A recent study from Baylor College of Medicine has identified a previously unknown structure inside leukemia cells that could offer a new target for treatment. Researchers found that different genetic mutations driving leukemia all use the same nuclear compartments, named "coordinating bodies" or C-bodies, to sustain cancer growth.
The research was led by Dr. Joshua Riback, assistant professor and CPRIT Scholar, and Dr. Margaret “Peggy” Goodell, chair of the Department of Molecular and Cellular Biology at Baylor. Their teams observed under high-resolution microscopes that leukemia cell nuclei displayed bright dots—C-bodies—not present in healthy cells. These structures are formed through phase separation, a physical process similar to how oil droplets form in water.
According to the researchers, these C-bodies act as control centers within the nucleus, gathering both mutant and normal proteins to activate genes necessary for leukemia development. Notably, they found that even with different underlying mutations, leukemia cells produced biophysically indistinguishable C-bodies.
“It was astonishing,” Riback said. “All these different leukemia drivers, each with its own recipe, ended up cooking the same droplet, or condensate. That’s what unites these leukemias and gives us a common target. If we understand the biophysics of the C-body, its general recipe, we’ll know how to dissolve it and reveal new insights for targeting many leukemias.”
Further experiments showed that disrupting these droplets—either by altering key proteins or using drugs—stopped leukemia cells from dividing and prompted them to mature into healthy blood cells.
“Seeing C-bodies in patient samples made the link crystal clear,” said Elmira Khabusheva, postdoctoral associate in the Goodell lab. “By putting existing drugs into the context of the C-body, we can see why they work across different leukemias and start designing new ones that target the condensate itself. It’s like finally seeing the whole forest instead of just the trees.”
“By identifying a shared nuclear structure that all these mutations depend on, we connect basic biophysics to clinical leukemia,” added Goodell. “It means we can target the structure itself – a new way of thinking about therapy.”
“Across every model we studied, the pattern was the same,” Datar said. “Once we saw those bright dots, we knew we were looking at something fundamental.”
The discovery suggests a unified mechanism behind various forms of leukemia despite their distinct genetic origins and could inform future drug development aimed at dissolving these essential droplets.
This research involved collaboration between Baylor College of Medicine labs and international partners such as Associazione Italiana per la Ricerca sul Cancro (AIRC), Trond Mohn Foundation and Norwegian Cancer Society. The findings have been published in Cell.
Funding for this project came from several sources including grants from national cancer research organizations in Italy and Norway as well as U.S.-based foundations supporting cancer research.
