2022
TP53-altered higher-risk myelodysplastic syndromes/neoplasms and acute myeloid leukemia: a distinct genetic entity with unique unmet needs
Ball S, Loghavi S, Zeidan A. TP53-altered higher-risk myelodysplastic syndromes/neoplasms and acute myeloid leukemia: a distinct genetic entity with unique unmet needs. Leukemia & Lymphoma 2022, 64: 540-550. PMID: 36323304, DOI: 10.1080/10428194.2022.2136969.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsAcute myeloid leukemiaMyelodysplastic syndromeVariant allele frequencyMyeloid leukemiaMDS/acute myeloid leukemiaIndependent poor prognostic factorBCL2 inhibitor venetoclaxPoor prognostic factorDisease-modifying therapiesIntensive chemotherapyBlast countClinical coursePrognostic factorsInvestigational agentsDisease entityClinical studiesInhibitor venetoclaxMyeloid neoplasmsResponse ratePathogenic alterationsNeoplasmsDistinct genetic entitiesLeukemiaGenetic characteristicsAllele frequenciesActivation of targetable inflammatory immune signaling is seen in myelodysplastic syndromes with SF3B1 mutations
Choudhary GS, Pellagatti A, Agianian B, Smith MA, Bhagat TD, Gordon-Mitchell S, Sahu S, Pandey S, Shah N, Aluri S, Aggarwal R, Aminov S, Schwartz L, Steeples V, Booher RN, Ramachandra M, Samson M, Carbajal M, Pradhan K, Bowman TV, Pillai MM, Will B, Wickrema A, Shastri A, Bradley RK, Martell RE, Steidl UG, Gavathiotis E, Boultwood J, Starczynowski DT, Verma A. Activation of targetable inflammatory immune signaling is seen in myelodysplastic syndromes with SF3B1 mutations. ELife 2022, 11: e78136. PMID: 36040792, PMCID: PMC9427103, DOI: 10.7554/elife.78136.Peer-Reviewed Original ResearchConceptsAcute myeloid leukemiaMyelodysplastic syndromeNF-kB activationLymphoma SocietyMDS/acute myeloid leukemiaNational InstitutePathogenesis of MDSInterleukin-1 receptor-associated kinase 4Expression of IRAK4Inflammatory-immune pathwaysInflammatory cytokine productionSpecific oncogenic pathwaysCareer development grantsHealth research trainingCritical downstream mediatorCytokine productionMyeloid leukemiaPreclinical modelsNew York State DepartmentXenograft modelImmune pathwaysNF-kB.MDS samplesTRAF6 activationLeukemic growthTP53 mutation defines a unique subgroup within complex karyotype de novo and therapy-related MDS/AML
Weinberg OK, Siddon A, Madanat Y, Gagan J, Arber DA, Dal Cin P, Narayanan D, Ouseph MM, Kurzer JH, Hasserjian RP. TP53 mutation defines a unique subgroup within complex karyotype de novo and therapy-related MDS/AML. Blood Advances 2022, 6: 2847-2853. PMID: 35073573, PMCID: PMC9092405, DOI: 10.1182/bloodadvances.2021006239.Peer-Reviewed Original ResearchConceptsAcute myeloid leukemiaMyelodysplastic syndromeOverall survivalTP53 mutationsComplex karyotypeBlast countWorse outcomesTherapy-related MDS/acute myeloid leukemiaDiagnosis of AMLMDS/acute myeloid leukemiaTherapy-related myeloid neoplasmsTherapy-related casesTP53-mutated patientsDe novo diseaseMarrow blast countLower hemoglobin levelsWorse overall survivalCK patientsNovo diseaseDifferent disease categoriesClinicopathologic featuresHemoglobin levelsMDS patientsMultivariable analysisAggressive diseaseIn vivo anti-tumor effect of PARP inhibition in IDH1/2 mutant MDS/AML resistant to targeted inhibitors of mutant IDH1/2
Gbyli R, Song Y, Liu W, Gao Y, Biancon G, Chandhok NS, Wang X, Fu X, Patel A, Sundaram R, Tebaldi T, Mamillapalli P, Zeidan AM, Flavell RA, Prebet T, Bindra RS, Halene S. In vivo anti-tumor effect of PARP inhibition in IDH1/2 mutant MDS/AML resistant to targeted inhibitors of mutant IDH1/2. Leukemia 2022, 36: 1313-1323. PMID: 35273342, PMCID: PMC9103411, DOI: 10.1038/s41375-022-01536-x.Peer-Reviewed Original ResearchConceptsAcute myeloid leukemiaMyelodysplastic syndromeMDS/acute myeloid leukemiaRefractory acute myeloid leukemiaPARP inhibitionVivo anti-tumor effectsAlternate therapeutic optionsSubset of AMLAnti-tumor effectsPre-clinical studiesRibose polymerase inhibitorsSerial transplantation assaysHomologous recombination defectsTherapeutic optionsTreatment optionsOverall engraftmentHigh relapseIDH inhibitionMyeloid leukemiaIsocitrate dehydrogenase 1Small molecule inhibitorsCell frequencyXeno-graftsIDH1/2 mutationsMalignant transformation
2020
Cyclosporine enhances the sensitivity to lenalidomide in MDS/AML in vitro
He X, Dou A, Feng S, Roman-Rivera A, Hawkins C, Lawley L, Zhang J, Wunderlich M, Mizukawa B, Halene S, Patel A, Fang J. Cyclosporine enhances the sensitivity to lenalidomide in MDS/AML in vitro. Experimental Hematology 2020, 86: 21-27.e2. PMID: 32437909, PMCID: PMC7335335, DOI: 10.1016/j.exphem.2020.05.001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell Line, TumorCyclosporineDNA-Binding ProteinsDrug Resistance, NeoplasmGene Expression Regulation, LeukemicHumansIkaros Transcription FactorLenalidomideLeukemia, Myeloid, AcuteMiceMice, Inbred NODMuscle ProteinsMyelodysplastic SyndromesNeoplasm ProteinsUp-RegulationXenograft Model Antitumor AssaysConceptsAcute myeloid leukemiaMDS/acute myeloid leukemiaMyelodysplastic syndromeT cell activationAML patient-derived xenograft modelsG protein-coupled receptor 68MDS/AML cellsPatient-derived xenograft modelsMDS/AML cell linesDegradation of IKZF1AML cell linesCell linesActivity of CaNBone marrow cellsMDS patientsPrimary bone marrow cellsHematologic malignanciesMyeloid leukemiaAML cellsLenalidomideXenograft modelDrug AdministrationSuppressive effectProsurvival pathwaysMarrow cells
2017
Bok Promotes Erythropoiesis in a Mouse Model of Myelodysplastic Syndrome
Kang S, Perales O, Michuad M, Katz S. Bok Promotes Erythropoiesis in a Mouse Model of Myelodysplastic Syndrome. Blood 2017, 130: 922. DOI: 10.1182/blood.v130.suppl_1.922.922.Peer-Reviewed Original ResearchAcute myeloid leukemiaNHD13 miceMean cell hemoglobin concentrationMouse modelBone marrowMean cell volumeMDS/acute myeloid leukemiaRBC progenitorsUnfolded protein responseSimilar overall survivalTransgenic mouse modelPathogenesis of myelodysplasiaER stressHigher mean cell volumeLower mean cell hemoglobin concentrationCell hemoglobin concentrationAnti-apoptotic Bcl-2Endoplasmic reticulum stressOverall survivalProgenitor stem cellsRed blood cellsLower hemoglobinMyelodysplastic syndromeMyeloid leukemiaRegulation of erythropoiesis
2016
Myelodysplastic Syndromes and Acute Myeloid Leukemia After Radiotherapy for Prostate Cancer: A Population‐Based Study
Wang R, Zeidan AM, Yu JB, Soulos PR, Davidoff AJ, Gore SD, Huntington SF, Gross CP, Ma X. Myelodysplastic Syndromes and Acute Myeloid Leukemia After Radiotherapy for Prostate Cancer: A Population‐Based Study. The Prostate 2016, 77: 437-445. PMID: 27868212, PMCID: PMC5785924, DOI: 10.1002/pros.23281.Peer-Reviewed Original ResearchConceptsMDS/acute myeloid leukemiaAcute myeloid leukemiaProstate cancer patientsElderly prostate cancer patientsImpact of radiotherapyCancer patientsMyelodysplastic syndromeNational Cancer Institute's SurveillanceSubsequent myelodysplastic syndromeEnd Results-MedicareRetrospective cohort studyRole of radiotherapyInformed treatment decisionsUnderwent radiotherapyIMRT groupCohort studyPatient characteristicsMedian timeMyeloid leukemiaProstate cancerTreatment decisionsPatientsRadiotherapyMyeloid malignanciesSurgery
2015
Secondary Myeloid Neoplasms in Older Women with Breast Cancer after Radiotherapy: A Population-Based Study
Zeidan A, Long J, Wang R, Yu J, Hall J, Abel G, Gore S, Gross C, Ma X, Davidoff A. Secondary Myeloid Neoplasms in Older Women with Breast Cancer after Radiotherapy: A Population-Based Study. Blood 2015, 126: 1676. DOI: 10.1182/blood.v126.23.1676.1676.Peer-Reviewed Original ResearchTherapy-related myeloid neoplasmsMDS/acute myeloid leukemiaSingle-modality radiotherapyAcute myeloid leukemiaBreast cancer patientsMonths of diagnosisEarly breast cancerCompeting-risk analysisMyelodysplastic syndromeBreast cancerCancer patientsBreast cancer diagnosisRisk factorsMyeloid neoplasmsRadiation therapyAML/myelodysplastic syndromeFemale breast cancer patientsNational Cancer Institute's SurveillanceRadiotherapy-treated patientsReceipt of radiotherapySecondary myeloid neoplasmsRetrospective cohort studyCancer diagnosisNumber of comorbiditiesBetter overall survival
2006
SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice
Ma Y, Cui W, Yang J, Qu J, Di C, Amin HM, Lai R, Ritz J, Krause DS, Chai L. SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice. Blood 2006, 108: 2726-2735. PMID: 16763212, PMCID: PMC1895586, DOI: 10.1182/blood-2006-02-001594.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAnimalsApoptosisBase Sequencebeta CateninCloning, MolecularColony-Forming Units AssayDNA-Binding ProteinsDNA, ComplementaryDNA, NeoplasmGene ExpressionHematopoiesisHumansLeukemia, Myeloid, AcuteMiceMice, TransgenicMyelodysplastic SyndromesNeoplasm TransplantationOncogenesProtein IsoformsRNA, MessengerRNA, NeoplasmSignal TransductionTranscription FactorsWnt ProteinsConceptsAcute myeloid leukemiaMyeloid leukemiaMurine modelTransgenic miceHuman primary acute myeloid leukemiaMDS/acute myeloid leukemiaPrimary acute myeloid leukemiaHuman acute myeloid leukemiaLeukemia stem cellsAML transformationMyelodysplastic syndromePolymerase chain reactionWnt/beta-catenin pathwayZinc finger transcriptional factorNovel oncogeneBeta-catenin pathwayLeukemogenic potentialConstitutive expressionChain reactionPathway's roleLeukemiaSALL4MiceStem cellsMouse marrow
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