grant
Identify Mechanisms Driving Resistance to AR Antagonists in CRPC
Organization BETH ISRAEL DEACONESS MEDICAL CENTERLocation BOSTON, UNITED STATESPosted 24 May 2013Deadline 31 Aug 2030
NIHUS FederalResearch GrantFY2025AR geneAddressAgonistAndrogen ReceptorAndrogenic AgentsAndrogenic CompoundsAndrogensAutomobile DrivingBasal Transcription FactorBasal transcription factor genesBindingBinding Site DomainBinding SitesCCAAT-Box Binding Transcription FactorCRISPR interferenceCRISPR-dCas9-mediated repressionCRISPR/dCas9 interferenceCRISPR/dCas9-mediated transcriptional inhibitionCRISPRiCell BodyCell Communication and SignalingCell SignalingCellsChromatinClustered Regularly Interspaced Short Palindromic Repeats interferenceCombined Modality TherapyCombining SiteComplexDNA mutationDataDevelopmentDihydrotestosterone ReceptorFamilyFundingGNRHGNRH1GNRH1 geneGene TranscriptionGeneral Transcription Factor GeneGeneral Transcription FactorsGenesGenetic ChangeGenetic TranscriptionGenetic defectGenetic mutationGenomicsGonadotropin Releasing Hormone 1ImpairmentIntracellular Communication and SignalingInvestigatorsKIAA1439KinasesLNRHLeadLengthLigand Binding DomainLuteinizing Hormone-Releasing HormoneMalignant neoplasm of prostateMalignant prostatic tumorMass Photometry/Spectrum AnalysisMass SpectrometryMass SpectroscopyMass SpectrumMass Spectrum AnalysesMass Spectrum AnalysisModelingModificationMolecular InteractionMultimodal TherapyMultimodal TreatmentMutationNF-I ProteinNFI Transcription FactorNFIANFIA geneNFIBNFIB geneNR3C4Nuclear Factor INuclear Factor I/ANuclear Factor I/BNucleosomesPDX modelPathway interactionsPatient derived xenograftPatientsPb elementPhosphorylationPhosphotransferase GenePhosphotransferasesPost-Translational Modification Protein/Amino Acid BiochemistryPost-Translational ModificationsPost-Translational Protein ModificationPost-Translational Protein ProcessingPosttranslational ModificationsPosttranslational Protein ProcessingProliferatingProstate CAProstate CancerProstate malignancyProtein ModificationProtein PhosphorylationProteinsRNA ExpressionRNA SplicingReactive SiteRecurrent Malignant NeoplasmRecurrent Malignant TumorResearch PersonnelResearchersResistanceRoleSMAX1Signal TransductionSignal Transduction SystemsSignalingSiteSplicingSteroid CompoundSteroidsTestingTherapeutic AndrogenTimeTranscriptionTranscription Factor NFIATranscription Factor NFIBTranscription Factor Proto-OncogeneTranscription factor genesTransphosphorylasesUpstream EnhancerVCaPVariantVariationXtandiabirateroneandrogen ablation therapyandrogen blockade therapyandrogen deprivation therapyandrogen deprivation treatmentandrogen independent prostate cancerandrogen indifferent prostate cancerandrogen insensitive prostate cancerandrogen receptor geneandrogen resistance in prostate cancerandrogen resistant prostate cancerantagonismantagonistbiological signal transductioncancer progressioncancer recurrencecastration resistant CaPcastration resistant PCacastration resistant prostate cancercombination therapycombined modality treatmentcombined treatmentdata sharingdevelopmentaldrivingenzalutamidegenome mutationglobal gene expressionglobal transcription profileheavy metal Pbheavy metal leadhormone refractory prostate cancerinhibitor druginhibitor therapeuticinhibitor therapyinsightmetermulti-modal therapymulti-modal treatmentneoplasm progressionneoplastic progressionneuroendocrine differentiationnew approachesnovelnovel approachesnovel strategiesnovel strategynuclear factor 1pathwaypatient derived xenograft modelprogramsprostate cancer cellprostate cancer progressionprostate cancer resistant to androgenprostate tumor cellreceptor expressionrepressing CRISPR-dCas9 systemresistantresponserestorationsocial roletargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmenttranscription factortranscriptometumortumor progression
Description preview
PROJECT SUMMARY/ABSTRACT
Prostate cancer (PCa) that recurs after standard androgen deprivation therapy (ADT) with a GnRH agonist or
antagonist (castration-resistant prostate cancer, CRPC) is in most cases still dependent on androgen receptor
(AR). AR activity in these patients can be further suppressed by agents such as abiraterone or by AR…
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