Stopping cancer-related fat loss caused by JAK/STAT signals
Official title: Identifying the Cellular and Molecular Targets of JAK/STAT-Driven Adipose Wasting to Reverse Cancer Cachexia
Funded at Ut Southwestern Medical Center · NIH-11175336 · Data updated 2026-11-12
This work aims to find ways to block JAK/STAT signals that make people with advanced cancer lose fat and weight.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Ut Southwestern Medical Center NIH-funded |
| Lab location | 1 site (Dallas, United States) |
| Project start | September 22, 2022 |
| Project end | August 31, 2027 |
| Funding year | 2025 |
| Award (this year) | $1,033,521 |
| NIH project number | 4R01CA266900-04 |
| Project ID | NIH-11175336 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with advanced cancer who are experiencing significant weight loss and loss of body fat from cancer cachexia are the most relevant candidates.
✕Less likely to help
Patients without cancer-related weight loss, those whose wasting is mainly muscle-only, or people whose weight loss comes from non-cancer causes are unlikely to benefit directly.
What this research studies
Researchers use lab-grown fat cells and several mouse models of cancer to find which cancer-released signals cause fat to break down. They screen substances secreted by tumors and have identified the cytokine LIF as a trigger that acts through the JAK/STAT pathway. The team will map which cells in fat tissue respond and test ways to block those molecular steps so fat loss is reduced or reversed. Promising lab and animal results could guide new drug development or future clinical trials for patients with cachexia.
Why it matters
Potential benefit: If successful, this work could lead to treatments that stop or reverse cancer-related fat loss, helping patients keep weight, strength, and potentially live longer.
How similar studies have gone: Preclinical lab and mouse studies have already linked LIF and JAK/STAT signaling to fat wasting, so this builds on promising but still early evidence with no approved human treatments yet.
Where this research is happening
-
Ut Southwestern Medical Center
Dallas, United States Active
Researchers
- Principal investigator: Infante, Rodney E — Ut Southwestern Medical Center
- Study coordinator: Infante, Rodney E
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.
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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.
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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.