Modeling the Effects of p14 and p53 on Common Oncogenic Pathways
Class of 2018
- Solon High School, Solon, OH 2014
- The College of Wooster, BA in Biochemistry and Molecular Biology, 2018
- Professional experience
- Vice President of Beta Beta Beta- Biology National Honors Society
- Track and Field Team CaptainCollege of Wooster Women’s
- North Coast Athletic Conference Honor Roll
IS Thesis Abstract
The cell cycle is a complex set of processes that regulate protein and signal interactions in order to maintain proper cell health and function. When a mutation occurs, problems arise that can often lead to cancer. Cancer cells have the ability to evade the regulatory aspects of the cell cycle, causing extensive damage which often leads to death of the individual. Our Boolean Model represents the interactions and regulatory components of the cell cycle. We wanted to investigate if our model had the ability to mimic common oncogenic pathways by inactivating p14 and p53. p14 did not demonstrate a great variance from the healthy cell, and overall had only minor differences from the healthy model: a dead cell opposed to a senescent phenotype when exposed to gamma at the boundary between telophase/cytokinesis and G1, and early G1. Conversely, p53 demonstrated an extreme difference from the healthy model in the form of great disorder and dysregulation. With some editing, this model can be used to investigate different aspects of cellular mutations that are difficult to explore through traditional lab work, expanding our knowledge. In addition, opportunities for new therapeutics to battle cancer can be developed, which will hopefully increase the survival rate of individuals diagnosed with cancer.
Figure 1. Stable phenotypes of the healthy (wild-type) model under different growth factor and ionizing radiation conditions.