2023
KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic
Zhang S, Cao J, Yan Q. KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic. Advances In Experimental Medicine And Biology 2023, 1433: 113-137. PMID: 37751138, DOI: 10.1007/978-3-031-38176-8_6.ChaptersConceptsPlant homeodomainFamily proteinsKey epigenetic markCell fate determinationHistone methylation marksCancer type-dependent mannerKetoglutarate-dependent dioxygenasesSelective KDM5 inhibitorsTumor suppressive functionType-dependent mannerEpigenetic marksTumor suppressive roleFate determinationJumonji CLysine 4Active chromatinMethylation marksHistone H3Lysine demethylasesCatalytic coreKDM5 inhibitorsDrug targetsKDM5Cancer metastasisSuppressive role
2020
KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer
Alam H, Tang M, Maitituoheti M, Dhar S, Kumar M, Han C, Ambati C, Amin S, Gu B, Chen T, Lin Y, Chen J, Muller F, Putluri N, Flores E, DeMayo F, Baseler L, Rai K, Lee M. KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer. Cancer Cell 2020, 37: 599-617.e7. PMID: 32243837, PMCID: PMC7178078, DOI: 10.1016/j.ccell.2020.03.005.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma of LungAnimalsAntimetabolitesApoptosisBiomarkers, TumorCell ProliferationDeoxyglucoseDNA-Binding ProteinsEnhancer Elements, GeneticGene Expression Regulation, NeoplasticGlycolysisHistone-Lysine N-MethyltransferaseHistonesHumansLung NeoplasmsMiceMice, KnockoutMice, NudeMutationMyeloid-Lymphoid Leukemia ProteinNeoplasm ProteinsPeriod Circadian ProteinsPrognosisTumor Cells, CulturedXenograft Model Antitumor AssaysConceptsLung cancerLung-specific lossHuman lung cancer cellsExpression of Per2Lung cancer cellsHistone methyltransferase KMT2DLung tumor suppressorTumor suppressive roleMultiple glycolytic genesLung tumorigenesisEpigenetic modifiersPharmacological inhibitionTherapeutic vulnerabilitiesGlycolytic inhibitorCancerCancer cellsKMT2DFunction mutationsTumor suppressorPer2GlycolysisGlycolytic genesMutationsMice
2017
Clinicopathological analysis of ATRX, DAXX and NOTCH receptor expression in angiosarcomas
Panse G, Chrisinger JS, Leung CH, Ingram DR, Khan S, Wani K, Lin H, Lazar AJ, Wang W. Clinicopathological analysis of ATRX, DAXX and NOTCH receptor expression in angiosarcomas. Histopathology 2017, 72: 239-247. PMID: 28796347, DOI: 10.1111/his.13337.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAdolescentAdultAgedAged, 80 and overBiomarkers, TumorCo-Repressor ProteinsDisease-Free SurvivalFemaleHemangiosarcomaHumansKaplan-Meier EstimateMaleMiddle AgedMolecular ChaperonesNuclear ProteinsPrognosisReceptors, NotchX-linked Nuclear ProteinYoung AdultConceptsNotch2 expressionWorse disease-specific survivalWorse event-free survivalDisease-specific survivalEvent-free survivalMalignant vascular tumorsPoor clinical outcomeATRX lossCase of angiosarcomaDeep soft tissuesPathogenesis of angiosarcomaTumor suppressive roleProtein 6 expressionNotch receptor expressionMental retardation syndrome XMultiple genetic alterationsSite of originInhibition of NotchAdvanced diseaseCutaneous sitesClinical outcomesPrognostic significanceClinicopathological analysisSyndrome XVascular tumors
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