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
2006
SLP65 deficiency results in perpetual V(D)J recombinase activity in pre-B-lymphoblastic leukemia and B-cell lymphoma cells
Sprangers M, Feldhahn N, Liedtke S, Jumaa H, Siebert R, Müschen M. SLP65 deficiency results in perpetual V(D)J recombinase activity in pre-B-lymphoblastic leukemia and B-cell lymphoma cells. Oncogene 2006, 25: 5180-5186. PMID: 16636677, DOI: 10.1038/sj.onc.1209520.Peer-Reviewed Original ResearchConceptsLymphoblastic leukemiaRecombinase activityRAG1/2 expressionB-cell lineage leukemiaDouble-strand break eventsLymphoma cellsSecondary genetic aberrationsB-cell lymphomaB-cell lymphoma cellsB-lymphoid malignanciesB-cell malignanciesB cell receptorVH gene rearrangementsMalignant progressionLeukemiaFrequent featureGenetic aberrationsGene rearrangementsCells resultsRearrangement activityLineage leukemiaMalignancyVH replacementDeficiencyExpression
2004
The BCR-ABL1 Kinase Bypasses Selection for the Expression of a Pre–B Cell Receptor in Pre–B Acute Lymphoblastic Leukemia Cells
Klein F, Feldhahn N, Harder L, Wang H, Wartenberg M, Hofmann WK, Wernet P, Siebert R, Müschen M. The BCR-ABL1 Kinase Bypasses Selection for the Expression of a Pre–B Cell Receptor in Pre–B Acute Lymphoblastic Leukemia Cells. Journal Of Experimental Medicine 2004, 199: 673-685. PMID: 14993251, PMCID: PMC2213306, DOI: 10.1084/jem.20031637.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAdolescentAdultAgedBase SequenceCarrier ProteinsChildChild, PreschoolDNA, NeoplasmFemaleFusion Proteins, bcr-ablGene ExpressionGene Rearrangement, B-Lymphocyte, Heavy ChainHumansMaleMembrane GlycoproteinsMiddle AgedPhosphoproteinsPre-B Cell ReceptorsPrecursor B-Cell Lymphoblastic Leukemia-LymphomaProtein-Tyrosine KinasesReceptors, Antigen, B-CellSelection, GeneticConceptsPre-B cell receptorVH region genesWide gene expression profilesPre-B cell receptor signalingFunctional B-cell receptorFunctional pre-B cell receptorCell receptorReceptor engagementAntigen receptor engagementLeukemia cellsCell receptor signalingGene expression profilesRegion genesCell receptor engagementBCR-ABL1 kinase activityB cell receptorImmature B cellsVH gene rearrangementsKinase activityGene expressionExpression profilesAcute lymphoblastic leukemiaReceptor signalingSerial analysisBCR-ABL1
2000
Rare Occurrence of Classical Hodgkin's Disease as a T Cell Lymphoma
Müschen M, Rajewsky K, Bräuninger A, Baur A, Oudejans J, Roers A, Hansmann M, Küppers R. Rare Occurrence of Classical Hodgkin's Disease as a T Cell Lymphoma. Journal Of Experimental Medicine 2000, 191: 387-394. PMID: 10637283, PMCID: PMC2195757, DOI: 10.1084/jem.191.2.387.Peer-Reviewed Original ResearchMeSH KeywordsAdultBase SequenceHodgkin DiseaseHumansLymphoma, T-CellMaleMiddle AgedMolecular Sequence DataReed-Sternberg CellsConceptsTCR beta locusMature B cellsGene rearrangementsCell-associated proteinsLight chain gene rearrangementsClassical Hodgkin's diseaseDJ gene rearrangementsIg gene rearrangementsSingle-cell polymerase chain reactionIgH locusCases of cHDClonal progenyBeta gene rearrangementsT cell receptorT cell moleculesLociGermline configurationCell phenotypeCell moleculesLineage derivationB cellsRS cellsCell receptorImmunoglobulin heavyCell markers
1998
Regulation of CD95 (Apo-1/Fas) Ligand and Receptor Expression in Human Embryonal Carcinoma Cells by Interferon γ and all-trans Retinoic Acid
Müschen M, Warskulat U, Schmidt B, Schulz W, Häussinger D. Regulation of CD95 (Apo-1/Fas) Ligand and Receptor Expression in Human Embryonal Carcinoma Cells by Interferon γ and all-trans Retinoic Acid. Biological Chemistry 1998, 379: 1083-1092. PMID: 9792441, DOI: 10.1515/bchm.1998.379.8-9.1083.Peer-Reviewed Original ResearchConceptsTrans retinoic acidTera-2 cellsTera-2 embryonal carcinoma cellsEmbryonal carcinoma cellsRetinoic acidT lymphocytesCarcinoma cellsJurkat T lymphocytesCD95 ligandReceptor isoformsCD95 receptorCD95 ligand expressionHuman embryonal carcinoma cellsAntitumor immunityControl conditionReceptor expressionInterferon γInterferon gammaLigand expressionProtein levelsDifferential regulationCD95 ligationIFNgammaLymphocytesApoptosis