Degree Name

Department

Computer Science

College

Physical and Mathematical Sciences

Defense Date

2025-02-28

Publication Date

2025-03-14

First Faculty Advisor

Matthew Bailey

First Faculty Reader

Amber Gonda

Honors Coordinator

Seth Holladay

Keywords

bioinformatics, cancer genomics, copy number variation (CNV), cell cycle reversal, ovarian cancer, pancreatic cancer

Abstract

Copy number variation is one of the main forms of genomic alteration in cancer genomes. The amplification of oncogenes or deletion of tumor suppressors commonly drives tumor formation. Average copy number variation events vary across cancer types; ovarian cancer has the highest average number of copy number changes, and pancreatic ductal adenocarcinoma has the least. With the copy number differences between cancer types, it is likely that different mechanisms of producing copy number changes exist. We propose that a possible mechanism is cell cycle reversal, which was recently shown to potentially occur during the G2 phase of the cell cycle after the genome has already been duplicated. Unintentional duplication of a genome would produce high copy number variation events characteristic of ovarian cancer. Though solid evidence for the occurrence of cell cycle reversal for ovarian cancer cells is yet to be found, our data analyses suggest the existence of mechanisms that prevent ovarian and pancreatic cancer cells from gaining additional copy number variation events since they are at the extremes of the copy number spectrum.