2016
Response to Programmed Cell Death-1 Blockade in a Murine Melanoma Syngeneic Model Requires Costimulation, CD4, and CD8 T Cells
Moreno B, Zaretsky JM, Garcia-Diaz A, Tsoi J, Parisi G, Robert L, Meeth K, Ndoye A, Bosenberg M, Weeraratna AT, Graeber TG, Comin-Anduix B, Hu-Lieskovan S, Ribas A. Response to Programmed Cell Death-1 Blockade in a Murine Melanoma Syngeneic Model Requires Costimulation, CD4, and CD8 T Cells. Cancer Immunology Research 2016, 4: 845-857. PMID: 27589875, PMCID: PMC5050168, DOI: 10.1158/2326-6066.cir-16-0060.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell Line, TumorDendritic CellsInterferon-gammaLymphocytes, Tumor-InfiltratingMacrophagesMelanomaMice, Inbred C57BLMutationProgrammed Cell Death 1 ReceptorProto-Oncogene Proteins B-rafXenograft Model Antitumor AssaysConceptsPD-1 blockade therapyPD-1 blockadeCD8 T cellsBlockade therapyDendritic cellsT cellsTumor modelEffector T cell functionSyngeneic murine tumor modelsAntitumor activityPD-L1 expressionT cell primingImmune cell recruitmentT cell functionTumor-associated macrophagesMurine tumor modelsTumor-host interactionsStrong antitumor activityCD80/86 costimulationL1 therapyInflammatory profileClinical benefitMHC-IIPeripheral tissuesCell recruitmentDNMT3b Modulates Melanoma Growth by Controlling Levels of mTORC2 Component RICTOR
Micevic G, Muthusamy V, Damsky W, Theodosakis N, Liu X, Meeth K, Wingrove E, Santhanakrishnan M, Bosenberg M. DNMT3b Modulates Melanoma Growth by Controlling Levels of mTORC2 Component RICTOR. Cell Reports 2016, 14: 2180-2192. PMID: 26923591, PMCID: PMC4785087, DOI: 10.1016/j.celrep.2016.02.010.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarrier ProteinsCell Line, TumorCell ProliferationDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDown-RegulationGene Expression Regulation, NeoplasticHumansMechanistic Target of Rapamycin Complex 2Melanoma, ExperimentalMice, 129 StrainMice, Inbred C57BLMice, NudeMicroRNAsMultiprotein ComplexesNeoplasm TransplantationProportional Hazards ModelsRapamycin-Insensitive Companion of mTOR ProteinRNA InterferenceSkin NeoplasmsTOR Serine-Threonine KinasesTumor BurdenConceptsMelanoma formationPotential therapeutic targetMiR-196b expressionMouse melanoma modelPro-tumorigenic roleMTORC2 component RictorMelanoma growthTherapeutic targetMelanoma modelLoss of RictorHuman melanomaCancer typesTumor cellsMelanomaSpecific signaling pathwaysMTORC2 signalingSignaling pathwaysTurn preventsMiR-196b promoterDNA methyltransferase DNMT3BRictorControlling LevelsDNMT3BMethyltransferase DNMT3BCancer
2011
β-Catenin Signaling Controls Metastasis in Braf-Activated Pten-Deficient Melanomas
Damsky WE, Curley DP, Santhanakrishnan M, Rosenbaum LE, Platt JT, Rothberg BE, Taketo MM, Dankort D, Rimm DL, McMahon M, Bosenberg M. β-Catenin Signaling Controls Metastasis in Braf-Activated Pten-Deficient Melanomas. Cancer Cell 2011, 20: 741-754. PMID: 22172720, PMCID: PMC3241928, DOI: 10.1016/j.ccr.2011.10.030.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, DifferentiationBenzamidesBeta CateninCell Transformation, NeoplasticColorectal NeoplasmsEnzyme ActivationGene Knockdown TechniquesHumansImatinib MesylateKaplan-Meier EstimateLung NeoplasmsLymphatic MetastasisMelanocytesMelanoma, ExperimentalMiceMice, 129 StrainMice, Inbred C57BLMice, TransgenicPhosphorylationPiperazinesProtein StabilityProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePyrimidinesSignal TransductionSkin NeoplasmsSplenic NeoplasmsTranscription, GeneticTumor Cells, CulturedConceptsΒ-catenin levelsPI3K/AktLymph nodesMetastatic tumorsFrequent metastasisTumor differentiationMalignant melanomaMAPK/ERKMelanoma metastasesMouse modelControl metastasisHuman melanomaMelanomaMetastasisΒ-catenin stabilizationPTEN lossCentral mediatorMetastasis regulatorsΒ-cateninSpecific changesFunctional implicationsWntLung
2001
Telomere dysfunction and evolution of intestinal carcinoma in mice and humans
Rudolph K, Millard M, Bosenberg M, DePinho R. Telomere dysfunction and evolution of intestinal carcinoma in mice and humans. Nature Genetics 2001, 28: 155-159. PMID: 11381263, DOI: 10.1038/88871.Peer-Reviewed Original ResearchConceptsHuman intestinal neoplasiaProgression of mouseTelomerase activationHuman colorectal carcinogenesisTelomere dysfunctionInitiated lesionsIntestinal carcinomaColorectal carcinogenesisIntestinal neoplasiaHuman colorectalDysfunctionAdvanced stageMalignant transformationTumor progressionChromosomal instabilityColon carcinomaCarcinoma transitionMacroscopic adenomasTransient telomere dysfunctionEarly carcinogenesisCancer initiationHuman cancersTelomerase activityCarcinomaDifferential effects