2025
Sex-specific effects of exogenous asparagine on colorectal tumor growth, 17β-estradiol levels, and aromatase
Aladelokun O, Benitez K, Wang Y, Jain A, Berardi D, Maroun G, Shen X, Roper J, Gibson J, Sumigray K, Khan S, Johnson C. Sex-specific effects of exogenous asparagine on colorectal tumor growth, 17β-estradiol levels, and aromatase. Pharmacological Research 2025, 107736. PMID: 40228761, DOI: 10.1016/j.phrs.2025.107736.Peer-Reviewed Original ResearchTumor-specific survivalColorectal cancerTumor growthR2G2 miceIncreased serum estradiol levelsSerum estradiol levelsSub-populations of macrophagesAssociated with cancer prognosisSuppressed tumor growthColorectal tumor growthExogenous asparagineColorectal cancer developmentColorectal cancer cellsNegative feed-back effectEstradiol levelsGlutamate levelsSex-related differencesSex-specific effectsMale miceCancer prognosisAsparagine supplementationCancer progressionMiceDecreased numberTumorThe development of an artificial intelligence auto-segmentation tool for 3D volumetric analysis of vestibular schwannomas
Jester N, Singh M, Lorr S, Tommasini S, Wiznia D, Buono F. The development of an artificial intelligence auto-segmentation tool for 3D volumetric analysis of vestibular schwannomas. Scientific Reports 2025, 15: 5918. PMID: 39966622, PMCID: PMC11836447, DOI: 10.1038/s41598-025-88589-x.Peer-Reviewed Original ResearchConceptsGround-truth datasetDice scoreVestibular schwannomaImage processing accuracyVolumetric analysisML-based algorithmsMeasuring tumor sizeMean dice scoreAuto-segmentation toolAccurate AIAI modelsTumor sizeTumor modelVS tumorsTumor growthTesting stageAI-LTumorImage processing softwareClinical practicePatient recruitmentProcessing softwareSchwannomaDatasetManual segmentationGPR55 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 ResearchConceptsEpithelial-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 mechanismsSorafenib 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 rate
2024
Impact of radiation therapy dose, fractionation, and immunotherapeutic partner in a mouse model of hormone receptor–positive mammary carcinogenesis
Buqué A, Bloy N, Petroni G, Jiménez-Cortegana C, Sato A, Iribarren C, Yamazaki T, Galassi C, Hensler M, Bhinder B, Guarracino A, Rippon B, Beltran-Visiedo M, Soler-Agesta R, Pannellini T, Fucikova J, Demaria S, Zhou X, Elemento O, Formenti S, Galluzzi L. Impact of radiation therapy dose, fractionation, and immunotherapeutic partner in a mouse model of hormone receptor–positive mammary carcinogenesis. Journal Of The National Cancer Institute 2024, djae329. PMID: 39661487, DOI: 10.1093/jnci/djae329.Peer-Reviewed Original ResearchImmune checkpoint inhibitorsRadiation therapyFocal RTOverall survivalMammary carcinogenesisPD-1Impact of radiotherapy doseMouse modelPD-1 blockerRT plus immunotherapyPrimary tumor growthPrimary disease controlIncrease local controlCheckpoint inhibitorsRadiotherapy doseHypofractionated RTOS benefitTumor burdenPrimary tumorBreast cancerTumor growthNeoplastic lesionsLocal controlICI sensitivityEffective immunityHuman HDAC6 senses valine abundancy to regulate DNA damage
Jin J, Meng T, Yu Y, Wu S, Jiao C, Song S, Li Y, Zhang Y, Zhao Y, Li X, Wang Z, Liu Y, Huang R, Qin J, Chen Y, Cao H, Tan X, Ge X, Jiang C, Xue J, Yuan J, Wu D, Wu W, Jiang C, Wang P. Human HDAC6 senses valine abundancy to regulate DNA damage. Nature 2024, 637: 215-223. PMID: 39567688, DOI: 10.1038/s41586-024-08248-5.Peer-Reviewed Original ResearchConceptsHuman histone deacetylase 6Active DNA demethylationDNA demethylationValine deprivationDNA damageTen-eleven translocationRegulating DNA damageHistone deacetylase 6Repeat domainTherapeutic efficacy of PARP inhibitorsBind valineEfficacy of PARP inhibitorsCellular functionsPatient-derived xenograft modelsCytoplasmic shuttlingInduce DNA damageBranched amino acidsProtein synthesisAmino acidsIntracellular levelsPARP inhibitorsDNALevels of valineTumor growthTherapeutic efficacyScavenger Receptor CD36 in Tumor-Associated Macrophages Promotes Cancer Progression by Dampening Type-I IFN Signaling.
Xu Z, Kuhlmann-Hogan A, Xu S, Tseng H, Chen D, Tan S, Sun M, Tripple V, Bosenberg M, Miller-Jensen K, Kaech S. Scavenger Receptor CD36 in Tumor-Associated Macrophages Promotes Cancer Progression by Dampening Type-I IFN Signaling. Cancer Research 2024, 85: 462-476. PMID: 39546763, PMCID: PMC11788022, DOI: 10.1158/0008-5472.can-23-4027.Peer-Reviewed Original ResearchTumor-associated macrophagesIFN-ITumor microenvironmentTumor growthHeterogeneous population of myeloid cellsPharmacological inhibition of CD36Population of myeloid cellsTumor cell quiescenceAnti-tumor immunityDelayed tumor growthTumor inflammatory microenvironmentElevated type I interferonReduced tumor growthMyeloid-specific deletionDeletion of CD36Type I interferon signalingInhibition of CD36Promote cancer progressionI interferon signalingIFN-I responseIFN-I signalingType I interferonScavenger receptor CD36TAM functionNatural suppressorCorrection: Methylglyoxal, a glycolysis side-product, induces Hsp90 glycation and YAP-mediated tumor growth and metastasis
Nokin M, Durieux F, Peixoto P, Chiavarina B, Peulen O, Blomme A, Turtoi A, Costanza B, Smargiasso N, Baiwir D, Scheijen J, Schalkwijk C, Leenders J, De Tullio P, Bianchi E, Thiry M, Uchida K, Spiegel D, Cochrane J, Hutton C, De Pauw E, Delvenne P, Belpomme D, Castronovo V, Bellahcène A. Correction: Methylglyoxal, a glycolysis side-product, induces Hsp90 glycation and YAP-mediated tumor growth and metastasis. ELife 2024, 13: e103327. PMID: 39312391, PMCID: PMC11419668, DOI: 10.7554/elife.103327.Peer-Reviewed Original ResearchTumor growthKeep 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 cytokinesCarbohydrate-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 platformSRBD1 Regulates the Cell Cycle, Apoptosis, and M2 Macrophage Polarization via the RPL11‐MDM2‐p53 Pathway in Glioma
Chen H, Gao S, Wang P, Xie M, Zhang H, Fan Y, Nie E, Lan Q. SRBD1 Regulates the Cell Cycle, Apoptosis, and M2 Macrophage Polarization via the RPL11‐MDM2‐p53 Pathway in Glioma. Environmental Toxicology 2024, 40: 66-78. PMID: 39258423, DOI: 10.1002/tox.24396.Peer-Reviewed Original ResearchRNA-binding proteinsP53 signalingInhibits Mdm2-mediated p53 ubiquitinationMDM2-mediated p53 ubiquitinationRPL11-MDM2-p53 pathwayElevated p53 levelsRibosomal protein expressionBinding to MDM2Tumor-associated macrophagesP53 signaling pathwayInactivation of p53P53 ubiquitinationRibosomal proteinsRNA translationM2 macrophage polarizationP53 levelsTumor growthRPL11Mouse xenograft modelEctopic expressionGlioma tumor growthCell cycleBinding proteinTarget genesSignaling pathwayA Minimalist Pathogen‐Like Sugar Nanovaccine for Enhanced Cancer Immunotherapy
Miao Y, Niu L, Lv X, Zhang Q, Xiao Z, Ji Z, Chen L, Liu Y, Liu N, Zhu J, Yang Y, Chen Q. A Minimalist Pathogen‐Like Sugar Nanovaccine for Enhanced Cancer Immunotherapy. Advanced Materials 2024, 36: e2410715. PMID: 39210649, DOI: 10.1002/adma.202410715.Peer-Reviewed Original ResearchCancer immunotherapyMaturation of antigen-presenting cellsVaccine carriersImmune checkpoint blockade therapyAntigen-specific immune responsesInhibition of tumor growthCheckpoint blockade therapyEnhanced cancer immunotherapyAntigen-presenting cellsVaccine delivery technologiesB16-OVABlockade therapyImmune activationTumor modelTumor growthAntigen loadNanovaccineImmune responseMeticulous screeningAntigenic peptidesImmunostimulatory characteristicsChain ratioDelivery technologiesImmunotherapyIn vivoOvercoming melanin interference in melanocyte photodynamic therapy with a pyrene-derived two-photon photosensitizer
Juvekar V, Cao Y, Koh C, Lee D, Kwak S, Kim S, Park T, Park S, Liu Z, Kim H. Overcoming melanin interference in melanocyte photodynamic therapy with a pyrene-derived two-photon photosensitizer. Chemical Engineering Journal 2024, 493: 152796. DOI: 10.1016/j.cej.2024.152796.Peer-Reviewed Original ResearchPhotodynamic therapyPhotodynamic therapy efficacyPlasma membrane of melanoma cellsMelanoma cellsInhibition of tumor growthReactive oxygen speciesConventional photodynamic therapyTails of miceTreatment of skin diseasesTumor modelTreat melanomaTumor growthMelanin contentMulticellular tumor spheroidsSkin cancerMelanomaVisible light irradiationPDT efficacySkin diseasesMelanin interferenceVisible light excitationBroad absorption spectraChlorin e6ROS generation efficiencyTP-PDTGrowth characteristics of HCT116 xenografts lacking asparagine synthetase vary according to sex
Aladelokun O, Lu L, Zheng J, Yan H, Jain A, Gibson J, Khan S, Johnson C. Growth characteristics of HCT116 xenografts lacking asparagine synthetase vary according to sex. Human Genomics 2024, 18: 67. PMID: 38886847, PMCID: PMC11184737, DOI: 10.1186/s40246-024-00635-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAspartate-Ammonia LigaseCarbon-Nitrogen Ligases with Glutamine as Amide-N-DonorCell ProliferationColorectal NeoplasmsFemaleGene Expression Regulation, NeoplasticHCT116 CellsHeterograftsHumansMaleMiceReceptors, EstrogenReceptors, G-Protein-CoupledSex FactorsXenograft Model Antitumor AssaysConceptsFemale tumor-bearing miceFemale CRC patientsTumor-bearing miceCRC patientsTumor growthInferior survivalAssociated with inferior survivalMetabolic reprogrammingG protein-coupled estrogen receptorTriggering metabolic reprogrammingSustained tumor growthSuppressed tumor growthExpression of asparagine synthetaseCancer cell linesBackgroundSex-related differencesSurvival improvementImpact of sexFemale miceEstrogen receptorCancer growthTranslational relevanceRewiring of metabolic pathwaysCancer burdenMetabolic pathwaysAsparagine synthetaseAutocatalytic, Brain Tumor‐Targeting Delivery of Bardoxolone Methyl Self‐Assembled Nanoparticles for Glioblastoma Treatment
Ye Z, Sheu W, Qu H, Peng B, Liu J, Zhang L, Yuan F, Wei Y, Zhou J, Chen Q, Xiao X, Zhang S. Autocatalytic, Brain Tumor‐Targeting Delivery of Bardoxolone Methyl Self‐Assembled Nanoparticles for Glioblastoma Treatment. Small Science 2024, 4 DOI: 10.1002/smsc.202400081.Peer-Reviewed Original ResearchBlood-brain barrierBardoxolone methylGlioblastoma multiformeBrain tumorsSurvival of miceSelf-assembled nanoparticlesInhibited GBM tumor growthEnhance drug penetrationGlioblastoma multiforme treatmentKill GBM cellsLack of effective drugsTumor growthDrug penetrationIntravenous administrationP28 peptideEffective drugsGlioblastoma treatmentTumorClinical applicationGBM cellsPeptide-conjugatesTreatmentBrainBardoxoloneGlioblastomaPerivascular NOTCH3+ Stem Cells Drive Meningioma Tumorigenesis and Resistance to Radiotherapy.
Choudhury A, Cady M, Lucas C, Najem H, Phillips J, Palikuqi B, Zakimi N, Joseph T, Birrueta J, Chen W, Oberheim Bush N, Hervey-Jumper S, Klein O, Toedebusch C, Horbinski C, Magill S, Bhaduri A, Perry A, Dickinson P, Heimberger A, Ashworth A, Crouch E, Raleigh D. Perivascular NOTCH3+ Stem Cells Drive Meningioma Tumorigenesis and Resistance to Radiotherapy. Cancer Discovery 2024, 14: 1823-1837. PMID: 38742767, PMCID: PMC11452293, DOI: 10.1158/2159-8290.cd-23-1459.Peer-Reviewed Original ResearchConceptsResistance to radiotherapyMeningioma tumorigenesisSystemic therapyTreating meningiomasStem cellsGenetically engineered mouse modelsTumor-initiating capacityHigh-grade meningiomasReduced tumor growthPrimary intracranial tumorsMeningioma growthImproved survivalIntracranial tumorsRadiotherapyTherapeutic vulnerabilitiesTumor growthMeningiomasMouse modelSingle-cell transcriptomicsLineage tracingNotch3TumorigenesisCell proliferationReduced survivalCell typesTumor-induced modifications of resting-state networks in patients with glioma
Pasquini L, Napolitano A, Schmid M, Jenabi M, Peck K, Holodny A. Tumor-induced modifications of resting-state networks in patients with glioma. Proceedings Of The International Society For Magnetic Resonance In Medicine ... Scientific Meeting And Exhibition. 2024 DOI: 10.58530/2024/3149.Peer-Reviewed Original ResearchBrain networksHealthy controlsResting-state functional MRITumor locationResting-state networksFunctional MRIAssociated with tumor locationTumor boundariesCognitive disabilitiesTumor-induced alterationsCognitive networksBrainChi-square testTumor effectWHO-gradeFunctional alterationsEloquent areasTumor growthGlioma patientsWidespread effectsTumorPatient networksPatientsGliomaAlterationsThe FLRT3-UNC5B Pathway is a Novel Regulator of T Immunosurveillance
Flies D, Yan C, Yang Q, Arbitman S, Fitzgerald D, Sharee S, Shaik J, Bosiacki J, Myers K, Paucarmayta A, Johnson D, O'Neill T, Cusumano Z, Langermann S, Langenau D, Patel S. The FLRT3-UNC5B Pathway is a Novel Regulator of T Immunosurveillance. The Journal Of Immunology 2024, 212: 0298_5492-0298_5492. DOI: 10.4049/jimmunol.212.supp.0298.5492.Peer-Reviewed Original ResearchT cell activationT cellsCell-derived xenograftsTumor growthT cell anti-tumor immunityInhibitor of T cell activationCell-derived xenograft modelControl T cell responsesHuman T cell functionT cell checkpointsAnti-tumor immunityT cell responsesT cell functionActivated T cellsTumor-immune interactionsPromote tumor growthHuman T cellsCAR-TUNC-5 netrin receptor BZebrafish tumor modelTumor cellsTumor modelReceptor BGain-of-function screenMonoclonal antibodiesTumor expressed BCAM impedes anti-tumor T cell immunity and can be targeted therapeutically
Flies D, Tian L, O'Neill R, Fitzgerald D, Sharee S, Shaik J, Bosiacki J, Paucarmayta A, Prajapati K, Langermann S, Mrass P. Tumor expressed BCAM impedes anti-tumor T cell immunity and can be targeted therapeutically. The Journal Of Immunology 2024, 212: 0517_5466-0517_5466. DOI: 10.4049/jimmunol.212.supp.0517.5466.Peer-Reviewed Original ResearchAnti-tumor immunityT cell immunityCytotoxic T cellsTumor microenvironmentT cellsTumor growthAnti-tumor T cell immunityT cell anti-tumor immunityExclusion of T cellsIncreased T-cell infiltrationRegulating T cell immunityHuman T cell functionT cell infiltrationInhibitor of T cell proliferationT cell suppressionHuman tumors in vitroT cell functionReduced tumor growthT cell proliferationDecreased tumor growthTumors in vitroTumor growth in vivoCancer escapeCheckpoint inhibitorsGrowth in vivo
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