2023
NRF2 controls iron homeostasis and ferroptosis through HERC2 and VAMP8
Anandhan A, Dodson M, Shakya A, Chen J, Liu P, Wei Y, Tan H, Wang Q, Jiang Z, Yang K, Garcia J, Chambers S, Chapman E, Ooi A, Yang-Hartwich Y, Stockwell B, Zhang D. NRF2 controls iron homeostasis and ferroptosis through HERC2 and VAMP8. Science Advances 2023, 9: eade9585. PMID: 36724221, PMCID: PMC9891695, DOI: 10.1126/sciadv.ade9585.Peer-Reviewed Original ResearchMeSH KeywordsApoferritinsFemaleFerroptosisHomeostasisHumansIronNF-E2-Related Factor 2Ovarian NeoplasmsR-SNARE ProteinsUbiquitin-Protein LigasesConceptsLabile iron poolNFE2L2/Human ovarian cancer tissuesCancer cellsOvarian cancer cell linesOvarian cancer tissuesIntracellular labile iron poolIron homeostasisCancer cell linesPreclinical modelsNrf2 inhibitionCancer tissuesNrf2 levelsCancer treatmentFerroptotic deathNrf2Ferroptosis resistanceKnockout cellsCell linesUntapped strategyFerroptosisIron poolCellsHomeostasisExpressionThe Poly (ADP-ribose) polymerase inhibitor olaparib and pan-ErbB inhibitor neratinib are highly synergistic in HER2 overexpressing epithelial ovarian carcinoma in vitro and in vivo
Han C, McNamara B, Bellone S, Harold J, Manara P, Hartwich T, Mutlu L, Yang-Hartwich Y, Zipponi M, Demirkiran C, Verzosa M, Altwerger G, Ratner E, Huang G, Clark M, Andikyan V, Azodi M, Dottino P, Schwartz P, Santin A. The Poly (ADP-ribose) polymerase inhibitor olaparib and pan-ErbB inhibitor neratinib are highly synergistic in HER2 overexpressing epithelial ovarian carcinoma in vitro and in vivo. Gynecologic Oncology 2023, 170: 172-178. PMID: 36706643, PMCID: PMC10023457, DOI: 10.1016/j.ygyno.2023.01.015.Peer-Reviewed Original ResearchConceptsCombination of olaparibOvarian cancerHER2 expressionSingle agentCell linesGynecologic cancer mortalityHER2-negative tumorsOvarian cancer cell linesOvarian cancer patientsEpithelial ovarian carcinomaNovel therapeutic optionsOC cell linesUnmet medical needPoly (ADP-ribose) polymerase (PARP) inhibitorsPan-ErbB inhibitorSingle-agent olaparibPolymerase inhibitor olaparibPoly (ADP-ribose) polymerase (PARP) inhibitor olaparibPrimary HER2Cancer cell linesNegative tumorsTherapeutic optionsCancer mortalityCancer patientsNeu expressionTrastuzumab 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
Homologous recombination deficiency (HRD) signature-3 in ovarian and uterine carcinosarcomas correlates with preclinical sensitivity to Olaparib, a poly (adenosine diphosphate [ADP]- ribose) polymerase (PARP) inhibitor
Tymon-Rosario JR, Manara P, Manavella DD, Bellone S, Hartwich TMP, Harold J, Yang-Hartwich Y, Zipponi M, Choi J, Jeong K, Mutlu L, Yang K, Altwerger G, Menderes G, Ratner E, Huang GS, Clark M, Andikyan V, Azodi M, Schwartz PE, Alexandrov LB, Santin AD. Homologous recombination deficiency (HRD) signature-3 in ovarian and uterine carcinosarcomas correlates with preclinical sensitivity to Olaparib, a poly (adenosine diphosphate [ADP]- ribose) polymerase (PARP) inhibitor. Gynecologic Oncology 2022, 166: 117-125. PMID: 35599167, DOI: 10.1016/j.ygyno.2022.05.005.Peer-Reviewed Original ResearchConceptsUterine carcinosarcomaCS cell linesSignature 3Cell linesPolymerase inhibitorsOverall animal survivalFresh tumor samplesPoly (ADP-ribose) polymerase (PARP) inhibitorsXenograft tumor growthG2/M phaseAggressive malignancyCS patientsPrimary tumorCell cycle arrestPrimary cell linesPoor survivalClinical studiesPreclinical sensitivityCarcinosarcomaTumor growthAnimal survivalOlaparib activityTumor samplesOlaparibAntitumor activity
2021
Progression of Cystadenoma to Mucinous Borderline Ovarian Tumor in Young Females: Case Series and Literature Review
Beroukhim G, Ozgediz D, Cohen PJ, Hui P, Morotti R, Schwartz PE, Yang-Hartwich, Vash-Margita A. Progression of Cystadenoma to Mucinous Borderline Ovarian Tumor in Young Females: Case Series and Literature Review. Journal Of Pediatric And Adolescent Gynecology 2021, 35: 359-367. PMID: 34843973, DOI: 10.1016/j.jpag.2021.11.003.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentChildCystadenoma, MucinousFemaleHumansNeoplasm Recurrence, LocalOvarian CystsOvarian NeoplasmsRetrospective StudiesConceptsMucinous borderline ovarian tumorsBorderline ovarian tumorsOvarian tumorsYale-New Haven HospitalRetrospective chart reviewBenign ovarian tumorsBenign ovarian lesionsRate of recurrenceNew Haven HospitalAbdominal painPreoperative characteristicsChart reviewDisease recurrenceRecurrent cystsCase seriesChief complaintClinical presentationClinicopathologic featuresFemale patientsMucinous cystadenomaOvarian cystsOvarian lesionsTumor stageAdolescent patientsSubsequent surveillancePersonalized models of heterogeneous 3D epithelial tumor microenvironments: Ovarian cancer as a model
Horst EN, Bregenzer ME, Mehta P, Snyder CS, Repetto T, Yang-Hartwich Y, Mehta G. Personalized models of heterogeneous 3D epithelial tumor microenvironments: Ovarian cancer as a model. Acta Biomaterialia 2021, 132: 401-420. PMID: 33940195, PMCID: PMC8969826, DOI: 10.1016/j.actbio.2021.04.041.Peer-Reviewed Original ResearchMeSH KeywordsExtracellular MatrixFemaleHumansNeoplasm Recurrence, LocalOvarian NeoplasmsPrecision MedicineTumor MicroenvironmentConceptsOptimal adjuvant treatmentTumor microenvironmentOvarian cancerCancer modelAdverse clinical outcomesHeterogeneous patient populationMinimal residual diseaseDifferent tumor locationsConventional cancer treatmentsEpithelial tumor microenvironmentModels of cancerAdjuvant treatmentDurable responsesTreatment failureClinical outcomesResidual diseasePatient populationTumor locationDisease progressionEffective therapyFundamental cancer biologyDiverse tumor microenvironmentsIndividual patientsSame patientPatient biopsies
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
2019
Tumor microenvironment and immunology of ovarian cancer: 12th Biennial Rivkin Center Ovarian Cancer Research Symposium
Mitra AK, Yang-Hartwich Y. Tumor microenvironment and immunology of ovarian cancer: 12th Biennial Rivkin Center Ovarian Cancer Research Symposium. International Journal Of Gynecological Cancer 2019, 29: s12. PMID: 31462543, DOI: 10.1136/ijgc-2019-000666.Peer-Reviewed Original ResearchInhibition of Heat Shock Protein 90 suppresses TWIST1 Transcription
Chong KY, Kang M, Garofalo F, Ueno D, Liang H, Cady S, Madarikan O, Pitruzzello N, Tsai CH, Hartwich T, Shuch B, Yang-Hartwich Y. Inhibition of Heat Shock Protein 90 suppresses TWIST1 Transcription. Molecular Pharmacology 2019, 96: 168-179. PMID: 31175180, DOI: 10.1124/mol.119.116137.Peer-Reviewed Original ResearchMeSH KeywordsBenzoquinonesCell Line, TumorDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansKidney NeoplasmsLactams, MacrocyclicNasopharyngeal NeoplasmsNuclear ProteinsOvarian NeoplasmsPhosphorylationPromoter Regions, GeneticSTAT3 Transcription FactorTissue Array AnalysisTranscription, GeneticTwist-Related Protein 1ConceptsEpithelial-mesenchymal transitionHsp90 inhibitorsTwist1 transcriptionMolecular chaperone heat shock protein 90Chaperone heat shock protein 90Involvement of Hsp90Heat shock protein 90Cancer cell linesRole of Hsp90Binding of STAT3Inhibition of Hsp90Shock protein 90Cell linesProximity ligation assayHsp90 inhibitor 17TWIST1 mRNA expressionTranscription factorsSignal transducerProtein 90Promoter activityTranscription 3New therapeutic opportunitiesHsp90Molecular mechanismsSTAT3 activityp53-Pirh2 Complex Promotes Twist1 Degradation and Inhibits EMT
Yang-Hartwich Y, Tedja R, Roberts C, Goodner-Bingham J, Cardenas C, Gurea M, Sumi NJ, Alvero AB, Glackin CA, Mor G. p53-Pirh2 Complex Promotes Twist1 Degradation and Inhibits EMT. Molecular Cancer Research 2019, 17: molcanres.0238.2018. PMID: 30131448, PMCID: PMC6800184, DOI: 10.1158/1541-7786.mcr-18-0238.Peer-Reviewed Original ResearchConceptsEpithelial-mesenchymal transitionTwist1 degradationInvasive cancer phenotypeEMT-inducing transcription factorsAbility of p53Tumor suppressor geneTumor cell invasivenessWild-type p53Proteasomal degradationTranscription factorsTwist1 proteinSuppressor geneEpithelial phenotypeInhibits epithelial-mesenchymal transitionCancer phenotypeMolecular levelCell invasivenessCancer progressionCancer metastasisWt p53Twist1P53Metastatic processTumor progressionNew insights
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
2011
Ovarian cancer stem cells and inflammation
Mor G, Yin G, Chefetz I, Yang Y, Alvero A. Ovarian cancer stem cells and inflammation. Cancer Biology & Therapy 2011, 11: 708-713. PMID: 21317559, PMCID: PMC3100563, DOI: 10.4161/cbt.11.8.14967.Peer-Reviewed Original ResearchConceptsEpithelial ovarian cancerOvarian cancerCancer stem cellsAdvanced stage ovarian cancerOvarian cancer stem cellsGynecologic cancer deathFourth leading causeCancer-related deathSource of recurrenceLack of responseStem cellsCancer deathDisease progressionLeading causeQuestion of recurrenceRecurrenceCancerChemotherapyDeathInflammationChemoresistanceCauseCellsProgressionWomen