Research Information
Research Interests
My laboratory investigates the molecular and cellular mechanisms driving colorectal cancer development, with particular emphasis on colitis-associated cancer and early-onset colorectal cancer. We seek to understand how chronic intestinal inflammation, epithelial–immune interactions, and dysregulated signaling pathways contribute to malignant transformation and tumor progression.
Our research integrates genetically engineered mouse models, human colorectal cancer tissues, patient-derived organoids, and single-cell and spatial transcriptomic approaches to identify mechanisms underlying colorectal carcinogenesis. We are particularly interested in the role of IL-1 signaling in inflammation-associated tumorigenesis and the contributions of metabolic dysfunction and bile acid signaling to early-onset colorectal cancer. Ultimately, our goal is to identify novel opportunities for colorectal cancer prevention and treatment.
Research Projects
Current Projects
- Define the role of epithelial IL-1/IL-1Ra signaling in inflammation-associated colorectal tumorigenesis using genetically engineered mouse models and patient-derived organoids.
- Characterize molecular and cellular alterations associated with colorectal cancer progression, with an emphasis on epithelial–immune interactions and the tumor microenvironment using single-cell and spatial transcriptomic approaches.
- Investigate the contributions of occult metabolic dysfunction and bile acid signaling to early-onset colorectal cancer using clinical data, metabolomic profiling, and patient-derived organoids.
- Evaluate novel and repurposed therapeutic strategies to prevent or suppress inflammation-associated colorectal tumorigenesis using preclinical mouse models and organoid systems.