Austin College hosted University of California assistant professor of microbiology and immunology and AC alumnus Kole Roybal for the Women’s Health and Cancer Forum Tuesday. In addition to the speaker, students in the cancer biology course at the college presented their research on the topic.


The cancer biology course was created by Associate Professor of Biology Lance Barton who began offering the course in 2014 after receiving support for the course from The Discovery Foundation of Dallas. Barton explained the course is for biology and biochemistry majors.


“We are really interested in trying to understand how cancer forms,” Barton said. “We have the availability here with the genetically modified mouse model. The mice lack one particular gene and it turns out that gene is really important for cancer formation. In the actual animals, if you would treat them with a carcinogen they don’t develop tumors like normal healthy animals do. We really want to understand more. The idea is to build the research question into the course.”


Students within the class, as well as those enrolled in the summer research component, generate new cancer cell lines through mutagenesis that can be further characterized in the course. For each new cell line generated, students collect data on genetic and genomic instability, metastatic potential and proliferative capacity. Students also learn the biological mechanisms behind these phenotypes of cancer and evaluate primary literature through classroom discussions.


Austin College senior Bethany Bundrant, who is majoring in biology, said her research project is centered around a particular protein called PA28-gamma.


“PA28-gamma has been found to be over-expressed in cancers,” Bundrant said. “There is too much of it. There’s a very cool experiment with mice who have PA28-gamma and ones who didn’t. The mice with PA28-gamma developed cancerous tumors while the ones without were almost completely resilient. The lack of PA28-gamma was somehow inhibiting the formation of tumors. That suggests that either PA28-gamma is important for how cancer cells become cancerous or it’s important for how cancer cells sustain themselves.”


Bundrant’s thesis is to evaluate whether PA28-gamma is important for a specific kind of DNA repair called Base Excision Repair. She explained Base Excision Repair is able to repair oxidative damage.


“My hypothesis is that PA28-gamma would be important for this type of repair,” Bundrant said. “I hypothesized that because PA28-gamma has been found to be important for other types of repair. When you damage a cell with a reactive oxygen species it’s response is to increase the expression of PA28-gamma. It’s how the cell is going to try to deal with it.”


The class is comprised of 14 students from six different teams. There are 11 seniors and three juniors. Barton said the projects are a culmination of the students’ work for the past 11 weeks.


“They create posters from their projects to describe the research that they did and what they learned from this process,” Barton said. “They share data amongst the different groups. They are working on slightly different questions. This is their opportunity to tell the public what they’ve learned, what they’ve accomplished.”


After the students presented their research, Roybal as the keynote speaker, addressed the attendees regarding his research at the University of California. Roybal received his doctorate in immunology from UT Southwestern Medical Center in 2013. His research is focused on synthetic and chemical biology to enhance the therapeutic potential of engineered immune cells. He also studies the safety and effectiveness of adoptive cell therapies.


Roybal explained tumor progression begins with cell transformation.


“Certain people have genetic abnormalities that predispose them for transformation of certain tissues, cancerous tissues,” Roybal said. “There may be some environmental stimulus over the course of your lifetime. Then you have a transformed cell that may become cancerous.”


Roybal went on to say there are intrinsic mechanisms within the cell that can cause them to either die or repair themselves.


“In a lot of cases what happens is, within these tissues that are transformed you have danger signals that occur and you have the infiltration of immune cells,” Roybal said. “In the best case scenario, your immune system can get rid of the cancer. But in many cases what you actually have, is your immune system is there but it doesn’t actually deplete the cancer cells.”


When this happens, immunotherapy can help identify and destroy the transformed cells. Roybal explained there are several types of immunotherapy.


“I work on taking out immune cells and modify them genetically,” Roybal said. “We can add certain genes into them such that it allows the cell to recognize the tumor. This is a case of making a T-cell that expresses a receptor that can detect this antigen on the surface of the tumor that can activate and kill a tumor cell.”


A T-cell is a cell that is involved in immunity. Roybal and his team are hoping to find a way to better equip cells to detect disease and subsequently customize behaviors in response to autoimmunity and cancer.


Roybal’s research is in direct relevance to the cancer biology course’s goal of learning how the immune system attacks cancer and how it is possible to engineer the immune system to be effective in trying to cure cancer.


Bundrant said research has become an important part of her education.


“I was always a student that liked the structure of the classroom,” Bundrant said. “I was very uncomfortable with ambiguity. Research is ambiguity. It is nuance. It is the unexpected. It’s all about how to deal with setbacks, how to look at things in a different light, think about things in new ways. I love research. It’s very near and dear to my heart because it really helps me grow in the places where I am weakest.”