2005
Molecular biomarkers for the study of childhood leukemia
Smith MT, McHale CM, Wiemels JL, Zhang L, Wiencke JK, Zheng S, Gunn L, Skibola CF, Ma X, Buffler PA. Molecular biomarkers for the study of childhood leukemia. Toxicology And Applied Pharmacology 2005, 206: 237-245. PMID: 15967214, DOI: 10.1016/j.taap.2004.11.026.Peer-Reviewed Original ResearchConceptsAcute myeloid leukemiaAcute lymphocytic leukemiaChildhood leukemiaLeukemia riskChildhood acute lymphocytic leukemiaC609T polymorphismLow folate intakeNeonatal blood spotsYears of lifeMethylenetetrahydrofolate reductase (MTHFR) geneDifferent cytogenetic subgroupsPerinatal exposureFolate intakeMyeloid leukemiaLymphocytic leukemiaT polymorphismUseful biomarkerInfectious agentsAberrant gene methylationLeukemiaCytogenetic subgroupsBlood spotsMolecular biomarkersIndoor pesticidesGene methylation
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
2003
Prenatal origin of childhood acute myeloid leukemias harboring chromosomal rearrangements t(15;17) and inv(16)
McHale CM, Wiemels JL, Zhang L, Ma X, Buffler PA, Feusner J, Matthay K, Dahl G, Smith MT. Prenatal origin of childhood acute myeloid leukemias harboring chromosomal rearrangements t(15;17) and inv(16). Blood 2003, 101: 4640-4641. PMID: 12756163, DOI: 10.1182/blood-2003-01-0313.Peer-Reviewed Original Research
2002
Site-specific translocation and evidence of postnatal origin of the t(1;19) E2A-PBX1 fusion in childhood acute lymphoblastic leukemia
Wiemels JL, Leonard BC, Wang Y, Segal MR, Hunger SP, Smith MT, Crouse V, Ma X, Buffler PA, Pine SR. Site-specific translocation and evidence of postnatal origin of the t(1;19) E2A-PBX1 fusion in childhood acute lymphoblastic leukemia. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 15101-15106. PMID: 12415113, PMCID: PMC137550, DOI: 10.1073/pnas.222481199.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentArtificial Gene FusionBase SequenceChildChild, PreschoolChromosome MappingChromosomes, Human, Pair 1Chromosomes, Human, Pair 19FemaleGene RearrangementHomeodomain ProteinsHumansImmunoglobulin Heavy ChainsInfantMaleMolecular Sequence DataOncogene Proteins, FusionPolymerase Chain ReactionPrecursor Cell Lymphoblastic Leukemia-LymphomaReceptors, Antigen, T-CellRestriction MappingTranslocation, GeneticConceptsAcute lymphoblastic leukemiaLymphoblastic leukemiaTime of birthChildhood acute lymphoblastic leukemiaE2A-PBX1 fusionSubtype of leukemiaAntigen receptor rearrangementNeonatal blood spotsIg heavy chainPediatric patientsTCR rearrangementsPrenatal originReceptor rearrangementPostnatal originCell originMolecular subgroupsLeukemiaNatural historyBlood spotsGuthrie cardsPatientsCell linesChromosomal translocationsPBX1 geneGenomic fusionIn utero origin of t(8;21) AML1-ETO translocations in childhood acute myeloid leukemia
Wiemels JL, Xiao Z, Buffler PA, Maia AT, Ma X, Dicks BM, Smith MT, Zhang L, Feusner J, Wiencke J, Pritchard-Jones K, Kempski H, Greaves M. In utero origin of t(8;21) AML1-ETO translocations in childhood acute myeloid leukemia. Blood 2002, 99: 3801-3805. PMID: 11986239, DOI: 10.1182/blood.v99.10.3801.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseChildChild, PreschoolChromosomes, Human, Pair 21Chromosomes, Human, Pair 8Core Binding Factor Alpha 2 SubunitDNA, NeoplasmHumansInfant, NewbornLeukemia, MyeloidOncogene Proteins, FusionRemission InductionRUNX1 Translocation Partner 1 ProteinTranscription FactorsTranslocation, GeneticConceptsChildhood acute myeloid leukemiaAcute myeloid leukemiaPrenatal originAML1–ETO translocationsMyeloid leukemiaGenomic fusion sequencesYears of ageTEL-AML1 translocationUtero originRemission samplesSecondary genetic alterationsGuthrie blood spotsBlood spotsGuthrie spotsPatientsLeukemiaLeukemia samplesGenetic alterationsRecent reportsFusion geneChildrenResultant fusion geneTranslocationInfantsUtero