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dc.contributor.authorBasecke, Jorg
dc.contributor.authorPodleschny, Martina
dc.contributor.authorClemens, Robert
dc.contributor.authorSchnittger, Susanne
dc.contributor.authorViereck, Volker
dc.contributor.authorTrumper, Lorenz
dc.contributor.authorGriesinger, Frank
dc.date.accessioned2009-04-16T12:24:33Z
dc.date.available2009-04-16T12:24:33Z
dc.date.issued2006-09
dc.identifier.citationLeuk. Res. 2006, 30 (9):1091-1096en
dc.identifier.issn0145-2126
dc.identifier.pmid16540167
dc.identifier.doi10.1016/j.leukres.2006.02.005
dc.identifier.urihttp://hdl.handle.net/10146/65057
dc.descriptionKEYWORDS CLASSIFICATION: Adult;Antigens,CD;blood;B-Lymphocytes;Female;Fetal Blood;genetics;Gene Duplication;Germany;Hematopoietic Stem Cells;Humans;Infant,Newborn;Leukemia;Leukemia,Myelocytic,Acute;Lymphoma,Mixed-Cell;metabolism;Male;mechanisms of carcinogenesis;Myeloid-Lymphoid Leukemia Protein;pathology;Research;T-Lymphocytes.en
dc.description.abstractAML-associated MLL-PTD contribute to leukemogenesis by a gain of function and confer an unfavorable prognosis. Like other leukemia associated aberrations they are also present in healthy adults. To delineate the leukemogenic mechanism we tracked down MLL-PTD in normal hematopoiesis and investigated cord blood samples. MLL-PTD were observed in 56/60 (93%) of all cord bloods. In contrast to AML, the transcript frequency in cord blood was four log scales lower as determined by real-time PCR. The CD34+ progenitor cell, CD33+ myeloid, CD19+ B-lymphoid and CD3+ T-lymphoid subfractions were positive. The ubiquitous presence of MLL-PTD in cord blood implicates a lifelong exposure, not an accumulation during lifetime. Since also present in the stem cell subfraction, these factors seem not to be major determinants in MLL-PTD leukemogenesis.
dc.language.isoenen
dc.relation.urlhttp://www.lrjournal.com/article/S0145-2126(06)00063-4/abstracten
dc.subjectMLL-PTDen
dc.subjectCord blooden
dc.subjectHealthy newbornen
dc.subjectLeukemogenesisen
dc.subject.meshAdult
dc.subject.meshAntigens, CD
dc.subject.meshB-Lymphocytes
dc.subject.meshFemale
dc.subject.meshFetal Blood
dc.subject.meshGene Duplication
dc.subject.meshHematopoietic Stem Cells
dc.subject.meshHumans
dc.subject.meshInfant, Newborn
dc.subject.meshLeukemia, Myeloid, Acute
dc.subject.meshLymphoma, Non-Hodgkin
dc.subject.meshMale
dc.subject.meshMyeloid-Lymphoid Leukemia Protein
dc.subject.meshT-Lymphocytes
dc.titleLifelong persistence of AML associated MLL partial tandem duplications (MLL-PTD) in healthy adults.en
dc.typeArticleen
dc.identifier.journalLeukemia researchen
html.description.abstractAML-associated MLL-PTD contribute to leukemogenesis by a gain of function and confer an unfavorable prognosis. Like other leukemia associated aberrations they are also present in healthy adults. To delineate the leukemogenic mechanism we tracked down MLL-PTD in normal hematopoiesis and investigated cord blood samples. MLL-PTD were observed in 56/60 (93%) of all cord bloods. In contrast to AML, the transcript frequency in cord blood was four log scales lower as determined by real-time PCR. The CD34+ progenitor cell, CD33+ myeloid, CD19+ B-lymphoid and CD3+ T-lymphoid subfractions were positive. The ubiquitous presence of MLL-PTD in cord blood implicates a lifelong exposure, not an accumulation during lifetime. Since also present in the stem cell subfraction, these factors seem not to be major determinants in MLL-PTD leukemogenesis.


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