2018
Cooperation between SYK and ZAP70 Kinases As a Driver of Oncogenic BCR-Signaling in B-Cell Malignancies
Sadras T, Cutler J, Aguade-Gorgorio J, Chen Z, Cosgun K, Pandey A, Muschen M. Cooperation between SYK and ZAP70 Kinases As a Driver of Oncogenic BCR-Signaling in B-Cell Malignancies. Blood 2018, 132: 3922. DOI: 10.1182/blood-2018-99-116954.Peer-Reviewed Original ResearchSpleen tyrosine kinaseSH2 domainZAP70 kinaseKinase domainCarboxy-terminal kinase domainLinker regionT cell receptorSurvival signalsBCR signalingTyrosine kinaseChronic lymphocytic leukemiaTandem SH2 domainsProximal signal transductionAmino acid insertB-cell malignanciesBCR-mediated signalsB cellsAlternative splice variantsNegative B cell selectionDifferential interactomeProteomic approachInterdomain BZAP70 proteinBCR componentsSignal transduction
2011
Compensatory Signaling From ROR1 and the Pre-B Cell Receptor Promote Survival of t(1;19) Acute Lymphoblastic Leukemia
Bicocca V, Chang B, Muschen M, Druker B, Tyner J. Compensatory Signaling From ROR1 and the Pre-B Cell Receptor Promote Survival of t(1;19) Acute Lymphoblastic Leukemia. Blood 2011, 118: 2466. DOI: 10.1182/blood.v118.21.2466.2466.Peer-Reviewed Original ResearchTyrosine kinaseAcute lymphoblastic leukemiaAkt activityPre-B cell receptor signalingCell linesLeukemogenic tyrosine kinasesProtein target identificationKinase inhibitor screenImmunoblot analysisCell receptor signalingCell viabilityKinase inhibitor screeningClinical trial contractsReceptor tyrosine kinasesTyrosine kinase activityPhospho-protein arraysSmall molecule inhibitorsROR1 knockdownSiRNA screeningAkt regulationLymphoblastic leukemiaDasatinib treatmentKinase domainPatient costsLeukemia patients
2008
Lymphoid Blast Crisis Transformation and Development of Drug- Resistance in Chronic Myeloid Leukemia Are Driven by Aberrant Somatic Hypermutation
Klemm L, Duy C, Feldhahn N, Groffen J, Kim Y, Hofmann W, Jumaa H, Lieber M, Casellas R, Muschen M. Lymphoid Blast Crisis Transformation and Development of Drug- Resistance in Chronic Myeloid Leukemia Are Driven by Aberrant Somatic Hypermutation. Blood 2008, 112: 571. DOI: 10.1182/blood.v112.11.571.571.Peer-Reviewed Original ResearchChronic phase chronic myeloid leukemiaPhase chronic myeloid leukemiaChronic myeloid leukemiaLymphoid blast crisisGerminal center B cellsAberrant somatic hypermutationSomatic hypermutationBCR-ABL1 kinase domainKinase domainEctopic expressionB cell lineage commitmentB-cell-specific transcription factor Pax5Lineage-specific activationCML cellsAID protein levelsImatinib resistanceAberrant activationB cellsTranscription factor Pax5AID expressionBCR-ABL1Cell lineage commitmentCytidine deaminase AIDDownstream regulatory elementsB-cell-specific activation
2007
PAX5-Mediated Lineage Conversion and Expression of AID Accelerates Clonal Evolution and Initiates Darwinian Selection of BCR-ABL1-Mutants in Chronic Myeloid Leukemia.
Klemm L, Feldhahn N, Hoffmann T, Hofmann W, Jumaa H, Muschen M. PAX5-Mediated Lineage Conversion and Expression of AID Accelerates Clonal Evolution and Initiates Darwinian Selection of BCR-ABL1-Mutants in Chronic Myeloid Leukemia. Blood 2007, 110: 1005. DOI: 10.1182/blood.v110.11.1005.1005.Peer-Reviewed Original ResearchLineage conversionCell lineagesDarwinian selectionKinase domainB-cell lineageCell linesSequence analysisEnzyme AIDCML cell linesRetroviral expression constructsTranscription factor Pax5CML linesAID expressionDrug-resistant cellsCell lineage conversionTumor suppressor gene CDKN2ABlast crisis chronic myeloid leukemiaBCR-ABL1 kinase