived factor-1alpha modulates VLA-4 integrin-dependent adhesion to fibronectin and VCAM-1 on bone marrow hematopoietic proge…

2001

Stromal cell-derived factor-1alpha (SDF-1alpha) is a potent chemoattractant for hematopoietic progenitor cells (HPC), suggesting that it could play an important role during their migration within or to the bone marrow (BM). The integrin VLA-4 mediates HPC adhesion to BM stroma by interacting with CS-1/fibronectin and VCAM-1. It is required during hematopoiesis and homing of HPC to the BM. As HPC migration in response to SDF-1alpha might require dynamic regulation of integrin function, we investigated if SDF-1alpha could modulate VLA-4 function on BM CD34(hi) cells.CD34(hi) BM cells and hematopoietic cell lines were tested for the effect of SDF-1alpha on VLA-4-dependent adhesion to CS-1/fibr…

Cancer ResearchIntegrinsReceptors CXCR4Stromal cellIntegrinCD34Receptors Lymphocyte HomingVascular Cell Adhesion Molecule-1Bone Marrow CellsIntegrin alpha4beta1Hematopoietic Cell Growth FactorsCell LineColony-Forming Units Assaychemistry.chemical_compoundMiceLeukemia Megakaryoblastic AcutePrecursor B-Cell Lymphoblastic Leukemia-LymphomaGeneticsCell AdhesionTumor Cells CulturedAnimalsHumansVCAM-1Cell adhesionMolecular BiologybiologyChemotaxisVLA-4Antibodies MonoclonalCell BiologyHematologyHematopoietic Stem CellsChemokine CXCL12Peptide FragmentsRecombinant ProteinsCell biologyFibronectinsFibronectinchemistryLiverbiology.proteinStromal CellsChemokines CXCHoming (hematopoietic)Signal TransductionExperimental hematology
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The BCL6 gene in B-cell lymphomas with 3q27 translocations is expressed mainly from the rearranged allele irrespective of the partner gene

2003

The BCL6 gene, which functions as a transcription repressor, is the target of multiple chromosomal translocations in non-Hodgkin's lymphomas (NHL). These translocations occur in the nontranslated region of the BCL6 gene, juxtaposing regulatory sequences of the diverse partner genes to the open reading frame of the BCL6 gene and thus are thought to deregulate BCL6 gene expression. The levels of expression of the BCL6 gene and protein have been demonstrated to predict the clinical outcome of diffuse large B-cell lymphomas. By contrast, the prognostic significance of BCL6 gene translocations is unclear. In this study we have sought an explanation for this apparent discrepancy. We examined tumo…

Cancer ResearchLymphoma B-CellBiologyTranslocation Geneticimmune system diseasesProto-Oncogene Proteinshemic and lymphatic diseasesGene expressionTumor Cells CulturedHumansRNA MessengerAllelePromoter Regions GeneticGeneAllelesGene RearrangementGeneticsRegulation of gene expressionPromoterHematologyGene rearrangementBCL6Neoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticRepressor ProteinsOncologyRegulatory sequenceMutationProto-Oncogene Proteins c-bcl-6Cancer researchChromosomes Human Pair 3Transcription FactorsLeukemia
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In vitro and in vivo purging of B lymphoma cells from stem-cell products using anti-CD20 Abs.

2000

Background Autologous stem-cell transplantation has proved curative therapy for relapsed NHL. However, recurrence of underlying disease remains the major cause of treatment failure in this setting. Methods Development of effective MAb therapy directed against the B cell surface antigen CD20 has added a valuable tool of clearing contaminating lymphoma cells from stem-cell products by either in vitro or in vivo application. Results Transplantation of successfully in vitro purged bone marrow using Mabs has been correlated with prolonged survival in large Phase-II study. So far, no randomized trial could demonstrate a therapeutic benefit for in vitro purging. The anti-CD20 Mab rituximab has bee…

Cancer ResearchLymphoma B-CellNeoplasm ResidualImmunologyAntineoplastic AgentsCell SeparationAntibodies Monoclonal Murine-DerivedClinical Trials Phase II as Topicimmune system diseaseshemic and lymphatic diseasesmedicineImmunology and AllergyHumansGenetics (clinical)B cellCD20Transplantationbiologybusiness.industryStem CellsBone Marrow PurgingAntibodies MonoclonalCell Biologymedicine.diseaseAntigens CD20LymphomaTransplantationHaematopoiesismedicine.anatomical_structureOncologyImmunologybiology.proteinRituximabBone marrowStem cellbusinessRituximabmedicine.drugStem Cell TransplantationCytotherapy
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Homozygous deletion of SOCS1 in primary mediastinal B-cell lymphoma detected by CGH to BAC microarrays

2005

Homozygous deletion of SOCS1 in primary mediastinal B-cell lymphoma detected by CGH to BAC microarrays

Cancer ResearchLymphoma B-Cellbusiness.industrySuppressor of cytokine signaling 1HomozygoteIntracellular Signaling Peptides and ProteinsSuppressor of Cytokine Signaling ProteinsHematologymedicine.diseaseMediastinal NeoplasmsLymphomaRepressor ProteinsSuppressor of Cytokine Signaling 1 ProteinOncologyhemic and lymphatic diseasesmedicineCancer researchHumansPrimary mediastinal B-cell lymphomaDNA microarraybusinessGene DeletionOligonucleotide Array Sequence AnalysisLeukemia
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In vivo targeting of human neutralizing antibodies against CD55 and CD59 to lymphoma cells increases the antitumor activity of rituximab.

2007

AbstractAn in vivo model of human CD20+ B-lymphoma was established in severe combined immunodeficiency mice to test the ability of human neutralizing miniantibodies to CD55 and CD59 (MB55 and MB59) to enhance the therapeutic effect of rituximab. The miniantibodies contained single-chain fragment variables and the hinge-CH2-CH3 domains of human IgG1. LCL2 cells were selected for the in vivo study among six B-lymphoma cell lines for their high susceptibility to rituximab-dependent complement-mediated killing enhanced by MB55 and MB59. The cells injected i.p. primarily colonized the liver and spleen, leading to the death of the animals within 30 to 40 days. Thirty percent of mice receiving bio…

Cancer ResearchLymphoma B-Cellmedicine.drug_classmedicine.medical_treatmentAntineoplastic AgentsCD59 AntigensAntigens CD59Mice SCIDPharmacologyMonoclonal antibodyAntigens CD55Antineoplastic AgentAntibodies Monoclonal Murine-DerivedMicerituximabIn vivomedicineAnimalsHumansantibodies against CD55 and CD59CD20Severe combined immunodeficiencyMice Inbred BALB CbiologyCD55 AntigensAnimalAntibody-Dependent Cell CytotoxicityAntibodies MonoclonalImmunotherapyrituximab; antibodies against CD55 and CD59medicine.diseaseDisease Models AnimalOncologyAnimals; Antibodies Monoclonal; Antibodies Monoclonal Murine-Derived; Antibody-Dependent Cell Cytotoxicity; Antigens CD55; Antigens CD59; Antineoplastic Agents; Disease Models Animal; Female; Humans; Lymphoma B-Cell; Mice; Mice Inbred BALB C; Mice SCID; Rituximab; Cancer Research; OncologyMonoclonalImmunologybiology.proteinRituximabFemaleAntibodymedicine.drugHuman
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Abstract LB-017: HSP110 sustains aberrant NFkB signaling in activated B-cell diffuse large B-cell lymphoma through MyD88 stabilization

2017

Abstract Diffuse large B cell lymphoma (DLBCL) is an aggressive lymphoproliferative disorder of B lymphocytes accounting for 30 % of adult Non Hodgkin Lymphoma (NHL). Among DLBCL, Activated B Cell - DLBCL (ABC-DLBCL) is the most aggressive form and has a poor prognosis. Heat-shock proteins (HSPs) are molecular chaperons highly expressed in cancer cells and implicated in resistance to radio- and chemotherapy. Therefore, HSPs are envisioned as therapeutic targets in many cancers. Among the different HSPs, HSP110 has been recently identified as a pro-survival factor in germinal center-derived DLBCL (GC-DLBCL), through stabilization of the GC-DLBCL oncogene Bcl-6. Here, we have explored if HSP1…

Cancer ResearchOncogeneBiologymedicine.diseaseLymphoma[ SDV.CAN ] Life Sciences [q-bio]/CancerSmall hairpin RNAmedicine.anatomical_structureOncologyCell cultureimmune system diseaseshemic and lymphatic diseasesCancer cellmedicineCancer researchGene silencingDiffuse large B-cell lymphomaneoplasmsB cell
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Genomic Abnormalities Acquired in the Blastic Transformation of Splenic Marginal Zone B-cell Lymphoma

2003

Among 20 cases of typical splenic marginal zone lymphoma (SMZL), two cases had blastic transformation. The genetic mechanisms underlying the morphologic transformation were investigated by comparing genetic changes in initial and blastic phases. A complex karyotype including trisomy of 3q and genomic gain of 17q22-q24 was seen in both cases at diagnosis. However, the extra copy of 3q was lost during the transformation process in both tumors. Additionally, the Karpas 1718 cell line, which was derived from a patient with transformed SMZL and carried a trisomy of 3q, also evidenced the spontaneous loss of the extra 3q during the culturing process. Other acquired abnormalities observed exclusiv…

Cancer ResearchPathologymedicine.medical_specialtyLymphoma B-CellTrisomyChromosomal translocationBiologyComplex KaryotypeTumor Cells CulturedmedicineChromosomes HumanHumansSplenic marginal zone lymphomaChromosome AberrationsLymphoma Non-HodgkinSplenic NeoplasmsHematologymedicine.diseaseTransformation (genetics)OncologyKaryotypingDisease ProgressionB-Cell Non-Hodgkin LymphomaChromosomes Human Pair 3Chromosome DeletionAbnormalityBlast CrisisTrisomyChromosomes Human Pair 17Comparative genomic hybridizationLeukemia & Lymphoma
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