grant
Elucidating the role of hepatic ketogenesis in pancreatic cancer cachexia and recovery
Organization ROSALIND FRANKLIN UNIV OF MEDICINE & SCILocation NORTH CHICAGO, UNITED STATESPosted 1 Feb 2024Deadline 28 Feb 2029
NIHUS FederalResearch GrantFY2026APRF proteinATAC sequencingATAC-seqATACseqAcute-Phase Response FactorAddressAffectAnti-Cachexia AgentsAnti-cachecticAnti-cachexia DrugsAnticachecticAnticachexia AgentAnticachexia DrugsAssayAssay for Transposase-Accessible Chromatin using sequencingB cell differentiation factorB cell stimulating factor 2B-Cell Differentiation FactorB-Cell Differentiation Factor-2B-Cell Stimulatory Factor-2BCDFBSF-2BSF2BindingBioassayBiological AssayBody TissuesCUT&RUNCachecticCachexiaCancer CachexiaCancer SurvivorCancer SurvivorshipCancersCell BodyCell Communication and SignalingCell SignalingCellsCirculationCleavage Targets and Release Using NucleaseCleavage Under Targets and Release Using NucleaseClinicalCo-ImmunoprecipitationsDNADNA AlterationDNA BindingDNA Binding InteractionDNA MethylationDNA MethyltransferaseDNA Modification MethylasesDNA Modification MethyltransferasesDNA Sequence AlterationDNA boundDNA-MethyltransferasesDataDeoxyribonucleic AcidDependenceDetectionDiagnosisDnmtDown-RegulationEpigeneticEpigenetic ChangeEpigenetic MechanismEpigenetic ProcessEstersEventFastingFatty AcidsFoundationsFunctional impairmentGene ExpressionGene InactivationGene SilencingGenesGenetic AlterationGenus HippocampusGoalsHPGFHepaticHepatic CellsHepatic Parenchymal CellHepatocyteHepatocyte-Stimulating FactorHybridoma Growth FactorIFN-beta 2IFNB2IL-6IL6 ProteinIL6-response factorImpairmentInflammationInflammatoryInterleukin-6Intermediary MetabolismInterventionIntracellular Communication and SignalingKetonesKnock-outKnockoutKnowledgeLIF-response factorLinkLipidsLiverLiver CellsMGI-2Malignant NeoplasmsMalignant Pancreatic NeoplasmMalignant TumorMalignant neoplasm of pancreasMeasuresMediatingMetabolicMetabolic PathwayMetabolic ProcessesMetabolic dysfunctionMetabolismMethylationMiceMice MammalsMitochondriaModelingModificationModification MethylasesMolecularMolecular InteractionMurineMusMuscleMuscle AtrophyMuscle TissueMuscular AtrophyMyeloid Differentiation-Inducing ProteinNutrient availabilityNutritionNutritionalOrganPDA modelPDAC ModelPancreas CancerPancreas Ductal AdenocarcinomaPancreatic CancerPancreatic Ductal AdenocarcinomaPatientsPatternPlasmacytoma Growth FactorPositionPositioning AttributePreclinical TestingProductionPromoter RegionsPromotor RegionsQOLQOL improvementQuality of lifeRecoveryRegulationResearchRoleSTAT1 proteinSeahorseSequence AlterationSignal Transducer and Activator of Transcription 3Signal TransductionSignal Transduction SystemsSignalingSite-Specific DNA-methyltransferaseSkeletal MuscleStat-1 proteinStat-91 proteinStat3 proteinStat91 proteinStimulusStressSupplementationSymptomsTechniquesTestingTherapeuticTherapeutic InterventionTissuesTrainingTranscription RepressorTranscriptional ControlTranscriptional RegulationTranscriptional RepressorTranslationsVoluntary MuscleWasting DiseaseWasting SyndromeWorkanti-cachexiaanticachexiaassay for transposase accessible chromatin followed by sequencingassay for transposase accessible chromatin seqassay for transposase accessible chromatin sequencingassay for transposase-accessible chromatin with sequencingbiological signal transductioncancer associated cachexiacancer induced cachexiacancer-associated muscle wastingcancer-induced muscle atrophycancer-induced muscle losscancer-induced muscle wastingcancer-related cachexiadetection of nutrientefficacious therapyefficacious treatmentepigeneticallyexperiencefastedfastsfatty acid oxidationgene locusgenetic locusgenetic promoter elementgenetic promoter sequencegenetic repressorgenomic alterationgenomic locationgenomic locushepatic body systemhepatic metabolismhepatic organ systemimplantationimprovedimprovements in QOLimprovements in quality of lifeinhibitorinnovateinnovationinnovativeinterferon beta 2intervention therapyketogenesisketogenicketogenticliver metabolismmalignancymitochondrialmortalitymouse modelmurine modelmuscle breakdownmuscle bulkmuscle degradationmuscle deteriorationmuscle formmuscle lossmuscle massmuscle wastingmuscularneoplasm/cancernovelnutrient sensingnutritiousoverexpressoverexpressionoxidationpancreatic cancer modelpancreatic ductal adenocarcinoma modelpancreatic malignancypancreatic tumor modelperception of nutrientspre-clinicalpre-clinical testingpreclinicalpreventpreventingprogramspromoter sequencequality of life improvementresponsesignal transducer and activator of transcription 1social rolesurvivorshipsystemic inflammationsystemic inflammatory responsetimelinetranscription factor Stat91transcriptional silencingtranslationtumortumor-induced cachexiatumor-induced muscle wastingwasting conditionwasting disorder
Description preview
PROJECT SUMMARY/ABSTRACT
80% of patients with Pancreatic Ductal Adenocarcinoma (PDAC) develop cachexia, which results in dispropor-
tionate skeletal muscle mass loss, relative to caloric deficits. Cachexia causes functional impairment and ineli-
gibility for anti-tumor therapeutic interventions, leading to drastically lower patient quality of life…
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