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Scientists co-led by St. Jude Children's Research Hospital have identified a potential therapeutic vulnerability in some forms of osteosarcoma. A combination approach described today in the Journal of Experimental Medicine slowed tumor growth and prolonged survival in preclinical models of this pediatric bone cancer. The therapies degraded EP300 (a protein that is co-opted to express oncogenes in many cancers) and inhibited AKT (a well-known cancer drug target), highlighting the combination's clinical potential.

Osteosarcoma has lower survival compared to many other cancers, with relapsed and metastatic disease showing especially poor outcomes. As no new treatments have been approved for the disease in the last 40 years, the findings provide a new therapeutic avenue to explore.

"We found a compound combination that looks promising for a disease that is exceptionally challenging to treat and has not had a major therapeutic improvement for a long time," said co-corresponding author Adam Durbin, M.D., Ph.D., St. Jude Department of Oncology. "It's especially exciting because the approach may have potential in patients who are metastatic and are least responsive to current therapies."

The study builds on previous work showing that EP300 can be targeted by a PROTAC , a type of compound that marks a protein for destruction. That approach had shown benefit in models of neuroblastoma, so researchers explored whether EP300 degradation could work in another setting. In osteosarcoma, they found that a small but meaningful subset of samples was disproportionately sensitive.

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