2021
The genome-wide impact of trisomy 21 on DNA methylation and its implications for hematopoiesis
Muskens IS, Li S, Jackson T, Elliot N, Hansen HM, Myint SS, Pandey P, Schraw JM, Roy R, Anguiano J, Goudevenou K, Siegmund KD, Lupo PJ, de Bruijn MFTR, Walsh KM, Vyas P, Ma X, Roy A, Roberts I, Wiemels JL, de Smith AJ. The genome-wide impact of trisomy 21 on DNA methylation and its implications for hematopoiesis. Nature Communications 2021, 12: 821. PMID: 33547282, PMCID: PMC7865055, DOI: 10.1038/s41467-021-21064-z.Peer-Reviewed Original ResearchMeSH KeywordsCase-Control StudiesCore Binding Factor Alpha 2 SubunitCpG IslandsDNA MethylationDown SyndromeEpigenesis, GeneticFemaleFetusGATA1 Transcription FactorGenome, HumanGenome-Wide Association StudyHematopoiesisHematopoietic Stem CellsHumansInfant, NewbornLiverMalePromoter Regions, GeneticProto-Oncogene Protein c-fli-1ConceptsDNA methylationGenome-wide impactGenome-wide effectsGenome-wide perturbationsPromoter/enhancer regionEpigenome-wide association studiesAssociation study resultsGene expression changesHematopoietic stem/progenitor cellsCell-type heterogeneityStem/progenitor cellsEpigenome-wide significant CpGsHematopoietic developmentDifferential methylationEpigenetic changesGene expressionPromoter regionEnhancer regionExpression changesAssociation studiesSignificant CpGsImportant regulatorSignificant hypermethylationHematopoietic cellsMethylation
2014
PTPRG inhibition by DNA methylation and cooperation with RAS gene activation in childhood acute lymphoblastic leukemia
Xiao J, Lee S, Xiao Y, Ma X, Houseman EA, Hsu L, Roy R, Wrensch M, de Smith A, Chokkalingam A, Buffler P, Wiencke JK, Wiemels JL. PTPRG inhibition by DNA methylation and cooperation with RAS gene activation in childhood acute lymphoblastic leukemia. International Journal Of Cancer 2014, 135: 1101-1109. PMID: 24496747, PMCID: PMC4776754, DOI: 10.1002/ijc.28759.Peer-Reviewed Original ResearchMeSH KeywordsCell Transformation, NeoplasticChildChild, PreschoolDNA MethylationDNA-Binding ProteinsEnzyme ActivationEpigenesis, GeneticExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, LeukemicHEK293 CellsHumansMutationPhosphorylationPrecursor Cell Lymphoblastic Leukemia-LymphomaPromoter Regions, GeneticRas ProteinsReceptor-Like Protein Tyrosine Phosphatases, Class 5Transcription FactorsTranscriptional ActivationConceptsDNA methylationPTPRG expressionDNA methylation profilesDNA methylation statusDephosphorylation of ERKMember genesEpigenetic mechanismsGene activationMutant RASRAS gene activationMethylation profilesGene expressionPtprg geneMethylation statusCell growthAdditional roleMethylationPotential therapeutic targetCell linesGenetic characteristicsGenesLeukemia phenotypeTherapeutic targetMutationsExpression
2004
Hypermethylation of the 5′ CpG Island of the FHIT Gene Is Associated with Hyperdiploid and Translocation-Negative Subtypes of Pediatric Leukemia
Zheng S, Ma X, Zhang L, Gunn L, Smith MT, Wiemels JL, Leung K, Buffler PA, Wiencke JK. Hypermethylation of the 5′ CpG Island of the FHIT Gene Is Associated with Hyperdiploid and Translocation-Negative Subtypes of Pediatric Leukemia. Cancer Research 2004, 64: 2000-2006. PMID: 15026336, DOI: 10.1158/0008-5472.can-03-2387.Peer-Reviewed Original ResearchMeSH KeywordsAcid Anhydride HydrolasesAdolescentAntimetabolites, AntineoplasticAzacitidineB-LymphocytesChildChild, PreschoolChromosomes, Human, Pair 12Chromosomes, Human, Pair 21CpG IslandsDecitabineDiploidyDNA MethylationDNA, NeoplasmFemaleGene DeletionGene Expression Regulation, NeoplasticHumansLeukemia, MyeloidMaleNeoplasm ProteinsPrecursor Cell Lymphoblastic Leukemia-LymphomaPromoter Regions, GeneticT-LymphocytesTranslocation, GeneticTumor Cells, CulturedConceptsPediatric leukemiaFHIT geneB cellsLeukemia cell linesFHIT methylation statusHigh WBC countPopulation-based casesChildhood leukemia patientsCell linesHyperdiploid B cellsHypermethylation of FHITPrognostic indicatorWBC countMethylation-specific PCRLeukemia patientsMyeloid leukemiaCytogenetic subtypesLoss of heterozygosityBone marrowFHIT expressionPrimary leukemiasFHIT inactivationFHIT methylationHuman malignanciesLeukemia