2021
Tumour antigen-induced T cell exhaustion — the archenemy of immune-hot malignancies
Lopez de Rodas M, Schalper KA. Tumour antigen-induced T cell exhaustion — the archenemy of immune-hot malignancies. Nature Reviews Clinical Oncology 2021, 18: 749-750. PMID: 34556846, PMCID: PMC9235859, DOI: 10.1038/s41571-021-00562-5.Peer-Reviewed Original ResearchConceptsT cell exhaustionCell exhaustionTumor antigen-specific effector T cellsAntigen-specific effector T cellsTissue-resident memory phenotypeT-cell alterationsEffector T cellsCell-specific antigensMemory phenotypeLung carcinomaClinical significanceT cellsHuman melanomaTumor microenvironmentCell alterationsSingle-cell strategyRecent studiesCD8CarcinomaMalignancyMelanomaExhaustionAntigen
2019
A novel mouse model demonstrates that oncogenic melanocyte stem cells engender melanoma resembling human disease
Sun Q, Lee W, Mohri Y, Takeo M, Lim CH, Xu X, Myung P, Atit RP, Taketo MM, Moubarak RS, Schober M, Osman I, Gay DL, Saur D, Nishimura EK, Ito M. A novel mouse model demonstrates that oncogenic melanocyte stem cells engender melanoma resembling human disease. Nature Communications 2019, 10: 5023. PMID: 31685822, PMCID: PMC6828673, DOI: 10.1038/s41467-019-12733-1.Peer-Reviewed Original ResearchConceptsMouse modelNovel mouse modelMelanoma progression modelDeadly skin cancerAnimal modelsSkin cancerBona fide sourceAdvanced stageMelanoma inductionMalignant transformationHuman melanomaMelanomaGene signatureAnagen onsetMolecular profilingMelanoma initiationMelanocyte stem cellsNormal WntStem cellsProgression modelHuman diseasesRecent studiesCancerDiseaseProgression
2018
Participation of xCT in melanoma cell proliferation in vitro and tumorigenesis in vivo
Shin S, Jeong B, Wall B, Li J, Shan N, Wen Y, Goydos J, Chen S. Participation of xCT in melanoma cell proliferation in vitro and tumorigenesis in vivo. Oncogenesis 2018, 7: 86. PMID: 30425240, PMCID: PMC6234219, DOI: 10.1038/s41389-018-0098-7.Peer-Reviewed Original ResearchMelanoma cell proliferationCell proliferationXCT expressionPhase II clinical trialDose-dependent decreasePost-treatment specimensTumor biopsy samplesXenograft-bearing animalsMelanoma cell growthHuman melanoma cell linesHuman tumor biopsy samplesCultured human melanomaStable diseaseMelanoma cell linesAggressive tumorsCancer stageClinical trialsTumor biopsiesXenograft studiesRiluzoleBiopsy samplesMost melanomasHuman melanomaTumor progressionWestern immunoblot analysisSomatic inactivating PTPRJ mutations and dysregulated pathways identified in canine malignant melanoma by integrated comparative genomic analysis
Hendricks W, Zismann V, Sivaprakasam K, Legendre C, Poorman K, Tembe W, Perdigones N, Kiefer J, Liang W, DeLuca V, Stark M, Ruhe A, Froman R, Duesbery N, Washington M, Aldrich J, Neff M, Huentelman M, Hayward N, Brown K, Thamm D, Post G, Khanna C, Davis B, Breen M, Sekulic A, Trent J. Somatic inactivating PTPRJ mutations and dysregulated pathways identified in canine malignant melanoma by integrated comparative genomic analysis. PLOS Genetics 2018, 14: e1007589. PMID: 30188888, PMCID: PMC6126841, DOI: 10.1371/journal.pgen.1007589.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell CycleCell ProliferationComparative Genomic HybridizationDNA Mutational AnalysisDog DiseasesDogsFemaleMaleMelanomaMutationProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)Receptor-Like Protein Tyrosine Phosphatases, Class 3Signal TransductionSkin NeoplasmsTissue Array AnalysisConceptsLow point mutation ratePowerful comparative modelComparative genomic analysisCell cycle controlPoint mutation rateSingle nucleotide polymorphism arrayNucleotide polymorphism arrayWhole-genome sequencingArray comparative genomic hybridizationHuman melanomaComparative genomic hybridizationGenomic analysisRNA sequencingCycle controlGenome sequencingMutation rateGenomic landscapePolymorphism arrayCopy numberMutational landscapeMutational signaturesGenomic hybridizationRecurrent alterationsMulti-platform analysisMutations
2016
A comprehensive system of congenic mouse melanoma models for evaluation of immune therapies
Bosenberg M, Meeth K, Damsky W. A comprehensive system of congenic mouse melanoma models for evaluation of immune therapies. The Journal Of Immunology 2016, 196: 144.19-144.19. DOI: 10.4049/jimmunol.196.supp.144.19.Peer-Reviewed Original ResearchImmune therapyMouse modelImmune systemImmune checkpoint inhibitorsSubset of patientsRenal cell carcinomaMouse melanoma modelMouse melanoma cell lineCheckpoint inhibitorsMelanoma cell linesMelanoma patientsCell carcinomaLung cancerCancer immunologyMalignant melanomaProstate cancerTherapeutic approachesMelanoma modelSkin cancerHuman melanomaTherapyTumor microenvironmentCancerFlow cytometryPatientsDNMT3b 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
2014
Dissection of Immune Gene Networks in Primary Melanoma Tumors Critical for Antitumor Surveillance of Patients with Stage II–III Resectable Disease
Sivendran S, Chang R, Pham L, Phelps RG, Harcharik ST, Hall LD, Bernardo SG, Moskalenko MM, Sivendran M, Fu Y, de Moll EH, Pan M, Moon JY, Arora S, Cohain A, DiFeo A, Ferringer TC, Tismenetsky M, Tsui CL, Friedlander PA, Parides MK, Banchereau J, Chaussabel D, Lebwohl MG, Wolchok JD, Bhardwaj N, Burakoff SJ, Oh WK, Palucka K, Merad M, Schadt EE, Saenger YM. Dissection of Immune Gene Networks in Primary Melanoma Tumors Critical for Antitumor Surveillance of Patients with Stage II–III Resectable Disease. Journal Of Investigative Dermatology 2014, 134: 2202-2211. PMID: 24522433, PMCID: PMC4291112, DOI: 10.1038/jid.2014.85.Peer-Reviewed Original ResearchConceptsStage IIResected stage IIDisease-specific survivalRecurrence-free survivalPrimary human melanomasPotential therapeutic targetPrimary tumor specimensIndependent test populationImmune gene networksDriver genesResectable diseaseIndependent predictorsCutaneous melanomaPrimary melanomaHigh riskTumor specimensTherapeutic targetAntitumor surveillanceHuman melanomaGene signaturePatientsBiomarker developmentMelanomaNanoString technologyTest population
2013
Low-copy piggyBac transposon mutagenesis in mice identifies genes driving melanoma
Ni TK, Landrette SF, Bjornson RD, Bosenberg MW, Xu T. Low-copy piggyBac transposon mutagenesis in mice identifies genes driving melanoma. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: e3640-e3649. PMID: 24003131, PMCID: PMC3780872, DOI: 10.1073/pnas.1314435110.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternDNA PrimersDNA Transposable ElementsGene Expression Regulation, NeoplasticGenetic TestingHEK293 CellsHumansImmunohistochemistryMAP Kinase Kinase Kinase 1MelanomaMiceMice, TransgenicMutagenesis, InsertionalReverse Transcriptase Polymerase Chain ReactionSignal TransductionSpecies SpecificityConceptsCancer-driving genesMitogen-activated protein kinase kinase kinase 1Membrane associated guanylate kinaseProtein kinase kinase kinase 1Kinase kinase kinase 1Protein tyrosine phosphataseTransposon mutagenesis approachKinase kinase 1Transposon mutagenesis screenHuman melanomaBackground mutation rateMelanoma driver genesUndescribed genesIdentifies genesMutagenesis screenPDZ domainGuanylate kinaseTyrosine phosphataseTransposon mutagenesisCellular transformationMutagenesis approachKinase 1Mutation rateERK signalingDriver genesImmune gene expression in primary melanomas to predict lower risk of recurrence and death.
Sivendran S, Chang R, Harcharik S, Hall L, Bernardo S, Moskalenko M, Phelps R, Sivendran M, Cohain A, DiFeo A, Parides M, Lebwohl M, Friedlander P, Banchereau J, Bhardwaj N, Oh W, Burakoff S, Palucka K, Merad M, Saenger Y. Immune gene expression in primary melanomas to predict lower risk of recurrence and death. Journal Of Clinical Oncology 2013, 31: 3014-3014. DOI: 10.1200/jco.2013.31.15_suppl.3014.Peer-Reviewed Original ResearchPrediction of non-recurrenceIndependent patient cohortReceiver Operating CharacteristicProlonged survivalMRNA copy numberNon-recurrenceTraining cohortPatient cohortGene panelLow risk of recurrencePrimary human melanomaStandard prognostic indicatorsImmune-related genesRisk of recurrenceReceiver operating characteristic curvePrimary melanomaImmunotherapy studiesMelanoma recurrencePrognostic indicatorImmune biomarkersRecurrence riskMitotic rateHuman melanomaPrevent recurrencePatient stratificationVesicular Stomatitis Virus Variants Selectively Infect and Kill Human Melanomas but Not Normal Melanocytes
Wollmann G, Davis JN, Bosenberg MW, van den Pol AN. Vesicular Stomatitis Virus Variants Selectively Infect and Kill Human Melanomas but Not Normal Melanocytes. Journal Of Virology 2013, 87: 6644-6659. PMID: 23552414, PMCID: PMC3676084, DOI: 10.1128/jvi.03311-12.Peer-Reviewed Original ResearchConceptsVesicular stomatitis virusReplication-competent vesicular stomatitis virusMetastatic malignant melanomaRecombinant vesicular stomatitis virusMouse melanoma modelHuman melanoma samplesGene mutation statusVSV-CT9Low viral concentrationsMelanoma typesMalignant melanomaSCID miceViral oncolysisMelanoma xenograftsViral infectionMelanoma modelMutation statusMalignant transformationHuman melanomaInfectionMelanomaVirus variantsComplete protectionMelanoma samplesGene mutations
2012
ALDH1A Isozymes are Markers of Human Melanoma Stem Cells and Potential Therapeutic Targets
Luo Y, Dallaglio K, Chen Y, Robinson WA, Robinson SE, McCarter MD, Wang J, Gonzalez R, Thompson DC, Norris DA, Roop DR, Vasiliou V, Fujita M. ALDH1A Isozymes are Markers of Human Melanoma Stem Cells and Potential Therapeutic Targets. Stem Cells 2012, 30: 2100-2113. PMID: 22887839, PMCID: PMC3448863, DOI: 10.1002/stem.1193.Peer-Reviewed Original ResearchMeSH KeywordsAldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyAldehyde OxidoreductasesAnimalsApoptosisCell Transformation, NeoplasticDacarbazineDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticGene SilencingHumansIsoenzymesMelanomaMiceMice, Inbred NODMice, SCIDNeoplasm TransplantationNeoplastic Stem CellsResponse ElementsRetinal DehydrogenaseRNA, Small InterferingSkin NeoplasmsTemozolomideTretinoinConceptsCancer stem cellsPositive melanoma cellsMelanoma cellsTherapeutic targetBiomarkers of CSCsHuman melanomaPatient-derived tumor specimensMelanoma cancer stem cellsNOD/SCID miceALDH-negative cellsHigh aldehyde dehydrogenase (ALDH) activityALDH isozymesNonobese diabetic/Potential therapeutic targetDrug-induced cell deathAttractive therapeutic targetNew molecular targetsHuman melanoma cellsStem cellsMelanoma stem cellsAldehyde dehydrogenase activityHuman melanoma stem cellsNSG miceCell cycle arrestImmunodeficiency mice
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 implicationsWntLungProinvasion Metastasis Drivers in Early-Stage Melanoma Are Oncogenes
Scott KL, Nogueira C, Heffernan TP, van Doorn R, Dhakal S, Hanna JA, Min C, Jaskelioff M, Xiao Y, Wu CJ, Cameron LA, Perry SR, Zeid R, Feinberg T, Kim M, Woude G, Granter SR, Bosenberg M, Chu GC, DePinho RA, Rimm DL, Chin L. Proinvasion Metastasis Drivers in Early-Stage Melanoma Are Oncogenes. Cancer Cell 2011, 20: 92-103. PMID: 21741599, PMCID: PMC3176328, DOI: 10.1016/j.ccr.2011.05.025.Peer-Reviewed Original ResearchMeSH KeywordsAcid PhosphataseAnimalsCell LineageConserved SequenceEvolution, MolecularGene Expression ProfilingGene Expression Regulation, NeoplasticGenomeHumansIsoenzymesKaplan-Meier EstimateMelanomaMiceNeoplasm InvasivenessNeoplasm MetastasisNeoplasm StagingOncogenesPhosphorylationReproducibility of ResultsSkin NeoplasmsTartrate-Resistant Acid PhosphataseTissue Array AnalysisConceptsFunctional genetic screensGenetic screenGlobal transcriptomeMetastatic potentialSuch genesGenomic evidenceExpression selectionTranscriptomic profilesHuman melanoma tissuesMetastasis driverCell invasionKey pathwaysOncogenic capabilitiesMelanoma tissuesGenesHuman melanomaHuman primary melanomasTranscriptomeMouse modelSpontaneous metastasisOncogeneEnhancerACP5PathwayInvasion
2010
Human melanoma-initiating cells express neural crest nerve growth factor receptor CD271
Boiko A, Razorenova O, van de Rijn M, Swetter S, Johnson D, Ly D, Butler P, Yang G, Joshua B, Kaplan M, Longaker M, Weissman I. Human melanoma-initiating cells express neural crest nerve growth factor receptor CD271. Nature 2010, 466: 133-137. PMID: 20596026, PMCID: PMC2898751, DOI: 10.1038/nature09161.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, NeoplasmBone and BonesBone TransplantationDNA-Binding ProteinsHumansLung NeoplasmsMelanomaMelanoma-Specific AntigensMiceMice, KnockoutNeoplasm MetastasisNeoplasm ProteinsNeoplasm TransplantationNeoplastic Stem CellsNerve Tissue ProteinsNeural CrestReceptors, Nerve Growth FactorSkinSkin TransplantationTransplantation, Heterologous
2008
Integrin Agonists as Adjuvants in Chemotherapy for Melanoma
Schwartz MA, McRoberts K, Coyner M, Andarawewa KL, Frierson HF, Sanders JM, Swenson S, Markland F, Conaway MR, Theodorescu D. Integrin Agonists as Adjuvants in Chemotherapy for Melanoma. Clinical Cancer Research 2008, 14: 6193-6197. PMID: 18829498, DOI: 10.1158/1078-0432.ccr-08-1285.Peer-Reviewed Original ResearchConceptsMelanoma linesExtracellular matrixMetastatic melanomaM21 tumorsTherapeutic responseImmunodeficient miceTumor volumeChemotherapyClonal growth assaysTherapy resistanceTumor growthHuman melanomaChemotherapeutic efficacyMelanomaTumor cellsDrug 1Survival assaysM21 cellsM21 melanomaSmall nestsIntegrin agonistsIntegrin-dependent adhesionTumorsMiceSnake venom
2005
Automated Quantitative Analysis of Activator Protein-2α Subcellular Expression in Melanoma Tissue Microarrays Correlates with Survival Prediction
Berger AJ, Davis DW, Tellez C, Prieto VG, Gershenwald JE, Johnson MM, Rimm DL, Bar-Eli M. Automated Quantitative Analysis of Activator Protein-2α Subcellular Expression in Melanoma Tissue Microarrays Correlates with Survival Prediction. Cancer Research 2005, 65: 11185-11192. PMID: 16322269, DOI: 10.1158/0008-5472.can-05-2300.Peer-Reviewed Original ResearchConceptsAP-2 expressionM.D. Anderson Cancer CenterCytoplasmic expression levelsAnderson Cancer CenterAP-2 levelsProgression of melanomaMelanoma tissue microarrayClinicopathologic factorsRetrospective cohortMetastatic groupPrognostic significanceBreslow depthCancer CenterNevi groupPoor prognosisMetastatic melanomaPrimary tumorPrimary melanomaDiagnosis groupsTissue microarrayTumor growthMelanoma specimensMalignant transformationHuman melanomaMelanoma progressionIntegrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma
Garraway LA, Widlund HR, Rubin MA, Getz G, Berger AJ, Ramaswamy S, Beroukhim R, Milner DA, Granter SR, Du J, Lee C, Wagner SN, Li C, Golub TR, Rimm DL, Meyerson ML, Fisher DE, Sellers WR. Integrative genomic analyses identify MITF as a lineage survival oncogene amplified in malignant melanoma. Nature 2005, 436: 117-122. PMID: 16001072, DOI: 10.1038/nature03664.Peer-Reviewed Original ResearchMeSH KeywordsCell Line, TumorCell LineageCell SurvivalChromosomes, Human, Pair 3Disease ProgressionDNA-Binding ProteinsGene AmplificationGene DosageGene Expression Regulation, NeoplasticGenomicsHumansIn Situ Hybridization, FluorescenceMelanomaMicrophthalmia-Associated Transcription FactorOncogenesPolymerase Chain ReactionPolymorphism, Single NucleotideTranscription FactorsConceptsMITF gene expressionDNA amplification eventsIntegrative genomic analysisLineage-survival oncogenePossible drug targetsGenomics effortsGenomic analysisGenetic dataGene expressionMelanoma formationAmplification eventsMelanoma genesDrug targetsCancer cell linesGenetic alterationsCell linesMITFMelanoma cellsHuman melanomaMalignant melanomaGenesMelanomaOncogeneExpressionCells
1993
KIT ligand (mast cell growth factor) inhibits the growth of KIT-expressing melanoma cells.
Zakut R, Perlis R, Eliyahu S, Yarden Y, Givol D, Lyman S, Halaban R. KIT ligand (mast cell growth factor) inhibits the growth of KIT-expressing melanoma cells. Oncogene 1993, 8: 2221-9. PMID: 7687762.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceCell DivisionHematopoietic Cell Growth FactorsHumansMelanomaMolecular Sequence DataNeoplasm ProteinsPhosphorylationProtein-Tyrosine KinasesProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-kitRNA, MessengerRNA, NeoplasmStem Cell FactorTumor Cells, CulturedConceptsMast cell growth factorMelanoma cell linesNormal melanocyte developmentMelanoma cellsAberrant signal transductionMetastatic melanoma cell linesCell linesActivation of KITMelanocyte developmentSignal transductionKIT proto-oncogeneKinase activationKIT mRNAKit ligandNormal melanocytesProto-oncogeneKIT kinaseCell growth factorBiological responsesGrowth factorHuman melanomaMelanocytesCellsKIT expressionNeoplastic melanocytesmet and HGF-SF in normal melanocytes and melanoma cells.
Halaban R, Rubin J, White W. met and HGF-SF in normal melanocytes and melanoma cells. 1993, 65: 329-39. PMID: 8380740.Peer-Reviewed Original ResearchConceptsHGF-SFFactor-dependent cellsMelanoma cellsNormal human melanocytesSignal transductionMouse melanocytesTumorigenic phenotypeHuman melanocytesHuman melanoma cellsNormal melanocytesAutocrine loopMelanocytesHuman melanomaMalignant conversionMelanin contentTyrosinase activityEctopic sitesCellsSynergistic factorExpressionBFGFERK2TransductionPhosphorylationProtein
1991
Induction of different morphologic features of malignant melanoma and pigmented lesions after transformation of murine melanocytes with bFGF-cDNA and H-ras, myc, neu, and E1a oncogenes.
Ramon y Cajal S, Suster S, Halaban R, Filvaroff E, Dotto G. Induction of different morphologic features of malignant melanoma and pigmented lesions after transformation of murine melanocytes with bFGF-cDNA and H-ras, myc, neu, and E1a oncogenes. American Journal Of Pathology 1991, 138: 349-58. PMID: 1992762, PMCID: PMC1886204.Peer-Reviewed Original ResearchConceptsMalignant tumorsMorphologic featuresDifferent morphologic featuresMalignant melanomaBenign lesionsNude miceSyngenic miceSame tumorMelanocytic lesionsSmall round cellsBasic fibroblast growth factorH-RasFibroblast growth factorBenign melanocytic lesionsHistologic typeHistologic featuresSubcutaneous injectionBiologic behaviorSpindle cellsPossible molecular mechanismsEpithelioid cellsIntradermal nevusHuman melanomaLesionsDifferent tumors
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