Investigation of p53 gene polymorphisms in colorectal cancer

Globally, colorectal cancer ranks third in incidence, and it's also the leading cause of cancer-related death. When colorectal polyps form, they are benign and do not cause cancer. However, they can evolve into advanced adenomas with high-grade dysplastic lesions and distant organ metastases. Oncogenes and tumor suppressor genes are believed to play a role in colorectal tumor progression. Genome-wide studies have identified APC, KRAS, SMAD4, and TP53 as genes that are often mutated in human colorectal tumors in 10 to 80 percent of non-hypermutated cases. The TP53 gene has been related to a poor prognosis in a range of malignancies, including colorectal tumors, according to new research. People with advanced colorectal cancer who had metastasized were found to have an 80 percent increase in TP53 mutations. However, This mutation is uncommon in benign colonic polyps, and the conversion rate to malignant polyps is 15-30 percent. It is believed that DNA damage and telomere erosion as well as hypoxia and malnutrition as well as oncogenic signals trigger the activation of p53. This results in cell cycle arrest and death, depending on the level and content of cellular stress During our research, we included six individuals with colorectal cancer in the study. Genotyping and polymorphism areas were determined when the patients' blood was isolated and DNA sequenced. Other than frequent polymorphisms, only three unusual polymorphic areas were found in Patient 3.