Kohei Kume, PhD
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Medical Oncology and Hematology
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Biography
Dr. Kohei Kume completed his PhD at Iwate University (Morioka, Japan) in 2011 with mentorship from Yasushi Saitoh, PhD. After a postdoctoral training at Iwate Medical University with mentorship from Satoshi S. Nishizuka MD, PhD, he joined Dr. Markus Müschen’s laboratory in 2017 at the Beckman Research Institute of the City of Hope. He is currently a Research Scientist in Dr. Müschen’s laboratory at Yale University, and studies the mechanisms and functional significance of autonomous Ca2+ oscillations in oncogenic signaling of multiple B-cell malignancies.
Last Updated on September 24, 2024.
Appointments
Medical Oncology and Hematology
Research ScientistPrimary
Other Departments & Organizations
- All Institutions
- Center of Molecular and Cellular Oncology
- Hematology
- Medical Oncology and Hematology
- Müschen Lab
Education & Training
- Associate Research Scientist
- Yale University
- Staff Scientist
- City of Hope
- Associate Instructor
- Iwate Medical University
- Postdoctoral Fellow
- Iwate Medical University
- PhD
- Iwate University, Bioresources Sciences (2011)
Research
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Overview
Medical Research Interests
Cell Size; Drug Resistance; Leukemia; Lipid Metabolism; Lymphoma; Oncogenes; Optogenetics; Protein Array Analysis; Proteogenomics
Public Health Interests
Biomarkers; Cancer
ORCID
0000-0003-2856-5970- View Lab Website
Lab Website
Research at a Glance
Yale Co-Authors
Frequent collaborators of Kohei Kume's published research.
Publications Timeline
A big-picture view of Kohei Kume's research output by year.
Research Interests
Research topics Kohei Kume is interested in exploring.
Markus Müschen, MD, PhD
Kadriye Nehir Cosgun, PhD
Mark Robinson, PhD
Jaewoong Lee, PhD
Etienne Leveille, MD
Shalin Kothari, MD
39Publications
604Citations
Protein Array Analysis
Drug Resistance
Publications
2026
Dynamic 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. PMID: 41666265, PMCID: PMC12924454, DOI: 10.1126/scisignal.adw5054.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsOncogenic 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 cellsTargeting 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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsProtein 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 vivo
2025
Alternating cycles of quiescent and proliferative cell states determine stemness and leukemia-initiation capacity in acute lymphoblastic leukemia
Cheng Z, Kume K, Shi R, Robinson M, Cosgun K, Bao Y, Chen S, Mishra P, Bewersdorf J, Xu M, Müschen M. Alternating cycles of quiescent and proliferative cell states determine stemness and leukemia-initiation capacity in acute lymphoblastic leukemia. Blood 2025, 146: 1485-1485. DOI: 10.1182/blood-2025-1485.Peer-Reviewed Original ResearchConceptsLeukemia-initiating cellsB-ALL cellsCell state transitionsAcute myeloid leukemiaLeukemia-initiating cell populationProliferative cell statesCell statesB-ALLFusion proteinTime-lapse imagingDry massKnockin alleleClonal hierarchyIntegrated ChIP-seqCatabolic metabolismMultiplex immunofluorescenceGene expression studiesDrug resistanceCellular dry massTime-lapse fluorescence imagingQuiescent cell stateLeukemia-initiating potentialChIP-seqDegron systemProtein synthesis pathwaysTargeted hyperactivation of oncogenic STAT5-signaling in acute lymphoblastic leukemia
Kume K, Cheng Z, Lin J, Xu L, Xiao G, Robinson M, Leveille E, Bramson E, Cosgun K, Geng H, Heinäniemi M, Graeber T, Abkowitz J, Chi H, Alexander W, Chiarle R, Leonard W, Müschen M. Targeted hyperactivation of oncogenic STAT5-signaling in acute lymphoblastic leukemia. Blood 2025, 146: 433-433. DOI: 10.1182/blood-2025-433.Peer-Reviewed Original ResearchConceptsLoss-of-functionB-ALL cellsLeukemia-initiating capacityCell statesER stressColony formationLoss of colony formationLeukemia cellsAmino acid metabolic pathwaysActivation of MYCExpression levelsGenetic deletionProliferative cell statesTime-lapse experimentsInhibitors of JAK2Oncogenic tyrosine kinasesActivation of BCL6Autophagosome biogenesisPtdEtn synthesisBCL6 target genesTCA cycleGene setsSTAT5 regulationCell-statesTranscriptional programsBidirectional glutamine transport enables B-cell activation and transformation 3034
Sun R, Deb G, Kume K, Feng Y, Scott J, Graeber T, Mäschen M. Bidirectional glutamine transport enables B-cell activation and transformation 3034. The Journal Of Immunology 2025, 214 DOI: 10.1093/jimmun/vkaf283.876.Peer-Reviewed Original ResearchConceptsCell fitnessImpair cell fitnessB cell activationProtein synthesisResistant to rapamycinPrimary resting B cellsAmino acid poolExpense of glutathioneIsotope tracingGlutamine deprivationProtein translationGlucosamine synthesisB cellsChemogenomic screensProteomic changesSynthetic lethalityNucleotide metabolismIntracellular glutaminePurine synthesisTransformed B cellsDeletionGlutamine transportAcid poolGlutamineGrowth inhibition
2024
Identification of Nuclear NAD+ Salvage As a Therapeutic Vulnerability in B-Lymphoid Malignancies
Robinson M, Li Q, Zhang C, Zhan C, Cheng Z, Kume K, Cosgun K, Kothari S, Agadzhanian N, Nakada D, Müschen M. Identification of Nuclear NAD+ Salvage As a Therapeutic Vulnerability in B-Lymphoid Malignancies. Blood 2024, 144: 4164-4164. DOI: 10.1182/blood-2024-205729.Peer-Reviewed Original ResearchConceptsB-ALL cell linesB-ALLB cellsCell linesTherapeutic vulnerabilitiesGene dependenciesNAD+ synthesisMature B-cell lymphomasElimination of B cellsTreatment of B-ALLNAD+ salvageChemotherapy-based regimensEffects of NAMPT inhibitionB-cell depletionB-cell lymphomaB-lymphoid malignanciesB-ALL cellsNAMPT inhibitorsInhibition of NAMPTATP-utilizing enzymesNAD+ salvage pathwayDrug repurposing platformNAD biosynthetic pathwayNear-complete ablationDe novo pathwayIdentification of High-Efficiency β-Catenin Protein Degradation As Critical Vulnerability in B-Cell Malignancies
Cosgun K, Robinson M, Agadzhanian N, Cheng Z, Oulghazi S, Berning P, Fonseca-Arce D, Kume K, Fontaine J, Chan L, Lee J, Yu F, Qian Z, Song J, Chan W, Chen J, Taketo M, Schjerven H, Müschen M. Identification of High-Efficiency β-Catenin Protein Degradation As Critical Vulnerability in B-Cell Malignancies. Blood 2024, 144: 4125-4125. DOI: 10.1182/blood-2024-208125.Peer-Reviewed Original ResearchConceptsProtein degradation pathwaysB-ALL cellsProtein degradationRepression of MYCTranscriptional activity of MYCCell deathAcute cell deathLoss of colony formationChIP-seq analysisActive enhancer marksB-cell malignanciesSuper-enhancer regionsActivation of MYCIkaros transcription factorB-lymphoid cellsCell linesB cell identityDefective protein degradationB-cateninNon-lymphoid cell linesDegradation pathwayMantle cell lymphomaProtein levelsB-ALLChIP-seqMechanism of Negative Feedback Regulation of Oncogenic BCR-Signaling in Mature B-Cell Lymphoma
Sun R, Lee J, Robinson M, Kume K, Zhan C, Cheng Z, Cosgun K, Chan L, Leveille E, Kothari S, Katz S, Ma N, Vykunta V, Shy B, Hodson D, Marson A, Vaidehi N, Müschen M. Mechanism of Negative Feedback Regulation of Oncogenic BCR-Signaling in Mature B-Cell Lymphoma. Blood 2024, 144: 3003-3003. DOI: 10.1182/blood-2024-211693.Peer-Reviewed Original ResearchConceptsB-cell lymphomaGC B cellsB-cell lymphoma cellsB cellsBCR signalingGerminal centersProteolytic cleavageNK cellsLymphoma cellsMantle cell lymphoma xenograftsAggressive B-cell lymphomasMature B-cell lymphomasB-cell lymphoma subtypesGerminal center B cellsSpontaneous germinal centersGlobal phosphoproteomic studiesActivation marker CD69Aggressiveness of diseaseCD25 surface expressionMechanism of negative feedback regulationB cell autoimmunityFollicular dendritic cellsHuman germinal centerCa2+ oscillationsExpressed increased levelsCell Growth Trajectories of B-Cell Lymphomas Are Defined By Oscillations between MYC- and BCL6-Dependent States
Cheng Z, Kume K, Shanmugam V, Müschen M. Cell Growth Trajectories of B-Cell Lymphomas Are Defined By Oscillations between MYC- and BCL6-Dependent States. Blood 2024, 144: 45-45. DOI: 10.1182/blood-2024-206563.Peer-Reviewed Original ResearchConceptsActivation of MYCCell divisionCell growthDNA damage-induced apoptosisTurnover of damaged organellesB-cell lymphomaTranscriptional activity of MYCChIP-seq dataDamage-induced apoptosisOscillatory expression patternsCell shrinkageDegradation of MycPhenotype to cellsTranscription of MYCInduce transcriptional activationAmino acid depletionTime-lapse confocal imagingLive-cell imagingStall cell growthB cell developmentChIP-seqB cellsDegron systemRepress transcriptionCell sizeTargeted Dynamic Phospho-Proteogenomic Analysis of Gastric Cancer Cells Suggests Host Immunity Provides Survival Benefit
Kume K, Iida M, Iwaya T, Yashima-Abo A, Koizumi Y, Endo A, Wade K, Hiraki H, Calvert V, Wulfkuhle J, Espina V, Siwak D, Lu Y, Takemoto K, Suzuki Y, Sasaki Y, Tokino T, Petricoin E, Liotta L, Mills G, Nishizuka S. Targeted Dynamic Phospho-Proteogenomic Analysis of Gastric Cancer Cells Suggests Host Immunity Provides Survival Benefit. Molecular & Cellular Proteomics 2024, 23: 100870. PMID: 39461475, PMCID: PMC11621936, DOI: 10.1016/j.mcpro.2024.100870.Peer-Reviewed Original ResearchCitationsAltmetricConceptsDNA-damaging drugsTotal lymphocyte countCell linesResistance to DNA damaging drugsPD-L1Adjuvant chemotherapyProtein dynamicsProtein-level regulationSurvival benefitCopy number lossExpression time courseGastric cancerRelapse-free survival rateGastric cancer cellsHost immunityAssociated with prolonged survivalIncreased STAT1 phosphorylationResistance to other drugsGlobal protein dynamicsImmune checkpoint blockadePD-L1 positivityPD-L1 expressionAdvanced gastric cancerExpression of STAT1Molecular targeted drugs
Academic Achievements & Community Involvement
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Honors
honor Nominated for full membership in Sigma Xi
09/09/2025National AwardSigma XiDetailsUnited Stateshonor ASH Abstract Achievement Award
10/23/2023, 11/12/2021, 11/29/2019, 10/29/2018, 10/31/2017National AwardAmerican Society of Hematologyhonor Research Grant from The Japan Prize Foundation
04/01/2012National AwardThe Japan Prize FoundationDetailsJapanhonor Sasakawa Scientific Research Grant
04/01/2009National AwardThe Japan Science SocietyDetailsJapan
News
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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
- February 26, 2025
Celebrating Yale Cancer Center Faculty, Research Scientists
- July 24, 2024
Yale Department of Internal Medicine Faculty Promotions and Appointments (July 2024)
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Müschen Lab
300 George Street
New Haven, CT 06511
United States