2025
SIMVI disentangles intrinsic and spatial-induced cellular states in spatial omics data
Dong M, Su D, Kluger H, Fan R, Kluger Y. SIMVI disentangles intrinsic and spatial-induced cellular states in spatial omics data. Nature Communications 2025, 16: 2990. PMID: 40148341, PMCID: PMC11950362, DOI: 10.1038/s41467-025-58089-7.Peer-Reviewed Original ResearchMeSH KeywordsB-LymphocytesCell CommunicationComputational BiologyDeep LearningGerminal CenterHumansMacrophagesMelanomaPalatine TonsilSingle-Cell AnalysisTumor MicroenvironmentConceptsOmics dataSpatial omics dataAnalysis of gene expressionSingle-cell resolutionDownstream analysisCellular statesSpatial interaction modelsGerminal center B cellsGene expressionCommunication machineryOmics technologiesIntercellular interactionsSpatial omics technologiesTumor microenvironmentB cellsSpatial dynamicsHuman tonsilsMacrophage stateSpatial effectsEpigenetic therapy sensitizes anti–PD-1 refractory head and neck cancers to immunotherapy rechallenge
Qin T, Mattox A, Campbell J, Park J, Shin K, Li S, Sadow P, Faquin W, Micevic G, Daniels A, Haddad R, Garris C, Pittet M, Mempel T, ONeill A, Sartor M, Pai S. Epigenetic therapy sensitizes anti–PD-1 refractory head and neck cancers to immunotherapy rechallenge. Journal Of Clinical Investigation 2025, 135: e181671. PMID: 40091844, PMCID: PMC11910227, DOI: 10.1172/jci181671.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic Combined Chemotherapy ProtocolsAzacitidineB7-H1 AntigenEpigenesis, GeneticFemaleHead and Neck NeoplasmsHumansImmune Checkpoint InhibitorsImmunotherapyMaleMiddle AgedProgrammed Cell Death 1 ReceptorSquamous Cell Carcinoma of Head and NeckTumor MicroenvironmentConceptsHead and neck squamous cell carcinomaTumor microenvironmentProlonged OSOverall survivalIFN-gCD8+ T cell infiltrationCD4+ T regulatory cellsOn-treatment tumor biopsiesNeck squamous cell carcinomaSystemic host immune responseBackgroundImmune checkpoint blockadeMetastatic (R/MMedian overall survivalPD-L1 expressionT cell infiltrationLocal tumor microenvironmentT regulatory cellsSquamous cell carcinomaBiologically effective dosePhase 1b clinical trialHost immune responseCheckpoint blockadeOS ratesPD-L1Tumor biopsiesBiological and clinical significance of tumour-infiltrating lymphocytes in the era of immunotherapy: a multidimensional approach
Lopez de Rodas M, Villalba-Esparza M, Sanmamed M, Chen L, Rimm D, Schalper K. Biological and clinical significance of tumour-infiltrating lymphocytes in the era of immunotherapy: a multidimensional approach. Nature Reviews Clinical Oncology 2025, 22: 163-181. PMID: 39820025, DOI: 10.1038/s41571-024-00984-x.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkers, TumorClinical RelevanceHumansImmune Checkpoint InhibitorsImmunotherapyLymphocytes, Tumor-InfiltratingNeoplasmsPrognosisTumor MicroenvironmentConceptsTumor-infiltrating lymphocytesImmune-checkpoint inhibitorsTumor-infiltrating lymphocyte subpopulationsClinical significance of tumor-infiltrating lymphocytesPredictive value of tumor-infiltrating lymphocytesSignificance of tumor-infiltrating lymphocytesStudy of tumor-infiltrating lymphocytesImmune-checkpoint inhibitor therapyImmune-mediated tumor eliminationEra of immunotherapyT cell dysfunctionBiomarkers of responseSolid tumor typesImmunotherapeutic approachesAntigen-reactiveTumor microenvironmentTumor typesClinical outcomesTumor eliminationClinical significanceSingle-cell transcriptomicsPredictive valueAnticancer mechanismClinical implicationsResistance mechanismsGPR55 in the tumor microenvironment of pancreatic cancer controls tumorigenesis
Ristić D, Bärnthaler T, Gruden E, Kienzl M, Danner L, Herceg K, Sarsembayeva A, Kargl J, Schicho R. GPR55 in the tumor microenvironment of pancreatic cancer controls tumorigenesis. Frontiers In Immunology 2025, 15: 1513547. PMID: 39885986, PMCID: PMC11779727, DOI: 10.3389/fimmu.2024.1513547.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaModel of pancreatic ductal adenocarcinomaImmune tumor microenvironmentTumor microenvironmentT cellsKO miceEndocannabinoid systemWT miceTumor growthCD8<sup>+</sup> T cellsG protein-coupled receptor 55Suppress T cell functionCancer cellsMurine pancreatic ductal adenocarcinomaCD3<sup>+</sup> T cellsExpression of PDL1T cell influxImmune cell compositionT cell functionTumor microenvironment cellsMigration of T cellsReduced tumor weightImmune cell populationsT cell activationCell linesHarnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition
Glaviano A, Lau H, Carter L, Lee E, Lam H, Okina E, Tan D, Tan W, Ang H, Carbone D, Yee M, Shanmugam M, Huang X, Sethi G, Tan T, Lim L, Huang R, Ungefroren H, Giovannetti E, Tang D, Bruno T, Luo P, Andersen M, Qian B, Ishihara J, Radisky D, Elias S, Yadav S, Kim M, Robert C, Diana P, Schalper K, Shi T, Merghoub T, Krebs S, Kusumbe A, Davids M, Brown J, Kumar A. Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition. Journal Of Hematology & Oncology 2025, 18: 6. PMID: 39806516, PMCID: PMC11733683, DOI: 10.1186/s13045-024-01634-6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionHumansMolecular Targeted TherapyNeoplasmsSignal TransductionTumor MicroenvironmentConceptsEpithelial-mesenchymal transitionTumor microenvironmentCancer progressionTherapeutic resistanceCancer therapyTumor microenvironment componentsTumor microenvironment modulationModulation of epithelial-mesenchymal transitionPromote tumor growthImprove treatment efficacyTumor microenvironment signalsTargeted cancer therapyTarget various componentsTherapeutic challengeTreatment responseTumor growthPromote metastasisTherapeutic strategiesTreatment efficacyEpithelial cellsMesenchymal traitsCancer cellsExtracellular matrix componentsCancerResistance mechanismsImmunogenomic determinants of exceptional response to immune checkpoint inhibition in renal cell carcinoma
Jammihal T, Saliby R, Labaki C, Soulati H, Gallegos J, Peris A, McCurry D, Yu C, Shah V, Poduval D, El Zarif T, El Ahmar N, Laimon Y, Eid M, Sheshdeh A, Krajewski K, Büttner F, Schwab M, Heng D, Casellas R, Rai K, Zacharias Millward N, Msaouel P, Karam J, Signoretti S, Van Allen E, Choueiri T, Braun D, Shukla S. Immunogenomic determinants of exceptional response to immune checkpoint inhibition in renal cell carcinoma. Nature Cancer 2025, 6: 372-384. PMID: 39789182, PMCID: PMC12121501, DOI: 10.1038/s43018-024-00896-w.Peer-Reviewed Original ResearchConceptsTertiary lymphoid structuresVascular endothelial growth factorRenal cell carcinomaCell carcinomaCytotoxic T-lymphocyte-associated protein 4 inhibitorsResponse to immune checkpoint inhibitionExceptional responseMetastatic clear cell renal cell carcinomaStandard-of-care immunotherapiesTertiary lymphoid structure formationCytotoxic T cell responsesClear cell renal cell carcinomaIO-based treatmentsTreatment-naive personsImmune checkpoint inhibitionImmune checkpoint inhibitorsCell renal cell carcinomaT cell responsesT-cell-directedEndothelial growth factorCell death proteinAntitumor immunityCheckpoint inhibitionCheckpoint inhibitorsNeoantigen loadBile acid synthesis impedes tumor-specific T cell responses during liver cancer
Varanasi S, Chen D, Liu Y, Johnson M, Miller C, Ganguly S, Lande K, LaPorta M, Hoffmann F, Mann T, Teneche M, Casillas E, Mangalhara K, Mathew V, Sun M, Jensen I, Farsakoglu Y, Chen T, Parisi B, Deota S, Havas A, Lee J, Chung H, Schietinger A, Panda S, Williams A, Farber D, Dhar D, Adams P, Feng G, Shadel G, Sundrud M, Kaech S. Bile acid synthesis impedes tumor-specific T cell responses during liver cancer. Science 2025, 387: 192-201. PMID: 39787217, DOI: 10.1126/science.adl4100.Peer-Reviewed Original ResearchMeSH KeywordsAcyltransferasesAnimalsBile Acids and SaltsCarcinoma, HepatocellularCD8-Positive T-LymphocytesCell Line, TumorEndoplasmic Reticulum StressHepatocytesHumansImmune Checkpoint InhibitorsImmunotherapyLithocholic AcidLiver NeoplasmsMiceOxidative StressProgrammed Cell Death 1 ReceptorTumor MicroenvironmentUrsodeoxycholic AcidConceptsTumor-specific T-cell responsesT cell responsesAnti-programmed cell death protein 1Ursodeoxycholic acidCell death protein 1CD8<sup>+</sup> T cellsBile acidsFeatures of human hepatocellular carcinomaImprove tumor immunotherapyInfluence antitumor immunityT cell functionReduced tumor growthBA synthesisLiver cancer modelCancer model systemsHuman hepatocellular carcinomaLandscape of cancerAntitumor immunityTumor immunotherapySecondary bile acidsOrgan-specific metabolitesEndoplasmic reticulum stressT cellsCancer modelsDietary intakeSorafenib Alters Interstitial Proton and Sodium Levels in the Tumor Microenvironment: A 1H/23Na Spectroscopic Imaging Study
Khan M, Walsh J, Kurdi S, Mishra S, Mihailović J, Coman D, Hyder F. Sorafenib Alters Interstitial Proton and Sodium Levels in the Tumor Microenvironment: A 1H/23Na Spectroscopic Imaging Study. NMR In Biomedicine 2025, 38: e5319. PMID: 39764672, DOI: 10.1002/nbm.5319.Peer-Reviewed Original ResearchConceptsU87 tumorsSorafenib-treated tumorsUpregulated aerobic glycolysisSodium-potassium pumpInterstitial spaceTumor microenvironmentIntracellular NaTumor growthSpectroscopic imaging studiesTumor invasionGlioblastoma modelSodium levelsTumorGlioblastoma therapyImaging studiesPlaceboSorafenibMetabolic changesImmune functionCancer hallmarksAerobic glycolysisProliferative stateMeasure treatment effectsIonic changesProliferation rateTrogocytosis-mediated immune evasion in the tumor microenvironment
Kim J, Park S, Kim J, Kim Y, Yoon H, Rayhan B, Jeong J, Bothwell A, Shin J. Trogocytosis-mediated immune evasion in the tumor microenvironment. Experimental & Molecular Medicine 2025, 57: 1-12. PMID: 39741180, PMCID: PMC11799389, DOI: 10.1038/s12276-024-01364-2.Peer-Reviewed Original ResearchConceptsCD4 T cellsT cellsMajor histocompatibility complexTumor microenvironmentImmune evasionMechanisms of immune evasionAnti-tumor immunityImmune regulatory moleculesAntigen-presenting cellsImmune-regulatory moleculesCTLA-4Cell-to-cell interactionsDonor cellsHistocompatibility complexTrogocytosisRecipient cellsTumorMembrane lossMembrane moleculesRegulatory moleculesMicroenvironmentSurface localizationPlasma membraneCellsTrogoptosisAdaptations of neutrophils in cancer
Ng M, Cerezo-Wallis D, Ng L, Hidalgo A. Adaptations of neutrophils in cancer. Immunity 2025, 58: 40-58. PMID: 39813993, DOI: 10.1016/j.immuni.2024.12.009.Peer-Reviewed Original Research
2024
Identification of HER2-positive breast cancer molecular subtypes with potential clinical implications in the ALTTO clinical trial
Rediti M, Venet D, Joaquin Garcia A, Maetens M, Vincent D, Majjaj S, El-Abed S, Di Cosimo S, Ueno T, Izquierdo M, Piccart M, Pusztai L, Loi S, Salgado R, Viale G, Rothé F, Sotiriou C. Identification of HER2-positive breast cancer molecular subtypes with potential clinical implications in the ALTTO clinical trial. Nature Communications 2024, 15: 10402. PMID: 39613746, PMCID: PMC11607438, DOI: 10.1038/s41467-024-54621-3.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic Agents, ImmunologicalBiomarkers, TumorBreast NeoplasmsClinical Trials, Phase III as TopicFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMiddle AgedNeoplasm Recurrence, LocalPrognosisRandomized Controlled Trials as TopicReceptor, ErbB-2TrastuzumabTumor MicroenvironmentConceptsHER2-positive breast cancerMolecular subtypesBreast cancerRate of pathological complete responseSensitive to HER2-targeted therapiesClinical trialsRisk of distant recurrenceBreast cancer molecular subtypesPathological complete responseHER2-targeted therapyCancer molecular subtypesPotential clinical implicationsNeoALTTO trialDistant recurrenceComplete responseAdjuvant trastuzumabPrognostic/predictive valueHeterogeneous biologySurvival outcomesI-SPY2Clinical outcomesMicroenvironment featuresGene expression profilesExternal cohortTumorTertiary Lymphoid Structures and Immunotherapy: Challenges and Opportunities
Ruddle N. Tertiary Lymphoid Structures and Immunotherapy: Challenges and Opportunities. Methods In Molecular Biology 2024, 2864: 299-312. PMID: 39527229, DOI: 10.1007/978-1-0716-4184-2_16.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsHumansImmune Checkpoint InhibitorsImmunotherapyNeoplasmsTertiary Lymphoid StructuresTumor MicroenvironmentConceptsImmune-related adverse eventsImmune checkpoint inhibitorsTertiary lymphoid structuresSecondary lymphoid organsTA-TLSSusceptibility to immune-related adverse eventsAssociated with favorable clinical outcomesPositive response to immunotherapyResponse to immunotherapyFavorable clinical outcomesCellular compositionVascular growth factorsAccumulation of lymphoid cellsCheckpoint inhibitorsLymphoid neogenesisLymphoid structuresProcess of lymphoid neogenesisClinical outcomesAdenovirus vectorLymphoid cellsTumor-associatedAdverse eventsTumor environmentOrgan rejectionChronic inflammationMouse Models Enable the Functional Investigation of Tertiary Lymphoid Structures in Cancer
Jeevanandam A, Yin Z, Connolly K, Joshi N. Mouse Models Enable the Functional Investigation of Tertiary Lymphoid Structures in Cancer. Methods In Molecular Biology 2024, 2864: 57-76. PMID: 39527217, DOI: 10.1007/978-1-0716-4184-2_4.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDisease Models, AnimalHumansLungMiceNeoplasmsTertiary Lymphoid StructuresTumor MicroenvironmentConceptsTertiary lymphoid structuresTertiary lymphoid structure formationSecondary lymphoid organsLymphoid structuresMurine modelFeatures of tertiary lymphoid structuresFunction of tertiary lymphoid structuresMouse modelPersistent inflammatory stimulationAssociated with positive clinical outcomesTissue-specific regulatory mechanismsPositive clinical outcomesPrognostic significanceClinical outcomesGut environmentNonlymphoid tissuesLymphoid aggregatesLymphoid organsMouse lungCancer patientsGenetic sequencesInflammatory stimulationRegulatory mechanismsTherapeutic modulationClinical effortsInterventional Oncology Meets Immuno-oncology: Combination Therapies for Hepatocellular Carcinoma.
Bitar R, Salem R, Finn R, Greten T, Goldberg S, Chapiro J. Interventional Oncology Meets Immuno-oncology: Combination Therapies for Hepatocellular Carcinoma. Radiology 2024, 313: e232875. PMID: 39560477, PMCID: PMC11605110, DOI: 10.1148/radiol.232875.Peer-Reviewed Original ResearchMeSH KeywordsCarcinoma, HepatocellularCombined Modality TherapyHumansImmunotherapyLiver NeoplasmsRadiology, InterventionalTumor MicroenvironmentConceptsManagement of hepatocellular carcinomaHepatocellular carcinomaLocoregional therapyClinical trialsImage-guided locoregional therapiesEnd pointsStages of hepatocellular carcinomaTumor microenvironment mechanismsCatheter-directed therapyCombination of immunotherapyProspective clinical trialImaging end pointsStandard of careAdjuvant settingNovel immunotherapiesCombination therapyTherapy resistanceInterventional radiologistsImmunotherapyDisease stageTherapyDisease evolutionNovel biomarkersCarcinomaMicroenvironment mechanismsNeoadjuvant vidutolimod and nivolumab in high-risk resectable melanoma: A prospective phase II trial
Davar D, Morrison R, Dzutsev A, Karunamurthy A, Chauvin J, Amatore F, Deutsch J, Das Neves R, Rodrigues R, McCulloch J, Wang H, Hartman D, Badger J, Fernandes M, Bai Y, Sun J, Cole A, Aggarwal P, Fang J, Deitrick C, Bao R, Duvvuri U, Sridharan S, Kim S, A Choudry H, Holtzman M, Pingpank J, O'Toole J, DeBlasio R, Jin Y, Ding Q, Gao W, Groetsch C, Pagliano O, Rose A, Urban C, Singh J, Divarkar P, Mauro D, Bobilev D, Wooldridge J, Krieg A, Fury M, Whiteaker J, Zhao L, Paulovich A, Najjar Y, Luke J, Kirkwood J, Taube J, Park H, Trinchieri G, Zarour H. Neoadjuvant vidutolimod and nivolumab in high-risk resectable melanoma: A prospective phase II trial. Cancer Cell 2024, 42: 1898-1918.e12. PMID: 39486411, PMCID: PMC11560503, DOI: 10.1016/j.ccell.2024.10.007.Peer-Reviewed Original ResearchConceptsPlasmacytoid dendritic cellsHigh-risk resected melanomaResected melanomaCD8<sup>+</sup> tumor-infiltrating lymphocytesAnti-PD-1 nivolumabAnti-tumor immune responseProspective phase II trialAnti-PD-1Associated with gene signaturesTumor-infiltrating lymphocytesPhase II trialResponse to therapySingle-arm studyAssociated with necrosisGut microbiotaClinical responseII trialPrimary endpointDendritic cellsTLR9 agonistsTumor microenvironmentT cellsMyeloid cellsPathological responseImmune activationThe neuroendocrine transition in prostate cancer is dynamic and dependent on ASCL1
Romero R, Chu T, González Robles T, Smith P, Xie Y, Kaur H, Yoder S, Zhao H, Mao C, Kang W, Pulina M, Lawrence K, Gopalan A, Zaidi S, Yoo K, Choi J, Fan N, Gerstner O, Karthaus W, DeStanchina E, Ruggles K, Westcott P, Chaligné R, Pe’er D, Sawyers C. The neuroendocrine transition in prostate cancer is dynamic and dependent on ASCL1. Nature Cancer 2024, 5: 1641-1659. PMID: 39394434, PMCID: PMC11584404, DOI: 10.1038/s43018-024-00838-6.Peer-Reviewed Original ResearchConceptsNeuroendocrine prostate cancerProstate cancerLineage plasticityAndrogen receptor signaling inhibitorsCancer progressionMouse prostate organoidsProstate cancer progressionRB1 deletionProstate organoidsMultiplex immunofluorescenceIn vivo platformTransient regressionDriver mutationsLuminal cellsSignaling inhibitorsAscl1Neuroendocrine transitionLineage transformationOrganoid culturesCancerTherapy outcomeProstateAdenocarcinomaTherapy timeIn vivo microenvironmentTranscriptional repression by HDAC3 mediates T cell exclusion from Kras mutant lung tumors
McGuire C, Meehan A, Couser E, Bull L, Minor A, Kuhlmann-Hogan A, Kaech S, Shaw R, Eichner L. Transcriptional repression by HDAC3 mediates T cell exclusion from Kras mutant lung tumors. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2317694121. PMID: 39388266, PMCID: PMC11494357, DOI: 10.1073/pnas.2317694121.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzamidesCell Line, TumorChemokine CXCL10Gene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHistone DeacetylasesHumansLung NeoplasmsMiceMutationProto-Oncogene Proteins p21(ras)PyridinesPyridonesPyrimidinonesT-LymphocytesTranscription, GeneticTumor MicroenvironmentConceptsT cell recruitmentLung tumorsHistone deacetylase 3Enhanced T cell recruitmentCombined treatmentLung tumors in vivoGenetically engineered mouse modelsT cell exclusionInhibition of histone deacetylase 3Tumor immune microenvironmentTumor growth controlKRAS mutant lung tumorsTumors in vivoLung cancer cellsImmune microenvironmentT cellsTissue-specific fashionMouse modelPathway inhibitorTumorPharmacological inhibitionCancer cellsFunction in vivoTranscriptional regulationTranscriptional repressionKeep It Moving: Physical Activity in the Prevention of Obesity-Driven Pancreatic Cancer.
Sogunro A, Muzumdar M. Keep It Moving: Physical Activity in the Prevention of Obesity-Driven Pancreatic Cancer. Cancer Research 2024, 84: 2935-2937. PMID: 39279380, DOI: 10.1158/0008-5472.can-24-1474.Peer-Reviewed Original ResearchConceptsPancreatic ductal adenocarcinomaTumor microenvironmentAntitumor effectPancreatic cancerObese micePhysical activityAdvanced tumor growthSystemic cytokine productionMyeloid cell infiltrationPancreatic ductal adenocarcinoma developmentEffect of obesityHigh-fat diet-induced obesityDiet-induced obesitySyngeneic allograftsAdvanced tumorsProtumorigenic effectsLean miceWhite adipose tissueCell infiltrationDuctal adenocarcinomaObesity-associatedTumor growthCytokine productionImpact of physical activityInflammatory cytokinesMutational Features and Tumor Microenvironment Alterations in High-Grade Appendiceal Cancers Treated With Iterative Hyperthermic Intraperitoneal Chemotherapy
Su D, Dhiman A, Bansal V, Zha Y, Shergill A, Polite B, Alpert L, Turaga K, Eng O. Mutational Features and Tumor Microenvironment Alterations in High-Grade Appendiceal Cancers Treated With Iterative Hyperthermic Intraperitoneal Chemotherapy. JCO Precision Oncology 2024, 8: e2400149. PMID: 39259912, PMCID: PMC11432692, DOI: 10.1200/po.24.00149.Peer-Reviewed Original ResearchConceptsHigh-grade appendiceal adenocarcinomaHyperthermic intraperitoneal chemotherapyProgression-free survivalImmunogenomic profilingAppendiceal cancerIntraperitoneal chemotherapyPeritoneal metastasisHigh-grade appendiceal cancerCD8<sup>+</sup> T cellsCytotoxic T cell populationsMutational signaturesAssociated with poor survivalElevated PD-L1Median overall survivalPD-L1 coexpressionPeritoneal tumour depositsT cell populationsTumor microenvironment alterationsNovel treatment approachesWhole-exome sequencingHIPEC treatmentAppendiceal adenocarcinomaOncological outcomesPD-L1Overall survivalImmune microenvironmental heterogeneity according to tumor DNA methylation phenotypes in microsatellite instability-high colorectal cancers
Kim J, Hong J, Lee J, Jung M, Choi E, Cho N, Kang G, Kim S. Immune microenvironmental heterogeneity according to tumor DNA methylation phenotypes in microsatellite instability-high colorectal cancers. Cancer Immunology, Immunotherapy 2024, 73: 215. PMID: 39235590, PMCID: PMC11377388, DOI: 10.1007/s00262-024-03805-3.Peer-Reviewed Original ResearchConceptsProgrammed death-ligand 1Tumor-infiltrating lymphocytesMicrosatellite instability-high colorectal cancerCombined positive scoreTumor proportion scoreTumor mutational burdenCD8+ tumor-infiltrating lymphocytesMicrosatellite instability-highTumor-infiltrating immune cellsCpG island methylator phenotypeColorectal cancerCIMP-high tumorsDensity of CD8+ tumor-infiltrating lymphocytesProgrammed death-ligand 1 tumor proportion scoreCIMP-highConsensus molecular subtype 1Cytolytic activity scoreWhole-slide immunohistochemistryDeath-ligand 1Tumor immune microenvironmentMethylator phenotypeMicrosatellite instability-high tumorsTumor DNA methylationDNA methylation phenotypeCpG island methylator phenotype status
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