Search results for " Ly"

showing 10 items of 2487 documents

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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Bispecific antibodies targeting tumor-associated antigens and neutralizing complement regulators increase the efficacy of antibody-based immunotherap…

2015

The efficacy of antibody-based immunotherapy is due to the activation of apoptosis, the engagement of antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity (CDC). We developed a novel strategy to enhance CDC using bispecific antibodies (bsAbs) that neutralize the C-regulators CD55 and CD59 to enhance C-mediated functions. Two bsAbs (MB20/55 and MB20/59) were designed to recognize CD20 on one side. The other side neutralizes CD55 or CD59. Analysis of CDC revealed that bsAbs could kill 4-25 times more cells than anti-CD20 recombinant antibody in cell lines or cells isolated from patients with chronic lymphocytic leukemia. The pharmacokinetics of the bsAbs was evaluate…

Cancer ResearchLymphomaMacrophageChronic lymphocytic leukemiamedicine.medical_treatmentAntibodieCell SeparationMice SCIDMiceAntibodies BispecificCloning MolecularCytotoxicityCD20LeukemiabiologyCD55 AntigensMedicine (all)HematologyFlow CytometryBurkitt LymphomaKiller Cells NaturalLeukemiaOncologyFemaleImmunotherapyAntibodybispecific antibodiesExperimental Lymphoma Mice MiceHumanComplement System ProteinCD59 AntigensEnzyme-Linked Immunosorbent AssayAntigens CD59Antigens CD55AntibodiesExperimentalAntigenbispecific antibodies; Leukemia; Experimental Lymphoma Mice Mice; complement systemmedicineAnimalsHumanscomplement systemAnimalMacrophagesAntibody-Dependent Cell CytotoxicityImmunotherapyComplement System Proteinsmedicine.diseaseAntigens CD20Complement systembispecific antibodieDisease Models AnimalAnesthesiology and Pain MedicineMicroscopy FluorescenceImmunologybiology.protein
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Blood T-cell Vβ transcriptome in melanoma patients

2004

Tumor-cells have been shown to elicit MHC-restricted and antigen-specific T-cell responses. In this article, we used a new approach to study T-cell responses in tumor-bearing patients based on a global representation of the Vβ-transcriptome, making it possible to grade CDR3-length distribution (CDR3-LD) alterations. Six patients with advanced melanoma disease, from whom blood samples were taken before and serially after tyrosinase-A peptide vaccination, were studied. The PBMC from patients displayed highly significant Vβ transcriptome alterations as compared to healthy individuals. Similar Vβ alterations could be detected both in PBMCs and at the tumor site. After vaccination, Vβ alteration…

Cancer ResearchMelanomaT cellT-cell receptorT lymphocyteBiologymedicine.diseasePeripheral blood mononuclear cellTranscriptomeImmune systemmedicine.anatomical_structureOncologyHypoxanthine-guanine phosphoribosyltransferaseImmunologymedicineInternational Journal of Cancer
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Can the plasma PD-1 levels predict the presence and efficiency of tumor-infiltrating lymphocytes in metastatic melanoma patients?

2019

e14035 Background: The immune response to melanoma has been shown to be locally affected by presence of tumor-infiltrating lymphocytes (TILs), generally divided into brisk (infiltrating the entire base of the invasive tumor), non-brisk (infiltrating only focally) and absent. Several studies showed that greater presence of TILs, especially brisk, in primary melanoma is associated with a better prognosis and a higher survival rate. Since recent studies revealed an association between PD-1/PD-L1 expression levels and tumor response, the aim of our study was to investigate the correlation between plasma PD-1 and presence/absence/class of TILs in metastatic melanoma patients. Methods: The plasm…

Cancer ResearchMetastatic melanomaTumor-infiltrating lymphocytesbusiness.industryMelanomahemic and immune systemschemical and pharmacologic phenomenamedicine.disease03 medical and health sciences0302 clinical medicineImmune systemOncology030220 oncology & carcinogenesisCancer researchmedicineplasma PD-1 tumor-infiltrating lymphocytes metastatic melanomabusiness030215 immunologyJournal of Clinical Oncology
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XPO1E571K Mutation Modifies Exportin 1 Localisation and Interactome in B-cell Lymphoma

2020

The XPO1 gene encodes exportin 1 (XPO1) that controls the nuclear export of cargo proteins and RNAs. Almost 25% of primary mediastinal B-cell lymphoma (PMBL) and classical Hodgkin lymphoma (cHL) cases harboured a recurrent XPO1 point mutation (NM_003400, chr2:g61718472C&gt

Cancer ResearchMutantXPO1/CRM1[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]CRISPR–Cas9[SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]lcsh:RC254-282Article03 medical and health sciencesXPO10302 clinical medicineproteomics[SDV.CAN] Life Sciences [q-bio]/Cancerimmune system diseasesExportin-1hemic and lymphatic diseases[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]medicine[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]B-cell lymphomaNuclear export signalproximity ligation assay030304 developmental biology0303 health sciencesimportin β1ChemistryB-cell lymphomaPoint mutationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseMolecular biologynuclear importindirect immunofluorescenceOncology030220 oncology & carcinogenesisMutation (genetic algorithm)nuclear exportNuclear transportCRISPR-Cas9
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Acute myeloid leukemia (AML)-reactive cytotoxic T lymphocyte clones rapidly expanded from CD8(+) CD62L((high)+) T cells of healthy donors prevent AML…

2008

Objective Current in vitro techniques for isolating leukemia-reactive cytotoxic T lymphocytes (CTLs) from healthy donors are of relatively low efficiency and yield responder populations with unknown biological significance. This study aimed at the development of a more reliable approach, allowing generation and expansion of acute myeloid leukemia (AML)-reactive CTLs using primary in vitro stimulation. Materials and Methods We established allogeneic mini-mixed lymphocyte-leukemia cultures (mini-MLLCs) by stimulating donor CD8 + T cells with human leukocyte antigen (HLA) class I–matched AML blasts in microtiter plates. Before culture, CD8 + T cells were separated into CD62L (high)+ and CD62L …

Cancer ResearchMyeloidGenes MHC Class Ichemical and pharmacologic phenomenaHuman leukocyte antigenMice SCIDBiologyCD8-Positive T-LymphocytesMiceImmune systemMice Inbred NODhemic and lymphatic diseasesGeneticsmedicineCytotoxic T cellAnimalsHumansL-SelectinMolecular BiologyAllelesCells CulturedMice KnockoutMyeloid leukemiahemic and immune systemsCell BiologyHematologyReference Standardsmedicine.diseaseCytotoxicity Tests ImmunologicClone CellsCTL*LeukemiaLeukemia Myeloid Acutemedicine.anatomical_structureImmunologyCD8Neoplasm TransplantationInterleukin Receptor Common gamma SubunitT-Lymphocytes CytotoxicExperimental hematology
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STAT5 is crucial to maintain leukemic stem cells in acute myelogenous leukemias induced by MOZ-TIF2.

2012

Abstract MOZ-TIF2 is a leukemogenic fusion oncoprotein that confers self-renewal capability to hematopoietic progenitor cells and induces acute myelogenous leukemia (AML) with long latency in bone marrow transplantation assays. Here, we report that FLT3-ITD transforms hematopoietic cells in cooperation with MOZ-TIF2 in vitro and in vivo. Coexpression of FLT3-ITD confers growth factor independent survival/proliferation, shortens disease latency, and results in an increase in the number of leukemic stem cells (LSC). We show that STAT5, a major effector of aberrant FLT3-ITD signal transduction, is both necessary and sufficient for this cooperative effect. In addition, STAT5 signaling is essent…

Cancer ResearchMyeloidOncogene Proteins Fusionmedicine.medical_treatmentArticleMyelogenousMicehemic and lymphatic diseasesmedicineSTAT5 Transcription FactorAnimalsSTAT5Mice Inbred BALB CbiologyGrowth factormedicine.diseaseFlow CytometryHaematopoiesisLeukemiaBlotting SouthernLeukemia Myeloid Acutemedicine.anatomical_structureCell Transformation NeoplasticOncologyCancer researchbiology.proteinNeoplastic Stem CellsSignal transductionStem cellSignal TransductionCancer research
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Role of SHP2 for FLT3-dependent proliferation and transformation in 32D cells.

2008

Fms-like tyrosine kinase 3 (FLT3) is a class III receptor tyrosine kinase, which plays a role in proliferation and differentiation of B-cell progenitors, myelomonocytic and dendritic cells, as well as in the maintenance of pluripotent hematopoietic stem cells (reviewed in Stirewalt and Radich,1and Schmidt-Arras et al.2). Recently, FLT3 has received much attention as an important oncoprotein. Mutations in FLT3 that lead to constitutive activation are among the most common molecular lesions found in acute myeloid leukemia.3 The most prevalent type of mutations result in internal tandem duplications (ITD) of amino-acid stretches in the juxtamembrane domain of FLT3. FLT3-ITD is constitutively a…

Cancer ResearchMyeloidProtein Tyrosine Phosphatase Non-Receptor Type 11Biologymedicine.disease_causeReceptor tyrosine kinaseCell LineMicefluids and secretionshemic and lymphatic diseasesmedicineAnimalsHumansRNA Small InterferingCell ProliferationMice Inbred C3Hhemic and immune systemsHematologyHaematopoiesismedicine.anatomical_structureCell Transformation NeoplasticOncologyfms-Like Tyrosine Kinase 3Trk receptorembryonic structuresCancer researchbiology.proteinStem cellSignal transductionCarcinogenesisTyrosine kinaseSignal TransductionLeukemia
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MLL-Rearranged Leukemia Is Dependent on Aberrant H3K79 Methylation by DOT1L

2011

SummaryThe histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations of the Mixed Lineage Leukemia (MLL) gene. We identified the MLL-fusion targets in an MLL-AF9 leukemia model, and conducted epigenetic profiling for H3K79me2, H3K4me3, H3K27me3, and H3K36me3 in hematopoietic progenitor and leukemia stem cells (LSCs). We found abnormal profiles only for H3K79me2 on MLL-AF9 fusion target loci in LSCs. Inactivation of Dot1l led to downregulation of direct MLL-AF9 targets and an MLL translocation-associated gene expression signature, whereas global gene expression remained largely unaffected. Suppression of MLL translocation-a…

Cancer ResearchOncogene Proteins FusionCellular differentiationApoptosisBiologyMethylationArticleHistonesMice03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesmedicineAnimalsHumansEpigeneticsMyeloid Ecotropic Viral Integration Site 1 ProteinneoplasmsMyeloid Progenitor Cells030304 developmental biologyGene RearrangementHomeodomain Proteins0303 health sciencesLysineMyelodysplastic syndromesCell CycleCell DifferentiationCell BiologyHistone-Lysine N-MethyltransferaseMethyltransferasesMethylationDOT1Lmedicine.diseaseMolecular biologyHematopoiesisNeoplasm Proteins3. Good healthLeukemiaCell Transformation NeoplasticOncologyGenetic Loci030220 oncology & carcinogenesisHistone methyltransferaseCancer researchH3K4me3Protein Processing Post-TranslationalMyeloid-Lymphoid Leukemia ProteinCancer Cell
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