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Increased Immune Cell Activity May Contribute to Duodenal Cancer Risk in Hereditary Disease

Increased Immune Cell Activity May Contribute to Duodenal Cancer Risk in Hereditary Disease

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Recent research highlights a potential link between immune system activity and the development of duodenal cancer in patients with familial adenomatous polyposis (FAP), a hereditary condition characterized by a high risk of tumor formation in the digestive tract. In patients with FAP, scientists have observed a significant increase in specific innate immune cells, notably type 3 innate lymphoid cells (ILC3), within the duodenal mucosa, especially near polyps and cancerous regions.

These ILC3 cells produce a neurotransmitter called interleukin-17A (IL-17A), which appears to stimulate intestinal cells to generate reactive oxygen species (ROS). Excessive ROS can damage the genetic material (DNA) within cells, creating conditions conducive to cancer development. This discovery suggests that immune responses, meant to defend against pathogens, might inadvertently promote carcinogenesis in the context of hereditary predispositions.

The study, published in Nature Communications, provides valuable insights into how the local immune environment influences cancer risk. It proposes that targeting IL-17A or modulating the activity of ILC3 cells could serve as innovative approaches to prevent duodenal cancer in FAP patients, supplementing existing monitoring therapies. Given that current treatments rely heavily on endoscopic surveillance and polyp removal—procedures associated with increased risks—these findings open pathways for emerging therapeutic strategies.

Dr. Benjamin Krämer from the University Hospital of Bonn emphasizes the importance of exploring immune-based interventions to reduce cancer risk, especially considering the variability in disease severity among FAP carriers. The research offers hope for developing pharmacological methods that can alter immune cell activity, ultimately aiming to lower the incidence of duodenal carcinoma in genetically predisposed individuals.

For more details, refer to the original study: Kaiser et al., IL-17A-producing NKp44(−) group 3 innate lymphoid cells accumulate in Familial Adenomatous Polyposis duodenal tissue, Nature Communications (2025). DOI: 10.1038/s41467-025-58907-y.

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