Lay summary
Inflammatory bowel disease (IBD) is a life-long condition that has significant health and economic impact worldwide including in New Zealand. Our previous studies show that there is a trend toward higher expression of a p53 variant, Δ133p53 in the inflamed bowel of IBD patients who had either dysplasia or colorectal cancer (CRC), compared to patients without progressive disease. Our studies in an animal model of colitis also show that mice overexpressing an analogue of the human Δ133p53 variant, Δ122p53, had elevated levels of inflammation and severe bowel damage. Here, we propose that Δ122p53/Δ133p53 drives an exaggerated immune response to promote the initiation and development of IBD. We will test our hypothesis using our animal colitis model and bowel tissue samples from IBD patients with and without CRC. The findings of this research provide significant knowledge and potential biomarker and/or target for diagnosis and better treatment options for IBD and CRC.