2025
An antibody–toxin conjugate targeting CD47 linked to the bacterial toxin listeriolysin O for cancer immunotherapy
Schrank B, Wang Y, Wu A, Tran N, Lee D, Edwards J, Huntoon K, Dong S, Ha J, Ma Y, Grippin A, Jeong S, Antony A, Chang M, Kang M, Gallup T, Koong A, Li J, Yun K, Kim B, Jiang W. An antibody–toxin conjugate targeting CD47 linked to the bacterial toxin listeriolysin O for cancer immunotherapy. Nature Cancer 2025, 6: 511-527. PMID: 40000910, DOI: 10.1038/s43018-025-00919-0.Peer-Reviewed Original ResearchConceptsAntibody-toxin conjugatesTumor cellsImmune recognition of tumor cellsEnhanced antigen cross-presentationRecognition of tumor cellsCancer cell phagocytosisTumor-derived antigensToxin listeriolysin OTumor-derived peptidesImproved animal survivalPromote immune recognitionCytosolic immune sensorsIntracellular bacterium Listeria monocytogenesTreatment in vivoTreating multiple cancersPhagocytosis checkpointsCheckpoint blockadeCancer immunotherapySignal CD47Listeriolysin OMetastatic breastMelanoma tumorsTherapeutic strategiesAnimal survivalCell phagocytosisInvestigation of ferroptosis and mTOR signaling in chromophobe renal cell carcinoma (ChRCC).
Madsen K, Labaki C, Saad E, Alchoueiry M, Bi K, Hobeika C, Bakouny Z, Priolo C, Khabibullin D, Schindler N, Camp S, Saliby R, Heng D, Van Allen E, Shukla S, Henske E, Choueiri T, Braun D. Investigation of ferroptosis and mTOR signaling in chromophobe renal cell carcinoma (ChRCC). Journal Of Clinical Oncology 2025, 43: 583-583. DOI: 10.1200/jco.2025.43.5_suppl.583.Peer-Reviewed Original ResearchInternational Metastatic RCC Database ConsortiumMetastatic clear cell RCCProgression-free survivalOverall survivalClear cell RCCCell of originMTOR inhibitorsTumor cellsChRCC tumorsEpithelial cellsScRNA-seq analysisCell RCCMetastatic ChRCCResponse to immune checkpoint inhibitorsDistal tubulesMechanisms of therapeutic responseChromophobe renal cell carcinomaTreated with mTOR inhibitorsResponse to mTOR inhibitorsImmune checkpoint inhibitorsScRNA-seqA intercalated cellsB intercalated cellsImproved overall survivalEvaluate survival outcomesComprehensive Molecular Profiling of Metastatic Pancreatic Adenocarcinomas
Antony V, Sun T, Dolezal D, Cai G. Comprehensive Molecular Profiling of Metastatic Pancreatic Adenocarcinomas. Cancers 2025, 17: 335. PMID: 39941707, PMCID: PMC11815932, DOI: 10.3390/cancers17030335.Peer-Reviewed Original ResearchMetastatic pancreatic ductal adenocarcinomaPancreatic ductal adenocarcinomaPrimary pancreatic ductal adenocarcinomaMolecular profilingGene mutationsGene copy number alterationsAdvanced-stage pancreatic cancerInsufficient tumor cellsOncomine Comprehensive AssayRate of TP53Copy number alterationsMetastatic diseasePDAC casesPIK3CA mutationsPancreatic cancerPoor prognosisTreatment optionsDuctal adenocarcinomaTumor cellsTumor progressionMolecular alterationsStudy cohortMolecular testingComprehensive assayTherapeutic target
2024
High p16INK4A expression in glioblastoma is associated with senescence phenotype and better prognosis
Park S, Roh T, Tanaka Y, Kim Y, Park S, Kim T, Eom S, Park T, Park I, Kim S, Kim J. High p16INK4A expression in glioblastoma is associated with senescence phenotype and better prognosis. Neoplasia 2024, 60: 101116. PMID: 39724755, PMCID: PMC11729681, DOI: 10.1016/j.neo.2024.101116.Peer-Reviewed Original ResearchConceptsP16<sup>INK4a</sup> expressionImmune cell infiltrationTumor cellsCell infiltrationImmunologically active tumor microenvironmentInfiltration of T cellsActive tumor microenvironmentTERT promoter mutationsExtended overall survivalIsocitrate dehydrogenase (IDH)-wildtypeSecretion of chemokinesSenescent phenotypeMalignant brain tumorsIn vitro studiesEGFR amplificationOverall survivalTumor microenvironmentCDKN2A/2B deletionT cellsPrognostic markerImprove prognosisP16INK4a expressionPromoter mutationsTumorBrain tumorsAfamin Ameliorates Testosterone Propionate (TP)-Induced Oxidative Stress and Mitochondrial Damage in Human Ovarian Granulosa Tumor Cells (KGN) by Upregulating the Expression of SIRT1
Ma Y, Li Z, Wang Z, Yang A. Afamin Ameliorates Testosterone Propionate (TP)-Induced Oxidative Stress and Mitochondrial Damage in Human Ovarian Granulosa Tumor Cells (KGN) by Upregulating the Expression of SIRT1. Molecular Biology 2024, 58: 1250-1267. DOI: 10.1134/s0026893324060074.Peer-Reviewed Original ResearchPCOS micePolycystic ovary syndromeGranulosa tumor cellsLuteinizing hormoneTumor cellsKGN cellsTestosterone propionateDevelopment of metabolic syndromeOxidative stressWomen of reproductive ageLevels of afaminExpression of SIRT1Reactive oxygen speciesLH/follicle-stimulating hormonePolycystic ovary syndrome patientsEndocrine disorder affecting women of reproductive ageMitochondrial damageLevels of 8-hydroxydeoxyguanosineEndocrine disorder affecting womenTreatment of polycystic ovary syndromeMetabolic syndromeReproductive ageCystic folliclesEstrous cycleTP-induced oxidative stressTargeting T-Cell Costimulation to the Surface of Tumor Cells.
Eguren-Santamaría I, Sanmamed M, Molero-Glez P, Perez-Gracia J, Melero I. Targeting T-Cell Costimulation to the Surface of Tumor Cells. Clinical Cancer Research 2024, 31: 231-233. PMID: 39531541, DOI: 10.1158/1078-0432.ccr-24-3003.Peer-Reviewed Original ResearchT lymphocytesTumor cellsTargeting T-cell costimulationSurface of tumor cellsT cell costimulationProportion of patientsT cell activationAntitumor responseT cellsSolid tumorsSurface antigensActivator receptorSignal 2CostimulationTumorTarget specificityCellsCD137HER2Novel evidencePatientsAntigenReceptorsCNSC-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 developmentGene Copy Number Alterations Identify Subsets of Mycosis Fungoides/Sézary Syndrome Patients with Worse Survival Outcomes
Kiwan A, Kewan T, Xu M, Siddon A, Girardi M, Sethi T, Foss F. Gene Copy Number Alterations Identify Subsets of Mycosis Fungoides/Sézary Syndrome Patients with Worse Survival Outcomes. Blood 2024, 144: 4440-4440. DOI: 10.1182/blood-2024-205144.Peer-Reviewed Original ResearchGene copy number alterationsAssociated with poor OSAbsolute lymphocyte countFluorescence in situ hybridization panelAssociated with worse OSCirculating tumor cellsFluorescence in situ hybridizationOverall survivalCopy number alterationsT cell receptorPoor OSSurvival outcomesTumor cellsMedian OSCox proportional hazardsBlood involvementATM deletionArid1a deletionT cellsElevated absolute lymphocyte countMedian absolute lymphocyte countAssociated with better OSMedian age of patientsMultivariate CPH modelZEB1 deletionSpatial Multiomics Profiling of Angioimmunoblastic T-Cell Lymphoma
Enninful A, Foss F, Fan R, Xu M. Spatial Multiomics Profiling of Angioimmunoblastic T-Cell Lymphoma. Blood 2024, 144: 1585-1585. DOI: 10.1182/blood-2024-211129.Peer-Reviewed Original ResearchAngioimmunoblastic T-cell lymphomaT follicular helper cellsT-cell lymphomaFollicular dendritic cellsHigh endothelial venulesT cellsTumor cellsTumor microenvironmentB cellsImmune surveillanceMultiplex immunofluorescenceCD21+ follicular dendritic cellsTumor evasion of immune surveillanceNon-neoplastic T cellsEvasion of immune surveillanceEBV-positive B cellsGene activity scoreTissue blocksActivity of tumor cellsReactive B cellsExpression of LMP1Positive B cellsComplex tumor microenvironmentT cell zonesLymph node samplingG9a/DNMT1 co-targeting inhibits non-small cell lung cancer growth and reprograms tumor cells to respond to cancer-drugs through SCARA5 and AOX1
Exposito F, Redrado M, Serrano D, Calabuig-Fariñas S, Bao-Caamano A, Gallach S, Jantus-Lewintre E, Diaz-Lagares A, Rodriguez-Casanova A, Sandoval J, San Jose-Eneriz E, Garcia J, Redin E, Senent Y, Leon S, Pio R, Lopez R, Oyarzabal J, Pineda-Lucena A, Agirre X, Montuenga L, Prosper F, Calvo A. G9a/DNMT1 co-targeting inhibits non-small cell lung cancer growth and reprograms tumor cells to respond to cancer-drugs through SCARA5 and AOX1. Cell Death & Disease 2024, 15: 787. PMID: 39488528, PMCID: PMC11531574, DOI: 10.1038/s41419-024-07156-w.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerNon-small cell lung cancer patientsCM-272Treatment of non-small cell lung cancerReprogram tumor cellsAssociated with poor prognosisResponse to chemotherapyCell lung cancerCancer drugsMonitor tumor progressionOverexpression of G9aNSCLC cell linesLung cancer growthCancer drug sensitivityNon-small cell lung cancer growthNon-invasive biomarkersTumor volumeAntitumor efficacyTargeted therapyPoor prognosisCancer modelsTumor cellsInduce cell deathTumor progressionLung cancerSpiculated Masses
Harigopal M, Andrejeva L, Lanjewar S, Podany P. Spiculated Masses. 2024, 127-158. DOI: 10.1007/978-3-031-65711-5_5.Peer-Reviewed Original ResearchInvasive ductal carcinomaInvasive lobular carcinomaDuctal carcinoma in situLobular carcinomaDuctal carcinomaSpiculated massesTumor cellsBenign entitySclerosing adenosisCorrelation of imaging findingsDesmoplastic stromal responseDiscohesive tumor cellsCore needle biopsyPseudoangiomatous stromal hyperplasiaCarcinoma in situInvasive mammary carcinomaFalse-negative mammogramsGranular cell tumorInvasive tumor cellsDiabetic mastopathyMucinous carcinomaStromal hyperplasiaInvasive cancerPleomorphic calcificationsDesmoplastic stromaTumor-Specific Antigen Delivery for T-cell Therapy via a pH-Sensitive Peptide Conjugate.
Yurkevicz A, Liu Y, Katz S, Glazer P. Tumor-Specific Antigen Delivery for T-cell Therapy via a pH-Sensitive Peptide Conjugate. Molecular Cancer Therapeutics 2024, 24: 105-117. PMID: 39382073, PMCID: PMC11695185, DOI: 10.1158/1535-7163.mct-23-0809.Peer-Reviewed Original ResearchMajor histocompatibility complexT cellsTumor cellsTreatment of tumor-bearing miceMajor histocompatibility complex class I pathwaySuppression of tumor growthTumor cells in vivoT-cell therapySyngeneic tumor modelsTumor-specific antigensTumor-bearing miceMelanoma tumor cellsT cell activationHealthy tissueTarget tumor cellsIn vivoIn vitroMicroenvironment of tumorsUnique delivery platformsClass I pathwayCell-based therapiesTargeted cancer therapyCells in vivoAntigen processing pathwayAcidic microenvironment of tumorsClinicopathologic features and prognosis of steatohepatitic hepatocellular carcinoma based on varying cutoffs of tumoral steatohepatitic changes
Zhang T, Niu N, Taddei T, Jain D, Zhang X. Clinicopathologic features and prognosis of steatohepatitic hepatocellular carcinoma based on varying cutoffs of tumoral steatohepatitic changes. American Journal Of Clinical Pathology 2024, 163: 411-418. PMID: 39418121, DOI: 10.1093/ajcp/aqae136.Peer-Reviewed Original ResearchSH-HCCSteatohepatitic hepatocellular carcinomaHepatocellular carcinomaLiver diseaseHepatitis C virus infectionC virus infectionStage of fibrosisPresence of steatohepatitisOverall survivalHistological subtypesPrognostic factorsHCC subtypesBackground liverHCC casesClinicopathological featuresConventional HCCHistopathological patternsHyaline globulesTumor cellsMallory-Denk bodiesGlycogenated nucleiSteatotic liver diseaseHCCSurvival analysisSteatohepatitisDeciphering craniopharyngioma subtypes: Single-cell analysis of tumor microenvironment and immune networks
Matsuda T, Kono T, Taki Y, Sakuma I, Fujimoto M, Hashimoto N, Kawakami E, Fukuhara N, Nishioka H, Inoshita N, Yamada S, Nakamura Y, Horiguchi K, Miki T, Higuchi Y, Tanaka T. Deciphering craniopharyngioma subtypes: Single-cell analysis of tumor microenvironment and immune networks. IScience 2024, 27: 111068. PMID: 39483146, PMCID: PMC11525618, DOI: 10.1016/j.isci.2024.111068.Peer-Reviewed Original ResearchTumor microenvironmentAnalysis of tumor microenvironmentImmune responseOccurrence of diabetes insipidusExpression of pro-inflammatory markersCell-cell interactionsPro-inflammatory markersComprehensive cell atlasM2 macrophage ratioSquamous papillaryDiabetes insipidusTumor cellsSingle cell RNA sequencingMacrophage ratioM1 macrophagesM2 macrophagesPituitary structureCell RNA sequencingCellular compositionSingle-cell clusteringCell typesDiverse cell typesTumorGene expression patternsMolecular characteristicsFeeding the wrath with myelin
Ghosh S, Rothlin C. Feeding the wrath with myelin. Trends In Immunology 2024, 45: 729-731. PMID: 39341708, PMCID: PMC11471388, DOI: 10.1016/j.it.2024.09.004.Peer-Reviewed Original ResearchCarbohydrate-Lectin Interactions Reprogram Dendritic Cells to Promote Type 1 Anti-Tumor Immunity
Lensch V, Gabba A, Hincapie R, Bhagchandani S, Basak A, Alam M, Noble J, Irvine D, Shalek A, Johnson J, Finn M, Kiessling L. Carbohydrate-Lectin Interactions Reprogram Dendritic Cells to Promote Type 1 Anti-Tumor Immunity. ACS Nano 2024, 18: 26770-26783. PMID: 39283240, PMCID: PMC11646345, DOI: 10.1021/acsnano.4c07360.Peer-Reviewed Original ResearchCellular immunityDendritic cellsToll-like receptorsVirus-like particlesCD8<sup>+</sup> T cellsTumor-specific cellular immunityVaccine developmentCancer vaccine developmentInfiltrate solid tumorsMurine melanoma modelT cell functionInhibited tumor growthActivate TLR signalingTumor controlCancer immunotherapyCD4<sup>+</sup>Melanoma modelTLR7 agonistDC activationT cellsSolid tumorsTumor cellsTumor growthHumoral immunityVLP platformImmune landscape of oncohistone-mutant gliomas reveals diverse myeloid populations and tumor-promoting function
Andrade A, Annett A, Karimi E, Topouza D, Rezanejad M, Liu Y, McNicholas M, Gonzalez Santiago E, Llivichuzhca-Loja D, Gehlhaar A, Jessa S, De Cola A, Chandarana B, Russo C, Faury D, Danieau G, Puligandla E, Wei Y, Zeinieh M, Wu Q, Hebert S, Juretic N, Nakada E, Krug B, Larouche V, Weil A, Dudley R, Karamchandani J, Agnihotri S, Quail D, Ellezam B, Konnikova L, Walsh L, Pathania M, Kleinman C, Jabado N. Immune landscape of oncohistone-mutant gliomas reveals diverse myeloid populations and tumor-promoting function. Nature Communications 2024, 15: 7769. PMID: 39237515, PMCID: PMC11377583, DOI: 10.1038/s41467-024-52096-w.Peer-Reviewed Original ResearchConceptsMyeloid populationsTumor microenvironmentExpression of immune checkpoint markersImmune checkpoint pathwaysImmune checkpoint markersSyngeneic mouse modelTumor-promoting functionsCheckpoint markersMyeloid infiltrationImmune landscapeImmune infiltrationImmune lineagesMyeloid cellsLymphoid cellsTumor cellsMouse modelTumor formationBenefit of patientsTherapeutic benefitBrain tumorsGliomaTumorDysregulated epigenomeDual inhibitionInfiltrationNovel immunotherapeutics against LGR5 to target multiple cancer types
Chen H, Mueller N, Stott K, Kapeni C, Rivers E, Sauer C, Beke F, Walsh S, Ashman N, O’Brien L, Rafati Fard A, Ghodsinia A, Li C, Joud F, Giger O, Zlobec I, Olan I, Aitken S, Hoare M, Mair R, Serrao E, Brenton J, Garcia-Gimenez A, Richardson S, Huntly B, Spring D, Skjoedt M, Skjødt K, de la Roche M, de la Roche M. Novel immunotherapeutics against LGR5 to target multiple cancer types. EMBO Molecular Medicine 2024, 16: 2233-2261. PMID: 39169164, PMCID: PMC11393416, DOI: 10.1038/s44321-024-00121-2.Peer-Reviewed Original ResearchConceptsHepatocellular carcinomaColorectal cancerTarget multiple cancer typesBispecific T-cell engagerCell killing in vitroChimeric antigen receptorT-cell engagersCancer cells in vitroPre-B-ALLAnti-tumor efficacyCancer cell killing in vitroKilling in vitroCells in vitroAntibody-drug conjugatesMultiple cancer typesLgr5 overexpressionTumor burdenAntigen receptorMurine modelNovel immunotherapeuticsCancer modelsTumor cellsEffective modalityEffective tumorLgr5Regulated induced proximity targeting chimeras—RIPTACs—A heterobifunctional small molecule strategy for cancer selective therapies
Raina K, Forbes C, Stronk R, Rappi J, Eastman K, Zaware N, Yu X, Li H, Bhardwaj A, Gerritz S, Forgione M, Hundt A, King M, Posner Z, Correia A, McGovern A, Puleo D, Chenard R, Mousseau J, Vergara J, Garvin E, Macaluso J, Martin M, Bassoli K, Jones K, Garcia M, Howard K, Yaggi M, Smith L, Chen J, Mayfield A, De Leon C, Hines J, Kayser-Bricker K, Crews C. Regulated induced proximity targeting chimeras—RIPTACs—A heterobifunctional small molecule strategy for cancer selective therapies. Cell Chemical Biology 2024, 31: 1490-1502.e42. PMID: 39116881, PMCID: PMC11371387, DOI: 10.1016/j.chembiol.2024.07.005.Peer-Reviewed Original ResearchProtein-protein interactionsTarget proteinsTernary complexChemical biology studiesExpressed intracellular proteinStable ternary complexAnti-proliferative responseEssential proteinsProtein proximityEffector ligandsIntracellular proteinsCDK inhibitorsTarget-expressing cellsHeterobifunctional small moleculesSmall moleculesCell survivalTumor cellsTherapeutic modalitiesProteinSelective therapySmall molecule strategiesLigandBiological studiesBSLM-10 MOLECULAR AND HISTOLOGICAL CHARACTERIZATION OF NSCLC PROGRESSION TO LEPTOMENINGEAL METASTASIS WITH COMORBID INTRAPARENCHYMAL DISEASE
Kandigian S, Chande S, Dolezal D, Tang T, Wang D, Arnal-Estapé A, Cheok S, McGuone D, Liu Y, Goldberg S, Blondin N, Chiang V, Nguyen D. BSLM-10 MOLECULAR AND HISTOLOGICAL CHARACTERIZATION OF NSCLC PROGRESSION TO LEPTOMENINGEAL METASTASIS WITH COMORBID INTRAPARENCHYMAL DISEASE. Neuro-Oncology Advances 2024, 6: i7-i7. PMCID: PMC11296776, DOI: 10.1093/noajnl/vdae090.020.Peer-Reviewed Original ResearchNon-small cell lung cancerLeptomeningeal diseaseCentral nervous systemLeptomeningeal metastasesParenchymal metastasesCerebrospinal fluidTumor cellsTyrosine kinase inhibitor treatmentCell lung cancerKinase inhibitor treatmentCerebrospinal fluid of patientsCell linesCerebral lateral ventriclesIntra-arterial injectionTGF-b signalingIn vivo passageIntraparenchymal diseaseMechanisms of progressionTumor microenvironmentMultiplex immunofluorescenceAggressive treatmentLeptomeningeal infiltrationPerivascular invasionIntraparenchymal metastasesMurine model
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