2025
Impact of peritoneal macrophage depletion on endometriotic lesion development in a mouse model
Stratopoulou C, Cacciottola L, Gawde N, Ngombo A, Brusa D, Donnez J, Taylor H, Dolmans M. Impact of peritoneal macrophage depletion on endometriotic lesion development in a mouse model. Journal Of Endometriosis And Uterine Disorders 2025, 10: 100113. DOI: 10.1016/j.jeud.2025.100113.Peer-Reviewed Original ResearchMacrophage depletionEndometriotic lesionsTreated miceMacrophage accumulationMouse modelVascular endothelial growth factor immunostainingEndometriosis developmentQuantification of immune cellsFlow cytometryMouse model of endometriosisClodronate-containing liposomesKi67-positive proliferating cellsNovel therapeutic optionsRate of fibrosisModel of endometriosisTUNEL-positive apoptotic cellsLevels of fibrosisPathogenesis of endometriosisReproductive-age womenMasson's trichrome stainingEndometriotic lesion developmentEnhanced cell deathPlacebo-ControlledUterine fragmentsT cells
2024
An explainable machine learning model for prediction of high-risk nonalcoholic steatohepatitis
Njei B, Osta E, Njei N, Al-Ajlouni Y, Lim J. An explainable machine learning model for prediction of high-risk nonalcoholic steatohepatitis. Scientific Reports 2024, 14: 8589. PMID: 38615137, PMCID: PMC11016071, DOI: 10.1038/s41598-024-59183-4.Peer-Reviewed Original ResearchConceptsNational Health and Nutrition Examination SurveyRisk of progression to cirrhosisClinical Risk IndexHealth and Nutrition Examination SurveyControlled attenuation parameter valuesNovel therapeutic optionsLiver stiffness measurementProgression to cirrhosisAspartate aminotransferase levelsNutrition Examination SurveyResource-limited settingsFIB-4Fibrosis scorePlatelet countAminotransferase levelsTherapeutic optionsWaist circumferenceClinically applicable modelExamination SurveyNonalcoholic steatohepatitisFAST scoreEarly identificationElastography measurementsStiffness measurementPatients
2023
Chronic Kidney Disease Management in the Middle East and Africa: Concerns, Challenges, and Novel Approaches
Al-Ghamdi S, Abu-Alfa A, Alotaibi T, AlSaaidi A, AlSuwaida A, Arici M, Ecder T, Koraie A, Ghnaimat M, Hafez M, Hassan M, Sqalli T. Chronic Kidney Disease Management in the Middle East and Africa: Concerns, Challenges, and Novel Approaches. International Journal Of Nephrology And Renovascular Disease 2023, 16: 103-112. PMID: 37051319, PMCID: PMC10084934, DOI: 10.2147/ijnrd.s363133.Peer-Reviewed Original ResearchChronic kidney diseaseManagement of CKDChronic kidney disease managementKidney disease managementManagement of patientsNovel therapeutic optionsTherapeutic optionsKidney diseaseProtective therapyOverall burdenEarly diagnosisAvailable evidenceDisease managementHealthcare specialistsHealthcare systemHealthcare policyPatientsSteering CommitteeBurdenRiskHypertensionComorbiditiesDiabetesReferralTherapyThe 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 expression
2022
Synergistic activity of neratinib in combination with olaparib in uterine serous carcinoma overexpressing HER2/neu
Yadav G, Roque DM, Bellone S, Manavella DD, Hartwich TMP, Zipponi M, Harold J, Tymon-Rosario J, Mutlu L, Altwerger G, Menderes G, Ratner E, Buza N, Hui P, Huang GS, Andikyan V, Clark M, Azodi M, Schwartz PE, Alexandrov LB, Santin AD. Synergistic activity of neratinib in combination with olaparib in uterine serous carcinoma overexpressing HER2/neu. Gynecologic Oncology 2022, 166: 351-357. PMID: 35641325, DOI: 10.1016/j.ygyno.2022.05.021.Peer-Reviewed Original ResearchConceptsUterine serous carcinomaHER2/neu expressionHER2/neuCombination of olaparibUSC xenograftsUSC cell linesNeu expressionSerous carcinomaLow HER2/neu expressionHER2/neu 3Cell linesHER2/neu gene amplificationNovel therapeutic optionsPolymerase inhibitor olaparibNeu gene amplificationDurable growth inhibitionNeratinib treatmentUSC cellsUSC patientsEndometrial cancerAggressive variantTherapeutic optionsPoor prognosisHER2/Single agent
2019
Temporal patterns and predictors of receiving no active treatment among older patients with acute myeloid leukemia in the United States: A population‐level analysis
Zeidan AM, Podoltsev NA, Wang X, Bewersdorf JP, Shallis RM, Huntington SF, Gore SD, Davidoff AJ, Ma X, Wang R. Temporal patterns and predictors of receiving no active treatment among older patients with acute myeloid leukemia in the United States: A population‐level analysis. Cancer 2019, 125: 4241-4251. PMID: 31483484, PMCID: PMC7733320, DOI: 10.1002/cncr.32439.Peer-Reviewed Original ResearchConceptsAcute myeloid leukemiaTime of diagnosisOlder patientsActive treatmentMyeloid leukemiaMultivariable logistic regression modelMedian overall survivalPercentage of patientsLow-intensity therapyMajority of patientsNovel therapeutic optionsQuality of careLogistic regression modelsIntensity therapyTherapy receiptOverall survivalWorse survivalClinical factorsInferior survivalEntire cohortTherapeutic optionsPatient populationRetrospective analysisHigher oddsProvider characteristics
2017
Management of myelofibrosis: JAK inhibition and beyond
Stahl M, Zeidan AM. Management of myelofibrosis: JAK inhibition and beyond. Expert Review Of Hematology 2017, 10: 459-477. PMID: 28395559, DOI: 10.1080/17474086.2017.1317590.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsBone marrow fibrosisMarrow fibrosisAbnormal cytokine expressionClinical trial evidenceJAK2 V617F allele burdenErythropoiesis stimulating agentsNovel therapeutic optionsAnti-fibrosis agentsV617F allele burdenJAK2 inhibitor ruxolitinibNovel therapeutic agentsJAK2 V617F mutationConstitutional symptomsCytoreductive drugsSymptom burdenImmunomodulatory drugsSurvival improvementJAK1/2 inhibitorMF patientsTherapeutic optionsTrial evidenceCytokine expressionExtramedullary hematopoiesisPrognostic assessmentRuxolitinib monotherapyOS07.3 Nivolumab in Combination With Radiotherapy With or Without Temozolomide in Patients With Newly Diagnosed Glioblastoma: Updated Results From CheckMate 143
Omuro A, Vlahovic G, Baehring J, Butowski N, Reardon D, Cloughesy T, Sahebjam S, Lim M, Zwirtes R, Sampson J. OS07.3 Nivolumab in Combination With Radiotherapy With or Without Temozolomide in Patients With Newly Diagnosed Glioblastoma: Updated Results From CheckMate 143. Neuro-Oncology 2017, 19: iii13-iii13. PMCID: PMC5463686, DOI: 10.1093/neuonc/nox036.044.Peer-Reviewed Original ResearchTreatment-related AEsAdverse eventsCheckMate 143Standard radiotherapyDisease progressionFirst prospective clinical trialHerpes simplex virus encephalitisTreatment-related adverse eventsTolerability of nivolumabTreatment-related deathsImmune checkpoint inhibitorsSimplex virus encephalitisDeath-1 receptorNew safety signalsPhase 2/3 studyProspective clinical trialsImmune cell infiltrationNovel therapeutic optionsMonoclonal antibody inhibitorMultiple cancer typesConcurrent temozolomideUnmethylated MGMTAdjuvant temozolomideCheckpoint inhibitorsRadiographic progression
2016
Dual CCNE1/PIK3CA targeting is synergistic in CCNE1-amplified/PIK3CA-mutated uterine serous carcinomas in vitro and in vivo
Cocco E, Lopez S, Black J, Bellone S, Bonazzoli E, Predolini F, Ferrari F, Schwab CL, Menderes G, Zammataro L, Buza N, Hui P, Wong S, Zhao S, Bai Y, Rimm DL, Ratner E, Litkouhi B, Silasi DA, Azodi M, Schwartz PE, Santin AD. Dual CCNE1/PIK3CA targeting is synergistic in CCNE1-amplified/PIK3CA-mutated uterine serous carcinomas in vitro and in vivo. British Journal Of Cancer 2016, 115: 303-311. PMID: 27351214, PMCID: PMC4973158, DOI: 10.1038/bjc.2016.198.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsCell Line, TumorClass I Phosphatidylinositol 3-KinasesCyclin EDNA Copy Number VariationsFemaleGene Knockdown TechniquesHeterograftsHumansIn Situ Hybridization, FluorescenceIn Vitro TechniquesMiceMutationOncogene ProteinsPhosphatidylinositol 3-KinasesRNA, MessengerTissue Array AnalysisUterine NeoplasmsConceptsUterine serous carcinomaSerous carcinomaTumor growthCyclin E1 (CCNE1) gene amplificationRecurrent uterine serous carcinomaPrimary USC cell linesNovel therapeutic optionsSingle-agent treatmentIdeal therapeutic targetUSC cell linesCyclin E1 expressionUSC patientsUSC xenograftsInhibited cell growthCell cycle analysisAggressive variantTherapeutic optionsCCNE1 amplificationEndometrial tumorsCYC065Therapeutic targetClinical optionPIK3CA driver mutationsDriver mutationsXenografts
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 linesThe Influence of Host Factors on the Prognosis of Breast Cancer: Stroma and Immune Cell Components as Cancer Biomarkers.
Karn T, Pusztai L, Rody A, Holtrich U, Becker S. The Influence of Host Factors on the Prognosis of Breast Cancer: Stroma and Immune Cell Components as Cancer Biomarkers. Current Cancer Drug Targets 2015, 15: 652-64. PMID: 26452382, DOI: 10.2174/156800961508151001101209.Peer-Reviewed Original ResearchConceptsBreast cancerPredictive markerImmune cellsStromal componentsHER2-positive breast cancerHigh lymphocytic infiltrationPositive breast cancerHER2-positive cancersImmune cell componentsNovel therapeutic optionsType breast cancerBreast cancer subtypesHost immunological responseImmunotherapeutic regimensClinical courseImmune markersLymphocytic infiltrationPositive cancersTherapeutic optionsInflammatory cellsClinical subtypingImmunological parametersClinical trialsImmune parametersImmunological response
2014
Intravenous mesenchymal stem cell administration exhibits therapeutic effects against 6-hydroxydopamine-induced dopaminergic neurodegeneration and glial activation in rats
Suzuki S, Kawamata J, Iwahara N, Matsumura A, Hisahara S, Matsushita T, Sasaki M, Honmou O, Shimohama S. Intravenous mesenchymal stem cell administration exhibits therapeutic effects against 6-hydroxydopamine-induced dopaminergic neurodegeneration and glial activation in rats. Neuroscience Letters 2014, 584: 276-281. PMID: 25449872, DOI: 10.1016/j.neulet.2014.10.039.Peer-Reviewed Original ResearchConceptsHuman bone marrow-derived mesenchymal stem cellsTherapeutic effectParkinson's diseaseCalcium binding adaptor molecule 1Mesenchymal stem cell administrationSubstantia nigra pars compactaHemi-parkinsonian rat modelParkinsonian model ratsTH-positive neuronsAdaptor molecule 1Anti-inflammatory factorsStem cell administrationNovel therapeutic optionsSham-operated ratsBone marrow-derived mesenchymal stem cellsMarrow-derived mesenchymal stem cellsGlial activationPars compactaCell administrationTherapeutic optionsDopaminergic neuronsModel ratsDopaminergic neurodegenerationNovel therapiesRat modelTaselisib, a selective inhibitor of PIK3CA, is highly effective on PIK3CA-mutated and HER2/neu amplified uterine serous carcinoma in vitro and in vivo
Lopez S, Schwab CL, Cocco E, Bellone S, Bonazzoli E, English DP, Schwartz PE, Rutherford T, Angioli R, Santin AD. Taselisib, a selective inhibitor of PIK3CA, is highly effective on PIK3CA-mutated and HER2/neu amplified uterine serous carcinoma in vitro and in vivo. Gynecologic Oncology 2014, 135: 312-317. PMID: 25172762, PMCID: PMC4270135, DOI: 10.1016/j.ygyno.2014.08.024.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnimalsAntineoplastic AgentsCarcinomaCell Cycle CheckpointsCell Line, TumorCell ProliferationClass I Phosphatidylinositol 3-KinasesDrug Screening Assays, AntitumorFemaleGene AmplificationHumansImidazolesIn Situ Hybridization, FluorescenceIn Vitro TechniquesMiceMiddle AgedNeoplasms, Cystic, Mucinous, and SerousOxazepinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsReceptor, ErbB-2Uterine NeoplasmsXenograft Model Antitumor AssaysConceptsHER2/neu gene amplificationUterine serous carcinomaUSC cell linesNeu gene amplificationCell linesHER2/neuPIK3CA mutationsGene amplificationPhosphorylation of S6Serous carcinomaPIK3CA wild typeG0/G1 phaseSelective inhibitorOncogenic PIK3CA mutationsS6 proteinCell cycle distributionPrimary uterine serous carcinomaWild typeDownstream signalingPrimary USC cell linesCell cycleNovel therapeutic optionsDose-dependent increaseDifferential growth inhibitionG1 phaseFacial and Hand Allotransplantation
Pomahac B, Gobble R, Schneeberger S. Facial and Hand Allotransplantation. Cold Spring Harbor Perspectives In Medicine 2014, 4: a015651. PMID: 24478387, PMCID: PMC3935393, DOI: 10.1101/cshperspect.a015651.Peer-Reviewed Original ResearchConceptsVascularized Composite AllotransplantationFacial transplantationLong-term immunosuppressionMinimization of immunosuppressionGood functional outcomeTreatment of patientsMultidisciplinary team approachNovel therapeutic optionsSevere facial disfigurementAllograft survivalHand allotransplantationSkin rejectionTherapeutic optionsFunctional outcomeLimb lossComposite allotransplantationSide effectsTeam approachTransplantationSurgical planningFacial disfigurementImmunosuppressionAllotransplantationComplex proceduresPatients
2013
Coordinated Targeting of the EGFR Signaling Axis by MicroRNA-27a*
Wu X, Bhayani MK, Dodge CT, Nicoloso MS, Chen Y, Yan X, Adachi M, Thomas L, Galer CE, Jiffar T, Pickering CR, Kupferman ME, Myers JN, Calin GA, Lai SY. Coordinated Targeting of the EGFR Signaling Axis by MicroRNA-27a*. Oncotarget 2013, 4: 1388-1398. PMID: 23963114, PMCID: PMC3824521, DOI: 10.18632/oncotarget.1239.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesCarcinoma, Squamous CellCell Growth ProcessesCell Line, TumorCell SurvivalDown-RegulationErbB ReceptorsHead and Neck NeoplasmsHumansMiceMicroRNAsProto-Oncogene Proteins c-aktRNA, MessengerSignal TransductionSquamous Cell Carcinoma of Head and NeckTOR Serine-Threonine KinasesXenograft Model Antitumor AssaysConceptsEpidermal growth factor receptorDownregulation of EGFRSolid tumorsTumor growthNeck squamous cell carcinomaMurine orthotopic xenograft modelHNSCC cell viabilityOral cavity cancerMultiple HNSCC cell linesSquamous cell carcinomaStar strandNovel therapeutic optionsNovel miRNAsMultiple solid tumorsOrthotopic xenograft modelOverexpression of EGFRCoordinated regulationHNSCC cell linesCoordinated targetingGrowth factor receptorComplex regulationDirect intratumoral injectionPathway componentsInducible expressionSignaling Axis
2012
A renaissance in therapeutic options for pancreatic neuroendocrine tumors.
Kunz PL. A renaissance in therapeutic options for pancreatic neuroendocrine tumors. American Society Of Clinical Oncology Educational Book 2012, 271-4. PMID: 24451747, DOI: 10.14694/edbook_am.2012.32.136.Peer-Reviewed Original ResearchProgression-free survivalPancreatic neuroendocrine tumorsNeuroendocrine tumorsTherapeutic optionsRandomized placebo-controlled studyPlacebo-controlled studyNovel therapeutic optionsChemotherapy backboneLocoregional diseaseAdvanced diseaseBiologic therapySurgical resectionSomatostatin analoguesClinical trialsDrug AdministrationU.S. FoodAntiproliferative agentsTumorsDiseaseFuture studiesResectionEverolimusSunitinibPatientsOptions
2009
Targeting Survivin Using ICG-001 May Overcome Drug Resistance in Primary B-Cell Acute Lymphoblastic Leukemia.
Jiang E, Park E, Scharman C, Hsieh Y, Kadavallore A, Nguyen C, Zhao Y, McMillan M, Groffen J, Heisterkamp N, Muschen M, Kahn M, Kim Y. Targeting Survivin Using ICG-001 May Overcome Drug Resistance in Primary B-Cell Acute Lymphoblastic Leukemia. Blood 2009, 114: 3072. DOI: 10.1182/blood.v114.22.3072.3072.Peer-Reviewed Original ResearchMedian survival timeAcute lymphoblastic leukemiaWhite blood cellsICG-001Control groupBlood cellsStandard chemotherapyRed blood cellsPeripheral bloodLymphoblastic leukemiaSmall molecule inhibitor ICG-001B-cell acute lymphoblastic leukemiaDrug resistanceCBP/β-cateninNormal hematopoiesisPromising therapeutic principleNormal white blood cellsConventional drug treatmentLeukemia cellsPrior intravenous injectionEnd of treatmentNovel therapeutic optionsNormal weight gainNew treatment modalitiesSubcutaneous osmotic pumpsBetaine for nonalcoholic fatty liver disease: Results of a randomized placebo‐controlled trial
Abdelmalek M, Sanderson S, Angulo P, Soldevila‐Pico C, Liu C, Peter J, Keach J, Cave M, Chen T, McClain C, Lindor K. Betaine for nonalcoholic fatty liver disease: Results of a randomized placebo‐controlled trial. Hepatology 2009, 50: 1818-1826. PMID: 19824078, DOI: 10.1002/hep.23239.Peer-Reviewed Original ResearchConceptsNonalcoholic steatohepatitisBetaine therapyHepatic steatosisAnimal studiesNonalcoholic fatty liver disease activity scoreBiopsy-proven nonalcoholic steatohepatitisRandomized placebo-controlled trialNonalcoholic fatty liver diseaseRandomized placebo-controlled studyPosttreatment liver biopsiesDisease Activity ScorePlacebo-controlled studyPlacebo-controlled trialFatty liver diseaseElevation of insulinNovel therapeutic optionsSecond hit mechanismsOral betaineWilcoxon rank testNASH patientsLiver biopsyActivity scoreLiver diseaseRemethylation of homocysteineSteatosis gradeTargeting of breast cancer with non-oncology drugs – possible novel therapeutic option for triple-negative breast cancer.
Liedtke C, Yan K, Wu Y, Hortobagyi G, Symmans W, Valero V, Goette M, Kiesel L, Pusztai L. Targeting of breast cancer with non-oncology drugs – possible novel therapeutic option for triple-negative breast cancer. Cancer Research 2009, 69: 2119. DOI: 10.1158/0008-5472.sabcs-2119.Peer-Reviewed Original ResearchTriple-negative breast cancerBreast cancerTherapeutic optionsCell linesEarly-stage breast cancerHuman triple-negative breast cancerCurrent chemotherapy agentsDrug targetsReceptor-positive cancersStage breast cancerBreast cancer cell line MCF-7Future therapeutic optionsNovel therapeutic optionsCancer cell line MCF-7TNBC cell linesBreast cancer cell linesGlutathione S-transferase piFine-needle biopsyDose-dependent inhibitionLack of ERCell line MCF-7Normal HER2 expressionCancer cell linesUnique drug targetsBiological presentation
2007
Preclinical Evaluation of CBP/β-catenin Inhibition as a New Strategy for Drug Resistant Acute Lymphoblastic Leukemia.
Kim Y, Park E, Lorentzen C, De La Torre B, Hsieh Y, Whang H, Klemm L, Nguyen C, McMillan M, Teo J, Muschen M, Kahn M. Preclinical Evaluation of CBP/β-catenin Inhibition as a New Strategy for Drug Resistant Acute Lymphoblastic Leukemia. Blood 2007, 110: 1596. DOI: 10.1182/blood.v110.11.1596.1596.Peer-Reviewed Original ResearchAcute lymphoblastic leukemiaMedian survival timeStandard chemotherapyICG-001Expression of survivinLymphoblastic leukemiaLeukemia cellsXenograft modelDrug-resistant acute lymphoblastic leukemiaSmall molecule inhibitor ICG-001NOD/SCID xenograft modelHuman preCBP/β-cateninPromising therapeutic principleBlood count analysisSCID xenograft modelSurvival of miceNovel therapeutic optionsNew treatment modalitiesΒ-cateninDrug-resistant leukemia cellsΒ-catenin inhibitionHigh death rateResistant leukemia cellsSurvivin mRNA expression
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