2025
PTEN mutations impair CSF dynamics and cortical networks by dysregulating periventricular neural progenitors
DeSpenza T, Kiziltug E, Allington G, Barson D, McGee S, O’Connor D, Robert S, Mekbib K, Nanda P, Greenberg A, Singh A, Duy P, Mandino F, Zhao S, Lynn A, Reeves B, Marlier A, Getz S, Nelson-Williams C, Shimelis H, Walsh L, Zhang J, Wang W, Prina M, OuYang A, Abdulkareem A, Smith H, Shohfi J, Mehta N, Dennis E, Reduron L, Hong J, Butler W, Carter B, Deniz E, Lake E, Constable R, Sahin M, Srivastava S, Winden K, Hoffman E, Carlson M, Gunel M, Lifton R, Alper S, Jin S, Crair M, Moreno-De-Luca A, Luikart B, Kahle K. PTEN mutations impair CSF dynamics and cortical networks by dysregulating periventricular neural progenitors. Nature Neuroscience 2025, 28: 536-557. PMID: 39994410, DOI: 10.1038/s41593-024-01865-3.Peer-Reviewed Original ResearchConceptsNeural progenitor cellsCongenital hydrocephalusCSF dynamicsIncreased CSF productionDe novo mutationsFrequent monogenic causeEverolimus treatmentCSF shuntingNonsurgical treatmentPTEN mutationsAqueductal stenosisInhibitory interneuronsVentriculomegalyProgenitor cellsChoroid plexusMonogenic causeCortical networksIncreased survivalBrain ventriclesCortical deficitsNeural progenitorsGene PTENCSF productionNkx2.1PTENChronic Rapamycin Prevents Electrophysiological and Morphological Alterations Produced by Conditional Pten Deletion in Mouse Cortex
Hauptman J, Antonios J, Mathern G, Levine M, Cepeda C. Chronic Rapamycin Prevents Electrophysiological and Morphological Alterations Produced by Conditional Pten Deletion in Mouse Cortex. Cells 2025, 14: 79. PMID: 39851507, PMCID: PMC11764219, DOI: 10.3390/cells14020079.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCerebral CortexElectrophysiological PhenomenaGene DeletionMiceMice, KnockoutPTEN PhosphohydrolasePyramidal CellsSirolimusTOR Serine-Threonine KinasesConceptsCortical pyramidal neuronsMice treated with rapamycinGABA releasePTEN deletionWhole-cell patch-clamp recordingsMiniature inhibitory postsynaptic currentsEx vivo slicesNeuronal somatic sizeReduced neuronal firingInhibitory postsynaptic currentsChronic rapamycin treatmentPatch-clamp recordingsIncreased input resistanceInhibitory synaptic inputsDevelopmental brain disordersRapamycin treatmentIncreased membrane capacitanceConditional mouse modelChronic treatmentPostsynaptic currentsClamp recordingsNaive miceSynaptic excitationBrain disordersControl mice
2023
PTEN Loss Confers Resistance to Anti-PD-1 Therapy in Non-Small Cell Lung Cancer by Increasing Tumor Infiltration of Regulatory T Cells.
Exposito F, Redrado M, Houry M, Hastings K, Molero-Abraham M, Lozano T, Solorzano J, Sanz-Ortega J, Adradas V, Amat R, Redin E, Leon S, Legarra N, Garcia J, Serrano D, Valencia K, Robles-Oteiza C, Foggetti G, Otegui N, Felip E, Lasarte J, Paz-Ares L, Zugazagoitia J, Politi K, Montuenga L, Calvo A. PTEN Loss Confers Resistance to Anti-PD-1 Therapy in Non-Small Cell Lung Cancer by Increasing Tumor Infiltration of Regulatory T Cells. Cancer Research 2023, 83: 2513-2526. PMID: 37311042, DOI: 10.1158/0008-5472.can-22-3023.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerLung squamous carcinomaAnti-PD-1 therapyRegulatory T cellsCell lung cancerImmunosuppressive microenvironmentLung cancerImmunotherapy resistanceT cellsWorse progression-free survivalCell death protein 1PTEN lossAnti-TGFβ antibodyConversion of CD4PI3K/AKT/mTOR pathwayProgression-free survivalDeath protein 1Treatment of miceImmunosuppressive tumor microenvironmentPTEN/PI3K/AKT/mTOR pathwayAKT/mTOR pathwayPD-L1TLR agonistsTumor rejectionSquamous carcinoma
2022
Loss of PTEN phosphorylation via single point mutation alters cortical connectivity and behaviour
Binder M, Bordey A. Loss of PTEN phosphorylation via single point mutation alters cortical connectivity and behaviour. Brain 2022, 145: 3343-3344. PMID: 36148582, PMCID: PMC10233246, DOI: 10.1093/brain/awac350.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements
2021
PTEN mutations in autism spectrum disorder and congenital hydrocephalus: developmental pleiotropy and therapeutic targets
DeSpenza T, Carlson M, Panchagnula S, Robert S, Duy PQ, Mermin-Bunnell N, Reeves BC, Kundishora A, Elsamadicy AA, Smith H, Ocken J, Alper SL, Jin SC, Hoffman EJ, Kahle KT. PTEN mutations in autism spectrum disorder and congenital hydrocephalus: developmental pleiotropy and therapeutic targets. Trends In Neurosciences 2021, 44: 961-976. PMID: 34625286, PMCID: PMC8692171, DOI: 10.1016/j.tins.2021.08.007.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutism Spectrum DisorderHumansHydrocephalusMammalsMutationNeurodevelopmental DisordersPhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseConceptsDevelopmental pleiotropyPTEN-PI3KMTOR pathwayMolecular pathophysiologyPTEN mutationsMolecular similarityTherapeutic targetCommon underlying mechanismNeurodevelopmental disordersUnderlying mechanismTherapeutic promisePleiotropyBiologyPhenotypicMutationsLimited understandingPathwayCommon neurodevelopmental disorderAutism spectrum disorderSimilarityTargetPrevalence and clinical/molecular characteristics of PTEN mutations in Turkish children with autism spectrum disorders and macrocephaly
Kaymakcalan H, Kaya İ, Binici N, Nikerel E, Özbaran B, Aksoy M, Erbilgin S, Özyurt G, Jahan N, Çelik D, Yararbaş K, Yalçınkaya L, Köse S, Durak S, Ercan‐Sencicek A. Prevalence and clinical/molecular characteristics of PTEN mutations in Turkish children with autism spectrum disorders and macrocephaly. Molecular Genetics & Genomic Medicine 2021, 9: e1739. PMID: 34268892, PMCID: PMC8404225, DOI: 10.1002/mgg3.1739.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAutism Spectrum DisorderChildChild, PreschoolFemaleGene FrequencyHumansMaleMegalencephalyMutationPTEN PhosphohydrolaseTurkeyCurrent Understandings of Core Pathways for the Activation of Mammalian Primordial Follicles
Zhao Y, Feng H, Zhang Y, Zhang J, Wang X, Liu D, Wang T, Li R, Ng E, Yeung W, Rodriguez-Wallberg K, Liu K. Current Understandings of Core Pathways for the Activation of Mammalian Primordial Follicles. Cells 2021, 10: 1491. PMID: 34199299, PMCID: PMC8231864, DOI: 10.3390/cells10061491.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsFemaleHumansInfertility, FemaleOvarian FolliclePhosphatidylinositol 3-KinasesPrimary Ovarian InsufficiencyPTEN PhosphohydrolaseSignal TransductionConceptsActivation of primordial folliclesPrimordial follicle activationPrimordial folliclesFollicular activityIn vitro activation of primordial folliclesFollicle activationPhosphatidylinositol 3-kinase (PI3K)/phosphatasePre-granulosa cellsPremature ovarian insufficiencyPoor ovarian responseOvarian endocrine functionIn vitro activityOvarian insufficiencyMammalian ovaryOvarian responsePI3K/PTEN signaling pathwayFollicular developmentMature oocytesEndocrine functionFolliclesSecrete hormonesTensin homologPrimary oocytesSignaling pathwayField of reproductionB2M overexpression correlates with malignancy and immune signatures in human gliomas
Zhang H, Cui B, Zhou Y, Wang X, Wu W, Wang Z, Dai Z, Cheng Q, Yang K. B2M overexpression correlates with malignancy and immune signatures in human gliomas. Scientific Reports 2021, 11: 5045. PMID: 33658560, PMCID: PMC7930032, DOI: 10.1038/s41598-021-84465-6.Peer-Reviewed Original ResearchMeSH Keywordsbeta 2-MicroglobulinBiomarkers, TumorBrain NeoplasmsCarcinogenesisCell Line, TumorDisease ProgressionGene Expression Regulation, NeoplasticGenomicsGliomaHumansImmune Checkpoint ProteinsImmune ToleranceImmunotherapyIsocitrate DehydrogenaseKaplan-Meier EstimateMutationPrognosisPTEN PhosphohydrolaseTumor MicroenvironmentConceptsB2M expressionImmune signaturesM expressionB2MAssociated with immune checkpoint moleculesAssociated with PTEN deletionSuppress anti-tumor immunityAnti-tumor immunityImmune checkpoint moleculesImmunotherapy of gliomaLimited treatment strategiesStromal cell typesCheckpoint moleculesEGFR amplificationClinical characteristicsPTEN deletionPatient prognosisTumor progressionTreatment strategiesGenomic profilingInflammatory activityImmunotherapySomatic mutationsCGGA databasesGlioma
2020
In vivo modeling of metastatic human high-grade serous ovarian cancer in mice
Kim O, Park EY, Klinkebiel DL, Pack SD, Shin YH, Abdullaev Z, Emerson RE, Coffey DM, Kwon SY, Creighton CJ, Kwon S, Chang EC, Chiang T, Yatsenko AN, Chien J, Cheon DJ, Yang-Hartwich Y, Nakshatri H, Nephew KP, Behringer RR, Fernández FM, Cho CH, Vanderhyden B, Drapkin R, Bast RC, Miller KD, Karpf AR, Kim J. In vivo modeling of metastatic human high-grade serous ovarian cancer in mice. PLOS Genetics 2020, 16: e1008808. PMID: 32497036, PMCID: PMC7297383, DOI: 10.1371/journal.pgen.1008808.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsCell Line, TumorChromosomal InstabilityCystadenocarcinoma, SerousDEAD-box RNA HelicasesDisease Models, AnimalDNA RepairDrug Resistance, NeoplasmDrug Screening Assays, AntitumorFeasibility StudiesFemaleHumansMiceMice, KnockoutMutationNeoplasm GradingNeoplasm MetastasisOvarian NeoplasmsPeritoneal NeoplasmsPrimary Cell CulturePTEN PhosphohydrolaseRibonuclease IIITumor Suppressor Protein p53ConceptsHigh-grade serous carcinomaHuman HGSCHigh-grade serous ovarian cancerSerous ovarian cancerOvarian cancerPeritoneal metastasisHuman high-grade serous ovarian cancerMetastatic ovarian cancerOvarian cancer typesHuman cancer metastasisHuman cancer mortalityHemorrhagic ascitesClinical metastasisHistopathological similaritiesSerous carcinomaCancer mortalityFallopian tubeMurine modelPeritoneal cavityMouse modelPotential therapyMouse deathMetastasisCancer typesCancer metastasisTumor Mutational Burden and PTEN Alterations as Molecular Correlates of Response to PD-1/L1 Blockade in Metastatic Triple-Negative Breast Cancer
Barroso-Sousa R, Keenan TE, Pernas S, Exman P, Jain E, Garrido-Castro AC, Hughes M, Bychkovsky B, Umeton R, Files JL, Lindeman NI, MacConaill LE, Hodi FS, Krop IE, Dillon D, Winer EP, Wagle N, Lin NU, Mittendorf EA, Van Allen EM, Tolaney SM. Tumor Mutational Burden and PTEN Alterations as Molecular Correlates of Response to PD-1/L1 Blockade in Metastatic Triple-Negative Breast Cancer. Clinical Cancer Research 2020, 26: 2565-2572. PMID: 32019858, PMCID: PMC7269810, DOI: 10.1158/1078-0432.ccr-19-3507.Peer-Reviewed Original ResearchConceptsMetastatic triple-negative breast cancerHigh tumor mutational burdenProgression-free survivalTumor mutational burdenObjective response rateImmune checkpoint inhibitorsAnti-PD-1/L1 therapyTriple-negative breast cancerOverall survivalL1 therapyPD-L1Breast cancerMutational burdenLow objective response rateLonger progression-free survivalShorter progression-free survivalDana-Farber Cancer InstituteTumor genomic featuresShorter overall survivalMutations/megabaseCheckpoint inhibitorsVisceral metastasesL1 blockadePerformance statusPrior linesInterplay of somatic alterations and immune infiltration modulates response to PD-1 blockade in advanced clear cell renal cell carcinoma
Braun DA, Hou Y, Bakouny Z, Ficial M, Sant’ Angelo M, Forman J, Ross-Macdonald P, Berger AC, Jegede OA, Elagina L, Steinharter J, Sun M, Wind-Rotolo M, Pignon JC, Cherniack AD, Lichtenstein L, Neuberg D, Catalano P, Freeman GJ, Sharpe AH, McDermott DF, Van Allen EM, Signoretti S, Wu CJ, Shukla SA, Choueiri TK. Interplay of somatic alterations and immune infiltration modulates response to PD-1 blockade in advanced clear cell renal cell carcinoma. Nature Medicine 2020, 26: 909-918. PMID: 32472114, PMCID: PMC7499153, DOI: 10.1038/s41591-020-0839-y.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntigen PresentationAntineoplastic Agents, ImmunologicalCarcinoma, Renal CellCD8-Positive T-LymphocytesChromosome DeletionChromosomes, Human, Pair 6Chromosomes, Human, Pair 9Class I Phosphatidylinositol 3-KinasesDNA-Binding ProteinsExome SequencingFemaleFluorescent Antibody TechniqueGene DeletionGenomicsHistocompatibility Antigens Class IIHistone DemethylasesHistone-Lysine N-MethyltransferaseHumansKidney NeoplasmsLymphocytes, Tumor-InfiltratingMaleMiddle AgedMutationNivolumabPrognosisProteasome Endopeptidase ComplexPTEN PhosphohydrolaseSequence Analysis, RNATOR Serine-Threonine KinasesTranscription FactorsTuberous Sclerosis Complex 1 ProteinTumor Suppressor ProteinsUbiquitin ThiolesteraseVon Hippel-Lindau Tumor Suppressor ProteinConceptsAdvanced clear cell renal cell carcinomaClear cell renal cell carcinomaPD-1 blockadeCell renal cell carcinomaRenal cell carcinomaCell carcinomaDegree of CD8Numerous chromosomal alterationsProspective clinical trialsSomatic alterationsInfiltrated tumorsClinical responseCell infiltrationTherapeutic responseClinical trialsTherapeutic efficacyBlockadeCcRCC tumorsTumorsPBRM1 mutationsModulates responseCD8Chromosomal alterationsImmunofluorescence analysisCarcinomaA DNA Repair Inhibitor Isolated from an Ecuadorian Fungal Endophyte Exhibits Synthetic Lethality in PTEN-Deficient Glioblastoma
Adaku N, Park HB, Spakowicz DJ, Tiwari MK, Strobel SA, Crawford JM, Rogers FA. A DNA Repair Inhibitor Isolated from an Ecuadorian Fungal Endophyte Exhibits Synthetic Lethality in PTEN-Deficient Glioblastoma. Journal Of Natural Products 2020, 83: 1899-1908. PMID: 32407116, DOI: 10.1021/acs.jnatprod.0c00012.Peer-Reviewed Original ResearchConceptsPTEN-deficient glioblastoma cellsPTEN-deficient cancersTumor suppressor PTENImportant molecular toolPTEN-deficient glioblastomaInhibitor of DNAHuman cancer developmentDNA repair inhibitorsFungal endophytesBreak repairGenomic levelSuppressor PTENMolecular toolsEndophytic fungiSynthetic lethalityPTEN deficiencyGlioblastoma cellsRepair inhibitorsCancer developmentPTEN lossCurrent cancer treatmentsLarger patient populationTherapeutic leadsMedicinal plantsNew therapeutic leads
2019
CFTR-PTEN–dependent mitochondrial metabolic dysfunction promotes Pseudomonas aeruginosa airway infection
Riquelme SA, Lozano C, Moustafa AM, Liimatta K, Tomlinson KL, Britto C, Khanal S, Gill SK, Narechania A, Azcona-Gutiérrez JM, DiMango E, Saénz Y, Planet P, Prince A. CFTR-PTEN–dependent mitochondrial metabolic dysfunction promotes Pseudomonas aeruginosa airway infection. Science Translational Medicine 2019, 11 PMID: 31270271, PMCID: PMC6784538, DOI: 10.1126/scitranslmed.aav4634.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarboxy-LyasesColony Count, MicrobialCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorHCT116 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitImmunityInterleukin-1betaLungMice, Inbred C57BLMiddle AgedMitochondriaOxidantsOxidative StressPseudomonas aeruginosaPseudomonas InfectionsPTEN PhosphohydrolaseReactive Oxygen SpeciesSuccinatesConceptsCystic fibrosis transmembrane conductance regulatorImmune-responsive gene 1Fibrosis transmembrane conductance regulatorEffect of PTENTransmembrane conductance regulatorPlasma membraneChromosome 10Reactive oxygen speciesConductance regulatorTumor suppressorTensin homologGene 1Mitochondrial functionMitochondrial activityAnti-inflammatory host responsesCell proliferationOxygen speciesPTENMyeloid cellsCFTR dysfunctionMetabolic defectsHost responseActivity contributesHomologComplexesTwo well-differentiated pancreatic neuroendocrine tumor mouse models
Wong C, Tang LH, Davidson C, Vosburgh E, Chen W, Foran DJ, Notterman DA, Levine AJ, Xu EY. Two well-differentiated pancreatic neuroendocrine tumor mouse models. Cell Death & Differentiation 2019, 27: 269-283. PMID: 31160716, PMCID: PMC7206057, DOI: 10.1038/s41418-019-0355-0.Peer-Reviewed Original ResearchConceptsMultiple endocrine neoplasia type 1Neuroendocrine tumorsMouse modelShort latencyPI3K/Akt/mTORPancreatic neuroendocrine tumorsPituitary neuroendocrine tumorsTumor mouse modelAkt/mTORMTOR inhibitor rapamycinCre-loxP systemNeuroendocrine cancerProlonged survivalProlonged latencyMEN1 patientsMouse insulin 1 promoterSame miceMen1 lossTherapeutic opportunitiesType 1Genetic syndromesPTEN lossEarly onsetTumorsTumor developmentROS play an important role in ATPR inducing differentiation and inhibiting proliferation of leukemia cells by regulating the PTEN/PI3K/AKT signaling pathway
Feng Y, Hua X, Niu R, Du Y, Shi C, Zhou R, Chen F. ROS play an important role in ATPR inducing differentiation and inhibiting proliferation of leukemia cells by regulating the PTEN/PI3K/AKT signaling pathway. Biological Research 2019, 52: 26. PMID: 31053167, PMCID: PMC6498685, DOI: 10.1186/s40659-019-0232-9.Peer-Reviewed Original ResearchConceptsPI3K/Akt pathwayPTEN/PI3K/AKT pathwayPTEN/PI3K/AKTPI3K/AktReactive oxygen speciesTrans retinoic acid (ATRA) derivativeAnti-AML effectAkt pathwayTreatment of AMLBackgroundAcute myeloid leukemiaCell proliferationAnti-tumor characteristicsIncurable hematological malignancyRetinoic acid derivativesG0/G1 phaseCCK-8 assayCell cycle distributionCell differentiationDifferentiation-related proteinFrequent relapsesStandard chemotherapyClinical outcomesCell line NB4Myeloid leukemiaNovel therapiesPTEN loss is associated with resistance to cetuximab in patients with head and neck squamous cell carcinoma
Eze N, Lee JW, Yang DH, Zhu F, Neumeister V, Sandoval-Schaefer T, Mehra R, Ridge JA, Forastiere A, Chung CH, Burtness B. PTEN loss is associated with resistance to cetuximab in patients with head and neck squamous cell carcinoma. Oral Oncology 2019, 91: 69-78. PMID: 30926065, PMCID: PMC6855599, DOI: 10.1016/j.oraloncology.2019.02.026.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntineoplastic Agents, ImmunologicalCetuximabFemaleHumansMaleMiddle AgedPTEN PhosphohydrolaseSquamous Cell Carcinoma of Head and NeckConceptsNeck squamous cell carcinomaEpidermal growth factor receptorSquamous cell carcinomaCell carcinomaCetuximab-based therapyTrial of cisplatinTrials (RCTs) of cetuximabPotential predictive biomarkersPTEN expressionLack of benefitPI3K mutationsPI3K p110αHigh PTEN expressionPI3K pathwayGrowth factor receptorHot spot mutationsStandard therapySuperior PFSMultivariable analysisPredictive biomarkersLoss of expressionSuch therapyCommon abnormalityCetuximabSide effectsNanoparticle-mediated intratumoral inhibition of miR-21 for improved survival in glioblastoma
Seo YE, Suh HW, Bahal R, Josowitz A, Zhang J, Song E, Cui J, Noorbakhsh S, Jackson C, Bu T, Piotrowski-Daspit A, Bindra R, Saltzman WM. Nanoparticle-mediated intratumoral inhibition of miR-21 for improved survival in glioblastoma. Biomaterials 2019, 201: 87-98. PMID: 30802686, PMCID: PMC6451656, DOI: 10.1016/j.biomaterials.2019.02.016.Peer-Reviewed Original ResearchConceptsEfficient intracellular deliveryDelivery systemPeptide nucleic acidNanoparticle productsNanoparticlesIntracellular deliveryConvection-enhanced deliveryDifferent delivery systemsNucleic acidsSignificant therapeutic efficacyMiR-21 suppressionTherapeutic efficacyLocal deliveryDeliverySystemic toxicityBlock copolymersDistinct advantagesPolyglycerolMiR-21
2018
PTEN Regulates Non-Homologous End Joining by Epigenetic Induction of NHEJ1/XLF
Sulkowski PL, Scanlon SE, Oeck S, Glazer PM. PTEN Regulates Non-Homologous End Joining by Epigenetic Induction of NHEJ1/XLF. Molecular Cancer Research 2018, 16: molcanres.0581.2017. PMID: 29739874, PMCID: PMC6072556, DOI: 10.1158/1541-7786.mcr-17-0581.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCHO CellsCricetinaeCricetulusDNA End-Joining RepairDNA Repair EnzymesDNA-Binding ProteinsEpigenomicsHumansPTEN PhosphohydrolaseConceptsDNA double-strand breaksKey DNA repair pathwaysCytotoxic DNA lesionsXRCC4-like factorPatient-derived melanomasDNA repair pathwaysDouble-strand breaksNovel regulatory roleTumor suppressor geneSuppression of PTENHistone acetyltransferasesDSB repairGenomic analysisNHEJ defectsNonhomologous endRepair pathwaysGene promoterNovel functionRegulatory acetylationNHEJ deficiencyDNA lesionsRegulatory roleSuppressor geneNHEJ DSB repairNHEJDKK2 imparts tumor immunity evasion through β-catenin-independent suppression of cytotoxic immune-cell activation
Xiao Q, Wu J, Wang WJ, Chen S, Zheng Y, Yu X, Meeth K, Sahraei M, Bothwell ALM, Chen L, Bosenberg M, Chen J, Sexl V, Sun L, Li L, Tang W, Wu D. DKK2 imparts tumor immunity evasion through β-catenin-independent suppression of cytotoxic immune-cell activation. Nature Medicine 2018, 24: 262-270. PMID: 29431745, PMCID: PMC5840007, DOI: 10.1038/nm.4496.Peer-Reviewed Original ResearchMeSH KeywordsAdenomatous Polyposis Coli Proteinbeta CateninCD8-Positive T-LymphocytesCell Line, TumorColorectal NeoplasmsCytotoxicity, ImmunologicGene Expression Regulation, NeoplasticHumansIntercellular Signaling Peptides and ProteinsIntestinal NeoplasmsKiller Cells, NaturalLow Density Lipoprotein Receptor-Related Protein-5MelanomaProgrammed Cell Death 1 ReceptorPTEN PhosphohydrolaseSignal TransductionSTAT5 Transcription FactorTumor EscapeMyeloid-targeted immunotherapies act in synergy to induce inflammation and antitumor immunity
Perry CJ, Muñoz-Rojas AR, Meeth KM, Kellman LN, Amezquita RA, Thakral D, Du VY, Wang JX, Damsky W, Kuhlmann AL, Sher JW, Bosenberg M, Miller-Jensen K, Kaech SM. Myeloid-targeted immunotherapies act in synergy to induce inflammation and antitumor immunity. Journal Of Experimental Medicine 2018, 215: 877-893. PMID: 29436395, PMCID: PMC5839759, DOI: 10.1084/jem.20171435.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD40 AntigensCell ProliferationImmunotherapyInflammationInterferon-gammaMacrophagesMelanoma, ExperimentalMiceMyeloid CellsNeoplasmsPhenotypeProto-Oncogene Proteins B-rafPTEN PhosphohydrolaseReceptors, Granulocyte-Macrophage Colony-Stimulating FactorRNA, MessengerSurvival AnalysisT-LymphocytesTranscription, GeneticTumor Necrosis Factor-alphaConceptsCombination therapyEffective antitumor immune responseProtective T cell responsesTumor-associated myeloid cellsM2-like stateCheckpoint inhibitor therapyAntitumor immune responseT cell responsesCSF-1R inhibitorAntitumor immunityInhibitor therapySuch patientsIL-12IL-6Cancer immunotherapyTAM subsetsUntreated tumorsT cellsImmune responseMouse modelTherapeutic targetTAM subpopulationsMyeloid cellsTumor growthCell responses
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply