BLOCK-ID: New Technique Finds Treatment Targets in Hard-to-Treat Cancers
When cancer is difficult to control, it’s often because the cancer cells have learned how to survive under intense stress. Even when their DNA is damaged or unstable — a situation that would normally cause a healthy cell to stop dividing or die — these cancer cells find ways to keep going.
This ability to survive under pressure is one reason some cancers become aggressive, resistant to treatment, or quick to return after therapy. Understanding how cancer cells manage this stress is a major focus of modern cancer research.
Researchers at Winship Cancer Institute of Emory University have now developed a powerful new research tool that helps explain how certain cancers adapt and survive under these extreme conditions. While this discovery is not a treatment yet, it offers important clues that may eventually lead to new targeted therapies for cancers that currently have limited options.
Why DNA copying matters in cancer
Every time a cell divides, it must make an exact copy of its DNA. In healthy cells, this process is carefully regulated to prevent mistakes. But in cancer cells, DNA copying often becomes chaotic.
DNA is copied at structures called replication forks, which are Y-shaped points where the DNA strands separate so new copies can be made. In many cancers, these replication forks frequently slow down, stall, or collapse. When this happens repeatedly, it creates DNA replication stress.
Replication stress is a double-edged sword. On one hand, it causes DNA damage and genetic instability — changes that can drive cancer growth and spread. On the other hand, cancer cells that learn how to survive replication stress gain a powerful advantage, allowing them to adapt, resist treatments, and continue dividing despite severe internal damage.
Many aggressive cancers exist in a constant state of replication stress. Understanding how they tolerate this stress — and which proteins help them survive it — is critical for finding new ways to disrupt cancer growth.
What is BLOCK-ID?
To better understand what happens when DNA is under stress or damage, researchers developed a new laboratory technique called BLOCK-ID, an Emory technique (short for biotinylation of lac operator array replication stress protein network identification).
In simpler terms, BLOCK-ID allows scientists to:
- Create stress in a cancer cell’s DNA on purpose.
- They then watch how cancer cells respond to that stress.
- This helps researchers see which proteins cancer cells use to survive.
This Emory technique solves a long-standing challenge in cancer research. Until now, it has been extremely difficult to identify which proteins are involved at replication forks during stress. BLOCK-ID provides a detailed and precise way to map the protein networks cancer cells rely on to survive.
A key discovery: TRIM24 and other proteins
Using BLOCK-ID, researchers identified multiple proteins that appear at stressed replication forks. One protein, called TRIM24, stood out as particularly important.
The team then applied this discovery to a specific cancer survival mechanism known as Alternative Lengthening of Telomeres (ALT).
Telomeres are protective caps at the ends of chromosomes. In normal cells, telomeres shorten each time a cell divides, which eventually limits how long a cell can continue reproducing. Cancer cells must overcome this limit to survive.
Some cancers — estimated at 10–15% — use the ALT pathway to maintain their telomeres without relying on the more common enzyme-based method. ALT is often seen in aggressive or difficult-to-treat cancers, including:
- Osteosarcoma
- Glioblastoma
- Pancreatic neuroendocrine tumors
The research showed that TRIM24 helps cancer cells protect their chromosome ends so they can keep dividing.
Why this is hopeful: four potential treatment targets
In addition to TRIM24, the researchers identified three other proteins involved in the ALT pathway. Together, these findings highlight four potential treatment targets in ALT-driven cancers.
Identifying targets is one of the most important early steps in cancer drug development. While it can take time to move from discovery to therapy, knowing which proteins are essential to cancer survival gives researchers a clearer path forward.
The next phase of research will focus on determining whether these targets can be safely disrupted — and whether doing so can slow or stop cancer growth.
What this could mean for patients
BLOCK-ID is not a new treatment, but it represents meaningful progress in understanding cancer biology. Research like this helps explain why some cancers behave aggressively and why they may stop responding to standard treatments.
For patients living with advanced or hard-to-treat cancers, this work supports a growing shift toward precision oncology — matching treatment strategies to the specific biological features of a tumor. Discoveries like this strengthen the importance of:
- Testing the cancer to learn what makes it grow
- Understanding how the cancer survives
- Looking into clinical trials when needed
As researchers uncover new weaknesses in cancer cells, new treatment options may become possible, even for patients who have been told there are few options left.
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References:
https://winshipcancer.emory.edu/newsroom/articles/2025/new-technique-identifies-potential-new-treatment-targets.php?
https://pubmed.ncbi.nlm.nih.gov/40614724/
