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Divergent Functions of ERK2 Substrate Binding Domains in Pathogenesis of KRAS-Driven Pancreatic Cancer
Organization RESEARCH INST OF FOX CHASE CAN CTRLocation PHILADELPHIA, UNITED STATESPosted 13 Dec 2023Deadline 30 Nov 2025 ⚠️
NIHUS FederalResearch GrantFY2025AddressAutomobile DrivingBindingBiologicalBloodBlood Reticuloendothelial SystemC-K-RASCRISPRCRISPR/Cas systemCancer GenesCancer InductionCancer TreatmentCancer-Promoting GeneCancersCell Communication and SignalingCell LineCell Senescence InductionCell SignalingCellLineCellular ExpansionCellular GrowthClinicClustered Regularly Interspaced Short Palindromic RepeatsDNA mutationDependenceDevelopmentDose LimitingDrug TargetingDrugsERK 1ERK 2ERK1ERK1 KinaseERK2ERT1EmbryoEmbryonicEngineeringEpithelial CellsExhibitsExtracellular Signal-Regulated Kinase 1Extracellular Signal-Regulated Kinase 2FibroblastsFutureGenesGenetic ChangeGenetic CrossesGenetic EngineeringGenetic Engineering BiotechnologyGenetic Engineering Molecular BiologyGenetic ModelsGenetic defectGenetic mutationGenetic studyHumanInterventionIntracellular Communication and SignalingK-RAS2AK-RAS2BK-RasK-Ras 2AK-Ras-2 OncogeneKI miceKPC genetically-engineered mouseKPC modelKPC mouseKPC murineKRASKRAS driven oncogenesisKRAS oncogenesisKRAS-driven tumorigenesisKRAS-mediated tumorigenesisKRAS2KRAS2 geneKi-RASKinasesKnock-inKnock-in MouseKnowledgeLSL-KrasG12D/+;LSL-Trp53R172H/+;Pdx-1-CreLSL-KrasG12D/+;LSL-p53R172H/+;Pdx-1-CreMAP Kinase 1MAP Kinase 2MAP Kinase 3MAPK1MAPK1 Mitogen-Activated Protein KinaseMAPK1 geneMAPK2MAPK2 Mitogen-Activated Protein KinaseMAPK3MAPK3 Mitogen-Activated Protein KinaseMAPK3 geneMalignant Neoplasm TherapyMalignant Neoplasm TreatmentMalignant NeoplasmsMalignant Pancreatic NeoplasmMalignant TumorMalignant neoplasm of pancreasMediatingMedicationMiceMice MammalsMitogen Activated Protein Kinase 1Mitogen-Activated Protein Kinase 2Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase 3 GeneMitogensModelingModern ManMolecularMolecular InteractionMurineMusMutationMyeloid DiseaseMyeloid MalignancyMyeloid NeoplasmMyeloid TumorMyeloproliferative DisordersMyeloproliferative TumorsMyeloproliferative diseaseOncogene K-RasOncogenesOncogenesisOncogenicP41MAPKP42MAPKP44ERK1PRKM1PRKM2PSTkinase p44mpkPancreasPancreas AdenocarcinomaPancreas CancerPancreaticPancreatic AdenocarcinomaPancreatic CancerPathogenesisPathway interactionsPatientsPharmaceutical PreparationsPhenotypePhosphotransferase GenePhosphotransferasesPlayPost-Transcriptional Gene SilencingProliferatingProteomicsRAS driven cancerRAS driven malignancyRASK2RNA InterferenceRNA SilencingRNAiRecombinant DNA TechnologyRoleSequence-Specific Posttranscriptional Gene SilencingSignal PathwaySignal TransductionSignal Transduction SystemsSignalingSolidStrains Cell LinesSubstrate InteractionTestingTherapeuticTherapeutic InterventionToxic effectToxicitiesTransforming GenesTransphosphorylasesWorkanti-cancer therapyattenuationbiologicbiological signal transductioncancer progressioncancer therapycancer-directed therapycarcinogenesiscell growthcell transformationcellular aging inductioncellular senescence inductionconditional knock-outconditional knockoutcostcultured cell linedevelopmentaldrivingdrug/agentgenetically engineeredgenome mutationglobal gene expressionglobal transcription profilein vitro Modelinhibitorinnovateinnovationinnovativeinsightintervention therapykinase inhibitorknockinknockin micemalignancymalignant phenotypemouse modelmurine modelmutantmutant mouse modelmyeloproliferative neoplasmneoplasm progressionneoplasm/cancerneoplastic progressionnew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapy approachesnew treatment approachnew treatment strategynovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapy approachoncogene induced senescenceoncogenic KRASoncogenic senescencep42 MAP Kinasep42 MAPKp44 MAPKpancreatic cancer cellspancreatic carcinogenesispancreatic malignancypancreatic oncogenesispancreatic tumor cellspancreatic tumorigenesisparalogparalogous genepathwaypharmacologicsenescencesenescence inductionsenescentsocial roletargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmenttooltranscriptometransformed cellstumor progressiontumorigenesisv-Ki-RAS2 Kirsten Rat Sarcoma 2 Viral Oncogene Homolog
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PROJECT SUMMARY/ABSTRACT
The central KRAS-ERK signaling axis is activated in most human pancreatic adenocarcinomas (PDAC).
Attempts to target ERK1 and ERK2 signaling with non-selective kinase inhibitors have produced only limited
efficacy in the clinic at the cost of dose-limiting toxicity. Our breakthrough discovery for this proposal is that…
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