Search results for "Cytotoxicity"

showing 10 items of 865 documents

Selective induction of apoptosis in multidrug resistant HL60R cells by the thiazolobenzoimidazole derivative 1-(2,6-difluorophenyl)-1H,3H-thiazolo [3…

1999

We investigated the antitumour effects of 1-(2,6-difluorophenyl)-1H,3H-thiazolo [3,4-a]benzimidazole (TBZ) a new anti-HIV-1 agent, on human promyelocytic HL60 leukaemia, both a parental and a multidrug resistant form (HL60R). HL60R overexpresses P-glycoprotein and, like HL60, lacks p53 protein expression. HL60 and HL60R show similar levels of Bcl-2 protein. In contrast to the conventional chemotherapeutic agents daunorubicin, etoposide and mitoxantrone, TBZ caused equal or even greater cytotoxicity in HL60R than in HL60, and this result was associated with a more marked induction of apoptosis in the drug resistant cells. The antitumour activity of TBZ occurred in the range of concentrations…

Cancer ResearchBenzimidazoleAnti-HIV AgentsDaunorubicinHL60ApoptosisHL-60 CellsDrug resistancePharmacologychemistry.chemical_compoundmedicineHumansATP Binding Cassette Transporter Subfamily B Member 1CytotoxicityP-glycoproteinbiologyFlow CytometryVirologyDrug Resistance MultipleMultiple drug resistanceThiazolesProto-Oncogene Proteins c-bcl-2OncologychemistryDrug Resistance NeoplasmApoptosisbiology.proteinBenzimidazolesDrug Screening Assays AntitumorTumor Suppressor Protein p53medicine.drugEuropean Journal of Cancer
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Induction of tumor-cell lysis by bi-specific antibody recognizing ganglioside GD2 and T-cell antigen CD3

1993

Human tumor cells expressing ganglioside GD2 were lysed by various effector populations targeted with an anti-CD3-anti-GD2 bi-specific antibody (BAb CD3 x GD2). This antibody-heteroconjugate was prepared by chemically cross-linking the OKT-3 monoclonal antibody (MAb) reactive with CD3 antigen on T lymphocytes with the ganglioside MAb ME 361, which binds preferentially to the tumor-associated ganglioside GD2. The specificity of target-cell lysis by the cytotoxic T cells (CTL) was mediated by the specificity of the targeting antibody: GD2-negative cells were not lysed in the presence of the CD3 x GD2 BAb. A dose-dependent response was observed in a range of 10 to 10,000 ng/ml. In contrast, 2 …

Cancer ResearchCD3 Complexmedicine.drug_classCross ReactionsBiologyMonoclonal antibodyAntibodiesImmunoglobulin GAntigenAntibody SpecificityGangliosidesNeoplasmsTumor Cells CulturedmedicineHumansCytotoxic T cellCytotoxicityMelanomaGangliosideT lymphocyteMolecular biologyKiller Cells NaturalOncologyImmunoglobulin GColonic Neoplasmsbiology.proteinImmunotherapyAntibodyT-Lymphocytes CytotoxicInternational Journal of Cancer
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The potential of acetaminophen as a prodrug in gene-directed enzyme prodrug therapy.

2000

Acetaminophen is oxidized by human CYP1A2 to the cytotoxic metabolite N-acetylbenzoquinoneimine (NABQI). Incubation of cells transfected with human CYP1A2 (H1A2 MZ cells) with 4-20 mM acetaminophen for 6 hours at 37 degrees C caused extensive cytotoxicity (cell viability10%). In contrast, nontransfected V79 MZ cells were unaffected (viability95%). By mixing H1A2 MZ cells with V79 MZ cells in various proportions and incubating with 4 mM acetaminophen, it was shown that the NABQI released from H1A2 MZ cells also caused cytotoxicity of bystander cells. Thus, in a mixture containing 5% H1A2 MZ cells, exposure to 4 mM acetaminophen for 6 hours resulted in complete cell killing by 24 hours. A sim…

Cancer ResearchCell SurvivalPharmacologyTransfectionCatalysisCell LineCricetulusCytochrome P-450 CYP1A2CricetinaemedicineTumor Cells CulturedCytotoxic T cellAnimalsHumansProdrugsViability assayCytotoxicityMolecular BiologyAcetaminophenChemistryCYP1A2TransfectionGenetic TherapyProdrugAcetaminophenCell killingMolecular Medicinemedicine.drugCancer gene therapy
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A sphingosine kinase inhibitor combined with temozolomide induces glioblastoma cell death through accumulation of dihydrosphingosine and dihydroceram…

2014

AbstractGlioblastomas (GBMs) are very aggressive tumors with low chemosensitivity. The DNA-alkylating agent temozolomide (TMZ) is currently the most efficient chemotoxic drug for GBM therapy; however, many patients develop resistance to TMZ. Combining TMZ with another agent could present an improved treatment option if it could overcome TMZ resistance and avoid side effects. Sphingosine kinase inhibitors (SKIs) have emerged as anticancer agents. Sphingosine kinases are often overexpressed in tumors where their activity of phosphorylating sphingosine (Sph) contributes to tumor growth and migration. They control the levels of the pro-apoptotic ceramide (Cer) and Sph and of the pro-survival sp…

Cancer ResearchCeramideProgrammed cell deathImmunologySphingosine kinaseAntineoplastic AgentsApoptosisBiologyCeramidesCellular and Molecular Neurosciencechemistry.chemical_compoundSphingosineCell Line TumorAutophagyTemozolomideHumansEnzyme InhibitorsCytotoxicitySphingosineCell DeathKinaseBrain NeoplasmsAutophagyCell BiologyEndoplasmic Reticulum StressCell biologyDacarbazinePhosphotransferases (Alcohol Group Acceptor)chemistryApoptosisDrug Resistance NeoplasmCancer researchDrug Therapy CombinationOriginal ArticleGlioblastomaCell deathdisease
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Analysis of antigens recognized on human melanoma cells by A2-restricted cytolytic t lymphocytes (CTL)

1993

We have pursued our analysis of potential tumor-rejection antigens recognized on human melanoma by autologous cytolytic T lymphocytes (CTL). We reported previously that 3 distinct antigens (A,B,C) were recognized on melanoma cell line SK29-MEL in association with HLA-A2. Selection for melanoma-cell variants resistant to anti-A CTL revealed that antigen A consists of at least 2 determinants (Aa, Ab) which can be lost separately. Genetic linkage between Aa and Ab was suggested by concomitant loss of Aa and Ab in an immunoselected tumor-cell variant. This variant was also resistant to an autologous CTL clone restricted by HLA-B45, indicating that this CTL may also recognize a determinant of an…

Cancer ResearchClone (cell biology)T lymphocyteBiologyCytotoxicity Tests ImmunologicTransfectionVirologyEpitopesCytolysisCTL*OncologyLytic cycleAntigenAntigens NeoplasmHLA-B AntigensHLA-A2 AntigenGene expressionImmunologyTumor Cells CulturedHumansCloning MolecularCytotoxicityMelanomaT-Lymphocytes CytotoxicInternational Journal of Cancer
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Impact of Extracellular Acidity on the Activity of P-glycoprotein and the Cytotoxicity of Chemotherapeutic Drugs

2006

AbstractThe expression and activity of P-glycoprotein (pGP) play a role in the multidrug resistance of tumors. Because solid-growing tumors often show pronounced hypoxia or extracellular acidosis, this study attempted to analyze the impact of an acidic environment on the expression and activity of pGP and on the cytotoxicity of chemotherapeutic agents. For this, prostate carcinoma cells were exposed to an acidic extracellular environment (pH 6.6) for up to 24 hours. pGP activity was more than doubled after 3 to 6 hours of incubation in acidic medium, whereas cellular pGP expression remained constant, indicating that increased transport rate is the result of functional modulation. In paralle…

Cancer ResearchDaunorubicinPharmacologyP-glycoproteinlcsh:RC254-282Calcium in biologyExtracellularmedicinepolycyclic compoundsintracellular Ca2+ concentrationCytotoxicityacidityProtein kinase CP-glycoproteinbiologyintegumentary systemChemistrychemotoxicitylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenscarbohydrates (lipids)BiochemistryCell culturebiology.proteinIntracellularmedicine.drugprotein kinase CNeoplasia
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Highly specific auto-antibodies against claudin-18 isoform 2 induced by a chimeric HBcAg virus-like particle vaccine kill tumor cells and inhibit the…

2011

Abstract Strategies for antibody-mediated cancer immunotherapy, such as active immunization with virus-like particle (VLP)-based vaccines, are gaining increasing attention. We developed chimeric hepatitis B virus core antigen (HBcAg)-VLPs that display a surface epitope of the highly selective tumor-associated cell lineage marker claudin-18 isoform 2 (CLDN18.2) flanked by a mobility-increasing linker. Auto-antibodies elicited by immunization with these chimeric HBcAg-VLPs in 2 relevant species (mouse and rabbit) bind with high precision to native CLDN18.2 at physiologic densities on the surface of living cells but not to the corresponding epitope of the CLDN18.1 splice variant that differs b…

Cancer ResearchHepatitis B virusLung Neoplasmsmedicine.medical_treatmentMolecular Sequence DataCHO CellsAdenocarcinomaActive immunizationCancer VaccinesEpitopeMiceCricetulusAntigenVirus-like particleCancer immunotherapyAntibody SpecificityStomach NeoplasmsCell Line TumorCricetinaemedicineAnimalsHumansProtein IsoformsAmino Acid SequenceVaccines Virus-Like ParticleAutoantibodiesMice Inbred BALB Cbiologybusiness.industryAntibody-Dependent Cell CytotoxicityMembrane ProteinsVirologyMolecular biologyHepatitis B Core AntigensHBcAgHEK293 CellsOncologyCell cultureClaudinsbiology.proteinRabbitsAntibodybusinessCancer research
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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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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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