2020
Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis
Li J, Huynh L, Cornwell WD, Tang MS, Simborio H, Huang J, Kosmider B, Rogers TJ, Zhao H, Steinberg MB, Thu Thi Le L, Zhang L, Pham K, Liu C, Wang H. Electronic Cigarettes Induce Mitochondrial DNA Damage and Trigger TLR9 (Toll-Like Receptor 9)-Mediated Atherosclerosis. Arteriosclerosis Thrombosis And Vascular Biology 2020, 41: 839-853. PMID: 33380174, PMCID: PMC8608030, DOI: 10.1161/atvbaha.120.315556.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAtherosclerosisDisease Models, AnimalDNA DamageDNA, MitochondrialE-Cigarette VaporFemaleHumansInflammationInflammation MediatorsMacrophagesMaleMiceMice, Inbred C57BLMice, Knockout, ApoEMiddle AgedMitochondriaRAW 264.7 CellsSignal TransductionSmokersToll-Like Receptor 9VapingConceptsECV exposureTLR9 expressionInflammatory cytokinesClassical monocytesTLR9 activationAtherosclerotic plaquesEight-week-old ApoEUpregulation of TLR9Expression of TLR9Atherosclerotic lesion developmentOil Red O stainingToll-like receptorsDays/weekE-cig exposureMonocytes/macrophagesNormal laboratory dietRed O stainingPotential pharmacological targetElectronic cigarette useHours/dayProinflammatory cytokinesCig vaporPlasma levelsTLR9 antagonistTLR9 inhibitor
2019
Enhancement of sorafenib-mediated death of Hepatocellular carcinoma cells by Carnosic acid and Vitamin D2 analog combination
Wu Q, Wang X, Pham K, Luna A, Studzinski GP, Liu C. Enhancement of sorafenib-mediated death of Hepatocellular carcinoma cells by Carnosic acid and Vitamin D2 analog combination. The Journal Of Steroid Biochemistry And Molecular Biology 2019, 197: 105524. PMID: 31704246, PMCID: PMC7015782, DOI: 10.1016/j.jsbmb.2019.105524.Peer-Reviewed Original ResearchConceptsHepatocellular carcinomaVitamin DOral multi-kinase inhibitorTreatment of HCCAutophagy markers Beclin1Vitamin D insufficiencyCarnosic acidAdvanced hepatocellular carcinomaPromising therapeutic optionVitamin D analogsMulti-kinase inhibitorCell linesElevated protein levelsAnti-oxidant propertiesHCC cell linesHuman neoplastic cellsD insufficiencyGlobal cancer mortalityHepatocellular carcinoma cellsSystemic treatmentTherapeutic optionsCancer mortalityHCC cell deathPreclinical studiesLiver cancerTumor-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
2018
RET rearrangements are actionable alterations in breast cancer
Paratala BS, Chung JH, Williams CB, Yilmazel B, Petrosky W, Williams K, Schrock AB, Gay LM, Lee E, Dolfi SC, Pham K, Lin S, Yao M, Kulkarni A, DiClemente F, Liu C, Rodriguez-Rodriguez L, Ganesan S, Ross JS, Ali SM, Leyland-Jones B, Hirshfield KM. RET rearrangements are actionable alterations in breast cancer. Nature Communications 2018, 9: 4821. PMID: 30446652, PMCID: PMC6240119, DOI: 10.1038/s41467-018-07341-4.Peer-Reviewed Original ResearchMeSH KeywordsAnilidesAnimalsAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMiceMice, NudeMitogen-Activated Protein KinasesNIH 3T3 CellsNuclear Receptor CoactivatorsOncogene Proteins, FusionPhosphatidylinositol 3-KinasesPiperidinesProto-Oncogene Proteins c-retPyridinesQuinazolinesRas Guanine Nucleotide Exchange FactorsReceptor, ErbB-2Signal TransductionXenograft Model Antitumor AssaysConceptsBreast cancerRET amplificationRET gene alterationsMetastatic breast cancerNCOA4-RET fusionXenograft tumor formationPI3K pathwayRadiographic responseActionable alterationsLung cancerRET fusionsRET alterationsRET inhibitionIndex caseTherapeutic targetRET rearrangementsCancerGenomic profilingGene alterationsK pathwayTumor formationGene RETNon-tumorigenic cellsSubsequent treatmentOncogenic potential
2015
VEGFR 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