grant
Mitochondrial Metabolism and Cancer
Organization NORTHWESTERN UNIVERSITYLocation CHICAGO, UNITED STATESPosted 1 Aug 2024Deadline 31 Jul 2029
NIHUS FederalResearch GrantFY202521+ years oldAddressAdenocarcinoma CellAdultAdult HumanAllograftingAntioncogene Protein p53AntioxidantsAspartateAutomobile DrivingAutoregulationB breveB. breveBacillus casei gBacillus gBackBetabacterium breveCRISPRCRISPR editing screenCRISPR screenCRISPR-based screenCRISPR/Cas systemCRISPR/Cas9 screenCancer GenesCancer cell lineCancer-Promoting GeneCancersCell BodyCell DifferentiationCell Differentiation processCell FunctionCell LineCell PhysiologyCell ProcessCell SurvivalCell ViabilityCellLineCellsCellular FunctionCellular PhysiologyCellular ProcessCellular Tumor Antigen P53Citric Acid CycleClustered Regularly Interspaced Short Palindromic RepeatsComplementComplement ProteinsComplexCytoplasmCytosolDataDevelopmentDorsumElectron TransportEngineeringEnzyme GeneEnzymesEpithelial CellsEssential GenesFerroprotoporphyrinFumaratesGeneralized GrowthGenerationsGenesGlutathioneGlycolysisGrantGrowthHemeHomeostasisHypoxiaHypoxicImmunocompetentImpairmentIn VitroIntermediary MetabolismInvestigationKRAS driven oncogenesisKRAS oncogenesisKRAS-driven tumorigenesisKRAS-mediated tumorigenesisKetosuccinatesKnock-outKnockoutKrebs CycleL breveL brevisL-AspartateL. breveL. brevisLactobacillus brevisLactobacterium breveLibrariesLinkLipidsLoxP-flanked alleleLungLung AdenocarcinomaLung Alveolar EpitheliaLung NeoplasmsLung Respiratory SystemLung TumorMaintenanceMalate DehydrogenaseMalate-Aspartate Shuttle PathwayMalate-aspartate shuttleMalatesMalic DehydrogenaseMalignant CellMalignant Glandular CellMalignant NeoplasmsMalignant TumorMalignant Tumor of the LungMalignant neoplasm of lungMetabolicMetabolic PathwayMetabolic ProcessesMetabolismMetastasisMetastasizeMetastatic LesionMetastatic MassMetastatic NeoplasmMetastatic TumorMiceMice MammalsMitochondriaMouse Cell LineMurineMusNAD-Malate DehydrogenaseNADHNADH oxidaseNatural regenerationNatureNeoplasm MetastasisNormal CellNucleotide SynthesisNucleotidesNutrient availabilityOncogenesOncoprotein p53OxaloacetatesOxosuccinatesOxygen DeficiencyP53Phosphoprotein P53Phosphoprotein pp53Physiological HomeostasisPlayPrimary NeoplasmPrimary TumorProcessProductionProliferatingProtein TP53ProtohemePublishingPulmonary CancerPulmonary NeoplasmsPulmonary malignant NeoplasmPurines/Pyrimidines/Nucleotides/Nucleic Acids MetabolismPyruvate CarboxylaseRegenerationResearchRespiratory EpitheliumRoleSecondary NeoplasmSecondary TumorSeriesSignal PathwayStrains Cell LinesStructure of respiratory epitheliumSubcellular ProcessSuccinatesTCA cycleTP53TP53 geneTRP53TestingTissue GrowthTransforming GenesTricarboxylic Acid CycleTumor ExpansionTumor PromotionTumor Protein p53Tumor Protein p53 GeneTumor Suppressor ProteinsWorkadulthoodaerobic glycolysisairway epitheliumalveolar epitheliumcancer cellcancer metastasiscancer microenvironmentcancer progressioncellular differentiationclustered regularly interspaced short palindromic repeats screencomplementationcultured cell linedevelopmentaldrivingelectron transferexperimentexperimental researchexperimental studyexperimentsferrohemefloxedfloxed allelefunctional genomicsgamma-L-Glu-L-Cys-Glygamma-L-Glutamyl-L-Cysteinylglycineimmune competentin vivolung cancermacromoleculemalignancymitochondrialmitochondrial metabolismmouse modelmurine modelneoplasm progressionneoplasm/cancerneoplastic progressionnovelnucleotide metabolismoncogenic KRASontogenyp53 Antigenp53 Genesp53 Tumor Suppressorprotein p53pyruvic carboxylaseregeneraterespiratory tract epitheliumsocial roletumortumor cell metastasistumor growthtumor initiationtumor microenvironmenttumor progressiontumor suppressor
Description preview
PROJECT SUMMARY/ABSTRACT
Transformation of normal cells to cancer cells involves complex changes influenced by oncogenes, inactivation
of tumor suppressors, and disrupted signaling pathways, imposing a metabolic demand that is sustained through
alterations in critical metabolic pathways and the availability of nutrients in the tumor…
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