Understanding how BACH1 controls lactate use in triple-negative breast cancer
Official title: Understanding lactate catabolism by BACH1 in triple negative breast cancer
Funded at George Washington University · NIH-11393880 · Data updated 2026-11-12
A research project aims to see how turning off BACH1 changes how cancer cells in triple-negative breast cancer use lactate, with the goal of making therapies targeting metabolism work better.
Quick facts
| Grant type | R37 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | George Washington University NIH-funded |
| Lab location | 1 site (Washington, United States) |
| Project start | August 1, 2022 |
| Project end | July 31, 2027 |
| Funding year | 2026 |
| Award (this year) | $485,832 |
| NIH project number | 5R37CA270536-05 |
| Project ID | NIH-11393880 on NIH RePORTER |
Who could benefit from this research
✓Could help
Patients with triple-negative breast cancer, especially those whose tumors show dependence on mitochondrial metabolism and lactate processing, may be eligible for future trials.
✕Less likely to help
Patients whose tumors do not rely on mitochondrial metabolism or lactate catabolism may see limited benefit.
What this research studies
This project looks at how cancer cells in triple-negative breast cancer manage their energy and how blocking a key regulator, BACH1, could make many cancer cells more vulnerable to metabolic drugs. Researchers will study how BACH1 affects lactate breakdown inside cancer cells and whether reducing BACH1 can harmonize cancer cell metabolism to boost drug response. The work combines molecular profiling and metabolic analyses to identify when tumors might be most susceptible to metabolic inhibitors. The ultimate aim is to reprogram cancer metabolism so more cells can be killed by existing anti-metabolic treatments.
Why it matters
Potential benefit: If successful, patients with TNBC could benefit from more effective metabolic therapies.
How similar studies have gone: Previous work suggests targeting metabolism can sensitize cancer cells to drugs, and this project builds on that concept with a novel focus on BACH1 and lactate pathways.
Where this research is happening
-
George Washington University
Washington, United States Active
Researchers
- Principal investigator: Lee, Jiyoung — George Washington University
- Study coordinator: Lee, Jiyoung
Related research
Other NIH-funded projects on the same topics.
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Genomic study to understand how genetics and epigenetics shape triple-negative breast cancer in African ancestry
This study looks at how inherited genes and gene activity affect triple-negative breast cancer in people of African ancestry to better understand why outcomes can be worse.
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A study aims to block two cancer-promoting pathways (IL-6 and CDK4/6) to prevent or reduce progression of triple-negative breast cancer in women veterans.
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Dormancy in Triple-Negative Breast Cancer: How Liver and Skin Metastases Go Quiet or Reactivate
Researchers will study how dormant cancer cells in liver and skin metastases of triple-negative breast cancer become quiescent or wake up, using organ-on-chip models and single-cell analysis to map chromatin states.
-
Rac-enhanced CAR-Macrophages against TNBC
A new cell therapy approach uses engineered macrophages with a CAR and Rac2 activation to target and kill triple-negative breast cancer cells expressing CSPG4.
-
A new peptide therapy to help treat metastatic triple-negative breast cancer
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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.