Search results for "Inbred NOD"

showing 10 items of 76 documents

Proliferation state and polo-like kinase1 dependence of tumorigenic colon cancer cells.

2012

Abstract Tumor-initiating cells are responsible for tumor maintenance and relapse in solid and hematologic cancers. Although tumor-initiating cells were initially believed to be mainly quiescent, rapidly proliferating tumorigenic cells were found in breast cancer. In colon cancer, the proliferative activity of the tumorigenic population has not been defined, although it represents an essential parameter for the development of more effective therapeutic strategies. Here, we show that tumorigenic colon cancer cells can be found in a rapidly proliferating state in vitro and in vivo, both in human tumors and mouse xenografts. Inhibitors of polo-like kinase1 (Plk1), a mitotic kinase essential fo…

Colorectal cancerCancer stem cellscolorectal cancercell proliferationcell cycle.Cell Cycle ProteinsMice0302 clinical medicineMice Inbred NODAC133 AntigenRNA Small Interfering0303 health scienceseducation.field_of_studyPteridinesCell CycleCell cycleImmunohistochemistry3. Good healthMitochondriaGene Expression Regulation Neoplastic030220 oncology & carcinogenesisColonic NeoplasmsMolecular MedicineFemaleStem cellPopulationTransplantation HeterologousCell Growth ProcessesBiologyProtein Serine-Threonine KinasesPLK103 medical and health sciencesCancer stem cellAntigens CDCell Line TumorProto-Oncogene ProteinsmedicineAnimalsHumanseducationProtein Kinase Inhibitors030304 developmental biologyGlycoproteinsSettore MED/04 - Patologia GeneraleCell growthCell Biologymedicine.diseaseTumor progressionImmunologyCancer researchPeptidesDevelopmental BiologyStem cells (Dayton, Ohio)
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Therapeutic afucosylated monoclonal antibody and bispecific T-cell engagers for T-cell acute lymphoblastic leukemia

2021

BackgroundT-cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease with a poor cure rate for relapsed/resistant patients. Due to the lack of T-cell restricted targetable antigens, effective immune-therapeutics are not presently available and the treatment of chemo-refractory T-ALL is still an unmet clinical need. To develop novel immune-therapy for T-ALL, we generated an afucosylated monoclonal antibody (mAb) (ahuUMG1) and two different bispecific T-cell engagers (BTCEs) against UMG1, a unique CD43-epitope highly and selectively expressed by T-ALL cells from pediatric and adult patients.MethodsUMG1 expression was assessed by immunohistochemistry (IHC) on a wide panel of normal t…

Cytotoxicity ImmunologicCancer Research2434T-LymphocytesMice SCIDafucosylated monoclonal antibodyLymphocyte ActivationPrecursor T-Cell Lymphoblastic Leukemia-LymphomaEpitopesJurkat CellsAntineoplastic Agents ImmunologicalAntibody SpecificityMice Inbred NODantigensAntibodies BispecificTumor MicroenvironmentImmunology and Allergyantibodieshematologic neoplasms1506RC254-282Antibody-dependent cell-mediated cytotoxicityLeukosialinbispecific T-cell engagersmedicine.diagnostic_testbiologyhematological malignancieNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.anatomical_structureantibodieOncologytranslational medical researchMolecular MedicineImmunohistochemistryFemaleimmunotherapyAntibodyT-ALLT-cell engagersT-cell acute lymphoblastic leukemiamedicine.drug_classT cellImmunologySettore MED/08 - Anatomia PatologicaMonoclonal antibodyAntibodies Monoclonal HumanizedFlow cytometryT Acute Lymphoblastic LeukemiaantigenAntigenPhagocytosismedicineAnimalsHumanshematological malignanciesCell ProliferationPharmacologyT-cell engagerbusiness.industryhematological malignancies; antibodies; antigens; hematologic neoplasms; immunotherapy; neoplasm; T-ALL; T-cell engagers; translational medical research; translational researchBasic Tumor ImmunologyXenograft Model Antitumor Assaystranslational researchCancer researchbiology.proteinneoplasmbusinesshematologic neoplasmneoplasm
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Both mature KIR+ and immature KIR- NK cells control pediatric acute B-cell precursor leukemia in NOD.Cg-Prkdcscid IL2rgtmWjl/Sz mice.

2014

Therapeutic natural killer (NK)-cell-mediated alloreactivity toward acute myeloid leukemia has largely been attributed to mismatches between killer immunoglobulin-like receptors (KIRs) on NK cells and their ligands, HLA class I molecules, on target cells. While adult acute B-cell precursor leukemia (BCP-ALL) appears to be resistant to NK-cell-mediated lysis, recent data indicate that pediatric BCP-ALL might yet be a target of NK cells. In this study, we demonstrate in a donor-patient-specific NOD.Cg-Prkdc(scid) IL2rg(tmWjl)/Sz (NSG) xenotransplantation model that NK cells mediate considerable alloreactivity toward pediatric BCP-ALL in vivo. Notably, both adoptively transferred mature KIR(+)…

Cytotoxicity ImmunologicGenotypeXenotransplantationmedicine.medical_treatmentImmunologyTransplantation HeterologousAntineoplastic AgentsGraft vs Leukemia EffectHuman leukocyte antigenBiochemistryMiceImmune systemReceptors KIRMice Inbred NODPrecursor B-Cell Lymphoblastic Leukemia-LymphomamedicineAnimalsHumansChildB cellSevere combined immunodeficiencybusiness.industryHematopoietic Stem Cell TransplantationMyeloid leukemiaCell BiologyHematologyDNA Methylationmedicine.diseasePrognosisTransplantationKiller Cells NaturalLeukemiaDisease Models Animalmedicine.anatomical_structureImmunologyAzacitidineCytokinesInterleukin-2businessBlood
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Human NK cells selective targeting of colon cancer-initiating cells: a role for natural cytotoxicity receptors and MHC class I molecules

2013

Abstract Tumor cell populations have been recently proposed to be composed of two compartments: tumor-initiating cells characterized by a slow and asymmetrical growth, and the “differentiated” cancer cells with a fast and symmetrical growth. Cancer stem cells or cancer-initiating cells (CICs) play a crucial role in tumor recurrence. The resistance of CICs to drugs and irradiation often allows them to survive traditional therapy. NK cells are potent cytotoxic lymphocytes that can recognize tumor cells. In this study, we have analyzed the NK cell recognition of tumor target cells derived from the two cancer cell compartments of colon adenocarcinoma lesions. Our data demonstrate that freshly p…

Cytotoxicity ImmunologicNKImmunologyGene ExpressionCancer Stem CellMice SCIDBiologyAdenocarcinomaInterleukin 21MiceNK-92Cancer stem cellMice Inbred NODTumor Cells CulturedImmunology and AllergyCytotoxic T cellAnimalsHumansCell LineageSettore MED/04 - Patologia GeneraleLymphokine-activated killer cellMicroscopy ConfocalNatural Cytotoxicity Triggering Receptor 3Natural Cytotoxicity Triggering Receptor 2Janus kinase 3Histocompatibility Antigens Class Inessuna parola chiaveKiller Cells NaturalOrgan SpecificityImmunologyCancer cellColonic NeoplasmsCancer researchInterleukin 12Neoplastic Stem Cellsimmunotherapy
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Overexpression of the truncated form of high mobility group a proteins (HMGA2) in human myometrial cells induces leiomyoma-like tissue formation

2014

The pathogenesis of uterine leiomyomas, the most common benign tumor in women, is still unknown. This lack of basic knowledge limits the development of novel non-invasive therapies. Our group has previously demonstrated that leiomyoma side population (SP) cells are present in tumor lesions and act like putative tumor-initiating stemcells in human leiomyoma. Moreover, accumulated evidence demonstrates that these benign tumors of mesenchymal origin are characterized by rearrangements of the High Mobility Group A proteins (HMGA). In this work, we tested the hypothesis that leiomyoma development may be due to overexpression of HMGA2 (encoding high mobility group AT-hook2) in myometrial stem cel…

EmbryologyMice SCID//purl.org/becyt/ford/1 [https]MiceMice Inbred NODProtein IsoformsUterine leiomyomaLeiomyomaStem CellsSOMATIC STEM CELLSObstetrics and GynecologyExonsBioquímica y Biología Molecularfemale genital diseases and pregnancy complicationsGene Expression Regulation NeoplasticCell Transformation NeoplasticLeiomyomaUterine NeoplasmsMyometriumNeoplastic Stem CellsFemaleStem cellHIGH MOBILITY GROUP A PROTEINSCIENCIAS NATURALES Y EXACTASPlasmidsAdult stem cellmedicine.medical_specialtyUTERINE LEIOMYOMASMyocytes Smooth MuscleTransplantation HeterologousBiologyTransfectionHUMAN MYOMETRIUMCiencias BiológicasHMGA2Side populationInternal medicineGeneticsmedicineAnimalsHumans//purl.org/becyt/ford/1.6 [https]neoplasmsMolecular BiologyHMGA2 ProteinMesenchymal stem cellHMGASIDE POPULATIONCell Biologymedicine.diseaseIntronsEndocrinologyReproductive MedicineCancer researchbiology.proteinDevelopmental Biology
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Tumour vascularization via endothelial differentiation of glioblastoma stem-like cells

2010

Glioblastoma is a highly angiogenetic malignancy, the neoformed vessels of which are thought to arise by sprouting of pre-existing brain capillaries. The recent demonstration that a population of glioblastoma stem-like cells (GSCs) maintains glioblastomas indicates that the progeny of these cells may not be confined to the neural lineage. Normal neural stem cells are able to differentiate into functional endothelial cells. The connection between neural stem cells and the endothelial compartment seems to be critical in glioblastoma, where cancer stem cells closely interact with the vascular niche and promote angiogenesis through the release of vascular endothelial growth factor(VEGF) and str…

EndotheliumAngiogenesisTransplantation HeterologousSettore MED/27 - NEUROCHIRURGIAMice TransgenicMice SCIDBiologyModels BiologicalMiceVasculogenesisNeural Stem CellsMice Inbred NODCell Line TumormedicineAnimalsHumansCell LineageVasculogenic mimicryglioblastoma tumor vascularizationIn Situ Hybridization FluorescenceChromosome AberrationsMultidisciplinaryNeovascularization PathologicEndothelial CellsCell DifferentiationVascular endothelial growth factor BEndothelial stem cellVascular endothelial growth factor Amedicine.anatomical_structureVascular endothelial growth factor CTumor Markers BiologicalImmunologyCancer researchEndothelium VascularGlioblastomaNeoplasm TransplantationNature
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MYC Activates Stem-like Cell Potential in Hepatocarcinoma by a p53-Dependent Mechanism

2014

Activation of c-MYC is an oncogenic hallmark of many cancers including liver cancer, and is associated with a variety of adverse prognostic characteristics. Despite a causative role during malignant transformation and progression in hepatocarcinogenesis, consequences of c-MYC activation for the biology of hepatic cancer stem cells (CSCs) are undefined. Here, distinct levels of c-MYC over-expression were established by using two dose-dependent tetracycline inducible systems in 4 hepatoma cell lines with different p53 mutational status. The CSCs were evaluated using side-population approach as well as standard in vitro and in vivo assays. Functional repression of p53 was achieved by lentivira…

Homeobox protein NANOGCancer ResearchCarcinoma HepatocellularCarcinogenesisMice SCIDBiologymedicine.disease_causeArticleMalignant transformationProto-Oncogene Proteins c-mycSide populationMice Inbred NODCancer stem cellmedicineAnimalsHumansLiver NeoplasmsHep G2 Cellsmedicine.diseaseTumor BurdenTransplantationPhenotypeOncologyImmunologyNeoplastic Stem CellsCancer researchTumor Suppressor Protein p53Liver cancerCarcinogenesisReprogrammingNeoplasm TransplantationCancer Research
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Evaluating Human T-Cell Therapy of Cytomegalovirus Organ Disease in HLA-Transgenic Mice

2015

Reactivation of human cytomegalovirus (HCMV) can cause severe disease in recipients of hematopoietic stem cell transplantation. Although preclinical research in murine models as well as clinical trials have provided 'proof of concept' for infection control by pre-emptive CD8 T-cell immunotherapy, there exists no predictive model to experimentally evaluate parameters that determine antiviral efficacy of human T cells in terms of virus control in functional organs, prevention of organ disease, and host survival benefit. We here introduce a novel mouse model for testing HCMV epitope-specific human T cells. The HCMV UL83/pp65-derived NLV-peptide was presented by transgenic HLA-A2.1 in the conte…

Human cytomegaloviruslcsh:Immunologic diseases. Allergymedicine.medical_treatmentT cellImmunologyCell- and Tissue-Based TherapyCytomegalovirusEpitopes T-LymphocyteMice TransgenicHematopoietic stem cell transplantationHuman leukocyte antigenMice SCIDBiologyMicrobiologyViral Matrix ProteinsMice Inbred NODVirologyHLA-A2 AntigenGeneticsmedicineCytotoxic T cellAnimalsHumansMolecular Biologylcsh:QH301-705.5ImmunotherapyViral Loadmedicine.diseaseMice Inbred C57BLDisease Models Animalmedicine.anatomical_structurelcsh:Biology (General)ImmunologyCytomegalovirus InfectionsParasitologylcsh:RC581-607Viral loadCD8Research ArticlePLoS Pathogens
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Protection from graft-versus-host disease by HIV-1 envelope protein gp120-mediated activation of human CD4+CD25+ regulatory T cells.

2009

AbstractNaturally occurring CD4+CD25+ regulatory T cells (Tregs) represent a unique T-cell lineage that is endowed with the ability to actively suppress immune responses. Therefore, approaches to modulate Treg function in vivo could provide ways to enhance or reduce immune responses and lead to novel therapies. Here we show that the CD4 binding human immunodeficiency virus-1 envelope glycoprotein gp120 is a useful and potent tool for functional activation of human Tregs in vitro and in vivo. Gp120 activates human Tregs by binding and signaling through CD4. Upon stimulation with gp120, human Tregs accumulate cyclic adenosine monophosphate (cAMP) in their cytosol. Inhibition of endogeneous cA…

ImmunologyTransplantation HeterologousGraft vs Host Diseasechemical and pharmacologic phenomenaCHO CellsMice SCIDBiologyHIV Envelope Protein gp120Lymphocyte ActivationBiochemistryT-Lymphocytes RegulatoryImmune tolerancechemistry.chemical_compoundMiceImmune systemCricetulusIn vivoMice Inbred NODCricetinaeCyclic AMPImmune ToleranceAnimalsHumansCyclic adenosine monophosphateIL-2 receptorhemic and immune systemsCell BiologyHematologyEnvelope glycoprotein GP120Cell biologyTransplantationchemistryImmunologyCD4 Antigensbiology.proteinHIV-1Signal transductionSignal TransductionBlood
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Interleukin-12 and -23 Control Plasticity of CD127(+) Group 1 and Group 3 Innate Lymphoid Cells in the Intestinal Lamina Propria.

2015

Human group 1 ILCs consist of at least three phenotypically distinct subsets, including NK cells, CD127(+) ILC1, and intraepithelial CD103(+) ILC1. In inflamed intestinal tissues from Crohn's disease patients, numbers of CD127(+) ILC1 increased at the cost of ILC3. Here we found that differentiation of ILC3 to CD127(+) ILC1 is reversible in vitro and in vivo. CD127(+) ILC1 differentiated to ILC3 in the presence of interleukin-2 (IL-2), IL-23, and IL-1β dependent on the transcription factor RORγt, and this process was enhanced in the presence of retinoic acid. Furthermore, we observed in resection specimen from Crohn's disease patients a higher proportion of CD14(+) dendritic cells (DC), whi…

Interleukin 2Receptors Retinoic AcidCellular differentiationCD14ImmunologyInterleukin-1betaRetinoic acidLipopolysaccharide Receptorschemical and pharmacologic phenomenaTretinoinMice SCIDBiologyInterleukin-12 Subunit p35Interleukin-7 Receptor alpha Subunitchemistry.chemical_compoundMiceIntestinal mucosaCrohn DiseaseMice Inbred NODmedicineImmunology and AllergyAnimalsHumansRetinoid X Receptor gammaLymphocytesIntestinal MucosaInterleukin-7 receptorCells CulturedMice KnockoutRetinoic Acid Receptor alphaInnate lymphoid cellvirus diseaseshemic and immune systemsCell DifferentiationDendritic CellsNuclear Receptor Subfamily 1 Group F Member 3Molecular biologyKiller Cells NaturalMice Inbred C57BLInfectious DiseaseschemistryLymphocyte TransfusionImmunologyInterleukin 12Interleukin-23 Subunit p19Interleukin-2medicine.drugImmunity
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