How Tuberous Sclerosis tumors use tryptophan to grow
Official title: Project 3 - Filippakis
Funded at University of New England · NIH-11251590 · Data updated 2026-11-12
This project looks at whether blocking the breakdown of the amino acid tryptophan can slow growth of tumors in people with tuberous sclerosis complex (TSC) and lymphangioleiomyomatosis (LAM).
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of New England NIH-funded |
| Lab location | 1 site (Biddeford, United States) |
| Project start | January 1, 2024 |
| Project end | December 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $253,362 |
| NIH project number | 5P20GM152330-03 |
| Project ID | NIH-11251590 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with tuberous sclerosis complex (TSC) or lymphangioleiomyomatosis (LAM), especially those with tumor manifestations such as angiomyolipomas, would be the most relevant candidates for related future trials or sample donation.
✕Less likely to help
Patients whose disease is not driven by TSC1/2-related mTORC1 activation or who are not eligible for future clinical trials may not see direct benefit from this specific approach.
What this research studies
From a patient perspective, researchers are studying why cells in TSC grow so much faster by looking at a cell process called macropinocytosis that lets cells gulp up nutrients. They focus on how the tryptophan-kynurenine pathway fuels that nutrient uptake in cells lacking the TSC2 gene, which overactivate mTORC1. In lab experiments with TSC2-deficient cells and related tumor models, they will block the kynurenine pathway and measure effects on nutrient uptake, cell proliferation, and tumor formation. The goal is to find whether shutting down this metabolic route can reduce tumor growth in TSC and LAM.
Why it matters
Potential benefit: If successful, this work could point to new treatments that slow or shrink TSC- and LAM-related tumors by targeting tryptophan metabolism.
How similar studies have gone: Drugs that block mTOR (like sirolimus) already help some TSC/LAM patients, but targeting macropinocytosis and the tryptophan-kynurenine pathway is a newer, preclinical strategy with promising early lab results but not yet proven in people.
Where this research is happening
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University of New England
Biddeford, United States Active
Researchers
- Principal investigator: Filippakis, Charilaos — University of New England
- Study coordinator: Filippakis, Charilaos
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.