2011
Reactive Oxygen Species Is Essential for Cycloheximide to Sensitize Lexatumumab-Induced Apoptosis in Hepatocellular Carcinoma Cells
Zhao X, Cao M, Liu J, Zhu H, Nelson D, Liu C. Reactive Oxygen Species Is Essential for Cycloheximide to Sensitize Lexatumumab-Induced Apoptosis in Hepatocellular Carcinoma Cells. PLOS ONE 2011, 6: e16966. PMID: 21347335, PMCID: PMC3037406, DOI: 10.1371/journal.pone.0016966.Peer-Reviewed Original ResearchAntibodies, MonoclonalApoptosisBcl-2 Homologous Antagonist-Killer ProteinBcl-2-Associated X ProteinCarcinoma, HepatocellularCaspasesCell Line, TumorCycloheximideDrug InteractionsGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansIntracellular SpaceLiver NeoplasmsReactive Oxygen SpeciesInterleukin-6 Modulates Graft-versus-Host Responses after Experimental Allogeneic Bone Marrow Transplantation
Tawara I, Koyama M, Liu C, Toubai T, Thomas D, Evers R, Chockley P, Nieves E, Sun Y, Lowler K, Malter C, Nishimoto N, Hill G, Reddy P. Interleukin-6 Modulates Graft-versus-Host Responses after Experimental Allogeneic Bone Marrow Transplantation. Clinical Cancer Research 2011, 17: 77-88. PMID: 21047980, PMCID: PMC3058832, DOI: 10.1158/1078-0432.ccr-10-1198.Peer-Reviewed Original ResearchConceptsAllogeneic bone marrow transplantationBone marrow transplantationDonor T cellsIL-6 deficiencyInterleukin-6MR16-1T cellsMarrow transplantationExperimental allogeneic bone marrow transplantationDonor regulatory T cellsBeneficial GVT effectsMR16-1 treatmentRegulatory T cellsProlongation of survivalDonor bone marrowEffector cell expansionRelevant murine modelIL-6 receptorBMT patientsGVT responseGVT effectHost diseaseBMT recipientsMAb therapyTumor effect
2010
Inhibition of Neovascularization to Simultaneously Ameliorate Graft-vs-Host Disease and Decrease Tumor Growth
Penack O, Henke E, Suh D, King C, Smith O, Na I, Holland A, Ghosh A, Lu S, Jenq R, Liu C, Murphy G, Lu T, May C, Scheinberg D, Gao D, Mittal V, Heller G, Benezra R, van den Brink M. Inhibition of Neovascularization to Simultaneously Ameliorate Graft-vs-Host Disease and Decrease Tumor Growth. Journal Of The National Cancer Institute 2010, 102: 894-908. PMID: 20463307, PMCID: PMC2886094, DOI: 10.1093/jnci/djq172.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAnimalsAntibodies, MonoclonalAntigens, CDBone Marrow TransplantationCadherinsFemaleFlow CytometryFluorescent Antibody TechniqueGraft vs Host DiseaseHematopoietic Stem Cell TransplantationMiceMice, Inbred C57BLNeoplasmsNeovascularization, PathologicTransplantation, HomologousConceptsTumor growthAllo-BMTHost diseaseAllogeneic hematopoietic stem cell transplantationHematopoietic stem cell transplantationEndothelial cellsAllo-BMT recipientsGVHD target tissuesAllogeneic BM transplantationStem cell transplantationEndothelial progenitor cellsDecreases tumor growthInhibition of neovascularizationTumor-bearing miceTissue endothelial cellsAmeliorate graftDonor BMBM transplantationCell transplantationGVHDBone marrowTherapeutic targetingNeovascularizationOverall outcomeTumor vasculature
2009
T helper17 Cells Are Sufficient But Not Necessary to Induce Acute Graft-Versus-Host Disease
Iclozan C, Yu Y, Liu C, Liang Y, Yi T, Anasetti C, Yu X. T helper17 Cells Are Sufficient But Not Necessary to Induce Acute Graft-Versus-Host Disease. Transplantation And Cellular Therapy 2009, 16: 170-178. PMID: 19804837, PMCID: PMC3876952, DOI: 10.1016/j.bbmt.2009.09.023.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalBody WeightBone Marrow TransplantationCD3 ComplexCells, CulturedGraft vs Host DiseaseGraft vs Host ReactionInterferon-gammaInterleukin-17MiceMice, Inbred StrainsMice, TransgenicNuclear Receptor Subfamily 1, Group F, Member 3Severity of Illness IndexSurvival AnalysisT-Lymphocyte SubsetsT-Lymphocytes, Helper-InducerTh1 CellsTime FactorsTumor Necrosis Factor-alphaWhole Body ImagingConceptsHost diseaseBALB/c recipientsBone marrow transplantation settingAcute Graft-VersusT helper17 cellsGVHD target organsInduction of graftPathogenesis of GVHDCD4 T cellsGraft-VersusGVHD developmentC recipientsT helperTh17 cellsAllogeneic recipientsAutoimmune diseasesC57BL/6 miceSyngeneic recipientsTransplantation settingGVHDT cellsIFN-gammaTarget organsSuperior expansionDisease
2007
The antigen for Hep Par 1 antibody is the urea cycle enzyme carbamoyl phosphate synthetase 1
Butler S, Dong H, Cardona D, Jia M, Zheng R, Zhu H, Crawford J, Liu C. The antigen for Hep Par 1 antibody is the urea cycle enzyme carbamoyl phosphate synthetase 1. Laboratory Investigation 2007, 88: 78-88. PMID: 18026163, DOI: 10.1038/labinvest.3700699.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, MonoclonalAntigensBase SequenceBlotting, WesternCarbamoyl-Phosphate Synthase (Ammonia)Chromatography, LiquidDNA PrimersFemaleHumansImmunoprecipitationLiver NeoplasmsMaleReverse Transcriptase Polymerase Chain ReactionSpectrometry, Mass, Electrospray IonizationTandem Mass SpectrometryConceptsHep Par 1 antibodyHep Par 1Carbamoyl phosphate synthetase 1Carcinoma cell linesHepatocellular carcinoma cell linesHuman hepatocellular carcinoma cell linePAR-1Cell linesHepatocyte paraffin 1Small intestinal tissueSurgical pathology practiceCPS1 expressionMurine monoclonal antibodiesHepatoid tumorsHuman liver tissueHepatocellular originIntestinal tissueRate-limiting enzymeLiver carcinogenesisSynthetase 1Liver tissuePathology practiceAntigenLiver pathobiologyMonoclonal antibodies
2005
Impact of Humoral Immune Response on Distribution and Efficacy of Recombinant Adeno-Associated Virus-Derived Acid -Glucosidase in a Model of Glycogen Storage Disease Type II
Cresawn K, Fraites T, Wasserfall C, Atkinson M, Lewis M, Porvasnik S, Liu C, Mah C, Byrne B. Impact of Humoral Immune Response on Distribution and Efficacy of Recombinant Adeno-Associated Virus-Derived Acid -Glucosidase in a Model of Glycogen Storage Disease Type II. Human Gene Therapy 2005, 16: 68-80. PMID: 15703490, DOI: 10.1089/hum.2005.16.68.Peer-Reviewed Original ResearchConceptsGlycogen storage disease type IIImmune-tolerant miceStorage disease type IIAntibody responseContractile functionImmune responseHumoral immune responseHind limb musclesAcid alpha-glucosidaseCardiorespiratory failureType IIAntibody formationReduced glycogenGlycogen reductionLysosomal storage diseaseSoleus muscleGAA levelsMiceEnzyme levelsSkeletal muscleStorage diseaseLevel of activityMuscleRecombinant adenoAlpha-glucosidase
2004
Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation
Min C, Maeda Y, Lowler K, Liu C, Clouthier S, Lofthus D, Weisiger E, Ferrara J, Reddy P. Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation. Blood 2004, 104: 3393-3399. PMID: 15280194, DOI: 10.1182/blood-2004-02-0763.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsAntibodies, MonoclonalApoptosisBone Marrow TransplantationCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesDisease Models, AnimalFemaleGraft vs Host DiseaseHistocompatibility Antigens Class IHistocompatibility Antigens Class IIInterleukin-18Interleukin-18 Receptor alpha SubunitMiceMice, Inbred C57BLReceptors, InterleukinReceptors, Interleukin-18Severity of Illness IndexT-Lymphocytes, CytotoxicTransplantation, HomologousConceptsAllogeneic bone marrow transplantationBone marrow transplantationExperimental allogeneic bone marrow transplantationDonor T cellsIL-18T cellsAcute GVHDAcute graftHost diseaseInterleukin-18Marrow transplantationClinical allogeneic bone marrow transplantationMajor histocompatibility complex class IIHistocompatibility complex class IIEndogenous IL-18Experimental acute graftT cell subsetsParadoxical effectFas-dependent mannerLess GVHDCytotoxic functionHistopathologic parametersGVHDClass IIFas expression
2001
Interleukin-18 Regulates Acute Graft-Versus-Host Disease by Enhancing Fas-mediated Donor T Cell Apoptosis
Reddy P, Teshima T, Kukuruga M, Ordemann R, Liu C, Lowler K, Ferrara J. Interleukin-18 Regulates Acute Graft-Versus-Host Disease by Enhancing Fas-mediated Donor T Cell Apoptosis. Journal Of Experimental Medicine 2001, 194: 1433-1440. PMID: 11714750, PMCID: PMC2193680, DOI: 10.1084/jem.194.10.1433.Peer-Reviewed Original ResearchConceptsDonor T cellsIL-18Acute GVHDHost diseaseT cellsDonor T cell expansionSerum tumor necrosis factorT helper type 1Acute Graft-VersusGamma knockout miceGVHD-related mortalityMurine bone marrow transplantation modelBone marrow transplantation modelHelper type 1T cell expansionTumor necrosis factorFas-deficient miceT cell apoptosisAcute graftGraft-VersusBMT recipientsIntestinal histopathologyTh2 responsesInterleukin-18Transplantation model