2016
Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells
Forloni M, Gupta R, Nagarajan A, Sun LS, Dong Y, Pirazzoli V, Toki M, Wurtz A, Melnick MA, Kobayashi S, Homer RJ, Rimm DL, Gettinger SJ, Politi K, Dogra SK, Wajapeyee N. Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells. Cell Reports 2016, 16: 457-471. PMID: 27346347, PMCID: PMC4945411, DOI: 10.1016/j.celrep.2016.05.087.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdenocarcinoma of LungAntineoplastic AgentsBrain NeoplasmsCCAAT-Enhancer-Binding ProteinsCell Line, TumorCpG IslandsDNA MethylationDrug Screening Assays, AntitumorErbB ReceptorsGene Expression Regulation, NeoplasticGene SilencingGlioblastomaHumansLung NeoplasmsMAP Kinase Signaling SystemMixed Function OxygenasesMutationOncogenesProtein Kinase InhibitorsProto-Oncogene ProteinsTranscription, GeneticTumor Suppressor ProteinsUp-RegulationConceptsOncogenic epidermal growth factor receptorMethylation-mediated transcriptional silencingEpidermal growth factor receptorTumor suppressorTranscriptional silencingActive DNA demethylationCancer cellsFamily member 1TET1 knockdownDNA demethylaseDNA demethylationTranscription factorsGrowth factor receptorEctopic expressionCytoplasmic localizationGlioblastoma tumor growthLung cancer cellsTET1 expressionFunctional roleSuppressorFactor receptorMember 1TET1SilencingLung cancer samplesEarly and multiple origins of metastatic lineages within primary tumors
Zhao ZM, Zhao B, Bai Y, Iamarino A, Gaffney SG, Schlessinger J, Lifton RP, Rimm DL, Townsend JP. Early and multiple origins of metastatic lineages within primary tumors. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: 2140-2145. PMID: 26858460, PMCID: PMC4776530, DOI: 10.1073/pnas.1525677113.Peer-Reviewed Original ResearchConceptsMetastatic lineagesGenetic changesEarly genetic divergenceMolecular evolutionary modelsSingle genetic changeDivergent lineagesTumor phylogeneticsDivergence timesAncestral stateGenetic divergenceCancer lineagesPhylogenetic analysisEvolutionary processesLineagesCancer evolutionMultiple originsDriver genesCancer biologyCancer progressionSomatic mutationsTumor developmentEvolutionary modelsDriver mutationsChronogramMutations
2011
Proinvasion 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
2005
Integrative 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"Lineage Addiction" in Human Cancer: Lessons from Integrated Genomics
GARRAWAY L, WEIR B, ZHAO X, WIDLUND H, BEROUKHIM R, BERGER A, RIMM D, RUBIN M, FISHER D, MEYERSON M, SELLERS W. "Lineage Addiction" in Human Cancer: Lessons from Integrated Genomics. Cold Spring Harbor Symposia On Quantitative Biology 2005, 70: 25-34. PMID: 16869735, DOI: 10.1101/sqb.2005.70.016.Peer-Reviewed Original ResearchMeSH KeywordsChromosomes, Human, Pair 3Cluster AnalysisDNA, NeoplasmGene AmplificationGene DosageGene Expression ProfilingGenomicsHumansIn Situ Hybridization, FluorescenceMelanomaMicrophthalmia-Associated Transcription FactorNeoplasmsOligonucleotide Array Sequence AnalysisOncogenesPolymorphism, Single NucleotideConceptsLineage addictionGenome-scale data setsHigh-density single nucleotide polymorphism arraysNovel cancer genesSingle nucleotide polymorphism arrayDNA microarray platformCell line collectionCell linesAdditional functional studiesTumor survival mechanismsSNP array dataDetailed genomic characterizationGene expression dataDistinct tissue typesIntegrated GenomicCopy number alterationsTissue of originGenome characterizationSurvival mechanismCancer genesGenomic characterizationMelanoma cell linesSurvival pathwaysExpression dataProgression of tumors