By digging into the complicated life of cell death, Rebecca Boohaker hopes to uncover alternatives to chemotherapy that ravages a patient’s body.

A doctoral student at the College of Medicine’s Burnett School of Biomedical Sciences, Rebecca was recently awarded the Rudy J. Wodzinski Memorial Endowed Scholarship for learning, creative problem solving and scientific inquiry. She will present her cell death research at the American Association for Cancer Research conference in Chicago on March 31.

Chemotherapy drugs normally target the surface of cancer cells, signaling the body’s immune system to respond and destroy diseased cells. But the treatment can leave patients with anemia, fatigue and infections, and can be rendered ineffective because cancer cells are experts at mutating to resist a drug.

Rebecca is investigating whether cancer cell death could be triggered from the cell’s interior instead of the surface, delivering a fatal blow that would not give the cancer a chance to mutate. Her research focuses on a peptide related to the BAX protein, which plays a key role in eliminating unnecessary, old and sickly cells.

This so-called programmed cell death is crucial to healthy organisms. It’s the reason humans have fingers instead of ducklike appendages. As embryos, the webbing that connects human digits dissolves before birth.

A cell’s interior is a tempting target because it holds the mitochondria, tiny saclike structures that provide the energy a cell needs to survive. A second metabolic pathway occurs in the cytosol, which is the liquid inside the cell. This source is faster than the mitochondria at producing energy, but the yield is lower.

Working with her advisor, associate professor Dr. Annette Khaled, Rebecca looked at two cell lines that were cancerous. One cell line had the BAX protein, the other did not.

Rebecca said she wanted to know what would happen if the missing protein was replaced in the BAX-free version to stimulate the mitochondria and promote cell suicide.

Rebecca focused on the full BAX protein and a truncated version that lacked the last 20 proteins. Both versions performed well in providing energy to the cell, but the shorter version had lost the ability to zero in on mitochondria and trigger cell death.

Working with Burnett school faculty members Dr. Suren Tatulian and Dr. Manny Perez , Rebecca is now investigating whether BAX can be manipulated to create a drug that would release its fatal punch inside mitochondria, breaking them apart and triggering “cell suicide.”

“This therapy goes straight to the heart of the matter – it targets the mitochondria,” Rebecca said. “There’s no workaround for cancer cells.”