2017
Aberrant DNA methylation in melanoma: biomarker and therapeutic opportunities
Micevic G, Theodosakis N, Bosenberg M. Aberrant DNA methylation in melanoma: biomarker and therapeutic opportunities. Clinical Epigenetics 2017, 9: 34. PMID: 28396701, PMCID: PMC5381063, DOI: 10.1186/s13148-017-0332-8.Peer-Reviewed Original ResearchConceptsAberrant DNA methylationDNA methylationMethylation changesDNA methylation changesEpigenetic hallmarkMelanoma formationMethylation signaturesMethylationImportant unresolved questionsBiomarker opportunitiesTherapeutic opportunitiesTherapeutic developmentMethylation methodUnresolved questionsTherapeutic potentialImportant roleRecent advancesPotential biomarkersGenesRecent developmentsHallmarkConsiderable effortDevelopmentBiomarkersAdvancesHistone demethylase KDM5B is critical for PI3K‐AKT‐mTOR signaling and stemness of melanoma
Yan Q, Zhang S, Meeth K, Micevic G, Bosenberg M. Histone demethylase KDM5B is critical for PI3K‐AKT‐mTOR signaling and stemness of melanoma. The FASEB Journal 2017, 31 DOI: 10.1096/fasebj.31.1_supplement.468.1.Peer-Reviewed Original ResearchKnockdown of KDM5BHistone demethylase KDM5BMTOR signalingPI3K-AktImmune checkpoint blockadeEpigenetic stateMouse melanoma cellsCancer stem cellsMouse melanoma modelMPC populationKDM5BMelanoma formationCheckpoint blockadeTumor initiationStem cellsMelanoma modelMelanoma cellsCareer Development AwardKnockdownSignalingPilot grantsMelanoma
2016
DNMT3b 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
2015
mTORC1 Activation Blocks Braf V600E -Induced Growth Arrest but Is Insufficient for Melanoma Formation
Damsky W, Micevic G, Meeth K, Muthusamy V, Curley DP, Santhanakrishnan M, Erdelyi I, Platt JT, Huang L, Theodosakis N, Zaidi MR, Tighe S, Davies MA, Dankort D, McMahon M, Merlino G, Bardeesy N, Bosenberg M. mTORC1 Activation Blocks Braf V600E -Induced Growth Arrest but Is Insufficient for Melanoma Formation. Cancer Cell 2015, 27: 41-56. PMID: 25584893, PMCID: PMC4295062, DOI: 10.1016/j.ccell.2014.11.014.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein KinasesAnimalsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p16HumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MelanocytesMelanoma, ExperimentalMiceMicroRNAsMolecular Sequence DataMultiprotein ComplexesMutationNevusProtein Serine-Threonine KinasesProto-Oncogene Proteins B-rafSignal TransductionSkin NeoplasmsTOR Serine-Threonine KinasesConceptsMelanoma formationGrowth arrestStable growth arrestMTORC2/AktSTK11 lossCDKN2A lossAkt activationIGF1R signalingMice resultsActivationArrestMTORC2Nevus developmentMTORC1/2SignalingAktMelanocytic nevus developmentMelanomagenesisMTORProgressionCDKN2AMelanocytesInactivationUpregulationComplete progression