Summary
This project aims to elucidate the role of hepatic ketogenesis and STAT3 signaling in pancreatic cancer cachexia and recovery, addressing the mechanisms of muscle loss and developing metabolic interventions.
Elucidating the role of hepatic ketogenesis in pancreatic cancer cachexia and recovery
US · IL
NIH
grant
awarded
#nih-5K99CA286709-02
What they want
The research will investigate how systemic inflammation in Pancreatic Ductal Adenocarcinoma (PDAC) prevents the liver from adapting to ketogenic metabolism, leading to muscle loss. It will specifically focus on the mechanism of STAT3-driven downregulation of lipid oxidation and study cachexia recovery in cancer survivors. Advanced epigenetic techniques combined with a novel mouse model of PDAC survivorship will be used to define epigenetic reprogramming events that persist after tumor clearance and increase muscle vulnerability to nutritional stress. The project includes pre-clinical testing of metabolic interventions.
Deliverables
- Defining the epigenetic reprogramming events that persist after tumor clearance and increase vulnerability of muscle to nutritional stress
- Pre-clinical testing of metabolic interventions to protect muscle during PDAC recovery
- Defining a previously undescribed action of STAT3 in hepatic metabolism control
- Linking long-term metabolic dysfunction to epigenetic reprogramming during PDAC cachexia
Technical requirements
- Advanced epigenetic techniques
- Novel mouse model of PDAC survivorship
Market context
inferred from NAICSProfessional, Scientific & Technical Services
NAICS 541714
- US market size
- $2.0T
- Typical award
- $25K – $50M
Typical buyers
All federal civilianDoDStates
Commonly required
8(a)WOSBSDVOSBPE/PMP
Sector-level estimate — full code lookup not yet in catalog.
