2023
Subsets of IFN Signaling Predict Response to Immune Checkpoint Blockade in Patients with Melanoma.
Horowitch B, Lee D, Ding M, Martinez-Morilla S, Aung T, Ouerghi F, Wang X, Wei W, Damsky W, Sznol M, Kluger H, Rimm D, Ishizuka J. Subsets of IFN Signaling Predict Response to Immune Checkpoint Blockade in Patients with Melanoma. Clinical Cancer Research 2023, 29: 2908-2918. PMID: 37233452, PMCID: PMC10524955, DOI: 10.1158/1078-0432.ccr-23-0215.Peer-Reviewed Original ResearchConceptsImmune checkpoint inhibitorsHuman melanoma cell linesMelanoma cell linesPD-L1Validation cohortYale-New Haven HospitalCombination of ipilimumabPD-L1 markersImmune checkpoint blockadePD-L1 biomarkerNew Haven HospitalSTAT1 levelsCell linesWestern blot analysisCheckpoint inhibitorsCheckpoint blockadeClinical responseOverall survivalImproved survivalResistance of cancersMetastatic melanomaMelanoma responsePredict responseTreatment responseDistinct patterns
2022
Isotope tracing reveals distinct substrate preference in murine melanoma subtypes with differing anti-tumor immunity
Zhang X, Halberstam A, Zhu W, Leitner B, Thakral D, Bosenberg M, Perry R. Isotope tracing reveals distinct substrate preference in murine melanoma subtypes with differing anti-tumor immunity. Cancer & Metabolism 2022, 10: 21. PMID: 36457136, PMCID: PMC9714036, DOI: 10.1186/s40170-022-00296-7.Peer-Reviewed Original ResearchTumor microenvironmentAnti-tumor immunityPotential prognostic factorsObesity-associated cancersPotential prognostic predictorPatient RNA-seq dataSubset of studiesImmunogenic tumorsCancer Genome AtlasLymphocyte infiltrationMelanoma cell linesPrognostic factorsPrognostic predictorMetabolic therapyMelanoma subtypesMurine modelImmune functionMetabolic gene expressionMelanoma progressionMelanomaSubstrate metabolismMetabolic flux studiesGene expressionGenome AtlasCell linesIntegrative molecular and clinical profiling of acral melanoma links focal amplification of 22q11.21 to metastasis
Farshidfar F, Rhrissorrakrai K, Levovitz C, Peng C, Knight J, Bacchiocchi A, Su J, Yin M, Sznol M, Ariyan S, Clune J, Olino K, Parida L, Nikolaus J, Zhang M, Zhao S, Wang Y, Huang G, Wan M, Li X, Cao J, Yan Q, Chen X, Newman AM, Halaban R. Integrative molecular and clinical profiling of acral melanoma links focal amplification of 22q11.21 to metastasis. Nature Communications 2022, 13: 898. PMID: 35197475, PMCID: PMC8866401, DOI: 10.1038/s41467-022-28566-4.Peer-Reviewed Original ResearchConceptsAcral melanomaMelanoma subtypesClinical profilingCommon melanoma subtypeImmune checkpoint blockadeCheckpoint blockadeInferior survivalMelanoma cell linesKey molecular driversPoor prognosisTherapeutic targetAnchorage-independent growthImmunomodulatory genesNon-white individualsHotspot mutationsMolecular driversCandidate oncogeneMelanomaApoptotic cell deathLZTR1Focal amplificationTumor promoterCell linesMetastasisTumor suppressor
2021
NEDD4 regulates ubiquitination and stability of the cell adhesion molecule IGPR-1 via lysosomal pathway
Sun L, Amraei R, Rahimi N. NEDD4 regulates ubiquitination and stability of the cell adhesion molecule IGPR-1 via lysosomal pathway. Journal Of Biomedical Science 2021, 28: 35. PMID: 33962630, PMCID: PMC8103646, DOI: 10.1186/s12929-021-00731-9.Peer-Reviewed Original ResearchConceptsCell adhesion molecule IGPR-1IGPR-1Lysosomal-dependent degradationUbiquitin E3Vivo co-immunoprecipitation assaysWild-type Nedd4Knockdown of NEDD4Polyproline-rich motifCritical cellular processesCell-cell adhesionCo-immunoprecipitation assaysTreatment of cellsCell surface levelsHEK-293 cellsA375 melanoma cellsWW domainsCellular processesRich motifLysosomal pathwayC-terminusNedd4Key regulatorLysosomal inhibitorsMolecular mechanismsMelanoma cell lines
2019
A novel anti-melanoma SRC-family kinase inhibitor
Halaban R, Bacchiocchi A, Straub R, Cao J, Sznol M, Narayan D, Allam A, Krauthammer M, Mansour TS. A novel anti-melanoma SRC-family kinase inhibitor. Oncotarget 2019, 10: 2237-2251. PMID: 31040916, PMCID: PMC6481345, DOI: 10.18632/oncotarget.26787.Peer-Reviewed Original ResearchSrc family kinase inhibitorMAPK inhibitorTranscription factor MITFPatient-derived melanoma cellsPI3K activityKinase inhibitorsSynergistic growth inhibitionGrowth arrestMelanoma cell linesK activityProteolytic degradationCell linesERBB2 inhibitionOncogene expressionMelanoma therapyTumor growthDrug resistanceMelanoma cellsGrowth inhibitionAlternative targetsActivity leadInhibitorsPP2ASHP2Inhibition
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 analysis
2017
UV‐induced somatic mutations elicit a functional T cell response in the YUMMER1.7 mouse melanoma model
Wang J, Perry CJ, Meeth K, Thakral D, Damsky W, Micevic G, Kaech S, Blenman K, Bosenberg M. UV‐induced somatic mutations elicit a functional T cell response in the YUMMER1.7 mouse melanoma model. Pigment Cell & Melanoma Research 2017, 30: 428-435. PMID: 28379630, PMCID: PMC5820096, DOI: 10.1111/pcmr.12591.Peer-Reviewed Original ResearchConceptsHigh somatic mutation burdenSomatic mutation burdenT cellsMutation burdenAnti-PD-1 therapyFunctional T cell responsesImmune checkpoint inhibitionAntitumor immune responseCD8 T cellsT cell responsesMouse melanoma modelCell numberSomatic mutationsMouse melanoma cell lineMelanoma cell linesTumor challengeAntitumor responseCheckpoint inhibitionImmune responseMelanoma modelHigh dosesImmune systemCell responsesMelanomas exhibitTumorsp90RSK Blockade Inhibits Dual BRAF and MEK Inhibitor-Resistant Melanoma by Targeting Protein Synthesis
Theodosakis N, Micevic G, Langdon CG, Ventura A, Means R, Stern DF, Bosenberg MW. p90RSK Blockade Inhibits Dual BRAF and MEK Inhibitor-Resistant Melanoma by Targeting Protein Synthesis. Journal Of Investigative Dermatology 2017, 137: 2187-2196. PMID: 28599981, PMCID: PMC6342201, DOI: 10.1016/j.jid.2016.12.033.Peer-Reviewed Original ResearchConceptsProtein synthesisRibosomal S6 kinase (RSK) familyPatient-derived melanoma cell linesDifferential protein expressionReverse phase protein arrayPhase protein arrayTranslation complexesKinase familyBI-D1870RSK inhibitorsMelanoma cell linesProtein arraysCell proliferationInhibitor treatmentProtein expressionCell linesNew targetsHuman melanoma patientsBRAF inhibitor vemurafenibAttenuation 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
2016
The YUMM lines: a series of congenic mouse melanoma cell lines with defined genetic alterations
Meeth K, Wang JX, Micevic G, Damsky W, Bosenberg MW. The YUMM lines: a series of congenic mouse melanoma cell lines with defined genetic alterations. Pigment Cell & Melanoma Research 2016, 29: 590-597. PMID: 27287723, PMCID: PMC5331933, DOI: 10.1111/pcmr.12498.Peer-Reviewed Original ResearchConceptsMouse melanoma cell lineMelanoma cell linesCell linesMouse cancer cell linesVariety of cancersCancer cell linesMouse melanoma linesImmune therapyTumor immunologyCancer immunologyHost miceMouse modelCancer modelMelanoma linesDriver mutationsGenetic alterationsCancer biologyImmunologyTherapyCancerMiceA 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 cytometryPatientsDownregulating FUK to Get Unstuck: Altered Fucosylation in Melanoma Promotes Tumor Development and Metastasis
Lau E, Feng Y, Claps G, Fukuda M, Perlina A, Donn D, Jilaveanu L, Kluger H, Freeze H, Ronai Z. Downregulating FUK to Get Unstuck: Altered Fucosylation in Melanoma Promotes Tumor Development and Metastasis. The FASEB Journal 2016, 30 DOI: 10.1096/fasebj.30.1_supplement.620.2.Peer-Reviewed Original ResearchActivating Transcription Factor 2Fucose salvage pathwayUpstream regulatory kinaseProtein kinase C epsilonTumor microarray analysisGDP-L-fucoseHuman melanoma specimensTranscription factor 2Cellular fucosylationRegulatory kinasesPrimary melanocytesGenetic manipulationMicroarray analysisMelanoma cell linesC epsilonSalvage pathwayPromotes tumor developmentCellular adhesionMelanoma developmentFactor 2Cell linesMelanoma specimensCell populationsTumor developmentFucosylation
2015
The broad‐spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF‐mutant melanoma cells in combination with other signaling pathway inhibitors
Langdon CG, Held MA, Platt JT, Meeth K, Iyidogan P, Mamillapalli R, Koo AB, Klein M, Liu Z, Bosenberg MW, Stern DF. The broad‐spectrum receptor tyrosine kinase inhibitor dovitinib suppresses growth of BRAF‐mutant melanoma cells in combination with other signaling pathway inhibitors. Pigment Cell & Melanoma Research 2015, 28: 417-430. PMID: 25854919, PMCID: PMC5215495, DOI: 10.1111/pcmr.12376.Peer-Reviewed Original ResearchConceptsBRAF-mutant melanomaBRAF inhibitorsCell linesCombination of dovitinibBRAF inhibitor treatmentBRAF mutant melanoma cellsBRAF inhibitor resistanceColorectal carcinoma cell linesBRAF-mutant melanoma cell linesMelanoma cell linesCarcinoma cell linesMetastatic melanomaEffective therapyWild-type BRAF cellsInhibitor treatmentAgent inhibitsPathway inhibitorDovitinibInhibitor resistanceMelanoma cellsMelanomaSecond agentInhibitorsTreatmentAbstract PR04: A melanoma transcriptional state distinction influences sensitivity to MAPK pathway inhibitors
Johannessen C, Konieczkowski D, Abudayyeh O, Kim J, Cooper Z, Piris A, Frederick D, Barzily-Rokni M, Straussman R, Haq R, Fisher D, Mesirov J, Hahn W, Flaherty K, Wargo J, Tamayo P, Garraway L. Abstract PR04: A melanoma transcriptional state distinction influences sensitivity to MAPK pathway inhibitors. Clinical Cancer Research 2015, 21: pr04-pr04. DOI: 10.1158/1557-3265.pms14-pr04.Peer-Reviewed Original ResearchBRAFV600-mutant melanomaMAPK pathway inhibitorsPathway inhibitorCell linesMelanocyte lineage transcription factor MITFPanel of melanoma cell linesResistance to MAPK pathway inhibitorsMAPK pathway inhibitionReceptor tyrosine kinase AXLDrug-resistant cell linesImprove cancer therapyTyrosine kinase AXLMelanoma cell linesSensitive cell linesNF-kB activationNF-kB signalingRAF/MEK inhibitionMelanoma patientsClinical responseTranscription factor MITFMalignant melanomaDrug susceptibilityAcquired resistancePatient biopsiesMEK inhibitors
2013
Gene Expression Profiling using Nanostring Digital RNA Counting to Identify Potential Target Antigens for Melanoma Immunotherapy
Beard R, Abate-Daga D, Rosati S, Zheng Z, Wunderlich J, Rosenberg S, Morgan R. Gene Expression Profiling using Nanostring Digital RNA Counting to Identify Potential Target Antigens for Melanoma Immunotherapy. Clinical Cancer Research 2013, 19: 4941-4950. PMID: 24021875, PMCID: PMC3778100, DOI: 10.1158/1078-0432.ccr-13-1253.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntigens, NeoplasmBiomarkers, TumorFemaleFlow CytometryGene Expression ProfilingHumansImmunoenzyme TechniquesImmunotherapyMaleMelanomaMiddle AgedNanotechnologyReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSkinTumor Cells, CulturedYoung AdultConceptsTumor samplesTarget antigenNormal tissuesTreatment of metastatic cancerPotential tumor antigensStudied tumor samplesMetastatic melanoma tumorsSuccess of immunotherapyPercentage of tumorsPotential target antigensTreatment of melanomaCell linesTissue samplesMelanoma cell linesMelanoma tumor samplesTissue gene expressionAnalysis of cell linesAdoptive immunotherapyMelanoma immunotherapyTumor antigensPotential immunotherapyMelanoma tumorsMetastatic cancerImmunotherapyDifferent malignanciesDistinct host cell fates for human malignant melanoma targeted by oncolytic rodent parvoviruses
Vollmers EM, Tattersall P. Distinct host cell fates for human malignant melanoma targeted by oncolytic rodent parvoviruses. Virology 2013, 446: 37-48. PMID: 24074565, PMCID: PMC3811133, DOI: 10.1016/j.virol.2013.07.013.Peer-Reviewed Original ResearchConceptsPrimary human melanoma cellsPatient-derived melanoma cell linesCurrent therapeutic regimensHuman malignant melanomaRodent parvovirusesHuman melanoma cellsLow response rateMelanoma cell linesOncolytic parvovirusTherapeutic regimensMetastatic melanomaMalignant melanomaResponse rateVirion uptakeViral protein synthesisHost cell fateChimeric virusesMelanoma cellsComplete lysisCell linesMelanomaViral transcriptionParvovirusProgeny virionsLow multiplicityPhase I trial of bortezomib and dacarbazine in melanoma and soft tissue sarcoma
Poklepovic A, Youseffian L, Winning M, Birdsell CA, Crosby NA, Ramakrishnan V, Ernstoff MS, Roberts JD. Phase I trial of bortezomib and dacarbazine in melanoma and soft tissue sarcoma. Investigational New Drugs 2013, 31: 937-942. PMID: 23315028, PMCID: PMC3844155, DOI: 10.1007/s10637-012-9913-8.Peer-Reviewed Original ResearchConceptsSoft tissue sarcomasPhase I trialTissue sarcomasPartial responseI trialPhase II dosesDurable complete responseAmine precursor uptakeTwenty-eight patientsProteasome inhibitor bortezomibHuman melanoma cell linesMurine xenograft tumor modelXenograft tumor modelCKIT mutationsDecarboxylation (APUD) tumorsProphylactic antiemeticsRECIST v1.0Eight patientsComplete responseMelanoma cell linesWeekly dosesDose escalationAgent dacarbazinePreclinical studiesDose levels
2012
Elucidating distinct tumorigenic pathways in nodular versus superficial spreading melanoma.
Farhadian J, O'Reilly K, Vega-Saenz de Miera E, Ye F, Zavadil J, Taunton J, Zhang D, Osman I. Elucidating distinct tumorigenic pathways in nodular versus superficial spreading melanoma. Journal Of Clinical Oncology 2012, 30: 8544-8544. DOI: 10.1200/jco.2012.30.15_suppl.8544.Peer-Reviewed Original ResearchRibosomal S6 kinaseMetastatic melanoma cell linesMelanoma cell linesTumorigenic pathwaysCell linesRadial growth phaseP90 ribosomal S6 kinaseDifferential protein expressionPrimary melanoma cell linesSmall molecule inhibitionSmall molecule inhibitorsVGP melanomasRGP melanomasWestern blotS6 kinaseConstitutive phosphorylationOverexpressed proteinsProtein Pathway ArrayMolecule inhibitionSerum starvationMolecule inhibitorsFunctional studiesPathway arrayDistinct tumorigenic pathwaysTumorigenic proteinsPreexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors
Shi H, Moriceau G, Kong X, Koya RC, Nazarian R, Pupo GM, Bacchiocchi A, Dahlman KB, Chmielowski B, Sosman JA, Halaban R, Kefford RF, Long GV, Ribas A, Lo RS. Preexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors. Cancer Discovery 2012, 2: 414-424. PMID: 22588879, PMCID: PMC3594852, DOI: 10.1158/2159-8290.cd-12-0022.Peer-Reviewed Original ResearchConceptsBRAF inhibitorsActivating mutationsObjective tumor responseMEK1/2 inhibitorMEK1 mutationsP-ERK1/2 levelsBRAF-mutant melanomaMelanoma cell linesAdvanced melanomaAntitumor responseExon 3 mutationsTumor responseDisease progressionMelanomaBRAFi resistanceDrug sensitivitySignificant alterationsPatientsCell linesInhibitorsBaselineMutationsExon 3Widespread use
2011
MicroRNA signatures differentiate melanoma subtypes
Chan E, Patel R, Nallur S, Ratner E, Bacchiocchi A, Hoyt K, Szpakowski S, Godshalk S, Ariyan S, Sznol M, Halaban R, Krauthammer M, Tuck D, Slack FJ, Weidhaas JB. MicroRNA signatures differentiate melanoma subtypes. Cell Cycle 2011, 10: 1845-1852. PMID: 21543894, PMCID: PMC3233487, DOI: 10.4161/cc.10.11.15777.Peer-Reviewed Original Research
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