2020
Enhancer hijacking determines extrachromosomal circular MYCN amplicon architecture in neuroblastoma
Helmsauer K, Valieva M, Ali S, Chamorro González R, Schöpflin R, Röefzaad C, Bei Y, Dorado Garcia H, Rodriguez-Fos E, Puiggròs M, Kasack K, Haase K, Keskeny C, Chen C, Kuschel L, Euskirchen P, Heinrich V, Robson M, Rosswog C, Toedling J, Szymansky A, Hertwig F, Fischer M, Torrents D, Eggert A, Schulte J, Mundlos S, Henssen A, Koche R. Enhancer hijacking determines extrachromosomal circular MYCN amplicon architecture in neuroblastoma. Nature Communications 2020, 11: 5823. PMID: 33199677, PMCID: PMC7669906, DOI: 10.1038/s41467-020-19452-y.Peer-Reviewed Original ResearchConceptsExtrachromosomal circular DNACore regulatory circuitEnhancer hijackingAmplicon structureDistal chromosomal fragmentsGene regulatory elementsMYCN amplificationChIP-seqShort readsHi-C.ATAC-seqChromatin landscapeNanopore sequencingRegulatory elementsRegulatory circuitsChromosome fragmentsMYCN ampliconGene copiesProximal enhancerCo-amplifiedCircular DNAAmpliconsMYCN overexpressionFunctional relevanceMYCN
2019
Extrachromosomal circular DNA drives oncogenic genome remodeling in neuroblastoma
Koche R, Rodriguez-Fos E, Helmsauer K, Burkert M, MacArthur I, Maag J, Chamorro R, Munoz-Perez N, Puiggròs M, Dorado Garcia H, Bei Y, Röefzaad C, Bardinet V, Szymansky A, Winkler A, Thole T, Timme N, Kasack K, Fuchs S, Klironomos F, Thiessen N, Blanc E, Schmelz K, Künkele A, Hundsdörfer P, Rosswog C, Theissen J, Beule D, Deubzer H, Sauer S, Toedling J, Fischer M, Hertwig F, Schwarz R, Eggert A, Torrents D, Schulte J, Henssen A. Extrachromosomal circular DNA drives oncogenic genome remodeling in neuroblastoma. Nature Genetics 2019, 52: 29-34. PMID: 31844324, PMCID: PMC7008131, DOI: 10.1038/s41588-019-0547-z.Peer-Reviewed Original ResearchProhibitin promotes de-differentiation and is a potential therapeutic target in neuroblastoma
MacArthur I, Bei Y, Garcia H, Ortiz M, Toedling J, Klironomos F, Rolff J, Eggert A, Schulte J, Kentsis A, Henssen A. Prohibitin promotes de-differentiation and is a potential therapeutic target in neuroblastoma. JCI Insight 2019, 5 PMID: 30998507, PMCID: PMC6542629, DOI: 10.1172/jci.insight.127130.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell Cycle CheckpointsCell DedifferentiationCell DifferentiationCell Line, TumorCell ProliferationChild, PreschoolChromosomes, Human, Pair 17HumansMAP Kinase Signaling SystemMiceNeuroblastomaProhibitinsProtein Kinase InhibitorsPyridonesPyrimidinonesRepressor ProteinsRNA-SeqRNA, MessengerSequence Analysis, RNAWhole Genome SequencingXenograft Model Antitumor AssaysConceptsLong arm of chromosome 17Neuroblastoma cellsSlow cell cycle progressionExpression of prohibitinImpaired ERK1/2 activationGene expression programsWhole genomeHigh-risk neuroblastomaChromosome 17Long armDe-differentiationPromote tumor cell proliferationTumor cell proliferationRNA sequencingAssociated with suppressionEctopic expressionProhibitinProliferation of neuroblastoma cellsCytogenetic hallmarkProhibitin expressionExpression programsAssociated with lossNeuronal developmentERK1/2 activationNeuroblastoma outcome
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