grant
Proteostasis Reprogramming in Mutant KRAS-Driven Cancers
Organization UNIVERSITY OF TX MD ANDERSON CAN CTRLocation HOUSTON, UNITED STATESPosted 1 Dec 2022Deadline 31 May 2028
NIHUS FederalResearch GrantFY20251-Phosphatidylinositol 3-KinaseAKTAblationAkt proteinBiochemicalBiologicalBypassC-K-RASCancersCell BodyCell Communication and SignalingCell SignalingCell SurvivalCell ViabilityCellsChronicClinicalColorectal CancerCombined Modality TherapyDNA mutationDataDevelopmentDose LimitingExtracellular Signal-Regulated Kinase GeneGEM modelGEMM modelGenesGeneticGenetic ChangeGenetic defectGenetic mutationGenetically Engineered MouseHSF1Heat ShockHeat-Shock ReactionHeat-Shock ResponseHumanIndividualIntracellular Communication and SignalingK-RAS2AK-RAS2BK-RasK-Ras 2AK-Ras-2 OncogeneKRASKRAS driven oncogenesisKRAS oncogenesisKRAS(G12D)KRAS-driven tumorigenesisKRAS-mediated tumorigenesisKRAS2KRAS2 geneKRASG12DKi-RASLaboratory StudyMAP Kinase GeneMAPKMalignant CellMalignant NeoplasmsMalignant Pancreatic NeoplasmMalignant TumorMalignant Tumor of the LungMalignant neoplasm of lungMalignant neoplasm of pancreasMediatingMembraneMitogen-Activated Protein Kinase GeneModern ManMolecularMonitorMultimodal TherapyMultimodal TreatmentMutateMutationNSCLCNSCLC - Non-Small Cell Lung CancerNon-Small Cell Lung CancerNon-Small-Cell Lung CarcinomaOncogene K-RasOncogenesisOncogenicPDX modelPI-3 KinasePI3-KinasePI3CGPI3KGammaPI3kPIK3PIK3CGPIK3CG genePancreas CancerPancreas Ductal AdenocarcinomaPancreatic CancerPancreatic Ductal AdenocarcinomaPathway interactionsPatient derived xenograftPatientsPhase 2 Clinical TrialsPhase II Clinical TrialsPhosphatidylinositol 3-KinasePhosphatidylinositol-3-OH KinasePhosphoinositide 3-HydroxykinasePhosphorylationPhosphorylation SitePost-Translational Modification Protein/Amino Acid BiochemistryPost-Translational ModificationsPost-Translational Protein ModificationPost-Translational Protein ProcessingPosttranslational ModificationsPosttranslational Protein ProcessingPre-Clinical ModelPreclinical ModelsProtein Kinase BProtein ModificationProtein PhosphorylationProtein SecretionProteinsProteomeProto-Oncogene Proteins c-aktPtdIns 3-KinasePulmonary CancerPulmonary malignant NeoplasmQuality ControlRAC-PK proteinRASK2RNA NucleasesRNaseRegulationRelapseResearchResistanceRibonuclease Family ProteinRibonucleasesSignal PathwaySignal TransductionSignal Transduction SystemsSignalingSpecificityStressTherapeuticToxic effectToxicitiesTreatment EfficacyType I Phosphatidylinositol KinaseType III Phosphoinositide 3-KinaseUbiquitilationUbiquitinationUbiquitinoylationbiologicbiological signal transductionc-akt proteincancer cellclinical relevanceclinically relevantcombination therapycombined modality treatmentcombined treatmentdevelopmentalgenetically engineered mouse modelgenetically engineered murine modelgenome mutationimprovedin vivoinhibitorinsightinsoluble aggregateintervention efficacylung cancermalignancymembrane structuremulti-modal therapymulti-modal treatmentmutantneoplasm/cancernew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapy approachesnew treatment approachnew treatment strategynovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapy approachoncogenic KRASpancreatic cancer modelpancreatic malignancypancreatic tumor modelpathwaypatient derived xenograft modelpatient responsepatient specific responsepharmacologicphase II protocolpre-clinicalpre-clinical trialpreclinicalpreclinical trialpreventpreventingprotein aggregateprotein aggregationprotein homeostasisproteostasisproteotoxicproteotoxicityproto-oncogene protein RACproto-oncogene protein aktrac protein kinaserefractory cancerrelated to A and C-proteinresistance mechanismresistance to therapyresistantresistant cancerresistant mechanismresistant to therapyresponseresponsive patienttherapeutic efficacytherapeutic resistancetherapy efficacytherapy resistanttreatment resistancetumortumor growthtumorigenesisubiquinationubiquitin conjugationv-Ki-RAS2 Kirsten Rat Sarcoma 2 Viral Oncogene Homolog
Description preview
ABSTRACT
KRAS is one of the most frequently mutated genes in human cancers. Despite advances in the development of
inhibitors that directly target mutant KRAS and the FDA approval of KRASG12C inhibitor sotorasib for KRASG12C-
mutant non-small cell lung cancer (NSCLC), cancer cell adaptation and resistance to KRAS inhibitors are almost
inevitable…
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