Search results for "disease model"

showing 10 items of 1116 documents

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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Deletion of the PER3 Gene on Chromosome 1p36 in Recurrent ER-Positive Breast Cancer

2010

El pdf del artículo es la versión de autor.-- et al.

Cancer ResearchMicroarrayGene DosageGene ExpressionEstrogen receptorBreast NeoplasmsGene dosageMiceBreast cancerOriginal ReportsAnimalsHumansMedicineGenetic Predisposition to DiseaseCopy-number variationskin and connective tissue diseasesSequence Deletionbusiness.industryCancerPeriod Circadian ProteinsPrognosismedicine.diseaseSurvival AnalysisDisease Models AnimalReceptors EstrogenOncologyChromosomes Human Pair 1Cancer researchFemaleBreast diseaseNeoplasm Recurrence LocalbusinessTamoxifenmedicine.drugJournal of Clinical Oncology
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Mesenchymal stromal-cell transplants induce oligodendrocyte progenitor migration and remyelination in a chronic demyelination model.

2013

Demyelinating disorders such as leukodystrophies and multiple sclerosis are neurodegenerative diseases characterized by the progressive loss of myelin that may lead toward a chronic demyelination of the brain’s white matter, impairing normal axonal conduction velocity and ultimately causing neurodegeneration. Current treatments modifying the pathological mechanisms are capable of ameliorating the disease; however, frequently, these therapies are not sufficient to repress the progressive demyelination into a chronic condition and permanent loss of function. To this end, we analyzed the effect that bone marrow-derived mesenchymal stromal cell (BM-MSC) grafts exert in a chronically demyelinate…

Cancer ResearchPathologymedicine.medical_specialtyNeurogenesisImmunologyNeural ConductionBiologyMesenchymal Stem Cell TransplantationModels Biologicaltrophic releaseCuprizoneMiceCellular and Molecular NeuroscienceMyelinNerve FibersCell MovementmedicineSubependymal zoneAnimalsNerve Growth FactorsStem Cell NicheProgenitor cellRemyelinationMyelin Sheathdemyelinating mouse modelMultiple sclerosisMesenchymal stem cellCell DifferentiationMesenchymal Stem CellsCell Biologymedicine.diseaseAxonsOligodendrocyteTransplantationDisease Models AnimalOligodendrogliaremyelinationmedicine.anatomical_structureChronic DiseaseDentate GyrusImmunologyoligodendrocyte activationOriginal Articlemesenchymal stromal cellsGenèticaDemyelinating Diseases
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Intestinal epithelial HuR modulates distinct pathways of proliferation and apoptosis and attenuates small intestinal and colonic tumor development.

2014

Abstract HuR is a ubiquitous nucleocytoplasmic RNA-binding protein that exerts pleiotropic effects on cell growth and tumorigenesis. In this study, we explored the impact of conditional, tissue-specific genetic deletion of HuR on intestinal growth and tumorigenesis in mice. Mice lacking intestinal expression of HuR (Hur IKO mice) displayed reduced levels of cell proliferation in the small intestine and increased sensitivity to doxorubicin-induced acute intestinal injury, as evidenced by decreased villus height and a compensatory shift in proliferating cells. In the context of Apcmin/+ mice, a transgenic model of intestinal tumorigenesis, intestinal deletion of the HuR gene caused a three-fo…

Cancer ResearchPost-translational regulationRNA-binding proteinContext (language use)ApoptosisCell Growth ProcessesBiologymedicine.disease_causeArticleAU-rich RNAMiceGene expressionIntestinal NeoplasmsmedicineAnimalsmRNA stabilityIntestinal MucosaMice KnockoutCell growthMolecular biologyPhenotypeProtein-RNA interactionSmall intestineDisease Models Animalmedicine.anatomical_structureOncologyELAV ProteinsApoptosisColonic NeoplasmsCancer researchCarcinogenesis
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Evaluation of genetic melanoma vaccines in cdk4-mutant mice provides evidence for immunological tolerance against authochthonous melanomas in the skin

2005

We evaluated the efficacy of a candidate melanoma vaccine approach in mice genetically prone to develop melanoma due to the introduction of an oncogenic mutation (R24C) in the germline sequence of the cyclin-dependent kinase 4 (cdk4), a protein critically involved in cell cycle regulation. Melanomas were induced in cdk4-mutant mice by chemical carcinogenesis and UVB irradiation. A genetic prime-boost strategy targeting the clinically relevant differentiation antigen tyrosinase-related protein 2 (TRP2) was performed which was able to stimulate a melanocyte-specific cellular immune response associated with localized autoimmune vitiligo-like depigmentation. However, significant destruction of …

Cancer ResearchSkin NeoplasmsUltraviolet Raysmedicine.medical_treatmentCancer VaccinesMelanoma VaccineDNA vaccinationMiceImmune systemDepigmentationAntigenImmune TolerancemedicineAnimalsGenetic Predisposition to DiseaseMelanomaneoplasmsGerm-Line MutationMice Knockoutbusiness.industryMelanomaCell CycleCyclin-Dependent Kinase 4Neoplasms ExperimentalImmunotherapymedicine.diseaseIntramolecular OxidoreductasesMice Inbred C57BLDisease Models AnimalOncologyImmunologyCarcinogensSkin cancermedicine.symptombusinessInternational Journal of Cancer
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T-cell Receptor Therapy Targeting Mutant Capicua Transcriptional Repressor in Experimental Gliomas

2021

Abstract Purpose: Gliomas are intrinsic brain tumors with a high degree of constitutive and acquired resistance to standard therapeutic modalities such as radiotherapy and alkylating chemotherapy. Glioma subtypes are recognized by characteristic mutations. Some of these characteristic mutations have shown to generate immunogenic neoepitopes suitable for targeted immunotherapy. Experimental Design: Using peptide-based ELISpot assays, we screened for potential recurrent glioma neoepitopes in MHC-humanized mice. Following vaccination, droplet-based single-cell T-cell receptor (TCR) sequencing from established T-cell lines was applied for neoepitope-specific TCR discovery. Efficacy of intravent…

Cancer ResearchT-LymphocytesT cellCellchemical and pharmacologic phenomenaRecurrent GliomaMajor histocompatibility complexImmunotherapy AdoptiveMiceGliomamedicineAnimalsMHC class IIReceptors Chimeric AntigenbiologyELISPOTT-cell receptorGliomamedicine.diseaseDisease Models Animalmedicine.anatomical_structureOncologybiology.proteinCancer researchImmunotherapyNeoplasm Recurrence LocalClinical Cancer Research
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Experimental models of kidney tumors.

1993

We here present in outline some outstanding results on the animal models of renal tumors submitted to the highest attention, which include two kinds of epithelial neoplams: those developed from the epithelium lining each the renal tubules (renal cell tumors) and pelvis; the mesenchymal tumor of rat; and tumors with embryonal appearance: the nephroplastoma as well as the variant of it known as the estrogen-induced tumor in the hamster. The review deals with methods for tumor induction and the pathobiology of tumors, the latter mainly focussed on the indendification of the precise types of renal cells committed in tumor origin. The existence of closely related counterparts of these animal tum…

Cancer Researchmedicine.medical_specialtyKidneyPathologyHematologyCellHamsterGeneral MedicineHistogenesisBiologymedicine.diseasemedicine.disease_causeEpitheliumKidney NeoplasmsRatsDisease Models Animalmedicine.anatomical_structureOncologyInternal medicineCricetinaemedicineBlastomaAnimalsRabbitsCarcinogenesisJournal of cancer research and clinical oncology
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Dendritic cell-tumor cell hybrids and immunotherapy: what's next?

2011

Dendritic cells (DC) are professional antigen-presenting cells currently being used as a cellular adjuvant in cancer immunotherapy strategies. Unfortunately, DC-based vaccines have not demonstrated spectacular clinical results. DC loading with tumor antigens and DC differentiation and activation still require optimization. An alternative technique for providing antigens to DC consists of the direct fusion of dendritic cells with tumor cells. These resulting hybrid cells may express both major histocompatibility complex (MHC) class I and II molecules associated with tumor antigens and the appropriate co-stimulatory molecules required for T-cell activation. Initially tested in animal models, …

Cancer Researchmedicine.medical_treatmentImmunologyAntigen-Presenting CellsHybrid CellsMajor histocompatibility complexAntigenCancer immunotherapyAntigens NeoplasmNeoplasmsmedicineImmunology and AllergyAnimalsHumansGenetics (clinical)TransplantationCell fusionMembrane GlycoproteinsbiologyHistocompatibility Antigens Class IHistocompatibility Antigens Class IICell BiologyDendritic cellImmunotherapyDendritic CellsCell biologyMembrane glycoproteinsDisease Models AnimalOncologybiology.proteinImmunotherapyAdjuvantCytotherapy
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A novel cell model to study the function of the adrenoleukodystrophy-related protein

2006

X-linked adrenoleukodystrophy (X-ALD) is a neurodegenerative disorder due to mutations in the ABCD1 (ALD) gene. ALDRP, the closest homolog of ALDP, has been shown to have partial functional redundancy with ALDP and, when overexpressed, can compensate for the loss-of-function of ALDP. In order to characterize the function of ALDRP and to understand the phenomenon of gene redundancy, we have developed a novel system that allows the controlled expression of the ALDRP-EGFP fusion protein (normal or non-functional mutated ALDRP) using the Tet-On system in H4IIEC3 rat hepatoma cells. The generated stable cell lines express negligible levels of endogenous ALDRP and doxycycline dosage-dependent lev…

Carcinoma Hepatocellularendocrine system diseasesRecombinant Fusion ProteinsBiophysicsGene redundancyATP-binding cassette transporterContext (language use)BiologyATP Binding Cassette Transporter Subfamily DProtein EngineeringTransfectionBiochemistryCell Line TumormedicineAnimalsAdrenoleukodystrophyMolecular BiologyGeneCell BiologyPeroxisomemedicine.diseaseFusion proteinRatsCell biologyDisease Models AnimalBiochemistryATP-Binding Cassette TransportersAdrenoleukodystrophyFunction (biology)
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Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardioto…

2015

Although treatment for heart failure induced by cancer therapy has improved in recent years, the prevalence of cardiomyopathy due to antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in cancer patients. The development of novel protective therapies requires testing putative therapeutic strategies in appropriate animal model…

Cardiac function curveACE inhibitorsCardiotonic AgentsNeuregulin-1CardiomyopathyAntineoplastic AgentsPreclinical modelsCardioprotectionCardiotonic AgentsPharmacologyBioinformaticsmedicine.disease_causeCancer therapy-induced cardiac injury ;Preclinical modelsMitochondria HeartBeta-blockersNeoplasmsCancer therapy-induced cardiac injuryMedicineAnimalsHumansCardiac stem cellsCardioprotectionCardiotoxicityACE inhibitors; Beta-blockers; Cancer therapy-induced cardiac injury; Cardiac stem cells; Cardioprotection; Mitochondria; Neuregulin-1; Oxidative stress; Preclinical models; Statinsbusiness.industryStatinsCancermedicine.diseaseCardiotoxicityMitochondriaCancer therapy-induced cardiac injury Preclinical models Cardioprotection Mitochondria Neuregulin-1 Oxidative stress Statins Beta-blockers ACE inhibitors Cardiac stem cellsDisease Models AnimalOxidative StressHeart failureCardiology and Cardiovascular MedicinebusinessOxidative stress
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