For David Plas, PhD, biomedical science is a constant adventure that never lulls. As an assistant professor of cancer and cell biology at the UC College of Medicine and researcher affiliated with the UC Cancer Institute, Plas studies the regulation of cell metabolism, cell growth and programmed cell death (apoptosis) as these processes relate to cancer and chemotherapeutic responses.
Plas joined UC in 2004 from the Abramson Family Cancer Research Institute at the University of Pennsylvania, where he also completed his postdoctoral training. He received his doctorate in immunology from Washington University and a bachelor’s of science from the University of Notre Dame.
Here, Plas tells us about why he became interested in the field of cancer biology and what keeps him motivated in the search for scientific answers to human diseases.
What influenced your decision to pursue cancer and cell biology as a career?
"While I was a graduate student, the study of programmed cell death exploded. The excitement of this new aspect of biology—together with its potential impact for cancer therapy—attracted me to the study of cancer and cell biology. Today, new biological problems are coming to light as genomic medicine and targeted chemotherapeutics are applied in cancer therapy. For me, these are exciting opportunities to apply mechanistic analysis and discover new ways to approach cancer therapy.”
Basic science takes time, patience and diligence. What keeps you motivated?
"One of the main attractions in science is the opportunity to work with smart people. I enjoy every chance to think and interact with colleagues from all sorts of backgrounds. Biomedical research would be a lot less rewarding if we didn't have appreciative colleagues with whom we can share our latest ideas.”
Give us some highlights of your current laboratory research projects in cell metabolism, cell growth and programmed cell death.
"We started out with a simple model: That oncogenic Akt activation worked through either the FOXO transcription factors or mTORC1/S6K1 to induce glucose-dependent survival in cancer cells. Shikha Khatri, the first graduate student in my lab, showed that the FOXOs actually can regulate mTORC1/S6K1 activation through pathway cross-talk. Then another graduate student, Preeti Tandon, showed that it is possible to reduce leukemia cell glycolysis by targeting S6K1. Most recently, Jen Barger's graduate thesis showed that reducing glycolysis via S6K1 is not always sufficient to kill leukemia cells, and that targeting fatty acid oxidative metabolism in combination with S6K1 inactivation is potentially more useful. So, the model has gotten more complicated, but we can still envision therapeutic targeting of specific signaling and metabolic pathways for cancer cell cytotoxic therapy. We're testing those new ideas now!”
Have you seen positive changes with the UC cancer program?
"Opportunities to interact with clinicians have been increasing. Recently, we've started great collaborations with physicians at both UC and Cincinnati Children’s Hospital Medical Center. These interactions are clearly helping to improve the clinical impact of our studies.”
What has been your proudest moment thus far in your career?
"I couldn't possibly pick a single moment. Every paper, grant and thesis defense is meaningful because we are fully invested in making progress in cancer biology and therapy. Each accomplishment means that we are a little bit closer to the ultimate goal of beating cancer.”
Tell us something we don’t know about you … any unexpected hobbies?
"It doesn't really look like it, but I enjoy medium distance running and road biking. I like to get a few colleagues together for the Reggae Run, a 5K that is held at the end of the summer in Ault Park. I’m always looking for runners out there …”
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