Improving CDK7-targeted treatments for estrogen receptor–positive (ER+) breast cancer
Official title: Optimizing CDK7 Inhibitor Therapeutic Strategies for ER+ Breast Cancer
Funded at Dana-Farber Cancer Inst · NIH-11304636 · Data updated 2026-11-12
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 start | August 16, 2019 |
| Project end | April 30, 2031 |
| Funding year | 2026 |
| Award (this year) | $442,427 |
| NIH project number | 2R01CA237414-06 |
| Project ID | NIH-11304636 on NIH RePORTER |
Who could benefit from this research
✓Could help
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.
✕Less likely to help
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.
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.
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 gone: 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
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Dana-Farber Cancer Inst
Boston, United States Active
Researchers
- Principal investigator: Jeselsohn, Rinath M. — Dana-Farber Cancer Inst
- Study coordinator: Jeselsohn, Rinath M.
Related research
Other NIH-funded projects on the same topics.
-
ER+ Breast Cancer Bone Metastasis in a Real Body Environment
This grant aims to understand why estrogen receptor alpha–positive breast cancer often spreads to bone and how the bone environment and immune system affect treatment resistance.
-
Targeting RAGE to fight obesity-related ER+ breast cancer and its drug resistance
A scientist team will explore how obesity-related inflammation involving RAGE and estrone interacts with ER+ breast cancer to drive growth and spread, aiming to find strategies to overcome therapy resistance.
-
Understanding estrogen signals in bone to stop ER+ breast cancer spread
This NIH grant aims to uncover how estrogen signals inside bone help ER-positive breast cancer cells grow and spread, with the goal of finding better ways to prevent bone metastasis.
-
Progesterone Receptor Signaling and Dormancy in ER+ Breast Cancer
Researchers are studying how hormone signals in ER+/PR+ breast cancer influence cancer cell dormancy and later recurrence.
-
Heavy Metals and Breast Cancer Treatment Resistance
This project explores how exposure to heavy metals might make ER+ breast cancer harder to treat and how we might overcome this challenge.
-
Turning ER-positive breast cancer into a viral target for immune attack
This project aims to wake up viral-like bits inside ER-positive breast cancer cells so the immune system can spot and attack them.
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.