Investigating how the complement system affects muscle loss in cancer patients
Official title: The Complement System and Cancer Cachexia
Funded at University of Florida · NIH-10898598 · Data updated 2026-11-12
This study is looking into how cancer can cause serious weight and muscle loss, and it aims to find new ways to help improve the lives of cancer patients by understanding the body's inflammation response.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Florida NIH-funded |
| Lab location | 1 site (Gainesville, United States) |
| Project start | August 1, 2022 |
| Project end | July 31, 2027 |
| Funding year | 2024 |
| Award (this year) | $462,810 |
| NIH project number | 5R01AR081648-03 |
| Project ID | NIH-10898598 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates for this research are cancer patients experiencing cachexia, particularly those with pancreatic cancer.
✕Less likely to help
Patients who are not currently experiencing significant muscle loss or cachexia may not benefit from this research.
What this research studies
This research focuses on understanding cancer cachexia, a condition that leads to severe muscle and weight loss in cancer patients. By examining the role of the complement system, which is involved in inflammation and tissue damage, the study aims to uncover the mechanisms that contribute to muscle wasting. Researchers will analyze muscle tissues from cancer patients and animal models to identify specific pathways and proteins that may be targeted for new treatments. The goal is to improve the quality of life and survival rates for those affected by this debilitating condition.
Why it matters
Potential benefit: If successful, this research could lead to new therapies that prevent or reverse muscle loss in cancer patients, enhancing their overall health and treatment outcomes.
How similar studies have gone: Previous research has shown promising results in understanding the role of the complement system in muscle wasting, indicating that this approach may lead to significant advancements in treatment.
Where this research is happening
-
University of Florida
Gainesville, United States Active
Researchers
- Principal investigator: Judge, Andrew Robert — University of Florida
- Study coordinator: Judge, Andrew Robert
Related research
Other NIH-funded projects on the same topics.
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Mitochondrial pores and muscle loss in cancer cachexia
A small US-based study will explore how changes in mitochondria contribute to muscle wasting in people with cancer cachexia and how this may be slowed.
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CANCAN: A Virtual Institute to Cure Cancer Cachexia
A broad, collaborative NIH initiative aims to uncover why cancer patients lose weight and muscle and to develop new ways to treat this serious condition.
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Spatial metabolism mapping in cancer cachexia tissues
Aims to map where and how metabolism changes in tissues affected by cancer cachexia using advanced imaging technology.
-
Nuclear receptors that may stop muscle wasting in cancer
This grant explores whether activating specific muscle-regulating receptors can prevent muscle loss in cancer patients.
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Stopping an enzyme called Transglutaminase 2 to prevent cancer-related muscle loss
This work explores whether blocking an enzyme called Transglutaminase 2 can stop or reverse the severe muscle wasting that often affects people with pancreatic cancer.
-
How the liver's ketone production affects muscle loss and recovery in pancreatic cancer
This project looks at whether helping the liver make ketones can prevent muscle wasting and aid recovery for people with pancreatic cancer.
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.