2019
Tumor-intrinsic PIK3CA represses tumor immunogenecity in a model of pancreatic cancer
Sivaram N, McLaughlin PA, Han HV, Petrenko O, Jiang YP, Ballou LM, Pham K, Liu C, van der Velden A, Lin RZ. Tumor-intrinsic PIK3CA represses tumor immunogenecity in a model of pancreatic cancer. Journal Of Clinical Investigation 2019, 129: 3264-3276. PMID: 31112530, PMCID: PMC6668699, DOI: 10.1172/jci123540.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsB7-1 AntigenCell Line, TumorClass I Phosphatidylinositol 3-KinasesHistocompatibility Antigens Class IHumansLymphocytes, Tumor-InfiltratingMiceMice, KnockoutMice, SCIDNeoplasms, ExperimentalPancreatic NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionT-LymphocytesXenograft Model Antitumor AssaysConceptsPancreatic cancerT cellsT cell-deficient miceTumor-infiltrating T cellsAntigen-experienced T cellsCell-deficient miceFavorable patient outcomesOrthotopic implantation modelComplete tumor regressionMost pancreatic cancersT cell surveillanceT cell recognitionPancreatic cancer cellsMHC class IAvailable immunotherapiesAdoptive transferEffective immunotherapyTumor immunogenicityTumor regressionPancreatic tumorsPatient outcomesHost miceImmunodeficient miceCell surveillanceTumors
2015
Patient-Derived Xenograft Models for Pancreatic Adenocarcinoma Demonstrate Retention of Tumor Morphology through Incorporation of Murine Stromal Elements
Delitto D, Pham K, Vlada AC, Sarosi GA, Thomas RM, Behrns KE, Liu C, Hughes SJ, Wallet SM, Trevino JG. Patient-Derived Xenograft Models for Pancreatic Adenocarcinoma Demonstrate Retention of Tumor Morphology through Incorporation of Murine Stromal Elements. American Journal Of Pathology 2015, 185: 1297-1303. PMID: 25770474, PMCID: PMC4419203, DOI: 10.1016/j.ajpath.2015.01.016.Peer-Reviewed Original ResearchConceptsPancreatic adenocarcinoma specimensStromal elementsTumor morphologyAdenocarcinoma specimensSuccessful engraftmentXenograft modelPatient-derived xenograft modelsCancer cellsPatient-derived xenograftsPancreatic adenocarcinoma xenograftsAdenocarcinoma xenograft modelTumor-stromal interactionsPatient demographicsClinicopathologic factorsPatient survivalNonobese diabeticPancreatic adenocarcinomaSurgical specimensImmunodeficiency miceInitial implantationPathological analysisPreclinical platformAdenocarcinoma xenograftsXenograft microenvironmentTumor growthVEGFR inhibitors upregulate CXCR4 in VEGF receptor-expressing glioblastoma in a TGFβR signaling-dependent manner
Pham K, Luo D, Siemann DW, Law BK, Reynolds BA, Hothi P, Foltz G, Harrison JK. VEGFR inhibitors upregulate CXCR4 in VEGF receptor-expressing glioblastoma in a TGFβR signaling-dependent manner. Cancer Letters 2015, 360: 60-67. PMID: 25676691, PMCID: PMC7294457, DOI: 10.1016/j.canlet.2015.02.005.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAngiogenesis InhibitorsAnimalsBenzylaminesBrain NeoplasmsCell Line, TumorCell MovementCyclamsFemaleGlioblastomaHeterocyclic CompoundsHumansInterleukin-2 Receptor alpha SubunitMaleMice, Inbred NODMice, KnockoutMice, SCIDMiddle AgedNeoplasm InvasivenessPiperidinesProtein Kinase InhibitorsQuinazolinesReceptor Cross-TalkReceptors, CXCR4Receptors, Transforming Growth Factor betaReceptors, Vascular Endothelial Growth FactorSignal TransductionTime FactorsUp-RegulationXenograft Model Antitumor AssaysConceptsTGFβ/TGFβRAnti-VEGF/VEGFR therapiesSignaling-dependent mannerMechanisms of crosstalkEnhanced invasive phenotypeVEGFR inhibitorsSurvival benefitHGF/METGBM cell linesInvasive phenotypeCXCL12/CXCR4 pathwayGreater survival benefitExpression of CXCR4VEGF/VEGFRMalignant phenotypeTumor-bearing animalsUpregulation of CXCR4Alternative therapeutic strategiesGBM progressionCell linesTGFβRRecurrent tumorsCXCR4 pathwayStandard treatmentCXCR4 antagonist
2013
Expression and Functional Heterogeneity of Chemokine Receptors CXCR4 and CXCR7 in Primary Patient-Derived Glioblastoma Cells
Liu C, Pham K, Luo D, Reynolds BA, Hothi P, Foltz G, Harrison JK. Expression and Functional Heterogeneity of Chemokine Receptors CXCR4 and CXCR7 in Primary Patient-Derived Glioblastoma Cells. PLOS ONE 2013, 8: e59750. PMID: 23555768, PMCID: PMC3605406, DOI: 10.1371/journal.pone.0059750.Peer-Reviewed Original ResearchConceptsFunction of CXCR4Chemokine receptor CXCR4CXCR4-CXCR7Receptor CXCR4Common primary brain tumorPrimary human GBM cellsPrimary brain tumorsPersonalized treatment approachesTube formationSurface expressionPatient-derived GBM cell linesNew therapeutic targetsCell linesHuman GBM cellsPatient-derived glioblastoma cellsGBM cell linesClinical benefitPoor prognosisSuccessful treatmentCell surface expressionCXCR7 axisCXCL12-CXCR4Intracranial tumorsGBM patientsBrain tumors