Exploring the role of TP53 mutations in the radioresistance of Diffuse Intrinsic Pontine Glioma (DIPG)
Mentor Name: Jessica Blackburn
The TP53 gene produces a protein that helps prevent cancer by repairing damaged DNA or killing off damaged cells. However, cancer often occurs due to mutations in TP53 that cause it to stop working. In a particularly deadly type of childhood brain cancer called Diffuse Intrinsic Pontine Glioma (DIPG), mutations in TP53 are associated with resistance to radiation therapy and poor outcomes for patients. Most TP53 mutations in DIPG are in the DNA binding domain. Our research team suspects that these mutations do more than just reduce the protein’s function, but actually change how p53 works to give it new ways to help cancer cells survive radiation therapy. During the POST program, our trainee Angelica Rivera-Martinez will use various techniques to study TP53 mutations in DIPG, including analyzing patient data, examining where the protein is located in cancer cells, and modeling the mutations in human cells to observe their effects on growth, DNA repair, and metabolism. Understanding how these mutations impact TP53 function could lead to new treatments that make radiation therapy more effective against DIPG.
