grant
Functional Interplay Between PARP, AR and DNA Damage
Organization BETH ISRAEL DEACONESS MEDICAL CENTERLocation BOSTON, UNITED STATESPosted 24 May 2013Deadline 31 Aug 2030
NIHUS FederalResearch GrantFY2025ATAC sequencingATAC-seqATACseqAgonistAndrogen ReceptorAndrogenic AgentsAndrogenic CompoundsAndrogensAssay for Transposase-Accessible Chromatin using sequencingBRCA 1/2 mutationsBRCA mutantsBRCA mutationsBRCA1BRCA1 Gene ProductBRCA1 MutationBRCA1 ProteinBRCA1 geneBRCA1 gene mutationBRCA1/2 mutationsBRCA1/2mutBRCA2BRCA2 MutationBRCA2 geneBRCA2 gene mutationBRCAmutBreast Cancer 1 GeneBreast Cancer 1 Gene ProductBreast Cancer 2 GeneBreast Cancer Type 1 Susceptibility GeneBreast Cancer Type 1 Susceptibility ProteinBreast Cancer Type 2 Susceptibility GeneBreast-Ovarian Cancer ProteinCRISPRCRISPR/Cas systemCastrate sensitive prostate cancerCell LineCellLineCessation of lifeChIP SequencingChIP-seqChIPseqChromatinChromatin StructureClustered Regularly Interspaced Short Palindromic RepeatsDNA DamageDNA InjuryDNA Repair PathwayDNA mutationDeathDefectDiseaseDisorderEarly Onset Gene Breast Cancer 1Early Onset Gene Breast Cancer 2Early Onset Protein Breast Cancer 1EffectivenessEndocrine Gland SecretionEnzyme GeneEnzymesEpithelial CellsEpithelium of Human Prostate GlandEquilibriumFANCD1Family memberGene ExpressionGene TranscriptionGeneralized GrowthGenesGenetic ChangeGenetic TranscriptionGenetic defectGenetic mutationGerm-Line MutationGlobal ChangeGrowthHereditary Breast Cancer 1Hereditary Breast Cancer 2Hereditary MutationHormonesMalignant neoplasm of prostateMalignant prostatic tumorMediatingModelingMutationOrganoidsOutcomePARP InhibitorPARP PolymerasePARP proteinPARP-1 inhibitorPARPiPARSPDX modelPathway interactionsPatient SelectionPatient derived xenograftPlayPoly(ADP-ribose) Polymerase InhibitorPoly(ADP-ribose) PolymerasesPoly(ADP-ribose) polymerase 1 inhibitorPoly(ADPribose) PolymerasePolymerase GeneProstateProstate CAProstate CancerProstate GlandProstate malignancyProstatic EpitheliumProstatic GlandRNA ExpressionRNA SeqRNA sequencingRNAseqRNF53Receptor SignalingRecurrenceRecurrentRegulationResistanceRoleSelection for TreatmentsStrains Cell LinesTestingTestosteroneTherapeutic AndrogenTherapeutic HormoneTherapeutic TestosteroneTissue GrowthTrans-TestosteroneTranscriptionTreatment EfficacyUncertaintyandrogen independent prostate cancerandrogen indifferent prostate cancerandrogen insensitive prostate cancerandrogen resistance in prostate cancerandrogen resistant prostate cancerandrogen sensitive prostate cancerantagonismantagonistassay for transposase accessible chromatin followed by sequencingassay for transposase accessible chromatin seqassay for transposase accessible chromatin sequencingassay for transposase-accessible chromatin with sequencingbalancebalance functionbrca 1 genebrca 2 genecastration resistant CaPcastration resistant PCacastration resistant prostate cancerchromatin immunoprecipitation coupled with sequencingchromatin immunoprecipitation followed by sequencingchromatin immunoprecipitation with sequencingchromatin immunoprecipitation-seqchromatin immunoprecipitation-sequencingclinical developmentcultured cell linedoubtfitnessgenome mutationgenome scalegenome-widegenomewidegerm-line defectgermline varianthigh risk menhomologous recombinationhomologous recombination deficiencyhomologous recombination repair deficiencyhormone refractory prostate cancerhormone sensitive prostate cancerimprovedinhibitorintervention efficacylife-time risklifetime riskmenmen at high riskmutation carriermutational statusmutations in BRCAontogenypathwaypatient derived xenograft modelpoly ADP polymerasepoly ADP ribose synthetaseprogramsprostate cancer cellprostate cancer cell lineprostate cancer progressionprostate cancer resistant to androgenprostate tumor cellreceptor functionrepairrepairedresistance mechanismresistantresistant mechanismresponseselection of treatmentsocial rolesynthetic lethal interactionsynthetic lethalitytargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmenttherapeutic efficacytherapy efficacytherapy selectiontranscriptome sequencingtranscriptomic sequencingtreatment selectiontumoryounger age
Description preview
Project Summary
Men carrying germline mutations in DNA damage response (DDR) genes including most notably BRCA2 and
BRCA1 have a very substantially increased lifetime risk of developing prostate cancer. BRCA1 and BRCA2
mutation carriers develop prostate cancer at a younger age and present with more aggressive disease. These
men are at higher risk…
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