2017
Antagonism of B cell enhancer networks by STAT5 drives leukemia and poor patient survival
Katerndahl CDS, Heltemes-Harris LM, Willette MJL, Henzler CM, Frietze S, Yang R, Schjerven H, Silverstein KAT, Ramsey LB, Hubbard G, Wells AD, Kuiper RP, Scheijen B, van Leeuwen FN, Müschen M, Kornblau SM, Farrar MA. Antagonism of B cell enhancer networks by STAT5 drives leukemia and poor patient survival. Nature Immunology 2017, 18: 694-704. PMID: 28369050, PMCID: PMC5540372, DOI: 10.1038/ni.3716.Peer-Reviewed Original ResearchAdaptor Proteins, Signal TransducingAgammaglobulinaemia Tyrosine KinaseAnimalsB-LymphocytesChromatin ImmunoprecipitationFlow CytometryGene Expression Regulation, NeoplasticHumansIkaros Transcription FactorInterferon Regulatory FactorsMiceMultiplex Polymerase Chain ReactionNF-kappa B p50 SubunitPAX5 Transcription FactorPre-B Cell ReceptorsPrecursor Cell Lymphoblastic Leukemia-LymphomaPrognosisProtein Kinase C betaProtein-Tyrosine KinasesProto-Oncogene ProteinsReal-Time Polymerase Chain ReactionSignal TransductionSTAT5 Transcription FactorSurvival RateTrans-Activators
2015
Mechanisms of clonal evolution in childhood acute lymphoblastic leukemia
Swaminathan S, Klemm L, Park E, Papaemmanuil E, Ford A, Kweon SM, Trageser D, Hasselfeld B, Henke N, Mooster J, Geng H, Schwarz K, Kogan SC, Casellas R, Schatz DG, Lieber MR, Greaves MF, Müschen M. Mechanisms of clonal evolution in childhood acute lymphoblastic leukemia. Nature Immunology 2015, 16: 766-774. PMID: 25985233, PMCID: PMC4475638, DOI: 10.1038/ni.3160.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAnimalsAntibody DiversityB-LymphocytesChildChild, PreschoolClonal EvolutionCytidine DeaminaseDNA-Binding ProteinsFemaleFlow CytometryHomeodomain ProteinsHumansImmunoblottingInfantMaleMice, Inbred NODMice, KnockoutMice, SCIDMice, TransgenicMicroscopy, FluorescencePrecursor Cell Lymphoblastic Leukemia-LymphomaPrecursor Cells, B-LymphoidReverse Transcriptase Polymerase Chain ReactionTumor Cells, Cultured
2007
Activation-induced cytidine deaminase acts as a mutator in BCR-ABL1–transformed acute lymphoblastic leukemia cells
Feldhahn N, Henke N, Melchior K, Duy C, Soh BN, Klein F, von Levetzow G, Giebel B, Li A, Hofmann WK, Jumaa H, Müschen M. Activation-induced cytidine deaminase acts as a mutator in BCR-ABL1–transformed acute lymphoblastic leukemia cells. Journal Of Experimental Medicine 2007, 204: 1157-1166. PMID: 17485517, PMCID: PMC2118573, DOI: 10.1084/jem.20062662.Peer-Reviewed Original ResearchMeSH KeywordsBase SequenceBlotting, WesternB-LymphocytesCytidine DeaminaseDNA Mutational AnalysisDNA-Binding ProteinsFlow CytometryFusion Proteins, bcr-ablGene Expression Regulation, NeoplasticGenes, mycHumansImmunoglobulin Variable RegionMolecular Sequence DataMutationOligonucleotide Array Sequence AnalysisOligonucleotidesPhiladelphia ChromosomePrecursor Cell Lymphoblastic Leukemia-LymphomaProtein-Tyrosine KinasesProto-Oncogene Proteins c-bcl-6Reverse Transcriptase Polymerase Chain ReactionRNA InterferenceSequence AlignmentConceptsAcute lymphoblastic leukemiaBCR-ABL1BCR-ABL1 kinaseUnfavorable prognosisActivation-induced cytidine deaminaseAcute lymphoblastic leukemia cellsAID expressionAberrant AID expressionBCR-ABL1 kinase activityIgH V region genesTumor suppressor gene CDKN2BGerminal center B cellsLymphoblastic leukemia cellsB cell precursorsImmunoglobulin heavy chain variable region genesLymphoblastic leukemiaLeukemia subsetsB cellsDNA single-strand breaksPH casesPhiladelphia chromosomeHeavy chain variable region genesAberrant expressionCell precursorsChain variable region genes
2004
A New Human Somatic Stem Cell from Placental Cord Blood with Intrinsic Pluripotent Differentiation Potential
Kögler G, Sensken S, Airey JA, Trapp T, Müschen M, Feldhahn N, Liedtke S, Sorg R, Fischer J, Rosenbaum C, Greschat S, Knipper A, Bender J, Degistirici O, Gao J, Caplan AI, Colletti EJ, Almeida-Porada G, Müller H, Zanjani E, Wernet P. A New Human Somatic Stem Cell from Placental Cord Blood with Intrinsic Pluripotent Differentiation Potential. Journal Of Experimental Medicine 2004, 200: 123-135. PMID: 15263023, PMCID: PMC2212008, DOI: 10.1084/jem.20040440.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAlbuminsAnimalsBlotting, WesternBone and BonesCell Culture TechniquesCell DifferentiationCell DivisionCell LineCell TransplantationCord Blood Stem Cell TransplantationFemurFetal BloodFlow CytometryGene Expression Regulation, DevelopmentalHematopoietic Stem CellsHippocampusHumansImmunophenotypingLeukocyte Common AntigensLeukocytes, MononuclearMyocardiumMyocytes, CardiacNeurotransmitter AgentsOsteoblastsPhenotypePlacentaPolymerase Chain ReactionRatsRats, WistarReverse Transcriptase Polymerase Chain ReactionSheepStem CellsTime FactorsUmbilical VeinsConceptsUnrestricted somatic stem cellsSomatic stem cellsHuman somatic stem cellsStem cellsPluripotent differentiation potentialSodium channel proteinEndodermal pathwayHuman cord bloodUSSC transplantationCord bloodChannel proteinsNeuron-like morphologyHomogeneous differentiationCell fusionIntact adult rat brainDifferentiation potentialRare populationParenchymal hepatic cellsTau-positive cellsVivo differentiationNeural cellsTumor formationPlacental cord bloodPreimmune fetal sheepAdult rat brain
2000
Somatic Mutation of the Cd95 Gene in Human B Cells as a Side-Effect of the Germinal Center Reaction
Müschen M, Re D, Jungnickel B, Diehl V, Rajewsky K, Küppers R. Somatic Mutation of the Cd95 Gene in Human B Cells as a Side-Effect of the Germinal Center Reaction. Journal Of Experimental Medicine 2000, 192: 1833-1840. PMID: 11120779, PMCID: PMC2213498, DOI: 10.1084/jem.192.12.1833.Peer-Reviewed Original ResearchConceptsDeath domainCD95 geneSomatic mutationsNegative selectionNon-Ig genesHuman B cellsSomatic hypermutation machineryApoptosis-resistant cellsTumor suppressor geneDD mutationsLast exonHypermutation machinerySuppressor geneApoptosis resistanceGenesB cellsImmunoglobulin genesGerminal center B cellsSomatic hypermutationMutationsCD95 pathwayGC B-cell lymphomasGC B cellsCellsGerminal center reactionCD95 ligand expression as a mechanism of immune escape in breast cancer
Müschen M, Moers C, Warskulat U, Even J, Niederacher D, Beckmann M. CD95 ligand expression as a mechanism of immune escape in breast cancer. Immunology 2000, 99: 69-77. PMID: 10651943, PMCID: PMC2327134, DOI: 10.1046/j.1365-2567.2000.00921.x.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisBreast NeoplasmsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesEnzyme-Linked Immunosorbent AssayFas Ligand ProteinFas ReceptorFemaleFlow CytometryHumansImmunohistochemistryJurkat CellsLymphocyte CountMembrane GlycoproteinsProtein IsoformsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerConceptsBreast cancer cellsT cellsBreast cancerCD95L expressionImmune escapeIFN-gammaCancer cellsJurkat T cellsTumor-infiltrating T cellsCD95L mRNA levelsDepletion of CD4Cultured breast cancer cellsBreast cancer patientsPeripheral blood lymphocytesCD95/CD95L systemBreast cancer cell linesNon-malignant mammary tissuesActivated T cellsCD95 ligand expressionRate of apoptosisBreast cancer sectionsCancer cell linesInteraction of CD95Systemic immunosuppressionCancer patients