How the ATM protein prevents lymphoid cancers
Official title: The role of ATM in the suppression of lymphoid malignancy
Funded at Columbia University Health Sciences · NIH-11164715 · Data updated 2026-11-12
Researchers are studying how changes in the ATM gene affect the development and treatment of lymphoid cancers, especially for people with ATM mutations or Ataxia‑Telangiectasia.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Columbia University Health Sciences NIH-funded |
| Lab location | 1 site (New York, United States) |
| Project start | March 1, 2011 |
| Project end | July 31, 2029 |
| Funding year | 2025 |
| Award (this year) | $429,756 |
| NIH project number | 5R01CA158073-12 |
| Project ID | NIH-11164715 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with inherited ATM mutations (Ataxia‑Telangiectasia) and patients whose lymphoid cancers show ATM mutations are the most relevant candidates for this research.
✕Less likely to help
Patients whose cancers do not involve ATM alterations or whose tumors are unlikely to respond to TopoI‑based strategies are less likely to benefit directly from this work.
What this research studies
From my perspective, researchers use mouse models with no ATM, kinase‑dead ATM, or ATM missense mutations to learn how ATM keeps lymphoid cells healthy. They examine how DNA damage and reactive oxygen species activate ATM and how inactive ATM proteins can physically block DNA repair, raising lymphoma risk. The team connects these lab findings to human cancers that carry ATM mutations and tests whether ATM‑defective cells are especially sensitive to topoisomerase I (TopoI) inhibitors. Those links aim to help match patients with ATM mutations to targeted drug strategies and to better predict lymphoma risk for people with A‑T.
Why it matters
Potential benefit: Could help identify targeted treatments for ATM‑mutant cancers (for example TopoI inhibitors) and improve prediction of lymphoma risk for people with ATM mutations.
How similar studies have gone: Preclinical studies have shown ATM‑defective cells can be hypersensitive to TopoI inhibitors, and early clinical trials targeting ATM‑mutant cancers are ongoing but results remain preliminary.
Where this research is happening
-
Columbia University Health Sciences
New York, United States Active
Researchers
- Principal investigator: Zha, Shan — Columbia University Health Sciences
- Study coordinator: Zha, Shan
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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.