The well-established link between inflammation and cancer is exemplified by Crohn’s disease, a severe intestinal disorder that afflicts millions world-wide. The chronic inflammation and repetitive tissue injury associated with this disease increase the risk of developing small intestinal and colorectal cancer. Although several mutations in genes have been identified that are important for Crohn’s disease, it remains unclear why these mutations cause disease in some people and not others.

Dr. Cadwell generated mice with mutations in the Crohn’s disease gene ATG16L1 during his time as a Damon Runyon Fellow.  He found that ATG16L1 mutant mice develop intestinal inflammatory disease, but only after infection with a virus called MNV.  Common viral infections underlie many chronic diseases and are prominent in cancer.  In this respect, the ATG16L1 mutant mouse model provides a tremendous opportunity to investigate a viral triggering event that leads to inflammation and disease.  His goal is to examine how viral infections and genetic susceptibility combine to generate inflammation, and by doing so, better understand the early events in disease.

 

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Project Title: "Characterization of mice deficient in autophagy protein Atg16L1"

Institution: New York University School of Medicine

Sponsor(s) / Mentor(s): n/a

Cancer Type: Colorectal, Gastric

Research Area: Infectious Disease