About
Titles
Research Scientist
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.
Appointments
Hematology
Research ScientistPrimary
Other Departments & Organizations
Education & Training
- Postdoctoral Fellow
- City of Hope
- Postdoctoral Fellow
- Iwate Medical University School of Medicine
- PhD
- Iwate University, Bioresources Sciences (2011)
Research
Overview
Medical Subject Headings (MeSH)
Cell Size; Drug Resistance; Leukemia; Lipid Metabolism; Lymphoma; Oncogenes; Optogenetics; Protein Array Analysis; Proteogenomics
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
Jaewoong Lee, PhD
Etienne Leveille, MD
Mark Robinson, PhD
Shalin Kothari, MD
34Publications
489Citations
Protein Array Analysis
Drug Resistance
Publications
2024
Targeted 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, 100870. PMID: 39461475, DOI: 10.1016/j.mcpro.2024.100870.Peer-Reviewed Original ResearchConceptsDNA-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 drugsDependence of lymphopoiesis on efficient β-catenin degradation
Cosgun K, Jumaa H, Robinson M, Klemm L, Oulghazi S, Fonseca-Arce D, Xu L, Xiao G, Khanduja D, Chan L, Lee J, Kume K, Song J, Chan W, Chen J, Taketo M, Kothari S. Dependence of lymphopoiesis on efficient β-catenin degradation. The Journal Of Immunology 2024, 212: 1195_4936-1195_4936. DOI: 10.4049/jimmunol.212.supp.1195.4936.Peer-Reviewed Original ResearchConceptsIkaros zinc fingersLymphoid cellsB-cateninChIP-seq analysisSuppression of MYC expressionRegulate lineage specificationInduce cell deathConstitutively low levelsDeletion of ApcChIP-seqTcf factorsZinc fingerProteasomal degradationBinding motifNucleosome remodelingDestruction complexSpecific genesWnt/b-catenin pathwayLineage specificationCell deathMYC expressionSuperenhancersLymphoid developmentEpithelial lineageEpithelial cellsDynamic recruitment of inhibitory complexes by CD25 controls B-cell development and selection
Sun R, Lee J, Robinson M, Kume K, Ma N, Cosgun K, Chan L, Antoshkina I, Khanduja D, Leveille E, Katz S, Vaidehi N, Müschen M. Dynamic recruitment of inhibitory complexes by CD25 controls B-cell development and selection. The Journal Of Immunology 2024, 212: 1253_4618-1253_4618. DOI: 10.4049/jimmunol.212.supp.1253.4618.Peer-Reviewed Original ResearchConceptsBCR signalingInhibitory complexInhibitory phosphatasesPositively charged tailITIM-bearing receptorsInitiation of BCR signalingNegatively charged residuesB cell developmentSH2 domainPhosphatase domainCytoplasmic tailITIM motifsGenetic studiesPhosphatase SHP1Co-IPBCR complexDynamic recruitmentIL2 receptorCell surfaceB cellsSHP1Surface-expressedTernary complexClonal expansionPhosphatase
2023
Optogenetic Control of Oncogenic Signaling in B-Cell Malignancies
Kume K, Lee J, Cheng Z, Robinson M, Leveille E, Cosgun K, Chan L, Feng Y, Arce D, Khanduja D, Toomre D, Müschen M. Optogenetic Control of Oncogenic Signaling in B-Cell Malignancies. Blood 2023, 142: 4138. DOI: 10.1182/blood-2023-190926.Peer-Reviewed Original ResearchConceptsB-cell malignanciesB-cell lymphomaMature B-cell lymphomasB cell deathB cellsB cell developmentGenetic deletionMantle cell lymphomaNF-kB signalingBCR signal inhibitorsB cell precursorsCell of originCell viabilityChronic active BCRB cell survivalB cell receptor signalsHodgkin's diseaseMultiple myelomaNormal B cell developmentPlasma cellsBtk tyrosine kinaseCell lymphomaBurkitt's lymphomaNF-kBSmall molecule inhibitorsSTAT5-Feedback Controls Distinct Metabolic States for Dynamic Transitions between Cellular Activation and Quiescence in Acute Lymphoblastic Leukemia
Kume K, Chen Z, Robinson M, Chan L, Leveille E, Cosgun K, Cheng Z, Arce D, Khanduja D, Graeber T, Müschen M. STAT5-Feedback Controls Distinct Metabolic States for Dynamic Transitions between Cellular Activation and Quiescence in Acute Lymphoblastic Leukemia. Blood 2023, 142: 2977. DOI: 10.1182/blood-2023-191006.Peer-Reviewed Original ResearchConceptsB-cell acute lymphoblastic leukemiaAcute lymphoblastic leukemiaLymphoblastic leukemiaPharmacological inhibitionGenetic deletionCellular activationReceptor signalingCell deathBone marrow relapsePoor overall outcomePoor clinical outcomeLeukemia-initiating capacityOncogenic STAT5Mass spectrometry-based metabolomics analysisExpression levelsPhosphorylation of STAT5Flow cytometry analysisMetabolic statePositive MRDRole of mTORMarrow relapseAggressive courseClinical outcomesExcessive protein synthesisMetabolic outcomesImmunoglobulin Light Chains Control Permissiveness to Malignant B-Cell Transformation By RAS-Pathway Lesions
Chan L, Kume K, Hurtz C, Robinson M, Cosgun K, Müschen M. Immunoglobulin Light Chains Control Permissiveness to Malignant B-Cell Transformation By RAS-Pathway Lesions. Blood 2023, 142: 2974. DOI: 10.1182/blood-2023-190163.Peer-Reviewed Original ResearchConceptsJeKo-1 cellsB cell precursorsMature B cellsB cellsMantle cell lymphoma cellsCell lymphoma cellsGenetic ablationImmunoglobulin light chainsRAS activationOncogenic RASMalignant transformationB-cell acute lymphoblastic leukemiaConventional light chainsRAS pathwayLymphoma cellsCell deathOncogenic RAS activationLight chainAcute lymphoblastic leukemiaMature B-cell lymphomasTransgenic mouse modelB-cell lymphomaB-cell malignanciesMalignant B-cell transformationKappa-LCRepurposing GSK3B Small Molecule Inhibitors for Refractory Lymphoid Malignancies
Cosgun K, Robinson M, Oulghazi S, Xu L, Xiao G, Chan L, Lee J, Kume K, Leveille E, Arce D, Khanduja D, Feldhahn N, Song J, Chan W, Chen J, Taketo M, Schjerven H, Jellusova J, Kothari S, Davids M, Müschen M. Repurposing GSK3B Small Molecule Inhibitors for Refractory Lymphoid Malignancies. Blood 2023, 142: 2818. DOI: 10.1182/blood-2023-190522.Peer-Reviewed Original ResearchConceptsFavorable safety profileSmall molecule inhibitorsT-lymphoid malignancyΒ-catenin degradationLymphoid malignanciesΒ-cateninInteractome studiesSafety profileClinical trialsMolecule inhibitorsLow nanomolar concentrationsΒ-catenin accumulationSolid tumorsRefractory B-cell malignanciesCell deathPK/PD profilesZinc finger proteinRefractory lymphoid malignanciesChIP-seq analysisPhase 2 trialMYC target genesT-cell lymphomaColony formationRapid nuclear accumulationWnt/β-catenin pathwayDynamic Recruitment of Inhibitory Complexes Controls Oncogenic Signaling in B-Cell Malignancies
Sun R, Lee J, Robinson M, Kume K, Ma N, Cosgun K, Chan L, Antoshkina I, Khanduja D, Leveille E, Katz S, Chen J, Paietta E, Vaidehi N, Müschen M. Dynamic Recruitment of Inhibitory Complexes Controls Oncogenic Signaling in B-Cell Malignancies. Blood 2023, 142: 719. DOI: 10.1182/blood-2023-189742.Peer-Reviewed Original ResearchConceptsB-cell malignanciesB-cell lymphomaHigher serum levelsMature B-cell lymphomasSoluble CD25Serum levelsOncogenic signalingMouse modelB cellsAggressive B-cell lymphomasAcceleration of diseaseActivation of inhibitoryPoor clinical outcomeCD25 surface expressionB cell subsetsRole of CD25Patient-derived xenograftsB cell populationsB-cell receptor signalingB-cell leukemiaGenetic mouse modelsKnockin mouse modelCell deathMature B cell populationClinical outcomesComputational Discovery and Validation of NAD+ Biosynthesis As Unique Vulnerability in B-Lymphoid Malignancies
Li Q, Robinson M, Leveille E, Zhang C, Sun R, Cheng Z, Kume K, Cosgun K, Kothari S, Khanduja D, Nakada D, Müschen M. Computational Discovery and Validation of NAD+ Biosynthesis As Unique Vulnerability in B-Lymphoid Malignancies. Blood 2023, 142: 418. DOI: 10.1182/blood-2023-190269.Peer-Reviewed Original ResearchConceptsSmall molecule inhibitorsDrug discovery toolNAMPT inhibitorsCompound screenCell type-specific targetsCell linesMolecule inhibitorsPurine/pyrimidine metabolismTumor cell linesEnergy metabolismSalvage biosynthesis pathwaySolid tumor cell linesB cell developmentCellular energy metabolismB cell signalingAmino acid metabolismCell cycle arrestDiscovery toolDepletion of metabolitesBiosynthesis pathwayCompetitive fitnessRate-limiting enzymeNAMPT deletionConditional mouse modelEnergy stressMYC to BCL6 State-Transitions Determine Cell Size and Metabolic Fluctuations and Define a Novel Biorhythm in B-Cell Malignancies
Cheng Z, Kume K, Müschen M. MYC to BCL6 State-Transitions Determine Cell Size and Metabolic Fluctuations and Define a Novel Biorhythm in B-Cell Malignancies. Blood 2023, 142: 2769. DOI: 10.1182/blood-2023-190972.Peer-Reviewed Original ResearchConceptsGerminal center-derived B-cell lymphomaB cell developmentCell size fluctuationsCell cycleImmunoglobulin light chain gene recombinationDNA damage-induced apoptosisDistinct cellular statesNormal B cell developmentDamage-induced apoptosisExit cell cycleCell sizeB cell transitionGene expression profilesQuiescent phenotypeOncogenic tyrosine kinasesCell cycle arrestActivation of autophagySingle-cell sortingCellular statesCell divisionHigher glycolysis activityMYC transcriptionB cell cycleSuppression of glycolysisExpression profiles
Academic Achievements & Community Involvement
honor ASH Abstract Achievement Award
National AwardDetails11/12/2021, 11/29/2019, 10/29/2018, 10/31/2017United Stateshonor Research Grant from The Japan Prize Foundation
International AwardDetails04/01/2012Japan
News
Get In Touch
Contacts
Email
Academic Office Number
Mailing Address
Müschen Lab
300 George Street
New Haven, CT 06511
United States