2024
Combined BET and MEK Inhibition synergistically suppresses melanoma by targeting YAP1
Hu R, Hou H, Li Y, Zhang M, Li X, Chen Y, Guo Y, Sun H, Zhao S, Liao M, Cao D, Yan Q, Chen X, Yin M. Combined BET and MEK Inhibition synergistically suppresses melanoma by targeting YAP1. Theranostics 2024, 14: 593-607. PMID: 38169595, PMCID: PMC10758063, DOI: 10.7150/thno.85437.Peer-Reviewed Original ResearchConceptsMEK inhibitor resistanceMEK inhibitor trametinibTrametinib treatmentInhibitor resistanceInhibitor trametinibMelanoma patientsYAP1 expressionMEK inhibitionBRAF-mutant melanoma patientsResistance to MEK inhibitionYAP1 inhibitionResistance to trametinibMelanoma growth <i>inInhibition of BRD4Trametinib resistanceAntitumor effectMelanoma growthTrametinibNHWD-870YAP1 inhibitorDrug resistanceMelanomaMelanoma samplesMelanoma cellsBRD4 depletion
2023
PTEN phosphatase inhibits metastasis by negatively regulating the Entpd5/IGF1R pathway through ATF6
Yu Y, Dai M, Huang L, Chen W, Yu E, Mendoza A, Michael H, Khanna C, Bosenberg M, McMahon M, Merlino G. PTEN phosphatase inhibits metastasis by negatively regulating the Entpd5/IGF1R pathway through ATF6. IScience 2023, 26: 106070. PMID: 36824269, PMCID: PMC9942123, DOI: 10.1016/j.isci.2023.106070.Peer-Reviewed Original ResearchProtein phosphatase activityPhosphatase activityPTEN protein phosphatase activityER stress sensor ATF6ER stressPTEN phosphatase activityPTEN expressionMelanoma cell invasivenessNovel candidate therapeutic targetInhibits metastasisIGF1R pathwayIGF1R levelsHuman melanoma samplesTumor suppressorCandidate therapeutic targetCell invasivenessATF6Melanoma samplesMetastatic progressionTherapeutic targetExpressionDose-dependent mannerPathwayMouse melanoma modelMutant melanoma
2021
Reprogramming of bivalent chromatin states in NRAS mutant melanoma suggests PRC2 inhibition as a therapeutic strategy
Terranova C, Tang M, Maitituoheti M, Raman A, Ghosh A, Schulz J, Amin S, Orouji E, Tomczak K, Sarkar S, Oba J, Creasy C, Wu C, Khan S, Lazcano R, Wani K, Singh A, Barrodia P, Zhao D, Chen K, Haydu L, Wang W, Lazar A, Woodman S, Bernatchez C, Rai K. Reprogramming of bivalent chromatin states in NRAS mutant melanoma suggests PRC2 inhibition as a therapeutic strategy. Cell Reports 2021, 36: 109410. PMID: 34289358, PMCID: PMC8369408, DOI: 10.1016/j.celrep.2021.109410.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorCell ProliferationChromatinEnhancer of Zeste Homolog 2 ProteinFemaleGTP PhosphohydrolasesHistonesHumansMelanocytesMelanomaMembrane ProteinsMesodermMice, NudeMitogen-Activated Protein Kinase KinasesMutationNeoplasm MetastasisPolycomb Repressive Complex 2Transcription, GeneticTumor BurdenConceptsHistone H3 lysine 27 trimethylationH3 lysine 27 trimethylationBivalent chromatin stateCell identity genesLysine 27 trimethylationKey epigenetic alterationsNRAS mutantsMaster transcription factorBivalent domainsChromatin statePRC2 inhibitionEpigenetic elementsTranscription factorsEpigenetic alterationsGenetic driversMesenchymal phenotypeNRAS-mutant melanomaState profilingTherapeutic vulnerabilitiesInvasive capacityPharmacological inhibitionMutantsTherapeutic strategiesMelanoma samplesMutant melanoma patients
2019
Potential MMP2-mediated availability of HLA binding, mutant ECM peptides reflects better melanoma survival rates and greater T-cell infiltrates
Zaman S, Chobrutskiy BI, Patel JS, Callahan BM, Mihyu MM, Diviney A, Blanck G. Potential MMP2-mediated availability of HLA binding, mutant ECM peptides reflects better melanoma survival rates and greater T-cell infiltrates. Laboratory Investigation 2019, 99: 1287-1295. PMID: 31019293, DOI: 10.1038/s41374-019-0248-3.Peer-Reviewed Original ResearchConceptsMutant amino acidsAmino acidsStructural proteinsExtracellular matrix structural proteinsMatrix metalloproteinase-2Cancer progressionLate-stage cancer developmentMutant peptidesECM structural proteinsMatrix structural proteinsBioinformatics approachProtein mutantsProtease functionECM peptidesSuch proteasesMutantsPotential substratesCancer developmentProteaseMelanoma samplesProteinSpread of cancerTumor samplesMetalloproteinase-2Cancer microenvironment
2015
Phosphorylation of eIF2α triggered by mTORC1 inhibition and PP6C activation is required for autophagy and is aberrant in PP6C-mutated melanoma
Wengrod J, Wang D, Weiss S, Zhong H, Osman I, Gardner LB. Phosphorylation of eIF2α triggered by mTORC1 inhibition and PP6C activation is required for autophagy and is aberrant in PP6C-mutated melanoma. Science Signaling 2015, 8: ra27. PMID: 25759478, PMCID: PMC4580977, DOI: 10.1126/scisignal.aaa0899.Peer-Reviewed Original ResearchMeSH KeywordsAmino AcidsAutophagyCell Line, TumorClustered Regularly Interspaced Short Palindromic RepeatsEnzyme ActivationEukaryotic Initiation Factor-2Gene Knock-In TechniquesHumansImmunoblottingImmunohistochemistryImmunoprecipitationMass SpectrometryMechanistic Target of Rapamycin Complex 1MelanomaMicroscopy, FluorescenceMultiprotein ComplexesMutationPhosphoprotein PhosphatasesPhosphorylationProtein Serine-Threonine KinasesSirolimusTOR Serine-Threonine KinasesTunicamycinConceptsKinase complex mTORC1Amino acid-sensing systemsProtein phosphatase 6Activation of GCN2Amino acid deprivationEukaryotic initiation factorPharmacological inhibitionWild-type alleleKinase GCN2Human melanoma samplesGCN2 activationRegulatory subunitCatalytic subunitInitiation factorsPathways downstreamPP6cGCN2MTORC1PhosphorylationAutophagyMutantsMelanoma samplesSubunitsMutationsActivation
2014
Rare SF3B1 R625 mutations in cutaneous melanoma
Kong Y, Krauthammer M, Halaban R. Rare SF3B1 R625 mutations in cutaneous melanoma. Melanoma Research 2014, 24: 332-334. PMID: 24709888, PMCID: PMC4101881, DOI: 10.1097/cmr.0000000000000071.Peer-Reviewed Original Research
2013
Vesicular 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
2011
Detecting copy number status and uncovering subclonal markers in heterogeneous tumor biopsies
Parisi F, Ariyan S, Narayan D, Bacchiocchi A, Hoyt K, Cheng E, Xu F, Li P, Halaban R, Kluger Y. Detecting copy number status and uncovering subclonal markers in heterogeneous tumor biopsies. BMC Genomics 2011, 12: 230. PMID: 21569352, PMCID: PMC3114747, DOI: 10.1186/1471-2164-12-230.Peer-Reviewed Original ResearchConceptsCopy number statusMelanoma samplesSingle nucleotide polymorphism arrayHigh-throughput technologiesNext-generation sequencing dataHigh-throughput techniquesCopy number profilesHigh-throughput assaysNucleotide polymorphism arrayNumber statusCopy number alterationsTranscriptome sequencingNext-generation sequencingRNA-seqSingle exonSNP arraySequencing dataMelanoma cell linesNumerous aberrationsPolymorphism arrayNovel aberrationsNumber alterationsSubclonal heterogeneitySitu hybridizationAllelic imbalance
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply