A groundbreaking study led by researchers at the University Hospital Bonn (UKB) sheds light on a potential mechanism behind duodenal cancer development in Familial Adenomatous Polyposis (FAP) patients. The investigation reveals an unexpected role of type 3 innate lymphoid cells (ILC3) and their production of interleukin-17A (IL-17A), which may contribute to genetic material damage and tumor formation. This discovery offers hope for new preventive strategies targeting these immune cells, potentially reducing the reliance on current endoscopic monitoring methods.

Scientists have long been searching for factors influencing the progression of FAP, a hereditary condition that significantly elevates the risk of both bowel and duodenal cancers. Dr. Benjamin Krämer, one of the study's co-leaders, highlights the variability in disease severity even among individuals sharing the same gene mutation, directing attention toward the local immune system as a critical player. The research team focused on ILC3 cells, uncovering their elevated presence in the duodenum of FAP patients.

In-depth analysis demonstrated that these ILC3 cells produce IL-17A, a neurotransmitter-like substance that appears to prompt intestinal cells into generating reactive oxygen species (ROS). These molecules are known to harm cellular DNA, thereby increasing cancer risk. According to Dr. Kim Melanie Kaiser, this finding elucidates how an increased concentration of IL-17A-producing ILC3 cells could foster a microenvironment conducive to cancer development in the duodenum of FAP sufferers.

The collaborative effort involved numerous institutions across Germany, including the ImmunoSensation² Cluster of Excellence at the University of Bonn, the German Center for Neurodegenerative Diseases (DZNE), and others. Prof. Jacob Nattermann emphasized the significance of these findings, suggesting that blocking IL-17A directly within the duodenum might offer a novel therapeutic avenue for preventing duodenal cancer in FAP patients.

This innovative approach could revolutionize the management of FAP-related duodenal cancer, providing much-needed alternatives beyond conventional endoscopic surveillance. By identifying the role of ILC3 cells and IL-17A in promoting carcinogenesis, the research paves the way for targeted interventions aimed at mitigating the adverse effects associated with this hereditary disorder.