grant
Molecular mechanisms of allele-specific NRAS signaling and tumorigenesis
Organization OHIO STATE UNIVERSITYLocation Columbus, UNITED STATESPosted 1 Jul 2024Deadline 30 Jun 2029
NIHUS FederalResearch GrantFY2025AML - Acute Myeloid LeukemiaAcute Myeloblastic LeukemiaAcute Myelocytic LeukemiaAcute Myelogenous LeukemiaAffectAffinityAllelesAllelomorphsAmino Acid SubstitutionAmino AcidsAnimalsAssayB-raf-1BRAFBRAF geneBindingBioassayBiochemicalBiochemistryBiologicalBiological AssayBiological ChemistryC-K-RASCancersCell BodyCell Communication and SignalingCell Death InductionCell SignalingCellsClinicalClinical TrialsCodonCodon NucleotidesComplementComplement ProteinsComplementarity Determining RegionsComplimentarity Determining RegionCysteineDNA mutationDataDependenceDimerizationDisparitiesDisparityDrug TargetingDrugsElementsExhibitsFrequenciesFutureGTP PhosphohydrolasesGTPasesGeneralized GrowthGenetic ChangeGenetic defectGenetic mutationGoalsGrowthGuanosine Triphosphate PhosphohydrolasesGuanosinetriphosphatasesH-rasH-ras GeneH-ras OncogeneHRASHRAS geneHRAS1Half-CystineHarvey Rat Sarcoma Viral Oncogene HomologHumanHypervariable LoopHypervariable RegionsImmune mediated therapyImmunoglobulin Hypervariable RegionImmunologically Directed TherapyImmunotherapyIn VitroIndividualInterventionIntracellular Communication and SignalingIsoformsK-RAS2AK-RAS2BK-RasK-Ras 2AK-Ras-2 OncogeneKRASKRAS2KRAS2 geneKi-RASKnowledgeL-CysteineLengthLinkMAP kinaseMAPK InhibitorsMalignant MelanomaMalignant NeoplasmsMalignant Thyroid Gland NeoplasmMalignant TumorMalignant Tumor of the ThyroidMalignant Tumor of the Thyroid GlandMalignant neoplasm of thyroidMapsMeasuresMediatingMedicationMelanomaMelanoma CellMelanotic NevusMiceMice MammalsMitogen-Activated Protein Kinase InhibitorMitogen-Activated Protein KinasesModelingModern ManMolecularMolecular Dynamics SimulationMolecular InteractionMurineMusMutateMutationNevusNucleotidesOncogene K-RasOncogene ProductsOncogene ProteinsOncogenesisOncogenicOncoproteinsPathway interactionsPeptidesPharmaceutical PreparationsPhenotypePreventative strategyPreventionPrevention strategyPreventive strategyPropertyProtein DimerizationProtein IsoformsRAFB1RAS driven cancerRAS driven malignancyRAS genesRASH1RASK2RNA SeqRNA sequencingRNAseqReporterReportingResearchRoentgen RaysSignal TransductionSignal Transduction SystemsSignalingSingle Crystal DiffractionSkinStructureTestingThyroid CancerTipifarnibTissue GrowthTranslatingVariantVariationX Ray CrystallographiesX-RadiationX-Ray CrystallographyX-Ray Diffraction CrystallographyX-Ray RadiationX-Ray/Neutron CrystallographyX-rayXrayXray Crystallographyacute granulocytic leukemiaacute myeloid leukemiaaminoacidbiologicbiological signal transductionbiophysical approachesbiophysical methodologybiophysical methodsbiophysical techniquescancer initiationcancer preventioncancer typecomplementationdrug/agentexperimentexperimental researchexperimental studyexperimentsgenome mutationglobal gene expressionglobal transcription profileguanosinetriphosphatasehigh riskimmune therapeutic approachimmune therapeutic interventionsimmune therapeutic regimensimmune therapeutic strategyimmune therapyimmune-based therapiesimmune-based treatmentsimmuno therapyimprovedin vivomalignancymelanocytemelanomagenesismolecular dynamicsmouse modelmurine modelmutantmutant mouse modelneoplasm/cancernovelontogenypathwaypharmacologicpreventpreventingprotein protein interactionresponse to therapyresponse to treatmentskin moletargeted cancer therapytargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmenttherapeutic responsetherapy responsethermolabilitythermostabilitytranscriptometranscriptome sequencingtranscriptomic sequencingtreatment responsetreatment responsivenesstumortumorigenesistumorigenicv-Ha-RAS Harvey Rat Sarcoma Viral Oncogene Homologv-Ki-RAS2 Kirsten Rat Sarcoma 2 Viral Oncogene Homologv-raf Murine Sarcoma Viral Oncogene Homolog B1
Description preview
ABSTRACT
Cancer-associated RAS mutants were once considered oncogenic equivalents. However, it is increasingly clear
that mutants of the same RAS isoform (H-, K- or NRAS) and amino acid (codon 12, 13) can exhibit distinct
GTPase, effector binding, signal transduction, and tumorigenic properties. These distinctions may contribute to
disparities in…
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