Inflammatory bowel disease and carcinogenesis

Colorectal cancer (CRC) is the third most common cancer and the fourth most common cause of cancer mortality worldwide. Colitis-associated colorectal cancer (CAC) is a subtype of CRC associated with inflammatory bowel disease (IBD). It is well known that individuals with IBD have a 2-3 times higher risk of developing CRC than those who do not, rendering CAC a major cause of death in this group. Although the etiology and pathogenesis of CAC are incompletely understood, animal models of chronic inflammation and human cohort data indicate that changes in the intestinal environment, including host response dysregulation and gut microbiota perturbations, may contribute to the development of CAC. Genomic alterations are a hallmark of CAC, with patterns that are distinct from those in sporadic CRC. The discovery of the biological changes that underlie the development of CAC is ongoing; however, current data suggest that chronic inflammation in IBD increases the risk of developing CAC. Therefore, a deeper understanding of the precise mechanisms by which inflammation triggers genetic alterations and disrupts intestinal homeostasis may provide insight into novel therapeutic strategies for the prevention of CAC.

Automated summary

Colorectal cancer is the third most common cancer worldwide and is closely associated with ulcerative colitis. Patients with ulcerative colitis have 2-3 times higher risk of developing colorectal cancer compared to those without the disease. Chronic inflammation is believed to be a major factor contributing to the development of colorectal cancer. Understanding the mechanisms by which inflammation triggers genetic alterations and disrupts intestinal homeostasis may lead to novel therapeutic strategies for the prevention of colorectal cancer.