2025
Preclinical Activity of Datopotamab Deruxtecan, an Antibody-Drug Conjugate Targeting Trophoblast Cell-Surface Antigen 2, in Uterine Serous Carcinoma.
Greenman M, Demirkiran C, Bellone S, Hartwich T, McNamara B, Ettorre V, Santin N, Sethi N, Yang-Hartwich Y, Papatla K, Ratner E, Santin A. Preclinical Activity of Datopotamab Deruxtecan, an Antibody-Drug Conjugate Targeting Trophoblast Cell-Surface Antigen 2, in Uterine Serous Carcinoma. Cancer Research Communications 2025, 5: 774-782. PMID: 40299780, PMCID: PMC12062949, DOI: 10.1158/2767-9764.crc-25-0057.Peer-Reviewed Original ResearchConceptsTrophoblast cell surface antigen 2Uterine serous carcinomaAntibody-dependent cell-mediated cytotoxicityAntibody-drug conjugatesCell-mediated cytotoxicitySerous carcinomaPreclinical activityCell linesTargets trophoblast cell-surface antigen-2Presence of peripheral blood lymphocytesTreatment of uterine serous carcinomaInduce antibody-dependent cell-mediated cytotoxicityPrimary USC cell linesRecurrent uterine serous carcinomaUSC xenograftsUterine serous carcinoma cell linesAntigen 2In vivoPrimary tumor cell linesTROP2 overexpressionBiomarker-targeted therapiesControl ADCChromium release assayHigher recurrence rateTumor growth suppression
2024
Preclinical evaluation of avutometinib and defactinib in high‐grade endometrioid endometrial cancer
Hartwich T, Mansolf M, Demirkiran C, Greenman M, Bellone S, McNamara B, Nandi S, Alexandrov L, Yang‐Hartwich Y, Coma S, Pachter J, Santin A. Preclinical evaluation of avutometinib and defactinib in high‐grade endometrioid endometrial cancer. Cancer Medicine 2024, 13: e70210. PMID: 39240189, PMCID: PMC11378359, DOI: 10.1002/cam4.70210.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsBenzamidesCarcinoma, EndometrioidCell Line, TumorCell ProliferationEndometrial NeoplasmsExome SequencingFemaleFocal Adhesion Kinase 1HumansImidazolesMiceNeoplasm GradingOxazepinesProtein Kinase InhibitorsPyrazinesSulfonamidesXenograft Model Antitumor AssaysConceptsFocal adhesion kinaseWhole-exome sequencingEndometrial cancer cell linesVS-4718Cell linesRas/MAPK pathwayPhosphorylated focal adhesion kinaseWestern blot assayWhole-exome sequencing resultsRAF/MEK inhibitionEAC cell linesBlot assayP-FAKGenetic landscapeCell cycleEndometrial cancerGenetic derangementsDefactinibP-MEKGrowth inhibitionRAF/MEKRas/MAPKCell viabilityP-ERKHigh-grade endometrial cancer
2023
Uterine leiomyosarcomas harboring MAP2K4 gene amplification are sensitive in vivo to PLX8725, a novel MAP2K4 inhibitor
McNamara B, Harold J, Manavella D, Bellone S, Mutlu L, Hartwich T, Zipponi M, Yang-Hartwich Y, Demirkiran C, Verzosa M, Yang K, Choi J, Dong W, Buza N, Hui P, Altwerger G, Huang G, Andikyan V, Clark M, Ratner E, Azodi M, Schwartz P, Burton E, Inagaki H, Albers A, Zhang C, Bollag G, Schlessinger J, Santin A. Uterine leiomyosarcomas harboring MAP2K4 gene amplification are sensitive in vivo to PLX8725, a novel MAP2K4 inhibitor. Gynecologic Oncology 2023, 172: 65-71. PMID: 36958197, PMCID: PMC10192120, DOI: 10.1016/j.ygyno.2023.03.009.Peer-Reviewed Original ResearchConceptsUterine leiomyosarcomaPDX modelsGain of functionMedian overall survivalPhase I trialOral gavage dailyVivo activityTumor growth inhibitionTumor volume differencesTumor cell proliferationOverall survivalTolerable toxicityI trialOral treatmentTreatment cohortsGavage dailyAggressive tumorsSCID miceULMS patientsPK studiesTumor samplesWestern blotCell proliferationControl vehicleLeiomyosarcomaTrastuzumab deruxtecan (DS-8201a), a HER2-targeting antibody–drug conjugate with topoisomerase I inhibitor payload, shows antitumor activity in uterine and ovarian carcinosarcoma with HER2/neu expression
Mauricio D, Bellone S, Mutlu L, McNamara B, Manavella D, Demirkiran C, Verzosa M, Buza N, Hui P, Hartwich T, Harold J, Yang-Hartwich Y, Zipponi M, Altwerger G, Ratner E, Huang G, Clark M, Andikyan V, Azodi M, Schwartz P, Santin A. Trastuzumab deruxtecan (DS-8201a), a HER2-targeting antibody–drug conjugate with topoisomerase I inhibitor payload, shows antitumor activity in uterine and ovarian carcinosarcoma with HER2/neu expression. Gynecologic Oncology 2023, 170: 38-45. PMID: 36610380, PMCID: PMC10445234, DOI: 10.1016/j.ygyno.2022.12.018.Peer-Reviewed Original ResearchConceptsHER2/neu expressionDS-8201aAntibody-drug conjugatesNeu expressionCS cell linesTrastuzumab deruxtecanOvarian carcinosarcomaTopoisomerase I inhibitor payloadCell linesAggressive gynecologic malignancyLimited therapeutic optionsEffective antibody-drug conjugatesCarcinosarcoma cell lineGynecologic malignanciesTherapeutic optionsIsotype controlSarcomatous elementsXenograft modelBystander killingFlow cytometryTumor cellsCarcinosarcomaAntitumor activityVivo studiesVivo activity
2022
Elimusertib (BAY1895344), a novel ATR inhibitor, demonstrates in vivo activity in ATRX mutated models of uterine leiomyosarcoma
Harold J, Bellone S, Manavella D, Mutlu L, McNamara B, Hartwich T, Zipponi M, Yang-Hartwich Y, Demirkiran C, Verzosa M, Choi J, Dong W, Buza N, Hui P, Altwerger G, Huang G, Andikyan V, Clark M, Ratner E, Azodi M, Schwartz P, Santin A. Elimusertib (BAY1895344), a novel ATR inhibitor, demonstrates in vivo activity in ATRX mutated models of uterine leiomyosarcoma. Gynecologic Oncology 2022, 168: 157-165. PMID: 36442427, PMCID: PMC9797429, DOI: 10.1016/j.ygyno.2022.11.014.Peer-Reviewed Original ResearchConceptsPatient-derived xenograftsUterine leiomyosarcomaVivo activityVehicle control treatmentMedian overall survivalTumor volume differencesOral scheduleWestern blot analysisOverall survivalOral gavageAggressive malignancyPDX modelsClinical trialsSCID miceTumor measurementsULMS patientsSignificant growth inhibitionNovel ATR inhibitorTumor samplesSignificant toxicityWestern blotKinase inhibitorsATRX mutationsGene mutationsControl vehicle
2021
A Benzenesulfonamide-based Mitochondrial Uncoupler Induces Endoplasmic Reticulum Stress and Immunogenic Cell Death in Epithelial Ovarian Cancer
Bi F, Jiang Z, Park W, Hartwich TMP, Ge Z, Chong KY, Yang K, Morrison MJ, Kim D, Kim J, Zhang W, Kril LM, Watt DS, Liu C, Yang-Hartwich Y. A Benzenesulfonamide-based Mitochondrial Uncoupler Induces Endoplasmic Reticulum Stress and Immunogenic Cell Death in Epithelial Ovarian Cancer. Molecular Cancer Therapeutics 2021, 20: molcanther.mct-21-0396-a.2021. PMID: 34625503, PMCID: PMC8643344, DOI: 10.1158/1535-7163.mct-21-0396.Peer-Reviewed Original ResearchConceptsEpithelial ovarian cancerImmunogenic cell deathOvarian cancerTumor progressionAntitumor adaptive immune responsesDamage-associated molecular patternsCancer cellsMitochondrial uncouplerAdaptive immune responsesOvarian cancer modelCause of deathCurrent chemotherapeutic agentsNew therapeutic strategiesOvarian cancer cellsCancer cell proliferationCell deathEndoplasmic reticulum stressGynecologic malignanciesClinical outcomesEndoplasmic reticulum stress sensorNew anticancer therapiesPeritoneal fluidInduces Endoplasmic Reticulum StressImmune responseAbdominal cavity
2020
Identification of miPEP133 as a novel tumor-suppressor microprotein encoded by miR-34a pri-miRNA
Kang M, Tang B, Li J, Zhou Z, Liu K, Wang R, Jiang Z, Bi F, Patrick D, Kim D, Mitra AK, Yang-Hartwich Y. Identification of miPEP133 as a novel tumor-suppressor microprotein encoded by miR-34a pri-miRNA. Molecular Cancer 2020, 19: 143. PMID: 32928232, PMCID: PMC7489042, DOI: 10.1186/s12943-020-01248-9.Peer-Reviewed Original ResearchConceptsNon-coding RNA transcriptsNasopharyngeal carcinomaCancer cell linesP53 transcriptional activationPrognostic markerTumor suppressor functionAmino acid residuesCell linesTumor growthNovel microproteinWild-type p53Cellular functionsMetastatic nasopharyngeal carcinomaTranscriptional activationPotential prognostic markerMitochondrial membraneUnfavorable prognostic markerCervical cancer cell linesRNA transcriptsMitochondrial massTumor suppressorMiR-34a expressionAcid residuesNormal human colonNPC clinical samplesIn vivo modeling of metastatic human high-grade serous ovarian cancer in mice
Kim O, Park EY, Klinkebiel DL, Pack SD, Shin YH, Abdullaev Z, Emerson RE, Coffey DM, Kwon SY, Creighton CJ, Kwon S, Chang EC, Chiang T, Yatsenko AN, Chien J, Cheon DJ, Yang-Hartwich Y, Nakshatri H, Nephew KP, Behringer RR, Fernández FM, Cho CH, Vanderhyden B, Drapkin R, Bast RC, Miller KD, Karpf AR, Kim J. In vivo modeling of metastatic human high-grade serous ovarian cancer in mice. PLOS Genetics 2020, 16: e1008808. PMID: 32497036, PMCID: PMC7297383, DOI: 10.1371/journal.pgen.1008808.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsCell Line, TumorChromosomal InstabilityCystadenocarcinoma, SerousDEAD-box RNA HelicasesDisease Models, AnimalDNA RepairDrug Resistance, NeoplasmDrug Screening Assays, AntitumorFeasibility StudiesFemaleHumansMiceMice, KnockoutMutationNeoplasm GradingNeoplasm MetastasisOvarian NeoplasmsPeritoneal NeoplasmsPrimary Cell CulturePTEN PhosphohydrolaseRibonuclease IIITumor Suppressor Protein p53ConceptsHigh-grade serous carcinomaHuman HGSCHigh-grade serous ovarian cancerSerous ovarian cancerOvarian cancerPeritoneal metastasisHuman high-grade serous ovarian cancerMetastatic ovarian cancerOvarian cancer typesHuman cancer metastasisHuman cancer mortalityHemorrhagic ascitesClinical metastasisHistopathological similaritiesSerous carcinomaCancer mortalityFallopian tubeMurine modelPeritoneal cavityMouse modelPotential therapyMouse deathMetastasisCancer typesCancer metastasis
2018
Mutational landscape of primary, metastatic, and recurrent ovarian cancer reveals c-MYC gains as potential target for BET inhibitors
Li C, Bonazzoli E, Bellone S, Choi J, Dong W, Menderes G, Altwerger G, Han C, Manzano A, Bianchi A, Pettinella F, Manara P, Lopez S, Yadav G, Riccio F, Zammataro L, Zeybek B, Yang-Hartwich Y, Buza N, Hui P, Wong S, Ravaggi A, Bignotti E, Romani C, Todeschini P, Zanotti L, Zizioli V, Odicino F, Pecorelli S, Ardighieri L, Silasi DA, Litkouhi B, Ratner E, Azodi M, Huang GS, Schwartz PE, Lifton RP, Schlessinger J, Santin AD. Mutational landscape of primary, metastatic, and recurrent ovarian cancer reveals c-MYC gains as potential target for BET inhibitors. Proceedings Of The National Academy Of Sciences Of The United States Of America 2018, 116: 619-624. PMID: 30584090, PMCID: PMC6329978, DOI: 10.1073/pnas.1814027116.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsAzepinesBRCA1 ProteinBRCA2 ProteinCell Line, TumorClass I Phosphatidylinositol 3-KinasesFemaleHumansMiceMutationNeoplasm MetastasisNeoplasm Recurrence, LocalOvarian NeoplasmsProteinsProto-Oncogene Proteins c-mycTriazolesTumor Suppressor Protein p53Xenograft Model Antitumor AssaysConceptsOvarian cancerWhole-exome sequencingC-myc amplificationRecurrent tumorsPrimary tumorBET inhibitorsChemotherapy-resistant diseaseRecurrent ovarian cancerLethal gynecologic malignancyBilateral ovarian cancerChemotherapy-resistant tumorsPrimary metastatic tumorsMutational landscapeSomatic mutationsFresh-frozen tumorsGynecologic malignanciesMetastatic tumorsPrimary cell linesC-MYC gainPIK3CA amplificationTranscoelomic metastasisTherapeutic targetPatientsMetastatic abilityTumors
2016
TRX-E-002-1 Induces c-Jun–Dependent Apoptosis in Ovarian Cancer Stem Cells and Prevents Recurrence In Vivo
Alvero AB, Heaton A, Lima E, Pitruzzello M, Sumi N, Yang-Hartwich Y, Cardenas C, Steinmacher S, Silasi DA, Brown D, Mor G. TRX-E-002-1 Induces c-Jun–Dependent Apoptosis in Ovarian Cancer Stem Cells and Prevents Recurrence In Vivo. Molecular Cancer Therapeutics 2016, 15: 1279-1290. PMID: 27196760, DOI: 10.1158/1535-7163.mct-16-0005.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell Line, TumorCell ProliferationCell SurvivalCisplatinDrug Resistance, NeoplasmDrug SynergismFemaleFlavonoidsGene Expression Regulation, NeoplasticHumansMiceNeoplasm Recurrence, LocalNeoplasm TransplantationNeoplastic Stem CellsOvarian NeoplasmsPhosphorylationProto-Oncogene Proteins c-junSignal TransductionXenograft Model Antitumor AssaysConceptsCancer stem cellsOvarian cancer cellsTumor burdenOvarian cancerCancer cellsChemoresistant cancer stem cellsOvarian cancer stem cellsIntraperitoneal tumor burdenRecurrent ovarian cancerBest therapeutic optionManagement of patientsCombination of cisplatinEpithelial ovarian cancerCell deathStem cellsTumor repairDisease recurrenceMaintenance treatmentPatient survivalTherapeutic optionsHigh mortalityStemness propertiesMonotherapyDeathVehicle control
2014
Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence
Sumi NJ, Lima E, Pizzonia J, Orton SP, Craveiro V, Joo W, Holmberg JC, Gurrea M, Yang-Hartwich Y, Alvero A, Mor G. Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence. Journal Of Visualized Experiments 2014, 51815. PMID: 25407815, PMCID: PMC4353409, DOI: 10.3791/51815.Peer-Reviewed Original ResearchConceptsRecurrent ovarian cancerOvarian cancerVisible light rangeAnatomical locationOptical imaging platformAvailable chemotherapy agentsLethal gynecologic malignancyOvarian cancer recurrenceEpithelial ovarian cancerNovel therapy optionsAppropriate animal modelsMultiple angular positionsLight rangeIdentification of tumorsGynecologic malignanciesRecurrent diseaseSurgical debulkingChemoresistant diseaseCombination chemotherapyClinical profileNon-invasive imagingTherapy optionsCancer recurrenceX-rayChemotherapy agentsp53 protein aggregation promotes platinum resistance in ovarian cancer
Yang-Hartwich Y, Soteras MG, Lin ZP, Holmberg J, Sumi N, Craveiro V, Liang M, Romanoff E, Bingham J, Garofalo F, Alvero A, Mor G. p53 protein aggregation promotes platinum resistance in ovarian cancer. Oncogene 2014, 34: 3605-3616. PMID: 25263447, DOI: 10.1038/onc.2014.296.Peer-Reviewed Original ResearchConceptsPro-apoptotic functionP53 aggregationProtein aggregationP53 aggregatesNormal transcriptional activationTwo-dimensional gel electrophoresisCancer cellsCancer cell survivalKey transcriptional factorGenetic mutationsHigh-grade serous ovarian carcinomaP53 inactivationP53 proteinStem cell propertiesCancer stem cell propertiesCellular homeostasisTranscriptional activationCancer stem cellsTranscriptional factorsTumor-initiating capacityP53 turnoverCell survivalHGSOC cellsStem cellsPotential therapeutic targetOvulation and extra-ovarian origin of ovarian cancer
Yang-Hartwich Y, Gurrea-Soteras M, Sumi N, Joo WD, Holmberg JC, Craveiro V, Alvero AB, Mor G. Ovulation and extra-ovarian origin of ovarian cancer. Scientific Reports 2014, 4: 6116. PMID: 25135607, PMCID: PMC4137344, DOI: 10.1038/srep06116.Peer-Reviewed Original ResearchConceptsOvarian cancerExtra-ovarian originMalignant cellsChemokines/cytokinesOvarian surface epitheliumBetter prevention strategiesPotential molecular mechanismsFallopian tubeLate diagnosisOvarian localizationGastrointestinal tractSDF-1Mortality ratePrevention strategiesSurface epitheliumMain chemoattractantVivo modelLethal diseaseEx vivoCancerEarly detectionSpecific markersOvulationOvariesTumors
2013
Phenotypic modifications in ovarian cancer stem cells following Paclitaxel treatment
Craveiro V, Yang-Hartwich Y, Holmberg JC, Joo WD, Sumi NJ, Pizzonia J, Griffin B, Gill SK, Silasi DA, Azodi M, Rutherford T, Alvero AB, Mor G. Phenotypic modifications in ovarian cancer stem cells following Paclitaxel treatment. Cancer Medicine 2013, 2: 751-762. PMID: 24403249, PMCID: PMC3892380, DOI: 10.1002/cam4.115.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Agents, PhytogenicCarcinoma, Ovarian EpithelialDrug Resistance, NeoplasmFemaleHEK293 CellsHumansHyaluronan ReceptorsMiceMice, NudeMyeloid Differentiation Factor 88Neoplasms, Glandular and EpithelialNeoplastic Stem CellsOvarian NeoplasmsPaclitaxelPhenotypeRecurrenceSnail Family Transcription FactorsTranscription FactorsTumor BurdenXenograft Model Antitumor AssaysConceptsEpithelial ovarian cancerRecurrent epithelial ovarian cancerOvarian cancer stem cellsEOC stem cellsCancer stem cellsQuantitative polymerase chain reactionRecurrent diseaseOvarian cancerEOC cellsVivo ovarian cancer modelsStem cellsDoses of paclitaxelLethal gynecologic malignancyOvarian cancer modelProcess of recurrenceWestern blot analysisMaintenance therapyGynecologic malignanciesPrimary diseaseAggressive diseaseEOC patientsPrimary tumorPolymerase chain reactionAggressive phenotypePaclitaxel treatmentTLR2 enhances ovarian cancer stem cell self-renewal and promotes tumor repair and recurrence
Chefetz I, Alvero A, Holmberg J, Lebowitz N, Craveiro V, Yang-Hartwich Y, Yin G, Squillace L, Soteras M, Aldo P, Mor G. TLR2 enhances ovarian cancer stem cell self-renewal and promotes tumor repair and recurrence. Cell Cycle 2013, 12: 511-521. PMID: 23324344, PMCID: PMC3587452, DOI: 10.4161/cc.23406.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinoma, Ovarian EpithelialDrug Resistance, NeoplasmFemaleHomeodomain ProteinsHumansHyaluronan ReceptorsInflammationMiceMice, NudeMyeloid Differentiation Factor 88Nanog Homeobox ProteinNeoplasm Recurrence, LocalNeoplasms, Glandular and EpithelialNeoplastic Stem CellsNF-kappa BOctamer Transcription Factor-3Ovarian NeoplasmsSOXB1 Transcription FactorsToll-Like Receptor 2Tumor Cells, CulturedTumor MicroenvironmentConceptsOvarian cancer stem cellsCancer stem cellsTumor repairEOC stem cellsTLR2-MyD88NFκB pathwaySpecific pro-inflammatory pathwaysStem cellsMajority of patientsEpithelial ovarian cancer stem cellsPrimary ovarian cancerPro-inflammatory pathwaysPro-inflammatory microenvironmentCell populationsStemness-associated genesChemoresistant recurrent diseaseRecurrent diseaseEOC patientsRecent compelling evidenceOvarian cancerTumor injuryRecurrenceCancer cell populationsTumor initiationCancer cells
2012
Constitutive proteasomal degradation of TWIST-1 in epithelial–ovarian cancer stem cells impacts differentiation and metastatic potential
Yin G, Alvero AB, Craveiro V, Holmberg JC, Fu HH, Montagna MK, Yang Y, Chefetz-Menaker I, Nuti S, Rossi M, Silasi DA, Rutherford T, Mor G. Constitutive proteasomal degradation of TWIST-1 in epithelial–ovarian cancer stem cells impacts differentiation and metastatic potential. Oncogene 2012, 32: 39-49. PMID: 22349827, PMCID: PMC3703656, DOI: 10.1038/onc.2012.33.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationFemaleHumansHyaluronan ReceptorsMiceMyeloid Differentiation Factor 88Neoplasm MetastasisNeoplasms, Glandular and EpithelialNeoplastic Stem CellsNuclear ProteinsOvarian NeoplasmsProteasome Endopeptidase ComplexProteolysisTumor Cells, CulturedTwist-Related Protein 1ConceptsEpithelial ovarian cancer stem cellsEpithelial-mesenchymal transitionCancer stem cellsMesenchymal-epithelial transitionEOC stem cellsStem cellsTwist-1Differentiation processEpithelial cancer stem cellsSpecific cell typesEpithelial cancer cellsSpheroid-forming cellsProteasomal degradationEpithelial stem cellsMolecular mechanismsCell typesProgenitor cellsMetastasis processCancer metastasisCancer cellsDifferentiationMetastatic potentialAdditional signalsCellsCritical process
2010
Kruppel-like Factor 4 (Klf4) Prevents Embryonic Stem (ES) Cell Differentiation by Regulating Nanog Gene Expression*
Zhang P, Andrianakos R, Yang Y, Liu C, Lu W. Kruppel-like Factor 4 (Klf4) Prevents Embryonic Stem (ES) Cell Differentiation by Regulating Nanog Gene Expression*. Journal Of Biological Chemistry 2010, 285: 9180-9189. PMID: 20071344, PMCID: PMC2838337, DOI: 10.1074/jbc.m109.077958.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Morphogenetic Protein 4Cell DifferentiationEmbryonic Stem CellsGene Expression RegulationHomeodomain ProteinsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsLeukemia Inhibitory FactorMiceModels, BiologicalNanog Homeobox ProteinSignal TransductionSTAT3 Transcription FactorConceptsES cell self-renewalES cell differentiationCell self-renewalSomatic cell reprogrammingCell differentiationKruppel-like factor 4Embryonic stemLeukemia inhibitory factorBone morphogenetic protein 4Cell reprogrammingPromoter region of NanogSelf-renewalTranscription factor Kruppel-like factor 4KLF4 gene expressionMaintenance of pluripotencyFamily proteinsFactor 4Differentiation of ES cellsPromoter regionGene expressionES cellsExpression of NanogOverexpressing KLF4Protein 4Nanog expression
2009
Klf4 Interacts Directly with Oct4 and Sox2 to Promote Reprogramming
Wei Z, Yang Y, Zhang P, Andrianakos R, Hasegawa K, Lyu J, Chen X, Bai G, Liu C, Pera M, Lu W. Klf4 Interacts Directly with Oct4 and Sox2 to Promote Reprogramming. Stem Cells 2009, 27: 2969-2978. PMID: 19816951, DOI: 10.1002/stem.231.Peer-Reviewed Original ResearchConceptsInduced pluripotent stemEndogenous KLF4Sets of transcription factorsInduced pluripotent stem cellsTandem zinc fingerEmbryonic stemDominant negative mutantInduced iPS cellsMouse ES cellsSomatic cell reprogrammingWild-type Klf4Zinc fingerPluripotent stemTranscription factorsC-terminusIPS cellsInhibit reprogrammingEctopic expressionTarget genesNanog promoterSomatic cellsSOX2Cell reprogrammingES cellsKLF4
2007
Combined effect of total alkaloids from Feculae Bombycis and natural flavonoids on diabetes
Geng P, Yang Y, Gao Z, Yu Y, Shi Q, Bai G. Combined effect of total alkaloids from Feculae Bombycis and natural flavonoids on diabetes. Journal Of Pharmacy And Pharmacology 2007, 59: 1145-1150. PMID: 17725858, DOI: 10.1211/jpp.59.8.0013.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, OralAlkaloidsAnimalsBlood GlucoseBombyxCholesterolDiabetes Mellitus, ExperimentalDrug SynergismDrug Therapy, CombinationFemaleFlavonoidsGlycoside Hydrolase InhibitorsIntestinal MucosaMaleMedicine, Chinese TraditionalMicePlant ExtractsPlants, MedicinalPostprandial PeriodRatsRats, WistarStarchConceptsInhibiting alpha-glucosidase activityAlpha-glucosidase activityDiabetic mice in vivoMice in vivoBlood glucoseStarch hydrolysateFlavonoidsFasting blood total cholesterolGlucose levelsIn vivoIndividual ingredientsBlood total cholesterolFasting blood glucoseDepressed blood glucose levelsNatural flavonoidPostprandial elevationBlood glucose levelsModel in vitroTherapy of diabetesTAFBShort-term studiesTotal cholesterolOral administrationBombycisBlood
2006
Identifying glucagon-like peptide-1 mimetics using a novel functional reporter gene high-throughput screening assay
Chen J, Bai G, Yang Y, Geng P, Cao Y, Zhu Y. Identifying glucagon-like peptide-1 mimetics using a novel functional reporter gene high-throughput screening assay. Peptides 2006, 28: 928-934. PMID: 17267075, DOI: 10.1016/j.peptides.2006.12.012.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsBlood GlucoseCHO CellsCricetinaeCricetulusDose-Response Relationship, DrugEnzyme-Linked Immunosorbent AssayFemaleGene Expression RegulationGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucose Tolerance TestGreen Fluorescent ProteinsHypoglycemic AgentsInjections, IntraperitonealMicePeptide LibraryPeptidesRatsReceptors, GlucagonTransfectionConceptsGlucagon-like peptide-1High-throughput screeningRounds of selectionChinese Kunming miceEGFP reporter geneHigh-throughput screening assayGreen fluorescent proteinDodecapeptide libraryPositional cloningResistant to DPP-IVRecombinant cell linesKS-12Reporter geneGlucagon-like peptide-1 mimeticsFluorescent proteinPeptide libraryGlucagon-like peptide-1 receptorGlucagon-like peptide-1 analogInhibit glucagon secretionMonitor receptor activityCell linesDPP-IVDipeptidyl peptidase IVDose-dependent mannerScreening assay
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