Berlin Berlin. Researchers in the laboratory of Michael Siegl at the Max Delbrück Center and the Charite-Universitätmedizin Berlin have discovered the importance of the p53 gene in ulcerative colitis. The work, published in Science Advances, proposes a potential new therapeutic target to prevent the disease from turning into cancer.
A team of researchers led by Kimberly Hartl, a graduate student at the Max Delbruck Center (MDC-BIMSB) and the Berlin Institute for Medical Systems Biology of the Charité-UniversitätMedien, shed new light on the role of the p53 tumor suppressor gene in the pathogenesis of ulcerative colitis (UC). IS – an inflammatory bowel disease that affects an estimated five million people worldwide and which is associated with an increased risk of colon cancer. The research points to a new way to stop the disease from progressing. The study was published in the journal Science Advances.
“In patients with ulcerative colitis, who are at high risk of developing cancer, we could potentially “Can target abnormal cells and get rid of them before they become cancer.”
Important role of p53: Ulcerative colitis affects the large intestine, specifically areas called “crypts,” which are tube-like glands within the epithelial tissue that lines the intestine. The crypts contain stem cells and other types of cells that maintain the health and normal function of the colon, such as absorbing nutrients or secreting mucus.
When the colon is injured, epithelial crypt cells enter “repair mode”. They start growing faster to heal the injury. However, in patients with UC and UC-related colon cancer, these cells become stuck in repair mode, what scientists call the “regenerative cell state.” As a result, there are very few mature cells. As a result, the colon struggles to function normally, which triggers even more stem cell proliferation in a toxic feedback loop.
In the current study, Hartl found that this defective repair mechanism is linked to a non-functional p53 gene, which plays an important role in regulating the cell cycle and DNA repair.
“If there is no p53, the cells remain in a proliferative state,” Sigal explained.
Sigal says existing tests to find precancerous lesions in UC patients, such as colonoscopy, can identify visible lesions that are sometimes not easy to spot. He said this study could be the first step in developing molecular tools for less invasive diagnostic testing that would allow physicians to identify abnormal cells much earlier, even before visible changes occur.
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