Kadriye Nehir Cosgun, PhD
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Targeting β-catenin degradation with GSK3β inhibitors induces cell death in acute lymphoblastic leukemia
Cosgun K, Jumaa H, Robinson M, Cheng Z, Oulghazi S, Kume K, Fonseca Arce D, Agadzhanian N, Kistner K, Leveille E, Drivet E, Yu F, Qian Z, Song J, Chan W, Xu L, Xiao G, Taketo M, Kothari S, Davids M, Schjerven H, Jellusova J, Müschen M. Targeting β-catenin degradation with GSK3β inhibitors induces cell death in acute lymphoblastic leukemia. Nature Cancer 2026, 7: 150-168. PMID: 41507538, PMCID: PMC12858398, DOI: 10.1038/s43018-025-01093-z.Peer-Reviewed Original ResearchConceptsProtein degradationCell deathProtein degradation machineryAcute lymphoblastic leukemiaGlycogen synthase kinase 3bB-ALLXenograft model in vivoDegradation machineryCRISPR screensMyc repressionProteasomal degradationHuman B-ALLLymphoblastic leukemiaPatient-derived xenograft models in vivoRefractory B-cell malignanciesB-cateninB-cell acute lymphoblastic leukemiaAcute cell deathWnt signalingGSK3BB-cell malignanciesMechanistic targetProteinMYCModel in vivoKit Regulates HSC Engraftment across the Human-Mouse Species Barrier
Cosgun KN, Rahmig S, Mende N, Reinke S, Hauber I, Schäfer C, Petzold A, Weisbach H, Heidkamp G, Purbojo A, Cesnjevar R, Platz A, Bornhäuser M, Schmitz M, Dudziak D, Hauber J, Kirberg J, Waskow C. Kit Regulates HSC Engraftment across the Human-Mouse Species Barrier. Cell Stem Cell 2014, 15: 227-238. PMID: 25017720, DOI: 10.1016/j.stem.2014.06.001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell LineageCrosses, GeneticEnzyme-Linked Immunosorbent AssayFetal BloodGene Expression RegulationHematopoietic Stem Cell TransplantationHematopoietic Stem CellsHumansLymphocytesMiceMice, Inbred C57BLMice, TransgenicMutationRNA, MessengerSpecies SpecificityStem Cell FactorThymocytesTime Factors
2026
BCR::ABL1‐Induced Enhancer Reprogramming Uncovers Hypersensitivity of Ph+B‐ALL Cells to Enhancer‐Targeting Drugs
Ng H, Glaser T, Zhu J, Robinson M, Cosgun K, Malysheva V, Deniz O, Crump N, Helian K, Innes A, Burt R, Sun L, John G, Zhou H, Kaneshige A, Bai L, Wang S, Spivakov M, Müschen M, Feldhahn N. BCR::ABL1‐Induced Enhancer Reprogramming Uncovers Hypersensitivity of Ph+B‐ALL Cells to Enhancer‐Targeting Drugs. Advanced Science 2026, e17231. PMID: 41764406, DOI: 10.1002/advs.202517231.Peer-Reviewed Original ResearchKinase-dependent activationTranscriptional programsB-ALLActivation of STAT5B-lineage leukemiasTranscriptional reprogrammingGenomic lesionsEnhancer reprogrammingKinase activityPoor prognosisCurrent therapiesMalignant transformationHematological cancersEnhancer deregulationKinase inhibitorsCurrent treatmentBlood cancerCancer initiationCancerEnhanced inhibitionEnhancer signaturesBCR::ABL1LesionsEnhanced activityGenesDynamic feedback control of oncogenic tyrosine kinase signaling in acute leukemia
Lee J, Sun R, Kume K, Robinson M, Cheng Z, Cosgun K, Ma N, Hurtz C, Geng H, Luger S, Litzow M, Paietta E, Chen J, Vaidehi N, Müschen M. Dynamic feedback control of oncogenic tyrosine kinase signaling in acute leukemia. Science Signaling 2026, 19: eadw5054-eadw5054. PMID: 41666265, PMCID: PMC12924454, DOI: 10.1126/scisignal.adw5054.Peer-Reviewed Original ResearchConceptsOncogenic tyrosine kinase signalingTyrosine kinase signalingPatient-derived xenograftsKinase signalingAcute leukemiaNatural killerInterleukin-2Tyrosine kinaseLeukemia cellsLeukemia-initiating capacityActivation of tyrosine kinasesGlobal phosphoproteome analysisOncogenic tyrosine kinasesPhosphatase activityInteractome analysisModels of acute leukemiaAntibody-drug conjugatesAcute leukemia cellsPhosphoproteomic analysisClonal fitnessRefractory leukemiaTransplant recipientsInhibitory phosphatasesMyeloid leukemiaT cells
2024
Tuning Responses to Polatuzumab Vedotin in B-cell Lymphoma.
Leveille E, Kothari S, Cosgun K, Mlynarczyk C, Müschen M. Tuning Responses to Polatuzumab Vedotin in B-cell Lymphoma. Cancer Discovery 2024, 14: 1577-1580. PMID: 39228298, DOI: 10.1158/2159-8290.cd-24-0644.Commentaries, Editorials and Letters
2021
Developmental partitioning of SYK and ZAP70 prevents autoimmunity and cancer
Sadras T, Martin M, Kume K, Robinson ME, Saravanakumar S, Lenz G, Chen Z, Song JY, Siddiqi T, Oksa L, Knapp AM, Cutler J, Cosgun KN, Klemm L, Ecker V, Winchester J, Ghergus D, Soulas-Sprauel P, Kiefer F, Heisterkamp N, Pandey A, Ngo V, Wang L, Jumaa H, Buchner M, Ruland J, Chan WC, Meffre E, Martin T, Müschen M. Developmental partitioning of SYK and ZAP70 prevents autoimmunity and cancer. Molecular Cell 2021, 81: 2094-2111.e9. PMID: 33878293, PMCID: PMC8239336, DOI: 10.1016/j.molcel.2021.03.043.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CD19AutoimmunityB-LymphocytesCalciumCell DifferentiationCell Transformation, NeoplasticEnzyme ActivationHumansImmune ToleranceLymphoma, B-CellMiceModels, GeneticNeoplasm ProteinsNeoplasmsNFATC Transcription FactorsPhosphatidylinositol 3-KinasesProtein BindingReceptors, Antigen, B-CellSignal TransductionSyk KinaseZAP-70 Protein-Tyrosine KinasePON2 subverts metabolic gatekeeper functions in B cells to promote leukemogenesis
Pan L, Hong C, Chan LN, Xiao G, Malvi P, Robinson ME, Geng H, Reddy ST, Lee J, Khairnar V, Cosgun KN, Xu L, Kume K, Sadras T, Wang S, Wajapeyee N, Müschen M. PON2 subverts metabolic gatekeeper functions in B cells to promote leukemogenesis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2016553118. PMID: 33531346, PMCID: PMC7896313, DOI: 10.1073/pnas.2016553118.Peer-Reviewed Original ResearchConceptsTransplant recipient miceDNA double-strand breaksNormal B cell developmentDouble-strand breaksB cell developmentGenetic deletionB cellsLymphoid transcription factorsGlucose transporter GLUT1Gatekeeper functionGlucose uptakeRecipient miceTranscription factorsSomatic recombinationSynthetic lethalityB-cell acute lymphoblastic leukemiaCell developmentMetabolic gatekeeperRefractory B-ALLDeficient murineCell acute lymphoblastic leukemiaPoor clinical outcomeCell typesAcute lymphoblastic leukemiaGlucose transport
2020
IFITM3 functions as a PIP3 scaffold to amplify PI3K signalling in B cells
Lee J, Robinson ME, Ma N, Artadji D, Ahmed MA, Xiao G, Sadras T, Deb G, Winchester J, Cosgun KN, Geng H, Chan LN, Kume K, Miettinen TP, Zhang Y, Nix MA, Klemm L, Chen CW, Chen J, Khairnar V, Wiita AP, Thomas-Tikhonenko A, Farzan M, Jung JU, Weinstock DM, Manalis SR, Diamond MS, Vaidehi N, Müschen M. IFITM3 functions as a PIP3 scaffold to amplify PI3K signalling in B cells. Nature 2020, 588: 491-497. PMID: 33149299, PMCID: PMC8087162, DOI: 10.1038/s41586-020-2884-6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CD19B-LymphocytesCell Transformation, NeoplasticFemaleGerminal CenterHumansIntegrinsMembrane MicrodomainsMembrane ProteinsMiceMice, Inbred C57BLMice, Inbred NODModels, MolecularPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPhosphorylationReceptors, Antigen, B-CellRNA-Binding ProteinsSignal TransductionConceptsPI3KCell leukemiaAntiviral effector functionsAntigen-specific antibodiesInterferon-induced transmembrane proteinsIFITM3 functionDevelopment of leukemiaCell surfacePoor outcomeOncogenic PI3KClinical cohortEffector functionsGerminal centersMouse modelB cellsExpression of IFITM3Malignant transformationAccumulation of PIP3PI3K signalsCell receptorNormal numbersLeukemiaDefective expressionEndosomal proteinIFITM3Signalling input from divergent pathways subverts B cell transformation
Chan LN, Murakami MA, Robinson ME, Caeser R, Sadras T, Lee J, Cosgun KN, Kume K, Khairnar V, Xiao G, Ahmed MA, Aghania E, Deb G, Hurtz C, Shojaee S, Hong C, Pölönen P, Nix MA, Chen Z, Chen CW, Chen J, Vogt A, Heinäniemi M, Lohi O, Wiita AP, Izraeli S, Geng H, Weinstock DM, Müschen M. Signalling input from divergent pathways subverts B cell transformation. Nature 2020, 583: 845-851. PMID: 32699415, PMCID: PMC7394729, DOI: 10.1038/s41586-020-2513-4.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsB-LymphocytesCell Line, TumorCell Transformation, NeoplasticEnzyme ActivationExtracellular Signal-Regulated MAP KinasesFemaleHumansLeukemia, B-CellMiceProtein Tyrosine Phosphatase, Non-Receptor Type 6Proto-Oncogene Proteins c-bcl-6Proto-Oncogene Proteins c-mycSignal TransductionSTAT5 Transcription FactorConceptsPre-B cell receptorPrincipal oncogenic driverDivergent pathwaysSignal transduction proteinsPro-B cell stageSingle-cell mutationTranscription factor MYCOncogenic driversDivergent signaling pathwaysSingle oncogenic pathwayCentral oncogenic driverMore mature cellsGenetic reactivationTranscriptional programsB-cell transformationProtein kinasePathway componentsERK activationIndividual mutationsOncogenic STAT5Signaling pathwaysCell transformationCytokine receptorsGenetic lesionsDivergent circuits
2018
Author Correction: Metabolic gatekeeper function of B-lymphoid transcription factors
Chan LN, Chen Z, Braas D, Lee JW, Xiao G, Geng H, Cosgun KN, Hurtz C, Shojaee S, Cazzaniga V, Schjerven H, Ernst T, Hochhaus A, Kornblau SM, Konopleva M, Pufall MA, Cazzaniga G, Liu GJ, Milne TA, Koeffler HP, Ross TS, Sánchez-García I, Borkhardt A, Yamamoto KR, Dickins RA, Graeber TG, Müschen M. Author Correction: Metabolic gatekeeper function of B-lymphoid transcription factors. Nature 2018, 558: e5-e5. PMID: 29849140, DOI: 10.1038/s41586-018-0164-5.Commentaries, Editorials and Letters
Academic Achievements & Community Involvement
News
News
- February 10, 2026
Yale Study Identifies a New Class of Drug Targets for Aggressive Leukemia
- January 08, 2026
Yale-Led Study Identifies a New Target for Treating Acute Leukemia
- December 09, 2025
Yale research advances presented at American Society of Hematology annual meeting
- February 26, 2025
Celebrating Yale Cancer Center Faculty, Research Scientists