Author(s): Peyton Jackson
Mentor(s): John Chaston
Institution BYU
This project explores a potential strategy for a new form of cancer treatment by increasing the copy number of the tumor suppressor gene p53. In humans, mutations in the p53 gene are linked to more than 50% of cancers including breast, ovarian, lung, and many more. Using Drosophila melanogaster (Fruit fly) as a model organism, we aim to test whether additional functional copies of Dmp53—the fly equivalent of human p53—can improve survivability even when the native gene is mutated. To simulate cancer-prone conditions, we will generate flies lacking functional Dmp53 (referred to as Dmp53¯ flies) and compare them to both wild-type (WT) flies and our experimental group: “Super Dmp53 Flies,” which possess two additional copies of Dmp53. The Super Dmp53 Flies are designed to compensate for any potential loss of function by providing redundant copies capable of initiating apoptosis in damaged cells. All three groups will be exposed to 4,000 rads of radiation to test their survivability under extreme carcinogenic stress. The biological inspiration for this proposed treatment method comes from African elephants, which carry 20 copies of the p53 gene instead of the mere one copy found in humans (Sulak et al., 2016). Despite size, lifespan, and exposure to UV radiation, elephants exhibit remarkably low cancer rates. This genetic abundance is believed to make these elephant cells more capable of recognizing and eliminating cells prone to cancer. This project aims to replicate a similar redundancy in Drosophila by creating flies with extra copies of Dmp53. By examining survival rates across the three groups in our experiment, we aim to assess whether increasing the gene dosage of p53 duplicates offers a viable strategy for cancer resistance. These findings could be the first step of many in developing a new, groundbreaking cancer treatment.