2023
Negative feedback regulation of MAPK signaling is an important driver of chronic lymphocytic leukemia progression
Ecker V, Brandmeier L, Stumpf M, Giansanti P, Moreira A, Pfeuffer L, Fens M, Lu J, Kuster B, Engleitner T, Heidegger S, Rad R, Ringshausen I, Zenz T, Wendtner C, Müschen M, Jellusova J, Ruland J, Buchner M. Negative feedback regulation of MAPK signaling is an important driver of chronic lymphocytic leukemia progression. Cell Reports 2023, 42: 113017. PMID: 37792532, DOI: 10.1016/j.celrep.2023.113017.Peer-Reviewed Original ResearchConceptsMitogen-activated protein kinaseChronic lymphocytic leukemiaCLL cellsMitochondrial reactive oxygen speciesChronic lymphocytic leukemia progressionApoptotic cell deathPoor clinical prognosisCLL cell survivalSmall molecule inhibitorsNegative feedback regulationProtein kinaseReactive oxygen speciesMAPK signalingMAPK activityPromising treatment conceptClinical prognosisClinical challengeLymphocytic leukemiaCell survivalAcute activationCell deathDNA damageDUSP6Treatment conceptFeedback regulation
2011
Targeting Inhibitory Phosphatases in Tyrosine Kinase-Driven Leukemias
Shojaee S, Buchner M, Geng H, Silvia B, Koeffler P, Muschen M. Targeting Inhibitory Phosphatases in Tyrosine Kinase-Driven Leukemias. Blood 2011, 118: 1382. DOI: 10.1182/blood.v118.21.1382.1382.Peer-Reviewed Original ResearchCell deathReactive oxygen speciesInducible deletionLeukemia cellsTyrosine kinase signalingActivation signalsSmall molecule inhibitionSubsequent cell deathMultiple new targetsLeukemia cell deathBCR-ABL1 oncogeneCytoplasmic tailKinase signalingTransplant recipient miceInduction of CreTyrosine kinase inhibitorsCellular senescenceMolecule inhibitionTyrosine kinasePTPN6Drastic upregulationINPP5DCurrent tyrosine kinase inhibitorsPTENDeletion
2009
Inducible Ablation of HSPA5 Suppresses BCR-ABL1-Driven Leukemia through Massive Accumulation of Reactive Oxygen Species.
Chang M, Wey S, Lee A, Müschen M. Inducible Ablation of HSPA5 Suppresses BCR-ABL1-Driven Leukemia through Massive Accumulation of Reactive Oxygen Species. Blood 2009, 114: 1976. DOI: 10.1182/blood.v114.22.1976.1976.Peer-Reviewed Original ResearchCML-like leukemiaBCR-ABL1Bone marrowLeukemia cellsReactive oxygen speciesImatinib sensitivityNOD/SCID recipientsG0/G1 cell cycle arrestNovel therapeutic approachesP210 BCR-ABL1G1 cell cycle arrestBone marrow cellsLevels of ROSBone marrow microenvironmentCell deathLeukemia cell survivalSCID recipientsCytokine primingFl miceCell cycle arrestOxygen speciesTherapeutic approachesCML cellsDay 4Leukemia growth