Publisher
The University of Arizona.Rights
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.Abstract
DNA repair is vital to the survival and proliferation of cells because it repairs damages that could lead to chromosomal abnormalities, loss of important gene information, and cell death. However, in some cases, DNA repair is not beneficial. For example, radiation therapy destroys cancer cells by introducing DNA damages, but the cellular ability to repair damaged DNA makes this treatment less effective. Additionally, improper repair of spontaneous DNA breaks can lead to oncogenic translocations. Therefore, the research focus is on finding a drug that disables DNA repair. To accomplish this, we are screening potential inhibitors designed to decrease the activity of Ku70/80, a vital DNA repair enzyme that mediates repair by physically attaching to the broken DNA ends and recruiting other repair enzymes. The goal is to find an inhibitor capable of preventing Ku70/80 from attaching to the DNA, which should inhibit the whole repair process. Theoretically, this novel approach should eliminate the cells’ abilities to counteract radiation, lower the radiation doses needed to destroy a tumor, and thereby lower the risk of collateral damage to surrounding healthy tissues. Thus far, five compounds have shown promising inhibitory activity and warrant further testing.Type
textElectronic Thesis
Degree Name
B.S.Degree Level
bachelorsDegree Program
Honors CollegeBiochemistry
