grant

Developmental transcription factors in Drosha-driven cancer

Organization UT SOUTHWESTERN MEDICAL CENTERLocation DALLAS, UNITED STATESPosted 1 Sept 2024Deadline 31 Aug 2029
NIHUS FederalResearch GrantFY202521+ years oldAblationAdultAdult HumanAffectAntioncogene Protein p53Automobile DrivingBasal Transcription FactorBasal transcription factor genesBindingBinding SitesBody TissuesBrainBrain Nervous SystemCCND2CCND2 geneCDK4CDK4 geneCancer CauseCancer EtiologyCancer GenesCancer-Promoting GeneCancersCell Division Kinase 4Cell LineCellLineCellular Tumor Antigen P53Childhood Brain NeoplasmChildhood Brain TumorChildhood CancersChromatinCollaborationsCombining SiteCyclin-Dependent Kinase 4DICER GeneDICER1DICER1 geneDNA BindingDNA Binding InteractionDNA boundDNA mutationDROSHADataDevelopmentDifferentiated GeneES cellEmbryoEmbryonicEncephalonEnzyme GeneEnzymesEpiphysis CerebriExhibitsExpression SignatureFamilyFutureGene Down-RegulationGene ExpressionGene Expression ProfileGeneral Transcription Factor GeneGeneral Transcription FactorsGeneralized GrowthGenesGeneticGenetic ChangeGenetic defectGenetic mutationGenomic SegmentGrowthHERNAHSA242976Helicase with RNase MotifHelicase-MOIHeterograftHeterologous TransplantationHumanImpairmentIn VitroK12H4.8-LikeKIAA0928KIAK0002KidneyKidney Urinary SystemLungLung Respiratory SystemMalignant Childhood NeoplasmMalignant Childhood TumorMalignant NeoplasmsMalignant Pediatric NeoplasmMalignant Pediatric TumorMalignant TumorMalignant childhood cancerMiceMice MammalsMicroRNAsModelingModern ManMolecular InteractionMurineMusMutationNeuroendocrine NeoplasmNeuroendocrine TumorsOncogenesOncogenesisOncogenicOncoprotein p53OvaryP53PSK-J3Pathway interactionsPatientsPhosphoprotein P53Phosphoprotein pp53Pineal BodyPineal Gland NeoplasmPineal Gland PNETPineal Gland TumorPineal NeoplasmsPineal PNETPineal Parenchymal Cell NeoplasmPineal Parenchymal Cell TumorPineal Parenchymal NeoplasmPineal Parenchymal TumorsPineal Primitive Neuroectodermal NeoplasmPineal Primitive Neuroectodermal TumorPineal TumorsPineal glandPineocytic NeoplasmPineocytic TumorPlayPrimitive Neuroectodermal Neoplasm of the Pineal GlandPrimitive Neuroectodermal Tumor of the Pineal GlandProliferatingProstateProstate GlandProstatic GlandProtein TP53RN3RNASE3LRNASE3L geneRNase III GeneReactive SiteRepressionRetinaRoleStrains Cell LinesTP53TP53 geneTRP53TestingTherapeuticTissue GrowthTissuesTranscription Factor Proto-OncogeneTranscription RepressionTranscription factor genesTransforming GenesTumor Protein p53Tumor Protein p53 GeneUndifferentiatedUpregulationXenograftXenograft ModelXenograft procedureXenotransplantationadulthoodcancer in a childcancer in childrencancer typechild with cancerchildhood malignancycultured cell linecyclin D2derepressiondevelopmentaldrivingembryo derived stem cellembryonal stem cellsembryonic progenitorembryonic stem cellgene expression patterngene expression signaturegene repressiongenetic approachgenetic strategygenome mutationgenome segmentgenomic regionhuman modelin vivomalignancymembermiRNAmodel of humanmouse modelmurine modelmutantneoplasm/cancerontogenyoverexpressoverexpressionp53 Antigenp53 Genesp53 Tumor Suppressorpathwaypediatric brain neoplasmpediatric brain tumorpediatric cancerpediatric malignancypineal body neoplasmpineal organpineoblastomaprogenitorprostate cancer cell lineprotein p53renalrestraintsmall moleculesocial rolestem cell of embryonic origintherapeutic targettranscription factortranscriptional profiletranscriptional signaturetumortumorigenesisxeno-transplantxeno-transplantationxenograft transplant modelxenotransplant model
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PROJECT SUMMARY/ABSTRACT
Pineoblastoma is one of a family of childhood cancers that can arise through mutations in

microRNA processing genes DROSHA and DICER1. It is unknown whether these tumors

develop through shared or distinct oncogenic pathways, and there are no ways to

therapeutically target such mutations. To understand how these mutations…

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