Over 14 million people in the United States are currently living with cancer, a disease not limited to humans. In fact, several other animals elicit the growth of tumors when exposed to cancer-causing compounds commonly referred to as carcinogens. However, the newt, a type of salamander, can remain cancer-free when exposed to carcinogenic substances at levels 100 times higher than what would induce tumor formation in mammals. Thus, the newt provides us with an innovative approach to traditional cancer research. Instead of looking for treatments for tumor formation, the newt provides us with the ability to discover methods of preventing tumor formation. To do this, we expose the newt iris to carcinogens and characterize the cellular and molecular events that orchestrate the tumor resistance in the newt iris. Initially, our hypothesis was that newt iris cells have adapted mechanisms preventing the harmful effects of carcinogen exposure, through tight control of cellular proliferation, cellular metabolism, and DNA damage repair. However, after experiments performed in our lab, recent epidemiological data in humans, and previously published data in mice, we now hypothesize the effects of carcinogen treatment in the newt are of epigenetic origin. Understanding the underlying mechanisms that allow the newt’s iris to be tumor-resistant can provide an increased understanding of cancer and lead to the generation of cancer fighting therapies. This project was of particular intrinsic value as it related to my future career as a physician, possibly even an oncologist specifically.
Author: Vayda Barker
Advisors: Drs. Katia Del Rio-Tsonis, Anthony Sallese, and George Tsissios, Department of Biology
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