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Tumors at distal colon after AOM/DSS treatment.
The Chen laboratory is interested in understanding how the host immune system and the gut microbiota modulate intestinal inflammation and carcinogenesis using mouse models.
The Chen laboratory is interested in understanding how the host immune system and the gut microbiota modulate intestinal inflammation and carcinogenesis using mouse models.
Specifically, we have focused on understanding the mechanism by which certain members of the Nod-like receptor (NLR) family that are largely involved in the sensing of bacteria or tissue damage protect against the development of inflammation-induced colon tumorigenesis using the AOM/DSS model.
Specifically, we have focused on understanding the mechanism by which certain members of the Nod-like receptor (NLR) family that are largely involved in the sensing of bacteria or tissue damage protect against the development of inflammation-induced colon tumorigenesis using the AOM/DSS model.
We are also investigating how the gut microbiota regulates colon tumorigenesis using germfree (GF) and gnotobiotic mice as well as attempting to identify tumor-suppressive and tumor-promoting bacterial populations through bacterial sequencing and analysis of stool from wildtype and NLR-deficient mice during the development of chemically-induced inflammation and tumors.
We are also investigating how the gut microbiota regulates colon tumorigenesis using germfree (GF) and gnotobiotic mice as well as attempting to identify tumor-suppressive and tumor-promoting bacterial populations through bacterial sequencing and analysis of stool from wildtype and NLR-deficient mice during the development of chemically-induced inflammation and tumors.
Ki67-stained colon sections of GF mice before DSS round 2. Arrows denote microadenomas.
Images from Zhan Y et al. Gut microbiota protects against gastrointestinal tumorigenesis caused by epithelial injury. Cancer Research. 2013;73(24):10.
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