What if one of the biggest obstacles to treating a childhood cancer is that its main cancer-causing protein won’t hold still long enough to target it?
That is part of the challenge facing researchers studying Ewing sarcoma, a rare and aggressive bone and soft-tissue cancer that primarily affects children and teenagers.
At the Greehey Children’s Cancer Research Institute, the Libich Lab, led by David S. Libich, PhD, studies highly dynamic protein interactions—molecular relationships that can be extremely difficult to capture with traditional structural biology.
One of the lab’s major targets is EWS::FLI1, the abnormal fusion protein that drives Ewing sarcoma. Unlike many proteins with relatively stable structures, EWS::FLI1 is highly flexible and constantly changing shape. That makes it extraordinarily difficult for conventional drug-development approaches to grab onto it.
Dr. Libich and his team are trying to change that.
In 2026, the lab received a $250,000 CPRIT award for a new approach to targeting Ewing sarcoma. Researchers are studying how EWS::FLI1 interacts with other proteins at extremely high resolution and combining that information with advanced computer modeling and artificial intelligence to design small engineered proteins capable of recognizing and binding specifically to EWS::FLI1.
If successful, the work could provide a detailed structural roadmap of how this elusive cancer-driving protein operates—and create a new generation of molecules specifically designed to target it. The long-term goal is straightforward but ambitious: safer, more precise treatments that improve survival and quality of life for children with Ewing sarcoma.
Sometimes the hardest targets in cancer are the ones worth pursuing most.
By figuring out how to hit a target that refuses to stand still, the Libich Lab is opening new possibilities for children facing one of the toughest pediatric cancers.
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