How early nerve over-activation during paclitaxel treatment may cause chemotherapy-related peripheral neuropathy
Official title: The role of acute excitation of sensory neurons in the development of paclitaxel-induced peripheral neuropathy
Funded at University of Texas Med Br Galveston · NIH-11174252 · Data updated 2026-11-12
This project looks at whether paclitaxel causes early over-activation of sensory nerves that leads to energy failure in nerve fibers and later painful peripheral neuropathy in people treated with paclitaxel.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Texas Med Br Galveston NIH-funded |
| Lab location | 1 site (Galveston, United States) |
| Project start | September 1, 2024 |
| Project end | August 31, 2029 |
| Funding year | 2025 |
| Award (this year) | $402,874 |
| NIH project number | 5R01CA273001-02 |
| Project ID | NIH-11174252 on NIH RePORTER |
Who could benefit from this research
✓Could help
People receiving paclitaxel chemotherapy, especially those who experience acute pain during infusion, would be the most relevant candidates for related future studies or recruitment.
✕Less likely to help
Patients not treated with paclitaxel or those with long-standing, severe neuropathy unlikely to be reversible may not benefit directly from findings focused on early paclitaxel effects.
What this research studies
From a patient perspective, scientists will study why some people who get paclitaxel develop a painful 'stocking-and-glove' numbness and pain. They will examine sensory neurons and axons to see if paclitaxel triggers over-activation by blocking KCNQ channels, causing ATP loss and impaired transport of mitochondria and other cargo. Experiments will use cellular and animal models and build on observations that acute pain during infusion predicts later neuropathy. The team will track neuronal activity, ATP levels, axonal transport, and mitochondrial clearance to link early events to later nerve damage.
Why it matters
Potential benefit: If correct, this work could point to new ways to prevent or reduce paclitaxel-induced nerve pain by protecting nerve energy supplies or blocking the early over-activation of sensory neurons.
How similar studies have gone: Preclinical studies have suggested paclitaxel can excite sensory neurons and implicate KCNQ channels, but translating these mechanisms into proven human treatments has not yet been achieved.
Where this research is happening
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University of Texas Med Br Galveston
Galveston, United States Active
Researchers
- Principal investigator: Yang, Qing — University of Texas Med Br Galveston
- Study coordinator: Yang, Qing
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Understanding how early nerve excitement during chemotherapy leads to painful nerve damage
A cancer treatment study looks at why the nerve pain some patients get after paclitaxel may develop, by studying how nerves react during the infusion.
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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.