2022
The Crossroads of Cancer Epigenetics and Immune Checkpoint Therapy.
Micevic G, Bosenberg M, Yan Q. The Crossroads of Cancer Epigenetics and Immune Checkpoint Therapy. Clinical Cancer Research 2022, 29: 1173-1182. PMID: 36449280, PMCID: PMC10073242, DOI: 10.1158/1078-0432.ccr-22-0784.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsImmune checkpoint inhibitorsImmune checkpoint therapyT cell exhaustionCheckpoint therapyAntitumor immune responseT cell populationsCell-intrinsic immunityTypes of cancerViral mimicry responseLow response rateCheckpoint inhibitorsCurrent immunotherapiesPancreatic cancerSustained responsePreclinical modelsTreatment outcomesImmune responseEndogenous antigensResponse rateTumor typesMultiple epigenetic regulatorsCritical mediatorLow immunogenicityTherapyCancer
2021
KDM5B promotes immune evasion by recruiting SETDB1 to silence retroelements
Zhang SM, Cai WL, Liu X, Thakral D, Luo J, Chan LH, McGeary MK, Song E, Blenman KRM, Micevic G, Jessel S, Zhang Y, Yin M, Booth CJ, Jilaveanu LB, Damsky W, Sznol M, Kluger HM, Iwasaki A, Bosenberg MW, Yan Q. KDM5B promotes immune evasion by recruiting SETDB1 to silence retroelements. Nature 2021, 598: 682-687. PMID: 34671158, PMCID: PMC8555464, DOI: 10.1038/s41586-021-03994-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorDNA-Binding ProteinsEpigenesis, GeneticGene SilencingHeterochromatinHistone-Lysine N-MethyltransferaseHumansInterferon Type IJumonji Domain-Containing Histone DemethylasesMaleMelanomaMiceMice, Inbred C57BLMice, KnockoutNuclear ProteinsRepressor ProteinsRetroelementsTumor EscapeConceptsImmune checkpoint blockadeImmune evasionCheckpoint blockadeImmune responseAnti-tumor immune responseRobust adaptive immune responseTumor immune evasionAnti-tumor immunityAdaptive immune responsesType I interferon responseDNA-sensing pathwayMouse melanoma modelImmunotherapy resistanceMost patientsCurrent immunotherapiesTumor immunogenicityImmune memoryMelanoma modelCytosolic RNA sensingRole of KDM5BConsiderable efficacyInterferon responseImmunotherapyEpigenetic therapyBlockade
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 effortDevelopmentBiomarkersAdvancesAttenuation of genome-wide 5-methylcytosine level is an epigenetic feature of cutaneous malignant melanomas
Micevic G, Theodosakis N, Taube JM, Bosenberg MW, Rodi N. Attenuation of genome-wide 5-methylcytosine level is an epigenetic feature of cutaneous malignant melanomas. Melanoma Research 2017, 27: 85-96. PMID: 27997431, PMCID: PMC5812886, DOI: 10.1097/cmr.0000000000000315.Peer-Reviewed Original ResearchConceptsS-adenosyl methionineMelanoma cell linesEpigenetic featuresCell linesInactive chromatin regionsGenome-wide increaseUniversal methyl group donorMethyl group donorChromatin regionsCancer epigenomeEpigenetic modificationsEpigenetic abnormalitiesCytosine residuesMelanoma cell growthEpigenome modulationMalignant melanomaCell growthCovalent changesGroup donorSubcytotoxic levelsChemical substratesMelanoma cellsCutaneous malignant melanomaDose-dependent increaseResidues