Researchers at The University of Texas at Austin and UT MD Anderson Cancer Center have identified a mechanism by which an experimental chemotherapy compound may recruit the immune system to attack cancer cells, a finding that could influence how chemotherapy doses and treatment strategies are designed in the future.

The study, published in the Proceedings of the National Academy of Sciences, found that Compound 1, an experimental agent that causes a build-up of reactive oxygen species in cancer cells, prompted those cells to release signals typically associated with viral infection. This effect, known as viral mimicry, appears to override the immune system’s self-tolerance mechanism, the built-in safeguard that normally prevents it from attacking the body’s own cells, including cancerous ones.

In mouse models, immune systems exposed to treated cancer cells remained primed to attack even when untreated cancer cells were subsequently introduced, suggesting a sustained immune response was generated.

The findings raise the possibility that lower chemotherapy doses, sufficient to trigger viral mimicry without depleting the immune system, could prove more effective than conventional high-dose approaches. Current chemotherapy strategies aim to eliminate all cancer cells, often at the cost of significant immune suppression. A viral mimicry-based approach could reduce the risk of treatment resistance, as tumours would have fewer opportunities to adapt when the immune system, rather than high-dose cytotoxic agents, serves as the primary mechanism of action.

The researchers plan to screen existing chemotherapy drugs for their capacity to induce viral mimicry and are seeking clinical collaborations to assess whether the effect correlates with patient survival outcomes.

Published in: Proceedings of the National Academy of Sciences