An extramedullary bone model of metastatic dormancy reveals an increased rate of metastatic reactivation upon distant insults.
Engineered extramedullary bone model reveals systemic inflammation increases metastatic reactivation by over 50% in dormant breast cancer cells.
- Why it matters: Understanding how dormant tumor cells reactivate is crucial for preventing metastatic relapse, which can occur years after initial treatment. The tissue microenvironment plays a key role in controlling dormancy, but its mechanisms are not fully understood.
- What they did: Researchers created a tunable, skeletal progenitor-based EM bone model in mice that mimics natural bone and induces dormancy in breast cancer cells, allowing controlled study of systemic influences like inflammation.
- The result: Systemic inflammation significantly increased the proliferative activity of dormant cells and metastatic incidence, with HMGB2 identified as a factor promoting overt metastasis, offering new targets for intervention.