Viruses and cancer have a surprising number of things in common: each can alter the metabolism of cells, cause rapid cellular proliferation, and also inactivate host immune defenses. Using viruses to better understand how cells work can lead to insights about what happens when functions and processes go wrong; and, even more importantly, lead to discoveries about how to interfere with cancer and stop its usurpation of normal cellular functions.
To better understand the high-stakes molecular chess match between viruses and host cells, molecular biologist Dustin Hancks was recruited in 2017 to The University of Texas Southwestern Medical Center Department of Immunology. He came to Dallas from the University of Utah School of Medicine, where he was a postdoctoral fellow in evolutionary biology, with the help of a First-Time Tenure-Track Award from CPRIT.
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Viruses and cancer have a surprising number of things in common: each can alter the metabolism of cells, cause rapid cellular proliferation, and also inactivate host immune defenses. Using viruses to better understand how cells work can lead to insights about what happens when functions and processes go wrong; and, even more importantly, lead to discoveries about how to interfere with cancer and stop its usurpation of normal cellular functions.
To better understand the high-stakes molecular chess match between viruses and host cells, molecular biologist Dustin Hancks was recruited in 2017 to The University of Texas Southwestern Medical Center Department of Immunology. He came to Dallas from the University of Utah School of Medicine, where he was a postdoctoral fellow in evolutionary biology, with the help of a First-Time Tenure-Track Award from CPRIT.
About five to 10 percent of cancers are caused by viruses, rather than mutations. But viruses are relevant to studying cancer not necessarily because they lead to cancer, but because viruses hijack the machinery of the cell in much the same ways that cancers do. “When a cell is infected by a virus,” Hancks says, “the cellular state strikingly resembles the state of the cell when it becomes cancerous.”
Viruses can actually steal genes from cells and incorporate them into future generations of virus genomes. Indeed, many of the first cancer-causing genes were discovered this way. Hancks identified a gene in a virus that infects squirrels — he studies other organisms because the cellular processes are the same as in humans — called squirrelpox.
The gene was interesting because it was originally stolen from squirrel cells and repurposed in the virus genome. It’s a gene that is normally turned on during infection and also rapidly evolves in response to infection. Hancks said this led him to discover a whole family of cellular proteins, metabolic switches that respond to cellular stressors like infection or low oxygen levels.
“Interestingly, this metabolic pathway is dysregulated in cancer,” he says. “We’re now trying to understand how these metabolic switches get turned on and off, which ultimately regulate cell growth and proliferation.”
He’s also trying to understand potential vulnerabilities in these proteins that could be exploited to interfere with cancer’s growth.
Hancks says, “UT Southwestern is one of the world leaders in studying host defenses and other pathogens,” so for me, “it’s the ideal spot where I can both learn from the experts and contribute new research. There are a lot of scientists but there is a cozy feeling here. And every day someone makes a significant discovery.”
He adds, “I’m extremely grateful to be here in Texas and be provided the resources from CPRIT to do my job and fund my passion. It rapidly increases the pace of what I can do and the quality of the people I can recruit to my lab.”
Hancks received his undergraduate degree in biological sciences from Southern Illinois University, and his Ph.D. in cell & molecular biology from the University of Pennsylvania. He began his postdoctoral fellowship in human genetics at the University of Utah in 2012.
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