2012
Cyclooxygenase‐2 and Akt mediate multiple growth‐factor‐induced epithelial‐mesenchymal transition in human hepatocellular carcinoma
Ogunwobi O, Wang T, Zhang L, Liu C. Cyclooxygenase‐2 and Akt mediate multiple growth‐factor‐induced epithelial‐mesenchymal transition in human hepatocellular carcinoma. Journal Of Gastroenterology And Hepatology 2012, 27: 566-578. PMID: 22097969, PMCID: PMC3288221, DOI: 10.1111/j.1440-1746.2011.06980.x.Peer-Reviewed Original ResearchMeSH KeywordsAlbuminsAlpha 1-AntitrypsinAnimalsCadherinsCarcinoma, HepatocellularCell MovementCell TransplantationCollagen Type ICyclooxygenase 2DinoprostoneEpidermal Growth FactorEpithelial-Mesenchymal TransitionFibroblast Growth Factor 2FibronectinsGene ExpressionHepatocyte Growth FactorHumansMiceOncogene Protein v-aktRNA, Small InterferingSignal TransductionTransforming Growth Factor beta1Tumor Cells, CulturedVimentinConceptsEpithelial-mesenchymal transitionCyclooxygenase-2Hepatocellular carcinomaBasic fibroblast growth factorGrowth factorProstaglandin E2Metastatic hepatocellular carcinomaProgression of HCCEffective therapeutic strategyExpression of vimentinHepatocyte growth factorGrowth factor βHuman hepatocellular carcinomaFibroblast growth factorAssociated hepatitisChemopreventive strategiesEpidermal growth factorMultiple growth factorsTherapeutic strategiesMesenchymal changesSignificant mortalityAkt pathwayMolecular targetingCancer invasionAkt
2011
Hepatocyte growth factor upregulation promotes carcinogenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via Akt and COX-2 pathways
Ogunwobi O, Liu C. Hepatocyte growth factor upregulation promotes carcinogenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via Akt and COX-2 pathways. Clinical & Experimental Metastasis 2011, 28: 721-731. PMID: 21744257, PMCID: PMC3732749, DOI: 10.1007/s10585-011-9404-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCadherinsCarcinoma, HepatocellularCell AdhesionCell DifferentiationCell Line, TumorCell MovementCell ProliferationCyclooxygenase 2Enzyme-Linked Immunosorbent AssayEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesHepatocyte Growth FactorLiver Neoplasms, ExperimentalMiceMice, Inbred BALB CNeoplasm InvasivenessPhosphorylationProto-Oncogene Proteins c-aktReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionUp-RegulationVimentinConceptsEpithelial-mesenchymal transitionHepatocyte growth factorCyclooxygenase-2Hepatocellular carcinomaBNL cellsMarkers of EMTDevelopment of HCCAdvanced hepatocellular carcinomaCOX-2 pathwayMetastatic hepatocellular carcinomaUpregulation of HGFMesenchymal characteristicsGrowth factor upregulationE-cadherinCharacteristic epithelial morphologyCancer mortalitySubsequent metastasisEMT markersImportant causeMigratory capacityHCC cellsBNL CLCancer progressionCollagen 1Growth factor
2009
The cytolytic molecules Fas ligand and TRAIL are required for murine thymic graft-versus-host disease
Na I, Lu S, Yim N, Goldberg G, Tsai J, Rao U, Smith O, King C, Suh D, Hirschhorn-Cymerman D, Palomba L, Penack O, Holland A, Jenq R, Ghosh A, Tran H, Merghoub T, Liu C, Sempowski G, Ventevogel M, Beauchemin N, van den Brink M. The cytolytic molecules Fas ligand and TRAIL are required for murine thymic graft-versus-host disease. Journal Of Clinical Investigation 2009, 120: 343-356. PMID: 19955659, PMCID: PMC2798682, DOI: 10.1172/jci39395.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow TransplantationCASP8 and FADD-Like Apoptosis Regulating ProteinCell MovementFas Ligand ProteinGraft vs Host DiseaseLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLReceptors, OX40Receptors, TNF-Related Apoptosis-Inducing LigandStromal CellsT-LymphocytesThymus GlandTNF-Related Apoptosis-Inducing LigandTransplantation, HomologousConceptsAlloreactive T cellsDonor alloreactive T cellsThymic stromal cellsHost diseaseT cellsDeath receptor 5Thymic graftsProfound T-cell deficiencySelectin glycoprotein ligand-1Stromal cellsPeripheral T cell functionCell adhesion molecule-1Allo-BMT recipientsAllogeneic BM transplantationT-cell reconstitutionT cell deficiencyT cell functionDeath receptor FasAdhesion molecule-1Fas/FasLApoptosis-inducing ligandBMT conditioningSystemic graftP-selectin glycoprotein ligand-1Cell reconstitution
2007
β2 integrins separate graft-versus-host disease and graft-versus-leukemia effects
Liang Y, Liu C, Djeu J, Zhong B, Peters T, Scharffetter-Kochanek K, Anasetti C, Yu X. β2 integrins separate graft-versus-host disease and graft-versus-leukemia effects. Blood 2007, 111: 954-962. PMID: 17928532, PMCID: PMC2200850, DOI: 10.1182/blood-2007-05-089573.Peer-Reviewed Original ResearchConceptsT cellsHost diseaseLeukemia effectMurine allogeneic bone marrow transplantation modelAllogeneic bone marrow transplantation modelWild-type donor T cellsAllogeneic hematopoietic stem cell transplantationDonor T-cell infiltrationDonor-derived T cellsHematopoietic stem cell transplantationBeta2 integrinsAnalysis of alloreactivityLess GVHD morbidityDevelopment of GVHDDonor T cellsGVHD target organsT cell infiltrationBone marrow transplantation modelStem cell transplantationWT T cellsT cell activationGVHD morbidityGVL activityGVL effectLess GVHDIFN-γ and Fas Ligand Are Required for Graft-versus-Tumor Activity against Renal Cell Carcinoma in the Absence of Lethal Graft-versus-Host Disease
Ramirez-Montagut T, Chow A, Kochman A, Smith O, Suh D, Sindhi H, Lu S, Borsotti C, Grubin J, Patel N, Terwey T, Kim T, Heller G, Murphy G, Liu C, Alpdogan O, van den Brink M. IFN-γ and Fas Ligand Are Required for Graft-versus-Tumor Activity against Renal Cell Carcinoma in the Absence of Lethal Graft-versus-Host Disease. The Journal Of Immunology 2007, 179: 1669-1680. PMID: 17641033, DOI: 10.4049/jimmunol.179.3.1669.Peer-Reviewed Original ResearchConceptsRenal cell carcinomaMurine renal cell carcinomaT cellsCell carcinomaGVT activityHost diseaseRenca cellsIFN-gammaTumor activityAllogeneic bone marrow transplantation modelFas ligandAbsence of graftRecipients of IFNBone marrow transplantation modelMechanism of graftMembrane-bound TNF-alphaTumor-bearing miceLethal graftLethal GVHDSevere GVHDTNF-alphaTransplantation modelTransplanted miceLytic capacitySolid tumors
2006
An effective cancer vaccine modality: Lentiviral modification of dendritic cells expressing multiple cancer-specific antigens
Wang B, He J, Liu C, Chang L. An effective cancer vaccine modality: Lentiviral modification of dendritic cells expressing multiple cancer-specific antigens. Vaccine 2006, 24: 3477-3489. PMID: 16530303, PMCID: PMC1850619, DOI: 10.1016/j.vaccine.2006.02.025.Peer-Reviewed Original ResearchConceptsTumor-associated antigensDendritic cellsModification of DCsMultiple tumor-associated antigensStrong anti-tumor responsesReactive dendritic cellsAnti-tumor responseT cell responsesLentiviral vectorsCancer-specific antigensCell antigen 2Tumor-bearing miceThymidine kinase suicide geneDC vaccinesVaccine modalitiesCancer immunotherapyCancer patientsTherapeutic injectionsTherapeutic effectExtended survivalAntigen 2Danger signalsVivo eliminationCell responsesTherapeutic potential
2005
CCR2 is required for CD8-induced graft-versus-host disease
Terwey T, Kim T, Kochman A, Hubbard V, Lu S, Zakrzewski J, Ramirez-Montagut T, Eng J, Muriglan S, Heller G, Murphy G, Liu C, Budak-Alpdogan T, Alpdogan O, van den Brink M. CCR2 is required for CD8-induced graft-versus-host disease. Blood 2005, 106: 3322-3330. PMID: 16037386, PMCID: PMC1895329, DOI: 10.1182/blood-2005-05-1860.Peer-Reviewed Original ResearchConceptsCC chemokine receptor 2Hematopoietic stem cell transplantationDevelopment of GVHDT cellsT cell migrationHost diseaseAllogeneic hematopoietic stem cell transplantationDonor-derived T cellsControl of CD8Donor-derived CD8GVHD target organsMurine bone marrow transplantation modelBone marrow transplantation modelStem cell transplantationChemokine receptor 2IFN-gamma productionWild-type CD8Alloreactive proliferationDonor CD8GVHD morbidityGVT activityTumor effectMajor complicationsCCR2 signalingCell transplantationA Role for CD54 (Intercellular Adhesion Molecule-1) in Leukocyte Recruitment to the Lung During the Development of Experimental Idiopathic Pneumonia Syndrome
Gerbitz A, Ewing P, Olkiewicz K, Willmarth N, Williams D, Hildebrandt G, Wilke A, Liu C, Eissner G, Andreesen R, Holler E, Guo R, Ward P, Cooke K. A Role for CD54 (Intercellular Adhesion Molecule-1) in Leukocyte Recruitment to the Lung During the Development of Experimental Idiopathic Pneumonia Syndrome. Transplantation 2005, 79: 536-542. PMID: 15753842, DOI: 10.1097/01.tp.0000151763.16800.b0.Peer-Reviewed Original ResearchConceptsDevelopment of IPSIdiopathic pneumonia syndromeGVHD target organsBone marrow transplantationMonoclonal blocking antibodyPulmonary vascular expressionICAM-1Pneumonia syndromeLeukocyte recruitmentBlocking antibodiesVascular expressionTarget organsBronchoalveolar lavage fluid levelsExperimental Idiopathic Pneumonia SyndromeMinor histocompatibility antigenic differencesAllogeneic bone marrow transplantationEndothelial cellsAllogeneic BMT recipientsMurine BMT systemLavage fluid levelsAdhesion molecules CD54ICAM-1 deficiencyICAM-1 expressionWild-type recipientsWild-type controls
2003
Role of CXCR3-induced donor T-cell migration in acute GVHD
Duffner U, Lu B, Hildebrandt G, Teshima T, Williams D, Reddy P, Ordemann R, Clouthier S, Lowler K, Liu C, Gerard C, Cooke K, Ferrara J. Role of CXCR3-induced donor T-cell migration in acute GVHD. Experimental Hematology 2003, 31: 897-902. PMID: 14550805, DOI: 10.1016/s0301-472x(03)00198-x.Peer-Reviewed Original ResearchConceptsRole of CXCR3T cellsAcute GVHDDonor T cell expansionDonor T cell migrationDonor T cellsExpression of CXCR3GVHD target organsDonor cellsEffector T cellsBone marrow transplantation modelDonor T-cell functionMinor histocompatibility antigensT cell expansionWild-type B6Chemokine receptor CXCR3T cell functionWild-type T cellsWild-type donor cellsT cell migrationMigration of donorWild-type donorsAcute graftHost diseaseBMT recipients