2023
Berberine protects mice against type 2 diabetes by promoting PPARγ-FGF21-GLUT2-regulated insulin sensitivity and glucose/lipid homeostasis
Chen Y, Li Q, Zhao S, Sun L, Yin Z, Wang X, Li X, Iwakiri Y, Han J, Duan Y. Berberine protects mice against type 2 diabetes by promoting PPARγ-FGF21-GLUT2-regulated insulin sensitivity and glucose/lipid homeostasis. Biochemical Pharmacology 2023, 218: 115928. PMID: 37979703, DOI: 10.1016/j.bcp.2023.115928.Peer-Reviewed Original ResearchConceptsType 2 diabetesInsulin sensitivityGlucose/lipid homeostasisInsulin resistanceLipid metabolismFibroblast growth factor 21Glucose/lipid metabolismFGF21-dependent mannerGlucose transporter 2 expressionLipid homeostasisGrowth factor 21Liver lipid accumulationMechanism of berberineEffects of berberineRole of berberineTransporter 2 expressionExpression of PPARγGlobal knockout miceFunction of berberineMultiple therapeutic actionsRegulation of glucoseT2D treatmentT2D miceDiabetic miceCarcinoma cell lines
2019
Blockade of ROCK inhibits migration of human primary keratinocytes and malignant epithelial skin cells by regulating actomyosin contractility
Srinivasan S, Das S, Surve V, Srivastava A, Kumar S, Jain N, Sawant A, Nayak C, Purwar R. Blockade of ROCK inhibits migration of human primary keratinocytes and malignant epithelial skin cells by regulating actomyosin contractility. Scientific Reports 2019, 9: 19930. PMID: 31882703, PMCID: PMC6934852, DOI: 10.1038/s41598-019-56447-2.Peer-Reviewed Original ResearchConceptsRho-Associated Protein KinaseMyosin light chain kinaseRegulates actomyosin contractilityMyosin light chainA-431 cellsActomyosin contractilityFocal adhesionsA-431Loss of migrationPhosphorylation of myosin light chainPhosphorylated myosin light chainPrimary keratinocytesLight chain kinaseMyosin light chain kinase expressionStress fibresCarcinoma cell linesProtein kinaseHuman primary keratinocytesSkin epithelial cellsKinaseMalignant skin cellsEpidermal carcinoma cell lineSkin cellsEpithelial skin cellsPhysiological processesHuman Ovarian Cancer Tumor Formation in Severe Combined Immunodeficient (SCID) Pigs
Boettcher AN, Kiupel M, Adur MK, Cocco E, Santin AD, Bellone S, Charley SE, Blanco-Fernandez B, Risinger JI, Ross JW, Tuggle CK, Shapiro EM. Human Ovarian Cancer Tumor Formation in Severe Combined Immunodeficient (SCID) Pigs. Frontiers In Oncology 2019, 9: 9. PMID: 30723704, PMCID: PMC6349777, DOI: 10.3389/fonc.2019.00009.Peer-Reviewed Original ResearchPreclinical animal modelsSCID pigsOvarian carcinomaAnimal modelsEar tissueLate-stage diseaseLethal gynecologic malignancyOvarian cancer researchImmunodeficient pigsGynecologic malignanciesCarcinoma cell linesImmunohistochemical phenotypeCytokeratin 7Ovarian cancerXenotransplantation modelNeck musclesOrthotopic modelTumor massOvCa cellsPapillary carcinoma cell lineCarcinomaControl pigsClaudin-4Claudin-3Tumors
2018
CDKN2A/p16 deletion in head and neck cancer cells is associated with Cdk2 activation, replication stress, and vulnerability to Chk1 inhibition
Gadhikar MA, Zhang J, Shen L, Rao X, Wang J, Zhao M, Kalu NN, Johnson FM, Byers LA, Heymach J, Hittelman WN, Udayakumar D, Pandita RK, Pandita TK, Pickering CR, Redwood AB, Piwnica-Worms H, Schlacher K, Frederick MJ, Myers JN. CDKN2A/p16 deletion in head and neck cancer cells is associated with Cdk2 activation, replication stress, and vulnerability to Chk1 inhibition. Cancer Research 2018, 78: canres.2802.2017. PMID: 29229598, PMCID: PMC5811346, DOI: 10.1158/0008-5472.can-17-2802.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsApoptosisBiomarkers, TumorCarcinoma, Squamous CellCell ProliferationCheckpoint Kinase 1Cyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p18DNA ReplicationEnzyme ActivationEnzyme InhibitorsHead and Neck NeoplasmsHumansS PhaseSequence DeletionTumor Cells, CulturedConceptsBiomarker-driven strategiesHNSCC patientsS-phase arrestEarly S-phase arrestCDKN2A/Neck squamous cell carcinoma cell linesSquamous cell carcinoma cell linesSingle-agent activityCell carcinoma cell linesCell linesHypersensitive cellsCarcinoma cell linesCdk2 activationHNSCC cellsDrug dosesCertain tumorsCancer ResCopy number lossCausative factorsHypersensitivityCHK inhibitorsPanel medianMonotherapyDrug ICReplication stress
2016
Mutational landscape of uterine and ovarian carcinosarcomas implicates histone genes in epithelial–mesenchymal transition
Zhao S, Bellone S, Lopez S, Thakral D, Schwab C, English DP, Black J, Cocco E, Choi J, Zammataro L, Predolini F, Bonazzoli E, Bi M, Buza N, Hui P, Wong S, Abu-Khalaf M, Ravaggi A, Bignotti E, Bandiera E, Romani C, Todeschini P, Tassi R, Zanotti L, Odicino F, Pecorelli S, Donzelli C, Ardighieri L, Facchetti F, Falchetti M, Silasi DA, Ratner E, Azodi M, Schwartz PE, Mane S, Angioli R, Terranova C, Quick CM, Edraki B, Bilgüvar K, Lee M, Choi M, Stiegler AL, Boggon TJ, Schlessinger J, Lifton RP, Santin AD. Mutational landscape of uterine and ovarian carcinosarcomas implicates histone genes in epithelial–mesenchymal transition. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: 12238-12243. PMID: 27791010, PMCID: PMC5087050, DOI: 10.1073/pnas.1614120113.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overCarcinosarcomaClass I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistonesHumansMiddle AgedMutationOvarian NeoplasmsPTEN PhosphohydrolaseTelomeraseTumor Suppressor Protein p53Uterine NeoplasmsConceptsEpithelial-mesenchymal transitionWhole-exome sequencingHistone gene clusterMutational landscapeStable transgenic expressionExcess of mutationsMultiregion whole-exome sequencingHistone genesEvolutionary historyPhylogenetic relationshipsGene clusterHistone H2AChromosome segmentsSeparate lineagesCancer genesGenetic landscapeUterine serous carcinoma cell linesTransgenic expressionGenesCarcinoma cell linesGene TP53Frequent amplificationFrequent deletionsChromosome 6pInvasive properties
2015
Dual HER2/PIK3CA Targeting Overcomes Single-Agent Acquired Resistance in HER2-Amplified Uterine Serous Carcinoma Cell Lines In Vitro and In Vivo
Lopez S, Cocco E, Black J, Bellone S, Bonazzoli E, Predolini F, Ferrari F, Schwab CL, English DP, Ratner E, Silasi DA, Azodi M, Schwartz PE, Terranova C, Angioli R, Santin AD. Dual HER2/PIK3CA Targeting Overcomes Single-Agent Acquired Resistance in HER2-Amplified Uterine Serous Carcinoma Cell Lines In Vitro and In Vivo. Molecular Cancer Therapeutics 2015, 14: 2519-2526. PMID: 26333383, PMCID: PMC4636465, DOI: 10.1158/1535-7163.mct-15-0383.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsCell CycleCell Line, TumorCell SurvivalClass I Phosphatidylinositol 3-KinasesCystadenocarcinoma, SerousDose-Response Relationship, DrugDrug SynergismFemaleGene AmplificationHumansImidazolesImmunoblottingMice, SCIDMutationOxazepinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationQuinolinesReceptor, ErbB-2Uterine NeoplasmsXenograft Model Antitumor AssaysConceptsHER2/neu gene amplificationNeu gene amplificationUSC xenograftsUterine serous carcinomaGene amplificationUterine serous carcinoma cell linesSingle-agent therapyNovel therapeutic optionsWild-type PIK3CADose-dependent increaseIdeal therapeutic targetUSC cell linesCell linesDose-dependent declineFlow cytometry assayG0-G1 phaseCell cycle distributionOncogenic PIK3CA mutationsPercentage of cellsUSC patientsEndometrial cancerAggressive variantSerous carcinomaTherapeutic optionsCarcinoma cell linesPIK3CA oncogenic mutations represent a major mechanism of resistance to trastuzumab in HER2/neu overexpressing uterine serous carcinomas
Black JD, Lopez S, Cocco E, Bellone S, Altwerger G, Schwab CL, English DP, Bonazzoli E, Predolini F, Ferrari F, Ratner E, Silasi DA, Azodi M, Schwartz PE, Santin AD. PIK3CA oncogenic mutations represent a major mechanism of resistance to trastuzumab in HER2/neu overexpressing uterine serous carcinomas. British Journal Of Cancer 2015, 113: 1020-1026. PMID: 26325104, PMCID: PMC4651122, DOI: 10.1038/bjc.2015.306.Peer-Reviewed Original ResearchConceptsUSC cell linesCell linesPIK3CA-mutated tumorsUterine serous carcinomaHER2/neuXenograft mouse modelOncogenic PIK3CA mutationsPrimary HER2Trastuzumab treatmentSerous carcinomaCarcinoma cell linesMechanisms of resistancePIK3CA mutationsTrastuzumab efficacyMouse modelTrastuzumabMouse xenograftsHER2Tumor growthMajor mechanismOncogenic mutationsWild-type cell linesSitu hybridisationSolitomab, an EpCAM/CD3 bispecific antibody construct (BiTE), is highly active against primary uterine serous papillary carcinoma cell lines in vitro
Bellone S, Black J, English DP, Schwab CL, Lopez S, Cocco E, Bonazzoli E, Predolini F, Ferrari F, Ratner E, Silasi DA, Azodi M, Schwartz PE, Santin AD. Solitomab, an EpCAM/CD3 bispecific antibody construct (BiTE), is highly active against primary uterine serous papillary carcinoma cell lines in vitro. American Journal Of Obstetrics And Gynecology 2015, 214: 99.e1-99.e8. PMID: 26272866, PMCID: PMC4698047, DOI: 10.1016/j.ajog.2015.08.011.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, BispecificAntigens, NeoplasmAntineoplastic AgentsAscitic FluidCarcinoma, PapillaryCD3 ComplexCD4-Positive T-LymphocytesCell Adhesion MoleculesCell Line, TumorCell ProliferationCell SurvivalCoculture TechniquesCytokinesCytotoxicity, ImmunologicEpithelial Cell Adhesion MoleculeFemaleFlow CytometryHumansLymphocyte ActivationNeoplasms, Cystic, Mucinous, and SerousT-Lymphocytes, CytotoxicUterine NeoplasmsConceptsUterine serous carcinoma cell linesUterine serous carcinomaEpithelial cell adhesion moleculeCell adhesion molecule expressionCarcinoma cell linesChromium release assaysSerous carcinoma cellsPeripheral blood lymphocytesAdhesion molecule expressionCell adhesion moleculeEpithelial cell adhesion molecule (EpCAM) expressionSerous carcinomaAdhesion moleculesBlood lymphocytesMolecule expressionT cellsAscitic fluidCell linesTumor-associated T cellsT cell-mediated killingT-cell activation markersFlow cytometryTumor cellsCarcinoma cellsRobust immunologic responsesPigment Epithelium-Derived Factor (PEDF) Inhibits Wnt/β-catenin Signaling in the Liver
Protiva P, Gong J, Sreekumar B, Torres R, Zhang X, Belinsky GS, Cornwell M, Crawford SE, Iwakiri Y, Chung C. Pigment Epithelium-Derived Factor (PEDF) Inhibits Wnt/β-catenin Signaling in the Liver. Cellular And Molecular Gastroenterology And Hepatology 2015, 1: 535-549.e14. PMID: 26473164, PMCID: PMC4604042, DOI: 10.1016/j.jcmgh.2015.06.006.Peer-Reviewed Original ResearchLow-density lipoprotein receptor-related protein 6Catenin signalingWnt coreceptor low-density lipoprotein receptor-related protein 6KO liversLipoprotein receptor-related protein 6Western diet feedingEpithelium-derived factorWnt/β-cateninHuman HCC cellsHuman HCC specimensInhibits Wnt/β-cateninMultiple tumor typesPEDF knockoutCarcinoma cell linesDiet feedingKO miceWestern dietHepatocellular carcinoma cell linesHCC formationHuman hepatocellular carcinoma cell lineTumor-suppressive propertiesPigment epitheliumTumor typesWnt5a proteinControl liversThe broad‐spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF‐mutant melanoma cells in combination with other signaling pathway inhibitors
Langdon CG, Held MA, Platt JT, Meeth K, Iyidogan P, Mamillapalli R, Koo AB, Klein M, Liu Z, Bosenberg MW, Stern DF. The broad‐spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF‐mutant melanoma cells in combination with other signaling pathway inhibitors. Pigment Cell & Melanoma Research 2015, 28: 417-430. PMID: 25854919, PMCID: PMC5215495, DOI: 10.1111/pcmr.12376.Peer-Reviewed Original ResearchConceptsBRAF-mutant melanomaBRAF inhibitorsCell linesCombination of dovitinibBRAF inhibitor treatmentBRAF mutant melanoma cellsBRAF inhibitor resistanceColorectal carcinoma cell linesBRAF-mutant melanoma cell linesMelanoma cell linesCarcinoma cell linesMetastatic melanomaEffective therapyWild-type BRAF cellsInhibitor treatmentAgent inhibitsPathway inhibitorDovitinibInhibitor resistanceMelanoma cellsMelanomaSecond agentInhibitorsTreatmentIncreased Expression of Androgen Receptor mRNA in Human Renal Cell Carcinoma Cells is Associated with Poor Prognosis in Patients with Localized Renal Cell Carcinoma
Ha Y, Lee G, Modi P, Kwon Y, Ahn H, Kim W, Kim I. Increased Expression of Androgen Receptor mRNA in Human Renal Cell Carcinoma Cells is Associated with Poor Prognosis in Patients with Localized Renal Cell Carcinoma. Journal Of Urology 2015, 194: 1441-1448. PMID: 25796113, DOI: 10.1016/j.juro.2015.03.078.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overBiomarkers, TumorBlotting, WesternCarcinoma, Renal CellCell Line, TumorDisease ProgressionFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansKidney NeoplasmsMaleMiddle AgedNeoplasm StagingPrognosisReal-Time Polymerase Chain ReactionReceptors, AndrogenRetrospective StudiesRNA, NeoplasmTime FactorsYoung AdultConceptsRenal cell carcinomaAndrogen receptor mRNA expressionReceptor mRNA expression levelsCancer-specific survivalCell carcinomaCell carcinoma cell linesReceptor mRNA expressionHuman renal cell carcinoma cell linesRenal cell carcinoma cell linesAndrogen receptorMRNA expression levelsSpecific survivalCarcinoma cell linesMultivariate Cox regression analysisLocalized Renal Cell CarcinomaMRNA expressionT2 renal cell carcinomaCell linesPathological stage T1Androgen receptor expressionCox regression analysisKaplan-Meier estimatesReceptor-positive cell linesChain reactionPositive renal cell carcinomas
2014
HRAS mutations and resistance to the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib in head and neck squamous cell carcinoma cells
Hah JH, Zhao M, Pickering CR, Frederick MJ, Andrews GA, Jasser SA, Fooshee DR, Milas ZL, Galer C, Sano D, William WN, Kim E, Heymach J, Byers LA, Papadimitrakopoulou V, Myers JN. HRAS mutations and resistance to the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib in head and neck squamous cell carcinoma cells. Head & Neck 2014, 36: 1547-1554. PMID: 24123531, PMCID: PMC4010580, DOI: 10.1002/hed.23499.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCarcinoma, Squamous CellCell Line, TumorCell ProliferationDown-RegulationDrug Resistance, NeoplasmErlotinib HydrochlorideHead and Neck NeoplasmsHumansMiceMolecular Targeted TherapyMutationProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)QuinazolinesSensitivity and SpecificitySignal TransductionSquamous Cell Carcinoma of Head and NeckTransfectionConceptsShort hairpin RNACell linesHRAS expressionErlotinib sensitivityErlotinib-sensitive cell linesErlotinib-resistant cell linesErlotinib resistanceHras mutationsNeck squamous cell carcinoma cellsEpidermal growth factor receptor tyrosine kinase inhibitorsGrowth factor receptor tyrosine kinase inhibitorsEpidermal growth factor receptor (EGFR) tyrosine kinase inhibitor erlotinibNeck squamous cell carcinoma cell linesSquamous cell carcinoma cellsTyrosine kinase inhibitor erlotinibPanel of headReceptor tyrosine kinase inhibitorsHairpin RNAHNSCC cell linesSquamous cell carcinoma cell linesCell carcinoma cell linesCarcinoma cell linesKinase inhibitor erlotinibTyrosine kinase inhibitorsMutationsThe ATP-Competitive mTOR Inhibitor INK128 Enhances In Vitro and In Vivo Radiosensitivity of Pancreatic Carcinoma Cells
Hayman T, Wahba A, Rath B, Bae H, Kramp T, Shankavaram U, Camphausen K, Tofilon P. The ATP-Competitive mTOR Inhibitor INK128 Enhances In Vitro and In Vivo Radiosensitivity of Pancreatic Carcinoma Cells. Clinical Cancer Research 2014, 20: 110-119. PMID: 24198241, PMCID: PMC3947297, DOI: 10.1158/1078-0432.ccr-13-2136.Peer-Reviewed Original ResearchConceptsCap-complex formationGene translationPancreatic carcinoma cellsMTOR activityPancreatic carcinoma cell linesCell linesDNA double-strand breaksATP-competitive mTOR inhibitorsCarcinoma cellsΓH2AX fociCarcinoma cell linesPolysome-bound mRNADouble-strand breaksRadiation-induced γH2AX fociAberrant mTOR activityComplex formationDNA repairFibroblast cell lineMicroarray analysisRegulatory roleINK128Normal fibroblast cell lineMTOR inhibitionVivo radiosensitivityClonogenic survival
2013
17Beta-Estradiol Promotes Aggressive Laryngeal Cancer Through Membrane-Associated Estrogen Receptor-Alpha 36
Schwartz N, Chaudhri RA, Hadadi A, Schwartz Z, Boyan BD. 17Beta-Estradiol Promotes Aggressive Laryngeal Cancer Through Membrane-Associated Estrogen Receptor-Alpha 36. Discover Oncology 2013, 5: 22-32. PMID: 24081562, PMCID: PMC3947116, DOI: 10.1007/s12672-013-0161-y.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsApoptosisCarcinogenesisCarcinomaCell ProliferationCell SurvivalDrug Resistance, NeoplasmEstradiolEstrogen Receptor alphaFemaleHeLa CellsHumansLaryngeal NeoplasmsLymphatic MetastasisMaleMembrane ProteinsMiddle AgedMolecular Targeted TherapyNeoplasm StagingNeovascularization, PathologicPhospholipase DProtein IsoformsProtein Kinase CVascular Endothelial Growth Factor AConceptsLaryngeal cancerMembrane associated estrogen receptorsLymph node metastasisRole of E2Estrogen receptor alphaLaryngeal carcinoma cell lineSecondary sex organsChemotherapy-induced apoptosisAntiestrogen therapyNode metastasisCarcinoma cell linesLaryngeal tumorsEstrogen receptorReceptor alphaERα36Metastatic factorsSimilar associationCompelling evidenceCytoplasmic receptorsCancerTumor samplesAntiapoptotic effectNovel drugsClinical analysisE2 responsivenessHER2/neu gene amplification determines the sensitivity of uterine serous carcinoma cell lines to AZD8055, a novel dual mTORC1/2 inhibitor
English DP, Roque DM, Carrara L, Lopez S, Bellone S, Cocco E, Bortolomai I, Schwartz PE, Rutherford T, Santin AD. HER2/neu gene amplification determines the sensitivity of uterine serous carcinoma cell lines to AZD8055, a novel dual mTORC1/2 inhibitor. Gynecologic Oncology 2013, 131: 753-758. PMID: 24012800, DOI: 10.1016/j.ygyno.2013.08.033.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsCarcinoma, PapillaryCell Line, TumorCystadenocarcinoma, SerousFemaleGene AmplificationHumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MorpholinesMultiprotein ComplexesProtein Kinase InhibitorsReceptor, ErbB-2TOR Serine-Threonine KinasesUterine NeoplasmsConceptsUSC cell linesC-erbB2 gene amplificationUterine serous carcinoma cell linesDual mTORC1/2 inhibitorCarcinoma cell linesC-erbB2Cell linesGene amplificationMTORC1/2 inhibitorsPrimary USC cell linesHER2/neu gene amplificationG0/G1 cell cycle phaseDose-dependent increaseHigh HER-2HER2/neuNeu gene amplificationDose-dependent declinePercentage of cellsUSC patientsHER-2Cell cycle profileDifferential growth inhibitionG1 cell cycle phasePS6 levelsTherapeutic agentsOncogenic PIK3CA gene mutations and HER2/neu gene amplifications determine the sensitivity of uterine serous carcinoma cell lines to GDC-0980, a selective inhibitor of Class I PI3 kinase and mTOR kinase (TORC1/2)
English DP, Bellone S, Cocco E, Bortolomai I, Pecorelli S, Lopez S, Silasi DA, Schwartz PE, Rutherford T, Santin AD. Oncogenic PIK3CA gene mutations and HER2/neu gene amplifications determine the sensitivity of uterine serous carcinoma cell lines to GDC-0980, a selective inhibitor of Class I PI3 kinase and mTOR kinase (TORC1/2). American Journal Of Obstetrics And Gynecology 2013, 209: 465.e1-465.e9. PMID: 23891627, DOI: 10.1016/j.ajog.2013.07.020.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntineoplastic AgentsBridged Bicyclo Compounds, HeterocyclicCarcinoma, PapillaryCell Line, TumorClass I Phosphatidylinositol 3-KinasesDrug Resistance, NeoplasmEndometrial NeoplasmsFemaleGene AmplificationGenes, erbB-2HumansIn Situ Hybridization, FluorescenceMiddle AgedMutationPhosphatidylinositol 3-KinasesPyrimidinesTOR Serine-Threonine KinasesConceptsClass I PI3-kinasePI3-kinaseC-erbB2 gene amplificationOncogenic PIK3CA mutationsMTOR kinaseCell linesGene amplificationUterine serous carcinoma cell linesDownstream cellular responsesCarcinoma cell linesUSC cell linesGene mutationsCellular responsesKinaseDifferential growth inhibitionDNA sequencingDirect DNA sequencingMutationsSitu hybridizationUse of GDCGrowth inhibitionExon 9HER2/neu gene amplificationFishPrimary USC cell linesAn Epithelial–Mesenchymal Transition Gene Signature Predicts Resistance to EGFR and PI3K Inhibitors and Identifies Axl as a Therapeutic Target for Overcoming EGFR Inhibitor Resistance
Byers LA, Diao L, Wang J, Saintigny P, Girard L, Peyton M, Shen L, Fan Y, Giri U, Tumula PK, Nilsson MB, Gudikote J, Tran H, Cardnell RJ, Bearss DJ, Warner SL, Foulks JM, Kanner SB, Gandhi V, Krett N, Rosen ST, Kim ES, Herbst RS, Blumenschein GR, Lee JJ, Lippman SM, Ang KK, Mills GB, Hong WK, Weinstein JN, Wistuba II, Coombes KR, Minna JD, Heymach JV. An Epithelial–Mesenchymal Transition Gene Signature Predicts Resistance to EGFR and PI3K Inhibitors and Identifies Axl as a Therapeutic Target for Overcoming EGFR Inhibitor Resistance. Clinical Cancer Research 2013, 19: 279-290. PMID: 23091115, PMCID: PMC3567921, DOI: 10.1158/1078-0432.ccr-12-1558.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxl Receptor Tyrosine KinaseCarcinoma, Non-Small-Cell LungCell Line, TumorCluster AnalysisDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionErbB ReceptorsGene Expression ProfilingHumansLung NeoplasmsMiceNeoplasm MetastasisPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProteomeProteomicsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesRecurrenceReproducibility of ResultsConceptsEpithelial-mesenchymal transitionPotential therapeutic targetEGFR inhibitor resistanceTherapeutic targetEMT signatureInhibitor resistanceMesenchymal transition gene signatureMesenchymal cellsCell linesBiomarker-Integrated ApproachesPI3K/Akt pathway inhibitorNon-small cell lung carcinoma cell lineEGFR mutation statusReceptor tyrosine kinase AXLNSCLC cell linesPI3K/Akt inhibitorCell lung carcinoma cell lineGene expression profilesTyrosine kinase AXLLung carcinoma cell linePI3K inhibitorsDrug response analysisAkt pathway inhibitorCarcinoma cell linesErlotinib resistance
2012
Targeted Delivery of Chemotherapy Agents Using a Liver Cancer-Specific Aptamer
Meng L, Yang L, Zhao X, Zhang L, Zhu H, Liu C, Tan W. Targeted Delivery of Chemotherapy Agents Using a Liver Cancer-Specific Aptamer. PLOS ONE 2012, 7: e33434. PMID: 22558072, PMCID: PMC3338807, DOI: 10.1371/journal.pone.0033434.Peer-Reviewed Original ResearchConceptsAptamer-drug conjugatesCancer-specific aptamersAntitumor agent doxorubicinDOX conjugatesIntercalation methodAptamerCell viability testTargeted deliveryConjugatesCancer cellsTarget proteinsAgent doxorubicinPotential candidateCell linesDOXEfficiency of chemotherapyLiver cancer cellsNonspecific uptakeTarget specificityAvailable aptamersCarcinoma cell linesChemotherapy agentsHepatocellular carcinoma cell linesHuman hepatocellular carcinoma cell linePromising method
2011
Primary human cervical carcinoma cells require human papillomavirus E6 and E7 expression for ongoing proliferation
Magaldi TG, Almstead LL, Bellone S, Prevatt EG, Santin AD, DiMaio D. Primary human cervical carcinoma cells require human papillomavirus E6 and E7 expression for ongoing proliferation. Virology 2011, 422: 114-124. PMID: 22056390, PMCID: PMC3229657, DOI: 10.1016/j.virol.2011.10.012.Peer-Reviewed Original ResearchConceptsCervical carcinoma cellsCervical cancer cellsHuman papillomavirus E6Human cervical carcinoma cellsCarcinoma cellsPrimary cervical cancer cellsCancer cellsPapillomavirus E6Cervical carcinoma cell linesE2 proteinHuman cervical cancer cellsCarcinoma cell linesE7 expressionE7 oncogenesLow passage numberSerum-free conditionsCell surface receptorsSV40 infectionTumor suppressor pathwayCell linesPrimary cellsViral vectorsE6Suppressor pathwayPassage numberHer2/neu extracellular domain shedding in uterine serous carcinoma: implications for immunotherapy with trastuzumab
Todeschini P, Cocco E, Bellone S, Varughese J, Lin K, Carrara L, Guzzo F, Buza N, Hui P, Silasi DA, Ratner E, Azodi M, Schwartz PE, Rutherford TJ, Pecorelli S, Santin AD. Her2/neu extracellular domain shedding in uterine serous carcinoma: implications for immunotherapy with trastuzumab. British Journal Of Cancer 2011, 105: 1176-1182. PMID: 21915118, PMCID: PMC3208497, DOI: 10.1038/bjc.2011.369.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overAntibodies, Monoclonal, HumanizedAntibody-Dependent Cell CytotoxicityAntineoplastic AgentsCulture Media, ConditionedFemaleFlow CytometryGenes, erbB-2HumansImmunohistochemistryImmunotherapyIn Situ Hybridization, FluorescenceMiddle AgedReal-Time Polymerase Chain ReactionTrastuzumabUterine NeoplasmsConceptsAntibody-dependent cell-mediated cytotoxicityTrastuzumab-mediated antibody-dependent cell-mediated cytotoxicityUSC cell linesHER2/neu expressionUSC patientsNeu expressionHER2/ECD levelsCell linesUterine serous carcinoma cell linesCell-mediated cytotoxicityUterine serous carcinomaChromium release assaysHER2/neuFISH-positive tumorsC-erbB2 gene amplificationTrastuzumab-induced cytotoxicityNeu tumorsHealthy womenSerous carcinomaCarcinoma cell linesReal-time PCRTherapeutic effectC-erbB2 genePatients
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply