2011
DUSP6-Mediated Negative Feedback to Oncogenic Tyrosine Kinase Signaling Prevents Excessive Accumulation of ROS and Enables Leukemia Cell Survival
Shojaee S, Buchner M, Geng H, Melnick A, Gery S, Molkentin J, Koeffler P, Muschen M. DUSP6-Mediated Negative Feedback to Oncogenic Tyrosine Kinase Signaling Prevents Excessive Accumulation of ROS and Enables Leukemia Cell Survival. Blood 2011, 118: 1479. DOI: 10.1182/blood.v118.21.1479.1479.Peer-Reviewed Original ResearchCellular senescenceEffects of BCIProtein levelsCpG methylation analysisLeukemia cellsOncogene-induced senescenceGene expression changesLineage leukemiaCpG methylation levelsOncogenic tyrosine kinasesPharmacological inhibitionTyrosine kinase activityActivation of p53Small molecule inhibitorsBone marrow progenitor cellsGenetic experimentsDUSP6 functionLeukemia cell survivalTherapeutic targetB-cell lymphoma cell linesMarrow progenitor cellsNormal growth kineticsHigh ROS levelsKinase activityPromoter region
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