P53 is a tumor suppressor and one of the most widely studied genes in cancer. It senses cell damage and activates mechanisms that stop cells dividing or start apoptosis, preventing damaged cells from entering the normal cell cycle. Mutations in the p53 gene can cause cell protection mechanisms to fail, possibly leading to cancer. Researchers at the University of Edinburgh School of medicine studied mutations in p53 to fully understand how the gene deactivates. The new findings may help predict clinical prospects.
Camille Bonneaud, a professor at the University of Edinburgh School of medicine, used big data to reveal that mutations in p53 were more frequent in patients with lower survival rates among all cancer types studied. At the same time, at the chromosome level, the research found that the p53 gene deletion obvious pattern. Studies have also shown that p53 mutations are closely related to genomic instability, suggesting that normal proteins play an important role in monitoring chromosome integrity. Meanwhile, in most patients with tumors caused by p53 mutations, other tumor suppressor genes were deleted and oncogenes amplified.
"P53 is one of the most important gatekeepers in cancer prevention, and understanding this gene will allow us to understand the pathogenesis of cancer, which will lead to better treatment of cancer," said professor Camille Bonneaud. The research could open up new avenues for cancer caused by mutations in the p53 gene.