2025
Chromosome 1p Loss and 1q Gain for Grading of Meningioma
Landry A, Wang J, Patil V, Liu J, Gui C, Ellenbogen Y, Ajisebutu A, Yefet L, Wei Q, Singh O, Sosa J, Mansouri S, Cohen-Gadol A, Tabatabai G, Tatagiba M, Behling F, Barnholtz-Sloan J, Sloan A, Chotai S, Chambless L, Mansouri A, Makarenko S, Yip S, Ehret F, Capper D, Tsang D, Moliterno J, Gunel M, Wesseling P, Sahm F, Aldape K, Gao A, Zadeh G, Nassiri F. Chromosome 1p Loss and 1q Gain for Grading of Meningioma. JAMA Oncology 2025, 11: 644-649. PMID: 40178835, PMCID: PMC11969356, DOI: 10.1001/jamaoncol.2025.0329.Peer-Reviewed Original ResearchConceptsClassification of central nervous system tumorsChromosomal copy number alterationsProgression-free survivalChromosome 1p lossCopy number alterationsLoss of chromosome 1pGrading of meningiomasWHO gradeWorld Health OrganizationChromosome 1pWorld Health Organization grade 1 meningiomasWorld Health Organization grade 1 tumorWorld Health Organization grade 2 tumorsGain of chromosome 1qHomozygous deletion of CDKN2AAssociated with significantly worse outcomesCentral nervous system tumorsHistopathological diagnosis of meningiomaGrade 3 tumorsGrade 1 tumorsGrade 2 tumorsLoss of 1pGrade 1 meningiomasOutcomes of patientsDeletion of CDKN2ADifferential links in 16p11.2 deletion carriers reveal aberrant connections between large-scale networks
Qureshi A, Nielsen J, Sepulcre J. Differential links in 16p11.2 deletion carriers reveal aberrant connections between large-scale networks. Cerebral Cortex 2025, 35: bhae474. PMID: 40007052, PMCID: PMC11859958, DOI: 10.1093/cercor/bhae474.Peer-Reviewed Original ResearchConceptsInferior parietal lobuleSuperior temporal gyrusLarge-scale networksDeletion carriersHeteromodal association areasDifferential linksHypo-connectivitySocial impairmentTemporal gyrusParietal lobulePosterior insulaAssociated with greater communicationAberrant connectivityAssociation areasCingulate sulcusBehavioral changesGlobal coherenceEntangled connectionsSulcusGreater communicationInsulaCingulateGyrusCopy number variationsImpairmentDecreased T helper 1 cell function underlies recurrent sinopulmonary infections in the 17q12 deletion syndrome
Shin J, Shin H, Gutierrez A, Yoo N, Par-Young J, Osmani L, Shin M, Sanchez-Lara P, Bucala R, Soffer G, Kang I. Decreased T helper 1 cell function underlies recurrent sinopulmonary infections in the 17q12 deletion syndrome. EBioMedicine 2025, 112: 105578. PMID: 39891996, PMCID: PMC11840234, DOI: 10.1016/j.ebiom.2025.105578.Peer-Reviewed Original ResearchConceptsCD4<sup>+</sup> T cellsRecurrent sinopulmonary infectionsT cell functionRNA-seq analysisT cellsHealthy controlsSinopulmonary infectionsRNA-seqT-betIFN-gFrequency of CD4<sup>+</sup> T cellsCD4<sup>+</sup> T cell functionTh1 transcription factor T-betDeletion syndromeFlow cytometryCompared to age-matched healthy controlsTranscription factor T-betDecreased T-betUrinary tract abnormalitiesAge-matched healthy controlsMultiplex assayDownstream effector cytokinesEffector cytokinesRecurrent infectionsTh17 cytokines
2024
Investigating social orienting in children with Phelan-McDermid syndrome and ‘idiopathic’ autism
San José Cáceres A, Wilkinson E, Cooke J, Baskett V, Blackmore C, Crawley D, Durkin A, Halpern D, Núñez M, Siper P, Murphy D, Foss-Feig J, Kolevzon A, Loth E. Investigating social orienting in children with Phelan-McDermid syndrome and ‘idiopathic’ autism. Journal Of Neurodevelopmental Disorders 2024, 16: 64. PMID: 39563223, PMCID: PMC11575217, DOI: 10.1186/s11689-024-09564-7.Peer-Reviewed Original ResearchConceptsNon-social stimuliPhelan-McDermid syndromeNeurotypical childrenIdiopathic autismAutistic featuresClinical groupsOrienting responseSocial orientationBackgroundPhelan-McDermid syndromeMental ageAutism groupSocial stimuliStimulus typeMotivational difficultiesAutismDevelopmental delay/intellectual disabilityDelayed speechSocial interactionStimuliPMS groupConclusionsThese findingsGroup levelSocial learningChildrenAtypicalityResolving the 22q11.2 deletion using CTLR-Seq reveals chromosomal rearrangement mechanisms and individual variance in breakpoints
Zhou B, Purmann C, Guo H, Shin G, Huang Y, Pattni R, Meng Q, Greer S, Roychowdhury T, Wood R, Ho M, Dohna H, Abyzov A, Hallmayer J, Wong W, Ji H, Urban A. Resolving the 22q11.2 deletion using CTLR-Seq reveals chromosomal rearrangement mechanisms and individual variance in breakpoints. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2322834121. PMID: 39042694, PMCID: PMC11295037, DOI: 10.1073/pnas.2322834121.Peer-Reviewed Original ResearchConceptsLong-read sequencingPulse-field gel electrophoresisBase-pair resolutionDNA methylation patternsCell-type specific analysisCell type-specificChromosomal interactionsSequence assemblySegmental duplicationsGenome sequenceGenomic rearrangementsGenomic regionsChromosomal breakpointsHuman genomeGenomic recombinationMethylation patternsSequence analysisHaplotype-specificDeletion haplotypesGel electrophoresisGenomeAmplification-freeBreakpoint locationsMicrodeletion disorderType-specificTranscriptomic dysregulation and autistic-like behaviors in Kmt2c haploinsufficient mice rescued by an LSD1 inhibitor
Nakamura T, Yoshihara T, Tanegashima C, Kadota M, Kobayashi Y, Honda K, Ishiwata M, Ueda J, Hara T, Nakanishi M, Takumi T, Itohara S, Kuraku S, Asano M, Kasahara T, Nakajima K, Tsuboi T, Takata A, Kato T. Transcriptomic dysregulation and autistic-like behaviors in Kmt2c haploinsufficient mice rescued by an LSD1 inhibitor. Molecular Psychiatry 2024, 29: 2888-2904. PMID: 38528071, PMCID: PMC11420081, DOI: 10.1038/s41380-024-02479-8.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutism Spectrum DisorderAutistic DisorderBehavior, AnimalBrainChromosome DeletionChromosomes, Human, Pair 9Craniofacial AbnormalitiesDisease Models, AnimalFemaleHaploinsufficiencyHeart Defects, CongenitalHistone DemethylasesHistone-Lysine N-MethyltransferaseIntellectual DisabilityMaleMiceMice, Inbred C57BLTranscriptomeConceptsLysine-specific histone demethylase 1Lysine‐specific histone demethylase 1 inhibitorAssociated with autism spectrum disorderHeterozygous loss-of-function variantsHistone H3 lysine 4Autistic-like behaviorsLoss-of-function variantsGenome-wide associationH3 lysine 4ASD risk genesRegulation of chromatinSingle-cell RNA sequencingHeterozygous frameshift mutationWorking memoryMutant miceChIP-seqLysine 4Downregulated DEGsCategories of psychiatric disordersExome sequencingPathogenesis of neurodevelopmental disordersTranscriptome analysisRisk genesDownregulated genesTranscriptomic dysregulation
2023
Beyond the Global Brain Differences: Intraindividual Variability Differences in 1q21.1 Distal and 15q11.2 BP1-BP2 Deletion Carriers
Boen R, Kaufmann T, van der Meer D, Frei O, Agartz I, Ames D, Andersson M, Armstrong N, Artiges E, Atkins J, Bauer J, Benedetti F, Boomsma D, Brodaty H, Brosch K, Buckner R, Cairns M, Calhoun V, Caspers S, Cichon S, Corvin A, Crespo-Facorro B, Dannlowski U, David F, de Geus E, de Zubicaray G, Desrivières S, Doherty J, Donohoe G, Ehrlich S, Eising E, Espeseth T, Fisher S, Forstner A, Fortaner-Uyà L, Frouin V, Fukunaga M, Ge T, Glahn D, Goltermann J, Grabe H, Green M, Groenewold N, Grotegerd D, Grøntvedt G, Hahn T, Hashimoto R, Hehir-Kwa J, Henskens F, Holmes A, Håberg A, Haavik J, Jacquemont S, Jansen A, Jockwitz C, Jönsson E, Kikuchi M, Kircher T, Kumar K, Le Hellard S, Leu C, Linden D, Liu J, Loughnan R, Mather K, McMahon K, McRae A, Medland S, Meinert S, Moreau C, Morris D, Mowry B, Mühleisen T, Nenadić I, Nöthen M, Nyberg L, Ophoff R, Owen M, Pantelis C, Paolini M, Paus T, Pausova Z, Persson K, Quidé Y, Marques T, Sachdev P, Sando S, Schall U, Scott R, Selbæk G, Shumskaya E, Silva A, Sisodiya S, Stein F, Stein D, Straube B, Streit F, Strike L, Teumer A, Teutenberg L, Thalamuthu A, Tooney P, Tordesillas-Gutierrez D, Trollor J, van ’t Ent D, van den Bree M, van Haren N, Vázquez-Bourgon J, Völzke H, Wen W, Wittfeld K, Ching C, Westlye L, Thompson P, Bearden C, Selmer K, Alnæs D, Andreassen O, Sønderby I, Group E. Beyond the Global Brain Differences: Intraindividual Variability Differences in 1q21.1 Distal and 15q11.2 BP1-BP2 Deletion Carriers. Biological Psychiatry 2023, 95: 147-160. PMID: 37661008, PMCID: PMC7615370, DOI: 10.1016/j.biopsych.2023.08.018.Peer-Reviewed Original ResearchMeSH KeywordsAbnormalities, MultipleBrainChromosome DeletionChromosomes, Human, Pair 15DNA Copy Number VariationsHumansMagnetic Resonance ImagingConceptsMedial visual cortexCortical surface areaBrain differencesCortical thicknessTemporal poleVisual cortexDeletion carriersGlobal brain measuresRegional brain differencesCopy number variantsSuperior temporal cortexSomatosensory cortexBrain valuesAltered neurodevelopmentAuditory cortexGlobal differencesRegional differencesTemporal cortexNumber variantsPosterior cingulateCortexBrain structuresBrain measuresStandardized differenceNoncarriersPRDM16 Deletion Is Associated With Sex-dependent Cardiomyopathy and Cardiac Mortality: A Translational, Multi-Institutional Cohort Study
Kramer R, Fatahian A, Chan A, Mortenson J, Osher J, Sun B, Parker L, Rosamilia M, Potter K, Moore K, Atkins S, Rosenfeld J, Birjiniuk A, Jones E, Howard T, Kim J, Scott D, Lalani S, Rouzbehani O, Kaplan S, Hathaway M, Cohen J, Asaki S, Martinez H, Boudina S, Landstrom A. PRDM16 Deletion Is Associated With Sex-dependent Cardiomyopathy and Cardiac Mortality: A Translational, Multi-Institutional Cohort Study. Circulation Genomic And Precision Medicine 2023, 16: 390-400. PMID: 37395136, PMCID: PMC10528350, DOI: 10.1161/circgen.122.003912.Peer-Reviewed Original ResearchConceptsConditional knockout miceKnockout miceCardiac transplantationCardiac mortalityRetrospective cohortIncreased risk of cardiomyopathyVentricular assist deviceDeletion syndromeAssociated with increased risk of deathMulti-institutional cohort studyReview cohortPediatric-onset cardiomyopathiesAssociated with increased riskRisk of cardiomyopathyPrevalence of cardiomyopathyRisk of deathSeverity of contractile dysfunctionPrognostic impactAssess fibrosisContractile dysfunctionCohort studyCardiomyopathyCardiac diseaseIncreased riskAssist device
2021
Cortical organoids model early brain development disrupted by 16p11.2 copy number variants in autism
Urresti J, Zhang P, Moran-Losada P, Yu N, Negraes P, Trujillo C, Antaki D, Amar M, Chau K, Pramod A, Diedrich J, Tejwani L, Romero S, Sebat J, Yates III J, Muotri A, Iakoucheva L. Cortical organoids model early brain development disrupted by 16p11.2 copy number variants in autism. Molecular Psychiatry 2021, 26: 7560-7580. PMID: 34433918, PMCID: PMC8873019, DOI: 10.1038/s41380-021-01243-6.Peer-Reviewed Original ResearchConceptsCortical organoidsCommon copy number variationNeural progenitorsRatio of neuronsPotential neurobiological mechanismsOrganoid sizeEarly brain developmentSynapse numberNeuronal maturationMigration deficitsBrain developmentNeurodevelopmental processesIon channel activityNeurobiological mechanismsNeuron migrationNeocortical developmentSkin fibroblastsChannel activityPatientsEarly neurogenesisMicrocephaly phenotypeNeurite outgrowthNeuronsAutism spectrum disorderSmall GTPase RhoAClinical effectiveness of DNA methyltransferase inhibitors and lenalidomide in older patients with refractory anemia with ring sideroblasts: a population-based study in the United States
Wang X, Zeidan AM, Wang R, Bewersdorf JP, Zhang C, Podoltsev NA, Huntington SF, Gore SD, Ma X. Clinical effectiveness of DNA methyltransferase inhibitors and lenalidomide in older patients with refractory anemia with ring sideroblasts: a population-based study in the United States. Leukemia & Lymphoma 2021, 62: 2438-2447. PMID: 33899659, DOI: 10.1080/10428194.2021.1913142.Peer-Reviewed Original ResearchConceptsPopulation-based studyDNA methyltransferase inhibitorRARS patientsRefractory anemiaRing sideroblastsRed blood cell transfusion independenceEnd Results-Medicare databaseLower-risk myelodysplastic syndromesPopulation-based cohortMethyltransferase inhibitorRBC-TIMedian durationMedian survivalOlder patientsTransfusion independenceTreatment initiationMyelodysplastic syndromeClinical effectivenessBetter survivalLenalidomideTreatment groupsPatientsRS statusOlder adultsAnemia
2020
Ring chromosome formation by intra‐strand repairing of subtelomeric double stand breaks and clinico‐cytogenomic correlations for ring chromosome 9
Chai H, Ji W, Wen J, DiAdamo A, Grommisch B, Hu Q, Szekely AM, Li P. Ring chromosome formation by intra‐strand repairing of subtelomeric double stand breaks and clinico‐cytogenomic correlations for ring chromosome 9. American Journal Of Medical Genetics Part A 2020, 182: 3023-3028. PMID: 32978894, DOI: 10.1002/ajmg.a.61890.Peer-Reviewed Original ResearchTranscriptional signatures of participant-derived neural progenitor cells and neurons implicate altered Wnt signaling in Phelan-McDermid syndrome and autism
Breen MS, Browne A, Hoffman GE, Stathopoulos S, Brennand K, Buxbaum JD, Drapeau E. Transcriptional signatures of participant-derived neural progenitor cells and neurons implicate altered Wnt signaling in Phelan-McDermid syndrome and autism. Molecular Autism 2020, 11: 53. PMID: 32560742, PMCID: PMC7304190, DOI: 10.1186/s13229-020-00355-0.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAutistic DisorderChildChild, PreschoolChromosome DeletionChromosome DisordersChromosomes, Human, Pair 22FemaleGene Expression ProfilingGene Expression RegulationHumansInduced Pluripotent Stem CellsMaleNeural Stem CellsNeuronsReproducibility of ResultsWnt Signaling PathwayConceptsNeural progenitor cellsTranscriptional signatureGene co-expression network analysisHiPSC-NPCsCo-expression network analysisIndependent biological samplesHiPSC-derived neural cellsProgenitor cellsPostsynaptic density genesDistinct transcriptional signaturesGenetic risk lociHuman-induced pluripotent stem cellsPluripotent stem cellsPotassium channel activityProtein translationSpecific neurobiological pathwaysTranscriptional differencesEmbryonic developmentLoss of SHANK3Risk lociHiPSC neuronsMorphological phenotypesWnt pathwayGenesHiPSC clonesInterplay of somatic alterations and immune infiltration modulates response to PD-1 blockade in advanced clear cell renal cell carcinoma
Braun DA, Hou Y, Bakouny Z, Ficial M, Sant’ Angelo M, Forman J, Ross-Macdonald P, Berger AC, Jegede OA, Elagina L, Steinharter J, Sun M, Wind-Rotolo M, Pignon JC, Cherniack AD, Lichtenstein L, Neuberg D, Catalano P, Freeman GJ, Sharpe AH, McDermott DF, Van Allen EM, Signoretti S, Wu CJ, Shukla SA, Choueiri TK. Interplay of somatic alterations and immune infiltration modulates response to PD-1 blockade in advanced clear cell renal cell carcinoma. Nature Medicine 2020, 26: 909-918. PMID: 32472114, PMCID: PMC7499153, DOI: 10.1038/s41591-020-0839-y.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntigen PresentationAntineoplastic Agents, ImmunologicalCarcinoma, Renal CellCD8-Positive T-LymphocytesChromosome DeletionChromosomes, Human, Pair 6Chromosomes, Human, Pair 9Class I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsExome SequencingFemaleFluorescent Antibody TechniqueGene DeletionGenomicsHistocompatibility Antigens Class IIHistone DemethylasesHistone-Lysine N-MethyltransferaseHumansKidney NeoplasmsLymphocytes, Tumor-InfiltratingMaleMiddle AgedMutationNivolumabPrognosisProteasome Endopeptidase ComplexPTEN PhosphohydrolaseSequence Analysis, RNATOR Serine-Threonine KinasesTranscription FactorsTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsUbiquitin ThiolesteraseVon Hippel-Lindau Tumor Suppressor ProteinConceptsAdvanced clear cell renal cell carcinomaClear cell renal cell carcinomaPD-1 blockadeCell renal cell carcinomaRenal cell carcinomaCell carcinomaDegree of CD8Numerous chromosomal alterationsProspective clinical trialsSomatic alterationsInfiltrated tumorsClinical responseCell infiltrationTherapeutic responseClinical trialsTherapeutic efficacyBlockadeCcRCC tumorsTumorsPBRM1 mutationsModulates responseCD8Chromosomal alterationsImmunofluorescence analysisCarcinomaClinical and genetic characterization of patients with Pierre Robin sequence and spinal disease: review of the literature and novel terminal 10q deletion
Yekula A, Grant C, Gupta M, Santiago-Dieppa DR, Duddleston PJ, Gonda D, Levy M. Clinical and genetic characterization of patients with Pierre Robin sequence and spinal disease: review of the literature and novel terminal 10q deletion. Child's Nervous System 2020, 36: 1367-1377. PMID: 32399800, PMCID: PMC7300078, DOI: 10.1007/s00381-020-04642-2.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAirway ObstructionChromosome DeletionChromosomes, Human, Pair 10FemaleHumansInfantInfant, NewbornPierre Robin SyndromeSpinal DiseasesConceptsPierre Robin sequenceSpinal diseaseTethered cordEarly genetic testingMagnetic resonance imagingOutpatient checkupsPRS patientsAirway obstructionNeurological assessmentPatient populationRobin sequenceClinical managementDisease burdenSpinal cordMotor functionSacral dimpleSpinal disordersSpinal pathologyPatientsSystematic reviewTerminal deletionResonance imagingClinical screeningChromosome 10qGenetic syndromes
2019
Inverted duplication, triplication and quintuplication through sequential breakage‐fusion‐bridge events induced by a terminal deletion at 5p in a case of spontaneous abortion
Chai H, Grommisch B, DiAdamo A, Wen J, Hui P, Li P. Inverted duplication, triplication and quintuplication through sequential breakage‐fusion‐bridge events induced by a terminal deletion at 5p in a case of spontaneous abortion. Molecular Genetics & Genomic Medicine 2019, 7: e00965. PMID: 31478360, PMCID: PMC6785443, DOI: 10.1002/mgg3.965.Peer-Reviewed Original Research1q21.1 Deletions and Duplications in 2 Siblings with Psychiatric Problems
Kaymakçalan H, Li P. 1q21.1 Deletions and Duplications in 2 Siblings with Psychiatric Problems. Indian Journal Of Pediatrics 2019, 86: 1068-1068. PMID: 31270733, DOI: 10.1007/s12098-019-03014-2.Peer-Reviewed Original ResearchPolysomy is associated with poor outcome in 1p/19q codeleted oligodendroglial tumors
Chen H, Thomas C, Munoz FA, Alexandrescu S, Horbinski CM, Olar A, McGuone D, Camelo-Piragua S, Wang L, Pentsova E, Phillips J, Aldape K, Chen W, Iafrate AJ, S AS, Zagzag D, Golfinos JG, Placantonakis DG, Rosenblum M, Ohman-Strickland P, Hameed M, Snuderl M. Polysomy is associated with poor outcome in 1p/19q codeleted oligodendroglial tumors. Neuro-Oncology 2019, 21: 1164-1174. PMID: 31140557, PMCID: PMC7571489, DOI: 10.1093/neuonc/noz098.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAged, 80 and overAneuploidyBrain NeoplasmsChemotherapy, AdjuvantChildChromosomal InstabilityChromosome DeletionChromosomes, Human, Pair 1Chromosomes, Human, Pair 19FemaleHumansIn Situ Hybridization, FluorescenceIsocitrate DehydrogenaseMaleMiddle AgedNeoadjuvant TherapyNeurosurgical ProceduresOligodendrogliomaPrognosisProgression-Free SurvivalRadiotherapy, AdjuvantSurvival RateYoung AdultConceptsProgression-free survivalOverall survivalOligodendroglial tumorsPrognostic significanceBetter progression-free survivalLonger progression-free survivalPolysomic cellsCodeletion of 1p/19qPresence of polysomyEarly recurrenceShorter survivalPoor outcomeEarly progressionPatientsTumorsSurvivalPolysomySitu hybridizationCodeletionChromosomal instabilityCellsGroupPrior studiesStatusRecurrence
2018
De novo truncating variants in WHSC1 recapitulate the Wolf–Hirschhorn (4p16.3 microdeletion) syndrome phenotype
Derar N, Al-Hassnan Z, Al-Owain M, Monies D, Abouelhoda M, Meyer B, Moghrabi N, Alkuraya F. De novo truncating variants in WHSC1 recapitulate the Wolf–Hirschhorn (4p16.3 microdeletion) syndrome phenotype. Genetics In Medicine 2018, 21: 185-188. PMID: 29892088, DOI: 10.1038/s41436-018-0014-8.Peer-Reviewed Original ResearchConceptsDe novo truncating variantsHaploinsufficiency of multiple genesSingle-gene levelMicrodeletion syndromeDisease genesGenomic disordersExome sequencingMultiple genesSingle-geneWHSC1Syndrome phenotypeCore phenotypePhenotypePhenotypic expressionLociWolf-HirschhornGenesPhenotypic componentsMicrodeletionHaploinsufficiencyVariantsMilder variantsHemizygosityConclusionOur studySequenceIris Hypoplasia as the Presenting Sign of Retinoblastoma in a Child With a 13q Deletion.
Shah S, Koban Y, Le BHA, Bechtold M, Zolfaghari E, Kim JW, Berry JL. Iris Hypoplasia as the Presenting Sign of Retinoblastoma in a Child With a 13q Deletion. Journal Of Pediatric Ophthalmology & Strabismus 2018, 55: e10-e13. PMID: 29684226, PMCID: PMC7444716, DOI: 10.3928/01913913-20180215-02.Peer-Reviewed Original ResearchChromosome DeletionChromosome DisordersChromosomes, Human, Pair 13Diagnosis, DifferentialDNA Mutational AnalysisDNA, NeoplasmFemaleFluorescein AngiographyFundus OculiHumansInfantIrisIris DiseasesMagnetic Resonance ImagingMutationPigmentation DisordersRetinoblastomaRetinoblastoma Binding ProteinsTomography, Optical CoherenceUbiquitin-Protein LigasesLenalidomide in non-deletion 5q lower-risk myelodysplastic syndromes: a glass quarter full or three quarters empty?
Shallis RM, Zeidan AM. Lenalidomide in non-deletion 5q lower-risk myelodysplastic syndromes: a glass quarter full or three quarters empty? Leukemia & Lymphoma 2018, 59: 2015-2017. PMID: 29411698, DOI: 10.1080/10428194.2018.1430797.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsAbnormalities, MultipleChromosome DeletionChromosomes, Human, Pair 2HumansLenalidomideMyelodysplastic Syndromes
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply