Cells normally require abundant energy and nutrients to grow and replicate. However, cancer cells can often manipulate their signaling pathways to allow them to grow in the absence of efficient energy production or the necessary growth signals. Furthermore, increasing evidence from epidemiological and animal studies have revealed causative links between metabolic disorders, including obesity and type 2 diabetes, and increased cancer incidence and worse prognosis, while conversely, energetic stresses, such as exercise and caloric restriction, can decrease tumor burden and improve survival. Two pathways critical for sensing the amount of energy in the cell and deciding whether cells should grow are the AMPK and mTOR pathways. Alterations in both of these pathways are implicated in cancer and metabolic disease.

Our research is aimed at studying the role of metabolic checkpoints triggered by AMPK and mTOR signaling in cancer and metabolic disease. We combine approaches in mouse genetics, biochemistry, cell biology, imaging, and metabolomics to dissect these biological processes. A deeper understanding of the interrelationship between cancer and metabolic disease will inform on how cells respond to energy stress and metabolic changes to suppress tumorigenesis and aid in establishing effective preventative and therapeutic strategies for cancer patients.

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