New Delhi: A team of researchers has linked a specific gene in the ulcerative colitis (UC) disease to an increased risk of colon cancer.
Ulcerative colitis is an inflammatory bowel disease that afflicts an estimated five million people worldwide and that is linked to an increased risk of colon cancer.
The research, published in the journal Science Advances, is a significant step forward in understanding of ulcerative colitis and its link to colon cancer. It suggests a new way to prevent the disease from progressing, marking a crucial development in the field of medical research.
Ulcerative colitis affects the large intestine, specifically areas called “crypts,” tube-like glands within the epithelial tissue that lines the intestine. When the colon is injured, epithelial crypt cells enter a “repair mode.” However, in patients with UC and UC-related colon cancers, these cells become stuck in repair mode, which scientists refer to as a “regenerative cell state.”
In the study, Kimberly Hartl from the Berlin Institute for Medical Systems Biology of the Max Delbruck Center (MDC-BIMSB) and Charite—Universitatsmedizin found that this defective repair mechanism is linked to a non-functional p53 gene. The p53 gene, often referred to as the ‘guardian of the genome ‘, plays a crucial role in regulating the cell cycle and repairing damaged DNA, thereby preventing the development of cancer.
“In patients with ulcerative colitis who are at high risk for developing cancer, we could potentially target aberrant cells and get rid of them early, before any cancer occurs,” said Professor Michael Sigal, a senior author of the paper. This promising approach could significantly improve patient care and outcomes.
“If there is no p53, cells remain in a proliferative state,” Sigal added. The study suggests a potential new drug target to stop disease progression to cancer.
Existing tests to find precancerous lesions in patients with UC such as colonoscopies can identify visible lesions that sometimes are not easy to remove.
This study could be a significant step towards developing molecular tools for a less invasive diagnostic test that would allow physicians to identify cells with defective p53 genes much earlier, even before visible alterations occur. This could lead to more effective and timely interventions, potentially reducing the risk of cancer in UC patients.
The next step is to transfer these findings to the human setting. The researchers are also now studying the repair process in more detail to develop more simple methods to identify cells with defective p53 genes in colon tissue.
–IANS
