Ulcerative colitis affects the large intestine, specifically areas called “crypts,” which are tube-like glands within the epithelial tissue that lines the intestine. When the colon is injured, the epithelial crypt cells enter “repair mode”. However, in patients with UC and UC-related colon cancer, these cells become stuck in repair mode, what scientists call the “regenerative cell state.”
In the study, Kimberly Hartl of the Berlin Institute for Medical Systems Biology and Charite-Universitätsmedizin at the Max Delbrück Center (MDC-BIMSB) found that this defective repair mechanism is linked to a non-functional p53 gene, which is involved in regulating the cell cycle and Plays an important role in DNA repair. Professor Michael Sigal, senior author of the research, said, “In ulcerative colitis patients, who are at high risk for developing cancer, we can potentially target abnormal cells and We can also get rid of cancer before it occurs.”
“If there is no p53, the cells remain in a proliferative state,” Sigal said. Study suggests a potential new drug target to prevent disease progression into cancer. Existing tests to find precancerous lesions in UC patients, such as colonoscopy, can identify visible lesions that are sometimes not easy to spot. It happens.
This study could be the first step toward developing molecular tools for a less invasive diagnostic test that would allow physicians to identify abnormal cells much earlier, even before visible changes occur. The next step is to transfer these findings to the human environment. Researchers are now studying the repair process in more detail with the goal of developing more simple methods to identify cells with a faulty p53 gene in colon tissue.
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