We study how interactions between skeletal and tumor cells promote tumor progression and identify targets to mitigate these effects. Metastatic cancer cells and cytotoxic therapies such as chemotherapy and radiation can induce senescence in skeletal cells, producing a growth-arrested yet metabolically altered state that can reprogram the local bone microenvironment and impact disease progression. A central focus of our research is to understand how these senescence-associated metabolic changes promote bone loss and tumor progression, with a primary focus on bone metastatic cancers, particularly breast cancer. Building on this mechanistic work, we also aim to explore nutritional strategies, including senotherapeutic-adjacent dietary approaches, that may help prevent or mitigate these effects.

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