Improving CDK7-targeted treatments for estrogen receptor–positive (ER+) breast cancer
Optimizing CDK7 Inhibitor Therapeutic Strategies for ER+ Breast Cancer
This project looks at whether drugs that block CDK7, alone or combined with other medicines, can overcome resistance in ER+ breast cancers that no longer respond to hormone therapy and CDK4/6 inhibitors.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Dana-Farber Cancer Inst NIH-funded |
| Lab location | 1 site (Boston, United States) |
| Project ID | NIH-11304636 on NIH RePORTER |
What this research studies
From a patient's perspective, the team is trying to understand why some ER+ breast cancers stop responding to standard hormone therapy and CDK4/6 blockers and whether blocking CDK7 can stop resistant tumors from growing. They use tumor samples, lab-grown and patient-derived tumor models, CRISPR genetic screens, and molecular tests to find biomarkers that predict who might benefit. They also test combinations — for example pairing CDK7 inhibitors with agents that affect NFKB/TNFα signaling such as SMAC mimetics — to identify drug pairs that kill resistant cancer cells. The goal is to identify biomarkers and treatment combinations that could move toward clinical trials and offer new options for people with metastatic ER+ breast cancer.
Who could benefit from this research
Good fit: Ideal candidates would be people with estrogen receptor–positive (ER+) breast cancer, especially those with metastatic disease that progressed on endocrine therapy and CDK4/6 inhibitors.
Not a fit: People with non–ER+ breast cancers (such as triple-negative or HER2-positive tumors), early-stage disease unlikely to need these combinations, or whose tumors lack the biomarkers of interest may not benefit.
Why it matters
Potential benefit: If successful, this work could lead to new targeted drug combinations and biomarkers to guide treatment for ER+ breast cancer patients who have become resistant to current therapies.
How similar studies have performed: Preclinical lab models and patient tumor analyses show that CDK7 inhibition can suppress MYC signaling and block growth in resistant ER+ cells, but clinical evidence in patients is still limited and this approach remains early-stage.
Where this research is happening
Boston, United States
- Dana-Farber Cancer Inst — Boston, United States (Active)
Researchers
- Principal investigator: Jeselsohn, Rinath M. — Dana-Farber Cancer Inst
- Study coordinator: Jeselsohn, Rinath M.
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 below.