28/01/2026
Ottawa, Ontario — Wednesday January 28, 2026
Rhabdomyosarcoma (RMS) is an aggressive cancer found in muscle cells that affects kids and young people. RMS happens when cells that should become skeletal muscle get stuck at an earlier stage because of genetic mis programming – so they keep dividing instead of maturing. But what if there were a way to guide these cells toward a less dangerous, more muscle‑like state and slow the progress of RMS?
To test this idea, a new study in Nature Oncogenesis led by Kyle Cowan explored if regulating a protein called APOBEC2 would lead to healthier, mature muscle cell development and push RMS cells past their stuck state. The research team found that using the signal protein PANX1 to lower the amount of APOBEC2 caused cancer cells to begin to fuse – a normal step in healthy muscle development and a sign of maturing.
“Discovering that PANX1 lowers APOBEC2 and helps RMS cells begin to fuse gives us a new way to potentially make these tumors less aggressive.” said Dr. Cowan. “We will continue to explore different methods to increase PANX1 or lower APOBEC2, and how these might help to improve treatment outcomes.”
Future studies will aim to further validate this pathway as a complementary tool to pair with standard treatments, aiming to steady tumor cells rather than only destroy them – potentially slowing disease progression and giving more time for therapies to work.