The cells in our body reproduce through a process known as mitosis, in which the DNA and organelles of a cell are duplicated before splitting into two new daughter cells. During this process, the DNA may become damaged, creating a mutation. Although there are different types of mutations, a cancer cell is defined by the mutation that allows it to rapidly reproduce. Cancer cells multiply and eventually form a tumor. As the tumor develops in size, it can spread and block off blood vessels or put pressure on nerve pathways and vital organs. In order to tackle this modern day problem, a USC Viterbi assistant professor is developing a new way to essentially starve and destroy cancer cells by using computational methods to predict their behavior.
For her groundbreaking work in computational cancer research, Stacey Finley has been named one of the 2015 Emerging Scholars by “Diverse: Issues in Higher Education.” “Diverse” magazine introduced the “Emerging Scholars” series in 2002. Each year, 12 scholars under the age of 40 are selected based on the impact they have had on their community, students and prospective field.
“I am excited to be recognized for this work and its potential to identify novel therapeutic targets, and optimize cancer treatment,” said Finley. “It is a privilege to pursue my research at USC, while encouraging women and students under-represented groups to pursue careers in STEM fields.”
Finley earned her bachelor’s degree in chemical engineering from Florida A&M University and her Ph.D. in chemical engineering from Northwestern University before becoming a postdoctoral research fellow at Johns Hopkins University. Finley joined USC Viterbi in 2013 as an assistant professor in the Department of Biomedical Engineering.
Finley’s research is focused on observing and prohibiting tumors from performing cellular metabolism and angiogenesis — the process of forming new blood vessels. Cancer cells are characterized by a hyperactive metabolic rate that allows them to quickly multiply and reproduce into a mass known as a tumor. Once formed, a tumor will begin producing a protein known as the vascular endothelial growth factor (VEGF). The VEGF protein stimulates angiogenesis. Like regular cells, mutated cancer cells still require oxygen to perform cellular functions. Without oxygen, the tumor will not exceed the size of a grain of sand. But with a bountiful supply of oxygen, the tumor can continue to expand and flourish. Angiogenesis is the key process that allows the tumor to form new blood vessels and redirect the blood supply to itself, giving it direct access to a continuous supply of oxygen.
A tumor is nothing more than a parasite created through an accidental mutation that lives off of its host’s nutrients. By targeting cellular metabolism and angiogenesis, Finley can essentially starve the tumor and prevent further growth. However, instead of directly experimenting with cancer cells, Finley uses a computational system to create a chemical kinetic model. Using this model, the concentration of the VEGF proteins can be predicted and used to investigate the effects of therapies that inhibit angiogenesis. An ultimate goal of this work is to use the model to predict the response in patient-specific tumors, enabling treatment decisions based on personalized medicine.