My name is Andrew Taylor and I’m currently a biology student at Florida State University pursuing a track in genetics/genomics with a minor in math. Since high school I’ve been fascinated by both disciplines for their ability to thread together ideas from multiple areas of study and across different levels of organization. More specifically, I’m enthralled by their capacity to explain the complexity spawned by the state of flux the natural world exists in.
Studying the sciences has provided me with the opportunity to understand the world through a more rigorous and holistic framework; one that in spite of its difficulty to attain, uncovers a transcendent beauty hidden in the structures that govern our reality: The interaction of molecules in a way that favors lower energy conformations, the pockets of decreasing entropy that define life, the eerie similarity between naturally occurring networks that differ in scale, the stochastic events whose outcomes irrevocably determine the unfolding of our reality. For me, the rapid development of science and technology is the validation of the human tendency to ask the question “why?” and find fascination in the irreducible complexity of the world, an age-old conviction that I think is worded most elegantly in the journal of the Roman emperor Marcus Aurelius: “He that sees things that are now, has seen all that either was, or ever shall be, for all things are one of a kind…Meditate often upon the connection of all things in the world; and upon the mutual relation they have, one unto another.”
My interest in cancer genetics began after taking general genetics with Dr. Erdem Bangi and learning about his research, which involves constructing multigenic models of colorectal cancer in fruit flies to explore mechanisms of tumor growth and drug
resistance. The complexity of dysregulation and variety of mutations seen in tumors is what makes cancer so difficult to treat and inspired the creation of the RPPA model in drosophila, which takes four of the most frequently observed mutations in human colorectal cancer and emulates them. This is done using an artificial genetic control system known as the GAL4-UAS system, which allows for spatially and temporally controlled induction of cancer in the drosophila hindgut, the anatomical equivalent of the human colon. By leveraging complex genetic tools, current molecular technology, and the practicality of fruit flies as model organisms, different combinations of mutations and their complicated interactions can be analyzed, allowing for the discovery of key components in the progression and functioning of cancer.
My project for the summer will involve working in the Bangi lab at FSU and modulating the expression of key DNA repair genes that are highly conserved in their functionality between humans and drosophila, using RNA mediated control to better understand the role of cell senescence in tumor growth and proliferation. Senescence is the cell arrest brought about by excessive stresses such as oncogene expression, chromatin dysregulation, and DNA damage, motivating the study of DNA repair genes in this project. Despite its functionality as a fail-safe to prevent the spread of cancer, senescence can result in the production of senescence- associated secretory phenotype (SASP), causing senescent cells to secrete molecules conducive to pathogenesis and the progression of cancer. Because of the positive relationship between the amount of DNA damage detected in a cell and SASP secretion, the goal in studying DNA repair genes is to identify key players in cancer disease states, providing a better understanding of the emergent dysregulation that makes treatment so challenging and paving the way for personalized therapeutics and drug discovery.