A new study published in Computational Biomedicine suggests that the interaction between two genes, SUCLA2 and USP10, may help explain why some breast cancer patients face a higher risk of distant metastasis while others with similar disease have better outcomes, according to an Aug. 7 report.
Researchers identified a relationship between SUCLA2 and USP10 that strongly correlates with distant metastasis-free survival in breast cancer patients. The study also found that this prognostic relationship changes significantly depending on whether patients receive treatment, highlighting the importance of considering molecular interactions when predicting clinical outcomes.
Breast cancer remains one of the leading causes of cancer-related death worldwide. While advances in surgery, chemotherapy, radiotherapy, endocrine therapy, and targeted therapies have improved survival rates, distant metastasis continues to be the primary cause of mortality. Reliable biomarkers for identifying high-risk patients are considered essential for guiding personalized treatment strategies.
The researchers analyzed gene expression and clinical data from four independent breast cancer cohorts with available distant metastasis-free survival information. Patients were stratified based on combined expression patterns of SUCLA2 and USP10 rather than evaluating each gene separately. The analysis showed that patients with low SUCLA2 expression together with high USP10 expression experienced significantly poorer distant metastasis-free survival if they did not receive treatment; however, among those who underwent treatment, this elevated metastatic risk was no longer observed. Neither gene alone consistently predicted patient outcomes across all cohorts.
"Our results indicate that molecular interactions may provide more informative biomarkers than single-gene measurements," the researchers said. "Considering gene interactions could improve risk stratification and support more personalized treatment decisions." The authors believe their findings provide important clinical evidence supporting interaction-based biomarker discovery and suggest that targeting the SUCLA2–USP10 pathway could contribute to strategies aimed at reducing metastatic progression.
