Our laboratory is interested in pathogenesis of gastrointestinal inflammation and cancer, mouse tumor models, role of lipid metabolism, microbiome, nutritional intervention.   My primary interests have been focused on examining the role of bioactive lipid signaling in colon carcinogenesis using both genetically engineered mouse models and cell culture systems.

My research focuses on pathogenesis of gastrointestinal inflammation and cancer, mouse tumor models, the role of lipid metabolism, microbiome, nutritional intervention.

Role of PGE2 on CRC development – genetic deletion of PGE2 synthase (mPGES-1) significantly suppress CRC in multiple mouse models, suggesting an alternative strategy to reduce PGE2 levels .  We are currently examining the potential mechanisms of tumor suppression using multiple mPGES-1 knockout mouse models.  Some of the focus on this project are;

1. Examining the source of PGE2 within the colon tumors; what are the effects of PGE2 on tumor microenvironment


2. Inhibition of PGE2 affects anti-tumor immunity within the tumor microenvironment; how does it affect the spatial architecture of immune cells

Differential susceptibility to colonic ulceration in mPGES-1 deficient mice – mPGES-1 KO mice develop colonic ulceration only in a specific strain.  We are examining the mechanisms of induction/protection of ulcer development, which may represent different susceptibility to NSAIDs in human population.

Accepting Lab Rotation Students: Fall Block 2024, Spring 1 and 2 Block 2025

Journal Articles

Conference Papers

Reviews