grant
Developing New Treatment Strategies for Neuroendocrine Prostate Cancer
Organization UNIVERSITY OF MICHIGAN AT ANN ARBORLocation ANN ARBOR, UNITED STATESPosted 1 Apr 2024Deadline 31 Mar 2029
NIHUS FederalResearch GrantFY20265 AZC5-AC5-Aza-cytidine5-AzacytidineAZCAndrogen ReceptorAnti-OncogenesAntioncogene Protein p53AntioncogenesAutoregulationAzacitidineAzacytidineBET bromodomain inhibitorBET inhibitorBETiBS-seqBasal Transcription FactorBasal transcription factor genesBindingBisulfite-based sequencingBromodomain and Extra-Terminal motif inhibitorBromodomains and extra-terminal domain inhibitorCRISPR interferenceCRISPR-dCas9-mediated repressionCRISPR/dCas9 interferenceCRISPR/dCas9-mediated transcriptional inhibitionCRISPRiCancer Suppressor GenesCancersCell BodyCell SurvivalCell ViabilityCellsCellular Tumor Antigen P53ChIP SequencingChIP-seqChIPseqChromatinClinicClinicalClinical TrialsClustered Regularly Interspaced Short Palindromic Repeats interferenceCombined Modality TherapyComplexDNADNA MethylationDNA MethyltransferaseDNA Methyltransferase 3BDNA Methyltransferase InhibitorDNA Modification MethylasesDNA Modification MethyltransferasesDNA methyltransferase inhibitionDNA-MethyltransferasesDNMT3B geneDNMT3aDNMT3bDeoxyribonucleic AcidDevelopmentDifferentiated GeneDiseaseDisorderDnmtDrugsE2F Transcription Factor 1E2F transcription factor 1 proteinE2F transcription factorsE2F-1E2F-1 proteinE2F1E2F1 geneE2F1 proteinENX-1EZH1EZH2EZH2 geneEarly-Stage Clinical TrialsEmerogenesEnhancer of Zeste 2 Polycomb Repressive Complex 2 SubunitEpigeneticEpigenetic ChangeEpigenetic MechanismEpigenetic ProcessEpithelial CellsEpitheliumEpithelium of Human Prostate GlandFutureGene Down-RegulationGene ExpressionGene InactivationGene SilencingGene TranscriptionGeneral Transcription Factor GeneGeneral Transcription FactorsGeneralized GrowthGenesGenetic TranscriptionGenomic SegmentGrowthHistologyHistonesHomeostasisIn VitroKMT6KMT6AMalignant CellMalignant NeoplasmsMalignant TumorMalignant neoplasm of prostateMalignant prostatic tumorMeasuresMedicationMesenchymalMetastasisMetastasizeMetastatic LesionMetastatic MassMetastatic NeoplasmMetastatic TumorMiceMice MammalsModelingModification MethylasesMolecularMolecular InteractionMultimodal TherapyMultimodal TreatmentMurineMusNeoplasm MetastasisNerve CellsNerve UnitNeural CellNeurocyteNeuroendocrine Prostate CancerNeuronal DifferentiationNeuronsNormal CellOnco-Suppressor GenesOncogenes-Tumor SuppressorsOncoprotein p53P53PBR3PRB-Binding Protein E2F-1Pathway interactionsPatientsPharmaceutical PreparationsPhase 1 Clinical TrialsPhase I Clinical TrialsPhosphoprotein P53Phosphoprotein pp53Physiological HomeostasisPost-Transcriptional Gene SilencingPredispositionProstate CAProstate CancerProstate malignancyProstatic EpitheliumProtein MethylasesProtein MethyltransferasesProtein TP53ProteinsRB1RB1 geneRBAP-1RBBP-3RBBP3RBP3RNA ExpressionRNA InterferenceRNA SeqRNA SilencingRNA sequencingRNAiRNAseqReaderReceptor SignalingRecessive OncogenesRepressionRepressor ProteinsResistanceRetinoblastoma Binding Protein 3Retinoblastoma-Associated Protein 1SafetySecondary NeoplasmSecondary TumorSequence-Specific Posttranscriptional Gene SilencingSite-Specific DNA-methyltransferaseSusceptibilityTP53TP53 geneTRP53TestingTissue GrowthToxic effectToxicitiesTranscriptionTranscription ActivatorTranscription CoactivatorTranscription Factor CoactivatorTranscription Factor Proto-OncogeneTranscription RepressionTranscription RepressorTranscription factor genesTranscriptional Activator/CoactivatorTranscriptional RepressorTranslatingTumor Protein p53Tumor Protein p53 GeneTumor Suppressing GenesTumor Suppressor GenesTumor Suppressor ProteinsVirulentWorkbisulfite sequencingbisulfite-seqbromodomain extra-terminal inhibitorcancer cellcancer metastasiscancer progressionchromatin immunoprecipitation coupled with sequencingchromatin immunoprecipitation followed by sequencingchromatin immunoprecipitation with sequencingchromatin immunoprecipitation-seqchromatin immunoprecipitation-sequencingcombination therapycombinatorialcombined modality treatmentcombined treatmentdemethylationdesigndesigningdevelopmentaldrug/agenteffective therapyeffective treatmentepigeneticallyepithelial to mesenchymal transitiongene repressiongenetic repressorgenome segmentgenomic regionhDNA methyltransferase 3ahDNA methyltransferase 3bhistone methylationin vivoinhibitorladakamycinloss of functionmalignancymembermenmulti-modal therapymulti-modal treatmentmutantneoplasm progressionneoplasm/cancerneoplastic progressionneuroendocrine differentiationneuronalnew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapy approachesnew treatment approachnew treatment strategynovelnovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapy approachoncosuppressor geneontogenyoverexpressoverexpressionp53 Antigenp53 Genesp53 Tumor Suppressorpathwaypatient subclasspatient subclusterpatient subgroupspatient subpopulationspatient subsetspatient subtypespharmacologicphase I protocolpluripotencypluripotent statepreventpreventingprogramsprostate cancer cellprostate tumor cellprotein p53recruitrepressing CRISPR-dCas9 systemrepressor complexresistance mechanismresistance to therapyresistantresistant mechanismresistant to therapyresponse biomarkerresponse markersretinoblastoma-1scRNA sequencingscRNA-seqscaffoldscaffoldingsingle cell RNA-seqsingle cell RNAseqsingle cell expression profilingsingle cell transcriptomic profilingsingle-cell RNA sequencingtargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmenttherapeutic resistancetherapeutically effectivetherapy resistanttranscription factortranscription factor E2F1transcriptional silencingtranscriptome sequencingtranscriptomic sequencingtreatment resistancetreatment strategytumortumor cell metastasistumor growthtumor progressiontumor suppressor
Description preview
Project Summary/Abstract
Neuroendocrine prostate cancer (NEPC) is the most virulent form of the disease. Loss of the tumor
suppressors TP53/RB1 is ubiquitous in NEPC, but molecular mechanisms that explain how loss of TP53/RB1
promotes NEPC development are largely unknown. Further, there are no effective therapies for NEPC. Thus,
there is a clear…
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