Researchers Discover How Chronic Gut Inflammation Could Increase Risk of Cancer

In tests, mice with chronic colitis were at more of a risk of developing tumors for longer than those without the condition.
March 25, 2026
2 min read

Key Highlights

  • Chronic gut inflammation activates AP-1 transcription factors, promoting tumor growth in mice models.
  • Epigenetic modifications in stem cells persist long after colitis symptoms subside, influencing cancer risk.
  • Altered stem cell activity may serve as an early biomarker for colorectal cancer in humans.
  • Targeting post-colitis molecular pathways could lead to new treatments to prevent tumor progression.
  • The study provides insights into how inflammation-induced epigenetic changes contribute to cancer development.

Researchers have uncovered a molecular mechanism that “could explain how chronic gut inflammation may increase the risk of colorectal cancer.”

For the study, researchers simulated the effects of chronic colitis in mice and noted an increase in activity in a specific group of proteins, called AP-1 transcription factors. Tumor growth was also promoted. The authors also found that the damage “caused alterations in stem cells, which new cells inherited for more than 100 days after colitis ceased. While an individual’s DNA generally stays the same over time, the collection of chemical annotations to their genome — called the epigenome — is dynamic.”

The researchers “closely examined more than 52,000 individual cells across the animals, identifying one epigenetic change that stood out from the rest. The results suggested that colitis led to an alteration in colonic stem cells that increased the activity of AP-1 transcription factors, which are known to steer cellular responses to stress.” They then found that colorectal tumor growth was “far more rapid in the colitis-recovered animals compared to the other group.”

The conclusion drawn was that “if this phenomenon plays out similarly in humans, then tests for these epigenetic memories could potentially inform patients of colorectal cancer risk early on.” Therapeutics aimed at “disrupting the post-colitis activity described in this study may help stall tumor growth.”

About the Author

Matt MacKenzie

Associate Editor

Matt is Associate Editor for Healthcare Purchasing News.

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