Featured Publications
Extrachromosomal DNA amplifications in cancer
Yi E, Chamorro González R, Henssen A, Verhaak R. Extrachromosomal DNA amplifications in cancer. Nature Reviews Genetics 2022, 23: 760-771. PMID: 35953594, PMCID: PMC9671848, DOI: 10.1038/s41576-022-00521-5.Peer-Reviewed Original ResearchConceptsExtrachromosomal DNA amplificationsNew therapeutic vulnerabilitiesCopy number heterogeneityEpigenetic architectureDNA amplificationCell divisionNuclear bodiesMost cancer typesNumber heterogeneityRegulatory landscapeTherapeutic vulnerabilitiesFunctional impactCancer typesDriver alterationsCircular structureEcDNAsChromatinizationChromosomesGenesAmplificationEcDNARecent investigationsEnhancerDeregulationCancerGlioma progression is shaped by genetic evolution and microenvironment interactions
Varn F, Johnson K, Martinek J, Huse J, Nasrallah M, Wesseling P, Cooper L, Malta T, Wade T, Sabedot T, Brat D, Gould P, Wöehrer A, Aldape K, Ismail A, Sivajothi S, Barthel F, Kim H, Kocakavuk E, Ahmed N, White K, Datta I, Moon H, Pollock S, Goldfarb C, Lee G, Garofano L, Anderson K, Nehar-Belaid D, Barnholtz-Sloan J, Bakas S, Byrne A, D’Angelo F, Gan H, Khasraw M, Migliozzi S, Ormond D, Paek S, Van Meir E, Walenkamp A, Watts C, Weiss T, Weller M, Palucka K, Stead L, Poisson L, Noushmehr H, Iavarone A, Verhaak R, Consortium T, Varn F, Johnson K, Martinek J, Huse J, Nasrallah M, Wesseling P, Cooper L, Malta T, Wade T, Sabedot T, Brat D, Gould P, Wöehrer A, Aldape K, Ismail A, Sivajothi S, Barthel F, Kim H, Kocakavuk E, Ahmed N, White K, Datta I, Moon H, Pollock S, Goldfarb C, Lee G, Garofano L, Anderson K, Nehar-Belaid D, Barnholtz-Sloan J, Bakas S, Byrne A, D’Angelo F, Gan H, Khasraw M, Migliozzi S, Ormond D, Paek S, Van Meir E, Walenkamp A, Watts C, Weiss T, Weller M, Alfaro K, Amin S, Ashley D, Bock C, Brodbelt A, Bulsara K, Castro A, Connelly J, Costello J, de Groot J, Finocchiaro G, French P, Golebiewska A, Hau A, Hong C, Horbinski C, Kannan K, Kouwenhoven M, Lasorella A, LaViolette P, Ligon K, Lowman A, Mehta S, Miletic H, Molinaro A, Ng H, Niclou S, Niers J, Phillips J, Rabadan R, Rao G, Reifenberger G, Sanai N, Short S, Smitt P, Sloan A, Smits M, Snyder J, Suzuki H, Tabatabai G, Tanner G, Tomaszewski W, Wells M, Westerman B, Wheeler H, Xie J, Yung W, Zadeh G, Zhao J, Palucka K, Stead L, Poisson L, Noushmehr H, Iavarone A, Verhaak R. Glioma progression is shaped by genetic evolution and microenvironment interactions. Cell 2022, 185: 2184-2199.e16. PMID: 35649412, PMCID: PMC9189056, DOI: 10.1016/j.cell.2022.04.038.Peer-Reviewed Original ResearchConceptsSpecific ligand-receptor interactionsMicroenvironment interactionsDNA sequencing dataGlioma progressionLigand-receptor interactionsNeoplastic cellsSignaling programsCell statesSequencing dataGenetic evolutionGenetic changesIDH wild-type tumorsIsocitrate dehydrogenaseMesenchymal transitionSomatic alterationsDistinct mannerActive tumor growthIDH-mutant gliomasPotential targetTherapy resistanceAdult patientsDisease progressionPossible roleCellsTumor growthSingle-cell multimodal glioma analyses identify epigenetic regulators of cellular plasticity and environmental stress response
Johnson K, Anderson K, Courtois E, Gujar A, Barthel F, Varn F, Luo D, Seignon M, Yi E, Kim H, Estecio M, Zhao D, Tang M, Navin N, Maurya R, Ngan C, Verburg N, de Witt Hamer P, Bulsara K, Samuels M, Das S, Robson P, Verhaak R. Single-cell multimodal glioma analyses identify epigenetic regulators of cellular plasticity and environmental stress response. Nature Genetics 2021, 53: 1456-1468. PMID: 34594038, PMCID: PMC8570135, DOI: 10.1038/s41588-021-00926-8.Peer-Reviewed Original ResearchMeSH KeywordsBrain NeoplasmsCell PlasticityClonal EvolutionDNA Copy Number VariationsDNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticGenetic HeterogeneityGenome, HumanGliomaHumansMutationPhylogenyPromoter Regions, GeneticSingle-Cell AnalysisStress, PhysiologicalTumor MicroenvironmentConceptsDNA methylation disorderEnvironmental stress responsesMethylation disordersEnvironmental stress response pathwaysStress responseStress response processesStress response pathwaysSingle-cell transcriptomesDNA methylation changesDNA methylation differencesDNA methylation dataMulti-omics profilesDNA methylomeTranscriptional disruptionEpigenetic instabilityEpigenetic heterogeneityEpigenetic regulatorsResponse pathwaysCellular plasticityMethylation changesMethylation differencesCell statesMethylation dataIrradiation stressWild-type gliomasExtrachromosomal DNA is associated with oncogene amplification and poor outcome across multiple cancers
Kim H, Nguyen N, Turner K, Wu S, Gujar A, Luebeck J, Liu J, Deshpande V, Rajkumar U, Namburi S, Amin S, Yi E, Menghi F, Schulte J, Henssen A, Chang H, Beck C, Mischel P, Bafna V, Verhaak R. Extrachromosomal DNA is associated with oncogene amplification and poor outcome across multiple cancers. Nature Genetics 2020, 52: 891-897. PMID: 32807987, PMCID: PMC7484012, DOI: 10.1038/s41588-020-0678-2.Peer-Reviewed Original ResearchConceptsOncogene amplificationPoor outcomeCancer typesEcDNA amplificationShorter survivalCancer patientsMost cancer typesExtrachromosomal DNA amplificationsClinical impactMultiple cancersPatientsNormal tissuesCancerTranscript fusionsEnhanced chromatin accessibilityIntratumoral genetic heterogeneityOncogene transcriptionChromosomal amplificationOutcomesGenetic heterogeneityHigh levelsDNA amplificationTissue typesBloodLongitudinal molecular trajectories of diffuse glioma in adults
Barthel FP, Johnson KC, Varn FS, Moskalik AD, Tanner G, Kocakavuk E, Anderson KJ, Abiola O, Aldape K, Alfaro KD, Alpar D, Amin SB, Ashley DM, Bandopadhayay P, Barnholtz-Sloan JS, Beroukhim R, Bock C, Brastianos PK, Brat DJ, Brodbelt AR, Bruns AF, Bulsara KR, Chakrabarty A, Chakravarti A, Chuang JH, Claus EB, Cochran EJ, Connelly J, Costello JF, Finocchiaro G, Fletcher MN, French PJ, Gan HK, Gilbert MR, Gould PV, Grimmer MR, Iavarone A, Ismail A, Jenkinson MD, Khasraw M, Kim H, Kouwenhoven MCM, LaViolette PS, Li M, Lichter P, Ligon KL, Lowman AK, Malta TM, Mazor T, McDonald KL, Molinaro AM, Nam DH, Nayyar N, Ng HK, Ngan CY, Niclou SP, Niers JM, Noushmehr H, Noorbakhsh J, Ormond DR, Park CK, Poisson LM, Rabadan R, Radlwimmer B, Rao G, Reifenberger G, Sa JK, Schuster M, Shaw BL, Short SC, Smitt PAS, Sloan AE, Smits M, Suzuki H, Tabatabai G, Van Meir EG, Watts C, Weller M, Wesseling P, Westerman BA, Widhalm G, Woehrer A, Yung WKA, Zadeh G, Huse JT, De Groot JF, Stead LF, Verhaak RGW. Longitudinal molecular trajectories of diffuse glioma in adults. Nature 2019, 576: 112-120. PMID: 31748746, PMCID: PMC6897368, DOI: 10.1038/s41586-019-1775-1.Peer-Reviewed Original ResearchConceptsAdult patientsDiffuse gliomasRecurrent gliomaOverall survivalPoor outcomeCurrent therapiesChromosome arms 1p/19qAcquired alterationsMajor subtypesTherapeutic resistanceGliomasGlioma developmentGene alterationsIDH mutationsGlioma subtypesPatientsHypermutator phenotypeDriver genesSubtypesClinical annotationSurvivalSubclonal selectionCell cycleAlterationsLittle evidence
2024
DNAR-16. TARGETING APOBEC CYTIDINE DEAMINASES TO ENHANCE RADIOSENSITIVITY IN GLIOMA
Marin B, Gujar A, Kocakavuk E, Johnson K, Amin S, Verhaak R. DNAR-16. TARGETING APOBEC CYTIDINE DEAMINASES TO ENHANCE RADIOSENSITIVITY IN GLIOMA. Neuro-Oncology 2024, 26: viii120-viii121. PMCID: PMC11553289, DOI: 10.1093/neuonc/noae165.0467.Peer-Reviewed Original ResearchApolipoprotein B mRNA-editing enzyme catalytic polypeptide-likeRadiation therapyNon-homologous end joiningRecurrent gliomaDNA-dependent protein kinaseMutational signaturesRT-induced DNA damageMonitoring response to treatmentRadiosensitivity in vitroEnhanced radiosensitivity in vitroA3GPromote tumor evolutionResponse to treatmentAutophosphorylation of DNA-dependent protein kinaseAPOBEC mutational signaturesAdult brain tumorsPrimary adult brain tumorGlioma Longitudinal Analysis ConsortiumFamily of cytidine deaminasesRadiosensitizing gliomasAPOBEC3G (A3GNon-homologous end-joining pathwayPost-RTGlioma cell linesWhole-genome sequencingEPCO-26. LONGITUDINAL SINGLE-CELL ANALYSES IDENTIFY DRIVERS OF GENETIC, EPIGENOMIC, AND CELLULAR EVOLUTION IN IDH-MUTANT GLIOMA
Johnson K, Spitzer A, Varn F, Nomura M, Garofano L, Chowdhury T, Anderson K, D’Angelo F, Bussema L, Gritsch S, Oh Y, Moon H, Paek S, Bielle F, Laurenge A, Di Stefano A, Mathon B, Picca A, Sanson M, Lipsa A, Hertel F, Zhao Z, Wang Q, Jiang T, Hermes B, Sanai N, Golebiewska A, Niclou S, Huse J, Yung W, Lasorella A, Suvà M, Iavarone A, Tirosh I, Verhaak R. EPCO-26. LONGITUDINAL SINGLE-CELL ANALYSES IDENTIFY DRIVERS OF GENETIC, EPIGENOMIC, AND CELLULAR EVOLUTION IN IDH-MUTANT GLIOMA. Neuro-Oncology 2024, 26: viii6-viii7. PMCID: PMC11552777, DOI: 10.1093/neuonc/noae165.0025.Peer-Reviewed Original ResearchIDH-mutant gliomasGenetic alterationsStem-like populationDifferentially accessible peaksChromatin accessibility dataCopy number alterationsCellular hierarchyCycling populationTumor microenvironment cell typesSingle nucleus RNA sequencingCell cycle alterationsMalignant cell differentiationHigh tumor gradeNucleus RNA sequencingDNA sequencesATAC sequencingGenetic analysisCellular statesAccessibility peaksMicroenvironment cell typesReduced differentiationRNA sequencingIntratumoral cellular heterogeneityCellular heterogeneityTumor gradeCNSC-54. CENTRAL AND BOUNDARY-DRIVEN GROWTH PATTERNS DOMINATE RESPECTIVELY IDH WILD-TYPE AND MUTANT GLIOMAS
Kyriakidou M, Urbaniak K, Mbegbu M, Rockne R, Wesseling P, Eijgelaar R, Anderson K, Verhaak R, de Witt-Hamer P, Verburg N, Branciamore S, Barthel F. CNSC-54. CENTRAL AND BOUNDARY-DRIVEN GROWTH PATTERNS DOMINATE RESPECTIVELY IDH WILD-TYPE AND MUTANT GLIOMAS. Neuro-Oncology 2024, 26: viii53-viii53. PMCID: PMC11553254, DOI: 10.1093/neuonc/noae165.0210.Peer-Reviewed Original ResearchConsistent with neutral evolutionDiffuse gliomasLocal treatmentEvolutionary processWhole-genome sequencingSpread to distant sitesIDH wild-typePrimary malignant brain tumorImage-guided samplingPhylogeographic relationshipsDN/dS ratiosMalignant brain tumorsNeutral evolutionSomatic variantsGenetic heterogeneityIDHmut tumorsTumor centerMRI abnormalitiesStochastic mutationsTumor diffusionAdult patientsPoor prognosisTumor cellsIDH mutantTumor developmentA brave new framework for glioma drug development
Hotchkiss K, Karschnia P, Schreck K, Geurts M, Cloughesy T, Huse J, Duke E, Lathia J, Ashley D, Nduom E, Long G, Singh K, Chalmers A, Ahluwalia M, Heimberger A, Bagley S, Todo T, Verhaak R, Kelly P, Hervey-Jumper S, de Groot J, Patel A, Fecci P, Parney I, Wykes V, Watts C, Burns T, Sanai N, Preusser M, Tonn J, Drummond K, Platten M, Das S, Tanner K, Vogelbaum M, Weller M, Whittle J, Berger M, Khasraw M. A brave new framework for glioma drug development. The Lancet Oncology 2024, 25: e512-e519. PMID: 39362262, DOI: 10.1016/s1470-2045(24)00190-6.Peer-Reviewed Original ResearchConceptsBrain tumorsBenefits of biopsyBrain tumor therapyLiquid biopsy technologiesTissue samplesPostoperative deficitsBiopsy techniqueBiopsy technologyEffective therapySurgical trialsClinical trialsTumor therapyResistance mechanismsTumorTherapyPatientsDrug developmentTissue analysisBrainTrialsTissueBiopsyGliomaRegulatory agenciesCASCADES, a novel SOX2 super‐enhancer‐associated long noncoding RNA, regulates cancer stem cell specification and differentiation in glioblastoma
Shahzad U, Nikolopoulos M, Li C, Johnston M, Wang J, Sabha N, Varn F, Riemenschneider A, Krumholtz S, Krishnamurthy P, Smith C, Karamchandani J, Watts J, Verhaak R, Gallo M, Rutka J, Das S. CASCADES, a novel SOX2 super‐enhancer‐associated long noncoding RNA, regulates cancer stem cell specification and differentiation in glioblastoma. Molecular Oncology 2024 PMID: 39323013, DOI: 10.1002/1878-0261.13735.Peer-Reviewed Original ResearchCancer stem cellsGlioma CSCsPresence of cancer stem cellsCancer stem cell compartmentPrimary malignant brain tumorGlioma cancer stem cellsMalignant brain tumorsCancer-specific mannerMedian survivalTumor recurrenceTreatment resistanceStem cell specificationRegulation of stemnessTumor developmentRegulation of Sox2Brain tumorsNeuronal lineageStem cellsGlioblastomaTherapeutic targetSOX2Cell RepositoryCell-specificTumorLong noncoding RNAs13. AmpliconSuite: Analyzing focal amplifications in cancer genomes
Luebeck J, Huang E, Dameracharla B, Kim F, Liefeld T, Ahuja R, Prasad D, Prasad G, Kim S, Kim H, Bailey P, Verhaak R, Deshpande V, Reich M, Mischel P, Mesirov J, Bafna V. 13. AmpliconSuite: Analyzing focal amplifications in cancer genomes. Cancer Genetics 2024, 286: s5. DOI: 10.1016/j.cancergen.2024.08.015.Peer-Reviewed Original ResearchWhole-genome sequencingWhole-genome sequencing dataFocal amplificationCancer genomesStructural variationsAmplification of oncogenesExtrachromosomal DNACopy numberEcDNAGenomeOncogene amplificationAmpliconArchitectCancer progressionAmplificationAmplification typeTumor samplesBiocondaNextflowPCAWGGenePatternRobust identificationDNACCLESequenceOncogeneOncogenic composite mutations can be predicted by co‐mutations and their chromosomal location
Küçükosmanoglu A, van der Borden C, de Boer L, Verhaak R, Noske D, Wurdinger T, Radonic T, Westerman B. Oncogenic composite mutations can be predicted by co‐mutations and their chromosomal location. Molecular Oncology 2024, 18: 2407-2422. PMID: 38757376, PMCID: PMC11459034, DOI: 10.1002/1878-0261.13636.Peer-Reviewed Original ResearchComposite mutationCo-mutationsMutation-specific drugsCell line dataChromosomal locationSub-clonal populationsGenetic heterogeneitySub-clonesTherapy resistanceSelection pressureGenetic eventsStratify patientsKRAS geneResistance-causing mutationsCancer patientsBiopsy samplesMutationsPatientsGenesPrecision medicineTherapyRiskChromosomeBiopsyBRAF
2023
QOL-09. QUALITY OF LIFE AFTER SURGERY FOR LOWER GRADE GLIOMAS
Heffernan A, Wu Y, Benz L, Verhaak R, Kwan B, Claus E. QOL-09. QUALITY OF LIFE AFTER SURGERY FOR LOWER GRADE GLIOMAS. Neuro-Oncology 2023, 25: v250-v250. PMCID: PMC10639580, DOI: 10.1093/neuonc/noad179.0961.Peer-Reviewed Original ResearchLow-grade gliomasGrade gliomasNon-malignant brain tumoursShort Form Health SurveyBackground Limited dataForm Health SurveyGeneral healthy populationGroup of patientsMedical Outcomes StudyCase/control studyLong-term qualityTime of interviewResidents of ConnecticutQOL outcomesSample average ageHealth SurveyOutcome studiesMeningioma casesTreatment groupsBrain tumorsAverage ageControl studyHealthy populationControl populationPrime of lifeCTNI-23. SINGLE CELL TRANSCRIPTOMICS, PHARMACOKINETICS, AND PHARMACODYNAMICS OF COMBINED CDK4/6 AND MTOR INHIBITION IN A PHASE 0 TRIAL OF RECURRENT HIGH-GRADE GLIOMA
Johnson K, Tien A, Jiang J, McNamara J, Chang Y, Montgomery C, DeSantis A, Elena L, Fujita Y, Kim S, Tovmasyan A, Li J, Mehta S, Verhaak R, Sanai N. CTNI-23. SINGLE CELL TRANSCRIPTOMICS, PHARMACOKINETICS, AND PHARMACODYNAMICS OF COMBINED CDK4/6 AND MTOR INHIBITION IN A PHASE 0 TRIAL OF RECURRENT HIGH-GRADE GLIOMA. Neuro-Oncology 2023, 25: v78-v79. PMCID: PMC10639373, DOI: 10.1093/neuonc/noad179.0305.Peer-Reviewed Original ResearchHigh-grade gliomasRecurrent high-grade gliomaPhase 0 trialsStandard therapyPharmacodynamic effectsSurgical specimensMTOR inhibitionAdult high-grade gliomasCDKN2A/B deletionsDose-escalation cohortsIDH wild-type tumorsPharmacokinetics/pharmacodynamicsUnbound drug concentrationsGlioma cell linesRibociclib treatmentCell cycle inhibitionPIK3CA mutationsPreoperative MRIGlioma patientsRibociclibEverolimus concentrationsUnbound concentrationsPatientsSurgical tissuesB deletionEPCO-09. CHARACTERIZING THE GBM CELLULAR LANDSCAPE BY LARGE-SCALE SINGLE-NUCLEUS RNA-SEQUENCING
Spitzer A, Nomura M, Garofano L, Johnson K, Nehar-Belaid D, Oh Y, Anderson K, Najac R, Bussema L, Varn F, D’Angelo F, Chowdhury T, Migliozzi S, Park J, Ermini L, Golebiewska A, Niclou S, Das S, Paek S, Moon H, Mathon B, Di Stefano A, Bielle F, Laurenge A, Sanson M, Tanaka S, Saito N, Keir S, Ashley D, Huse J, Yung W, Lasorella A, Verhaak R, Iavarone A, Tirosh I, Suva M. EPCO-09. CHARACTERIZING THE GBM CELLULAR LANDSCAPE BY LARGE-SCALE SINGLE-NUCLEUS RNA-SEQUENCING. Neuro-Oncology 2023, 25: v125-v125. PMCID: PMC10639394, DOI: 10.1093/neuonc/noad179.0473.Peer-Reviewed Original ResearchCellular statesSingle-cell RNA sequencing technologySpecific cellular statesCell typesDNA sequence dataRNA sequencing technologyMalignant cell statesWhole-genome sequencing dataNucleus RNA sequencingRNA sequencing datasetsFunctional enrichment analysisScRNA-seq datasetsScRNA-seq studiesGBM tumor samplesCertain genetic eventsHallmark of glioblastomaCellular landscapeRNA sequencingCell statesEnrichment analysisBaseline expression profilesSequencing dataExpression profilesGlial developmentIntra-tumor heterogeneityEPCO-22. LONGITUDINAL MOLECULAR CHARACTERIZATION IDENTIFIES TREATMENT DRIVEN EVOLUTION OF OLIGODENDROGLIOMA
Chowdhury T, Johnson K, Kocakavuk E, Heo C, Ye G, Ghospurkar P, Wade T, Barnholtz-Sloan J, Costello J, Elliott C, French P, Golebiewska A, Hermes B, Hong C, Horbinski C, Khasraw M, LaViolette P, Li K, Lipp E, Lowman A, McCortney K, Moon H, Ng H, Padovan M, Paek S, Vallentgoed W, Vaubel R, Wesseling P, Westcott K, Consortium G, Varn F, Verhaak R. EPCO-22. LONGITUDINAL MOLECULAR CHARACTERIZATION IDENTIFIES TREATMENT DRIVEN EVOLUTION OF OLIGODENDROGLIOMA. Neuro-Oncology 2023, 25: v128-v128. PMCID: PMC10639435, DOI: 10.1093/neuonc/noad179.0485.Peer-Reviewed Original ResearchWhole-exome sequencingPI3K pathwaySingle-nucleus RNA sequencingStem-like cellsPatient mortalityChromosome 4 lossPIK3R1 mutationsTreatment resistanceFUBP1 mutationsAggressive phenotypeMost oligodendrogliomasOligodendroglioma patientsChromosome arms 1pRecurrenceAdministration dateSomatic copy number alterationsCopy number alterationsMutational signature analysisOligodendrogliomasRecurrent samplesTERT promoterExome sequencingK pathwayCommon mutationsMolecular changesEPCO-34. IMAGE-BASED PHENOTYPIC HIGH-CONTENT CRISPR-CAS9 SCREEN FOR CHARACTERIZING CANCER DRIVERS IN PEDIATRIC HIGH-GRADE GLIOMA
Amin S, Gujar A, Yi E, Kang W, Costa M, Gabriel P, Sjogren G, Maher L, Lee C, Robson P, Dickinson P, Packer R, Courtois E, Verhaak R. EPCO-34. IMAGE-BASED PHENOTYPIC HIGH-CONTENT CRISPR-CAS9 SCREEN FOR CHARACTERIZING CANCER DRIVERS IN PEDIATRIC HIGH-GRADE GLIOMA. Neuro-Oncology 2023, 25: v131-v131. PMCID: PMC10639707, DOI: 10.1093/neuonc/noad179.0497.Peer-Reviewed Original ResearchKnockout phenotypesWhole genome sequencing datasetsPediatric high-grade gliomasCancer Dependency MapCancer aneuploidyCell morphological featuresKnockout screensOntology analysisCancer driversSequencing datasetsHigh-content screening systemTumor suppressorFocal amplificationDriver genesGenomic landscapeHigh-grade glioma cell linesGenesLive cell imagesGlioma cell linesCell membraneDependency MapSingle cellsApoptotic cellsCell linesCRISPREPCO-37. DISSECTING GBM EVOLUTION FOLLOWING STANDARD-OF-CARE BY LARGE-SCALE LONGITUDINAL SINGLE NUCLEUS RNA-SEQUENCING
Nomura M, Spitzer A, Johnson K, Garofano L, Nehar-Belaid D, Oh Y, Anderson K, Najac R, Bussema L, Varn F, D’Angelo F, Chowdhury T, Migliozzi S, Park J, Ermini L, Golebiewska A, Niclou S, Das S, Paek S, Moon H, Mathon B, Di Stefano A, Bielle F, Laurenge A, Sanson M, Tanaka S, Saito N, Keir S, Ashley D, Huse J, Yung W, Lasorella A, Iavarone A, Verhaak R, Suva M, Tirosh I. EPCO-37. DISSECTING GBM EVOLUTION FOLLOWING STANDARD-OF-CARE BY LARGE-SCALE LONGITUDINAL SINGLE NUCLEUS RNA-SEQUENCING. Neuro-Oncology 2023, 25: v132-v132. PMCID: PMC10639295, DOI: 10.1093/neuonc/noad179.0499.Peer-Reviewed Original ResearchSingle-nucleus RNA sequencingLarge-scale longitudinal cohortTME compositionRecurrent samplesGood clinical courseInitial tumor resectionMajority of patientsTumor microenvironment cellsPrimary tumor samplesMGMT methylation statusTME changesClinical courseRNA sequencingTherapy failureLikely respondersTumor resectionDisease progressionNucleus RNA sequencingLongitudinal cohortReciprocal increaseTumor samplesMicroenvironment cellsMalignant cell fractionGlioblastomaRecurrenceDISP-04. EXPLORING ENGAGEMENT IN LOW GRADE GLIOMA GENOMIC RESEARCH: A COMPARATIVE ANALYSIS OF THREE APPROACHES
Kwan B, Barnard J, Ritger C, Begum A, Salmi L, Fischmann R, Garcia-Hernandez S, Gay N, Gonzalez-Fisher R, Helmkamp L, Johnson K, Lennox L, Lipof G, Ostmeyer J, Perkins I, Pyle L, Reno J, Roth T, Claus E, Verhaak R, DeCamp M. DISP-04. EXPLORING ENGAGEMENT IN LOW GRADE GLIOMA GENOMIC RESEARCH: A COMPARATIVE ANALYSIS OF THREE APPROACHES. Neuro-Oncology 2023, 25: v137-v137. PMCID: PMC10639326, DOI: 10.1093/neuonc/noad179.0519.Peer-Reviewed Original ResearchDISP-10. ENHANCING TRUST AND REPRESENTATIVE PARTICIPATION IN THE INTERNATIONAL LOW GRADE GLIOMA REGISTRY: COMMUNITY ENGAGEMENT STRATEGIES AND RECOMMENDATIONS
Salmi L, Barnard J, Ritger C, Fischmann R, Garcia-Hernandez S, Gay N, Gonzalez-Fisher R, Johnson K, Lennox L, Lipof G, Ostmeyer J, Perkins I, Reno J, Roth T, Begum A, Claus E, Verhaak R, Kwan B. DISP-10. ENHANCING TRUST AND REPRESENTATIVE PARTICIPATION IN THE INTERNATIONAL LOW GRADE GLIOMA REGISTRY: COMMUNITY ENGAGEMENT STRATEGIES AND RECOMMENDATIONS. Neuro-Oncology 2023, 25: v138-v139. PMCID: PMC10639948, DOI: 10.1093/neuonc/noad179.0525.Peer-Reviewed Original Research