Pathophysiology of colitis-associated colorectal cancer.

Journal: Nature reviews. Gastroenterology & hepatology

This review focuses on colitis-associated colorectal cancer (caCRC), a form of colorectal malignancy arising in the setting of chronic inflammatory bowel disease (ulcerative colitis and Crohn’s disease), whose incidence is expected to grow with the rising global burden of IBD.

The authors synthesize current understanding of caCRC pathophysiology, emphasizing how it differs from sporadic colorectal cancer. They move from clinical characteristics to tumor biology, describing:

  • Distinctive features of caCRC tumor epithelium compared with sporadic CRC, including differences in how chronic inflammation shapes initiation and progression.
  • The central role of stromal elements (fibroblasts, endothelial cells, extracellular matrix components) within the tumor microenvironment in driving or modulating tumor growth.
  • Dual roles of immune cells in both tumor control and tumor promotion, reflecting the complex interplay between anti-tumor immunity and chronic inflammatory signaling in IBD.
  • Contributions of the gut microbiome, including how microbial signals may support or inhibit tumor development in the inflamed colon.

The review also highlights the biological and clinical heterogeneity of caCRC and discusses how these mechanistic insights may inform therapeutic decision-making and the development of future personalized medicine approaches, including tailoring surveillance, prevention, and treatment strategies specifically for patients with IBD-associated colorectal cancer.

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