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New Therapeutic Target Could Prevent Transition from Chronic Gut Inflammation to Cancer

New Therapeutic Target Could Prevent Transition from Chronic Gut Inflammation to Cancer

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Researchers at Charité Berlin have identified a new immune pathway involving interleukin-22 and oncostatin M that could lead to targeted therapies for preventing cancer in chronic gut inflammation cases, offering hope for high-risk patients.

2 min read

Chronic inflammatory bowel diseases such as Crohn's disease and ulcerative colitis are complex conditions that pose significant treatment challenges and carry an increased risk of developing bowel cancer. These diseases often begin insidiously, with symptoms like severe abdominal pain, diarrhea, weight loss, fatigue, and emotional distress, typically affecting young individuals between 15 and 29 years old—an age critical for personal development.

Researchers at Charité—Universitätsmedizin Berlin have identified a promising therapeutic target that may stop the harmful progression of chronic gut inflammation. Their recent study, published in Nature Immunology, highlights the role of immune system interactions in driving these conditions.

Chronic inflammation results from a mix of genetic and environmental factors, leading to tissue damage and raising cancer risk. While traditional treatments suppress immune activity broadly, newer therapies aim to interrupt specific inflammatory pathways. This research zeroes in on the interaction between two immune signaling molecules: Interleukin-22, which protects and maintains the gut lining, and oncostatin M, involved in tissue repair and cell differentiation.

The team discovered that a disbalance and uncontrolled interaction between these molecules creates a persistent inflammatory cycle. Elevated levels of oncostatin M, particularly around tumors in inflamed tissue, suggest its involvement in cancer progression. Furthermore, high oncostatin M levels are associated with poor response to conventional therapies, marking it as a potential biomarker for severe disease.

Utilizing animal models and patient tissue samples, the researchers unraveled how oncostatin M triggers a chain reaction amplifying inflammation in the gut. They found that disrupting this interaction in laboratory models significantly reduced inflammation and the risk of cancer.

This insight opens the door to developing targeted treatments that block the harmful effects of oncostatin M and interleukin-22. Such therapies could be especially beneficial for patients with high-risk inflammatory bowel disease, potentially preventing the progression to colorectal cancer. A clinical trial is currently underway testing an antibody that inhibits oncostatin M receptors, marking a step forward in precision medicine for intestinal inflammation.

These findings mark a promising advance in understanding the molecular basis of gut inflammation and its link to cancer, paving the way for innovative therapies that address the root causes of these chronic conditions.

Source: Medical Xpress

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