2011
Kinase inhibitor Sorafenib modulates immunosuppressive cell populations in a murine liver cancer model
Cao M, Xu Y, Youn J, Cabrera R, Zhang X, Gabrilovich D, Nelson D, Liu C. Kinase inhibitor Sorafenib modulates immunosuppressive cell populations in a murine liver cancer model. Laboratory Investigation 2011, 91: 598-608. PMID: 21321535, PMCID: PMC3711234, DOI: 10.1038/labinvest.2010.205.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzenesulfonatesBone Marrow CellsCarcinoma, HepatocellularCell DivisionCell Line, TumorDisease ProgressionImmunity, CellularLiver NeoplasmsMiceMice, Inbred BALB CMyeloid CellsNiacinamidePhenylurea CompoundsProtein Kinase InhibitorsPyridinesSorafenibSpleenT-Lymphocytes, RegulatoryConceptsMyeloid-derived suppressor cellsImmunosuppressive cell populationsAnti-tumor immunityTumor-bearing hostsImmune cell populationsLiver cancer modelMurine liver cancer modelHepatocellular carcinomaCell populationsCancer modelNovel multi-kinase inhibitorSuppressive immune cell populationBALB/c miceDepletion of TregsImpact of sorafenibRegulatory T cellsAdvanced hepatocellular carcinomaTreatment of sorafenibKinase inhibitor sorafenibMulti-kinase inhibitorHCC cell growthSuppressor cellsTumor burdenC miceCancer patients
2004
A Role for Tumor Necrosis Factor-&agr;-Mediated Endothelial Apoptosis in the Development of Experimental Idiopathic Pneumonia Syndrome
Gerbitz A, Nickoloff B, Olkiewicz K, Willmarth N, Hildebrandt G, Liu C, Kobzik L, Eissner G, Holler E, Ferrara J, Cooke K. A Role for Tumor Necrosis Factor-&agr;-Mediated Endothelial Apoptosis in the Development of Experimental Idiopathic Pneumonia Syndrome. Transplantation 2004, 78: 494-502. PMID: 15446306, DOI: 10.1097/01.tp.0000128839.13674.02.Peer-Reviewed Original ResearchConceptsExperimental Idiopathic Pneumonia SyndromeAllogeneic bone marrow transplantationIdiopathic pneumonia syndromeBone marrow transplantationTumor necrosis factorLung injuryTNF-alphaPneumonia syndromeNecrosis factorVascular endotheliumBronchoalveolar lavage fluid tumor necrosis factorDevelopment of IPSPulmonary vascular endothelial cell apoptosisAlloreactive donor T cellsInflammatory mediators TNF-alphaMinor histocompatibility antigenic differencesMurine BMT systemPulmonary vascular endotheliumDonor T cellsEC apoptosisVascular endothelial cell apoptosisEndothelial cell apoptosisHost diseaseLung histopathologyPulmonary histopathologyIncreasing T-cell age reduces effector activity but preserves proliferative capacity in a murine allogeneic major histocompatibility complex-mismatched bone marrow transplant model
Friedman J, Alpdogan O, van den Brink M, Liu C, Hurwitz D, Boyd A, Kupper T, Burakoff S. Increasing T-cell age reduces effector activity but preserves proliferative capacity in a murine allogeneic major histocompatibility complex-mismatched bone marrow transplant model. Transplantation And Cellular Therapy 2004, 10: 448-460. PMID: 15205666, DOI: 10.1016/j.bbmt.2004.03.005.Peer-Reviewed Original ResearchConceptsOld T cellsT cellsSurface antigen expressionCD8 cellsAntigen expressionEffector activityT cell receptor repertoireBone marrow transplant modelCD4 T cell expansionT-cell doseSeverity of GVHDType 1 cytokinesT cell expansionAntigen-driven proliferationT-cell groupAdult T-cellT-cell ageSuccinimidyl ester labelingYoung T cellsAge-dependent declineLethal GVHDHost diseasePathologic evidenceTransplant modelCytolytic functionStabilized β-catenin promotes hepatocyte proliferation and inhibits TNFα-induced apoptosis
Shang X, Zhu H, Lin K, Tu Z, Chen J, Nelson D, Liu C. Stabilized β-catenin promotes hepatocyte proliferation and inhibits TNFα-induced apoptosis. Laboratory Investigation 2004, 84: 332-341. PMID: 14767485, DOI: 10.1038/labinvest.3700043.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBeta CateninCarcinoma, HepatocellularCell DivisionCell LineCell Line, TumorCell Transformation, NeoplasticCyclin D1Cytoskeletal ProteinsDrug StabilityGene Expression RegulationGenes, mycHepatocytesHumansLiver NeoplasmsMiceMice, SCIDMutationTrans-ActivatorsTransfectionTumor Necrosis Factor-alphaConceptsHuman hepatocellular carcinomaHepatocyte proliferationCell linesCommon malignant tumorCell proliferationImmune-deficient miceCell survival abilityLiver cell growthMurine hepatocyte cell lineCell growthHepatocyte cell lineAnchorage-independent cell growthMalignant tumorsHepatocellular carcinomaLiver cancerCyclin D1Inhibits TNFαOncogenic transformationCell apoptosisBeta-catenin mutationsAct DΒ-cateninPotential roleC-MycTumors
2003
Repifermin (keratinocyte growth factor-2) reduces the severity of graft-versus-host disease while preserving a graft-versus-leukemia effect
Clouthier S, Cooke K, Teshima T, Lowler K, Liu C, Connolly K, Ferrara J. Repifermin (keratinocyte growth factor-2) reduces the severity of graft-versus-host disease while preserving a graft-versus-leukemia effect. Transplantation And Cellular Therapy 2003, 9: 592-603. PMID: 14506661, DOI: 10.1016/s1083-8791(03)00230-1.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow TransplantationCD4 Lymphocyte CountCD8-Positive T-LymphocytesCell DivisionCell Line, TumorDisease Models, AnimalFemaleFibroblast Growth Factor 10Fibroblast Growth FactorsGraft vs Host DiseaseGraft vs Leukemia EffectHumansInterferon-gammaInterleukin-2IntestinesLipopolysaccharidesLiverLymphocyte CountMiceMice, Inbred C57BLMice, Inbred StrainsRecombinant ProteinsSpleenT-LymphocytesT-Lymphocytes, CytotoxicTransplantation, HomologousTumor Necrosis Factor-alphaConceptsBone marrow transplantationAllogeneic bone marrow transplantationAllogeneic BMT recipientsSystemic GVHDGVL effectHost diseaseBMT recipientsTumor necrosis factor alphaBeneficial GVL effectInduction of GVHDSeverity of graftToxicity of GVHDMurine BMT modelBone marrow inoculumNecrosis factor alphaT cell proliferationRecombinant human keratinocyte growth factorHuman keratinocyte growth factorKeratinocyte growth factorLeukemia effectLeukemia responseSerum levelsMarrow transplantationControl miceOrgan histopathology
2002
Flt3 ligand therapy for recipients of allogeneic bone marrow transplants expands host CD8α+ dendritic cells and reduces experimental acute graft-versus-host disease
Teshima T, Reddy P, Lowler K, KuKuruga M, Liu C, Cooke K, Ferrara J. Flt3 ligand therapy for recipients of allogeneic bone marrow transplants expands host CD8α+ dendritic cells and reduces experimental acute graft-versus-host disease. Blood 2002, 99: 1825-1832. PMID: 11861301, DOI: 10.1182/blood.v99.5.1825.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAdjuvants, ImmunologicAnimalsBone Marrow TransplantationCD8 AntigensCell DivisionCoculture TechniquesDendritic CellsDisease Models, AnimalFemaleGraft vs Host DiseaseLymphocyte ActivationMembrane ProteinsMiceMice, Inbred C57BLSurvival RateT-LymphocytesTransplantation, HomologousConceptsDendritic cellsT cell responsesAcute graftHost diseaseDonor T-cell responsesAllogeneic bone marrow transplantationAllogeneic T-cell responsesAllogeneic bone marrow transplantExperimental acute graftHost dendritic cellsPoor stimulatory capacityNormal dendritic cellsAllogeneic T cellsBone marrow transplantationTreatment of miceBone marrow transplantFL treatmentAcute GVHDGVHD mortalityDC subsetsAllogeneic lymphocytesDC numbersMarrow transplantationLigand therapyMarrow transplant