PhD candidate Ashari Kannangara came to BYU from Sri Lanka to study how to make chemotherapy more effective. “I have seen a lot of people go through the pain of cancer,” she said. One of those was her uncle, who battled bladder cancer for several years. She witnessed not only her uncle’s suffering, but also how “their family went through this miserable pain.”
But even before her family’s life was impacted by cancer, she was fascinated by biochemistry. “Since my childhood, I was curious to know how tiny, little cells carry out huge functions to sustain our lives,” she said, “and that curiosity led me to study biochemistry.”
Kannangara heard about BYU from her friend Vajira Weerasekara, who completed his PhD at BYU in biochemistry. She began exploring BYU’s website, and she liked what she saw. However, reading about BYU’s cancer research lab is really what inspired her to apply to the PhD program.
In the Fritz B. Burns Cancer Research Laboratory, led by Dr. Joshua Andersen, researchers focus on understanding and targeting mechanisms of chemo resistance in cancer. One mechanism of chemo resistance is a cell recycling process called autophagy. The purpose of autophagy is to help cells maintain cellular homeostasis and to survive under stress conditions.
Autophagy is a natural process that assists with the turnover of cells. However, when a person has cancer and is being treated by chemotherapy, cancerous cells in tumors can hijack the process of autophagy and can lead the disease to progress. In this situation, autophagy enables the cancer cells to survive, effectively overriding the effects of chemotherapy.
Once she read about the Fritz B. Burns laboratory, she knew she had found the program that was right for her. Kannangara is now in her fourth year of her PhD program. Her research focuses on a set of proteins called ATG, a significant player in initiating autophagy. Autophagy pathway is mediated by a set of proteins called ATG. In her research, she focuses on how autophagy is regulated by ATG9A. ATG9A is a transmembrane protein which plays a very important role in autophagosome formation.
According to Kannangara, the factors that initiate the molecular mechanism of autophagy are poorly understood. Her research aims to increase understanding, which will enable developers of chemotherapy better understand how to prevent cancerous cells initiating autophagy.
She and her team discovered a previously unknown bi-modal interaction of ATG9A with the canonical ULK1 complex and an ATG13-ATG101 subcomplex. Further, they revealed that an ATG9A-ATG13-ATG101 subcomplex is required for ATG9A to traffic away from early endosomes. This mechanism can be used as a potential therapeutic target to develop drugs to inhibit the autophagy pathway.
As a graduate student, Kannangara balances teaching, researching, and coursework. Although she has worked hard to end up where she is, her eyes and heart are focused on gratitude. She expressed thanks for the recent gift of $5 million from the Fritz B. Burns Foundation. That gift enabled the chemistry department to build the research lab where Andersen and his students work. She also expressed appreciation for the Simmons Center for Cancer Research for the Spring and Summer fellowship that she received in 2017 and 2018. Kannangara also wishes to thank her mentor and professor, Dr. Andersen. “Part of my success is because of his excellent guidance,” she expressed.
Moving forward Kannangara hopes to continue researching cancer as a postdoc. Eventually, she hopes to run a cancer research lab of her own. Her work in reversing the process of autophagy is one vital piece to finding a cure for cancer.