The Pew Charitable Trusts and the Alexander and Margaret Stewart Trust have named Damon Runyon-Dale F. Frey Breakthrough Scientist Shruti Naik, PhD, and Former Damon Runyon Fellow Jihye Yun, PhD, as part of the 2020 class of the Pew-Stewart Scholars Program for Cancer Research. Each will each receive a four-year grant to advance innovative research into the development, diagnosis, and treatment of cancer. “Despite the gains of recent years, cancer remains a relentless disease that takes millions of lives across the globe every year,” said Rebecca W. Rimel, Pew’s president and CEO. “I am confident these promising researchers will help uncover effective diagnosis and treatment strategies to advance progress toward a cure.”
The Naik, lab at New York University, will explore whether prior inflammatory reactions can predispose tissues to becoming more susceptible to cancer. The skin, for example, routinely encounters inflammation-inducing stressors and is a common site of tumorigenesis. However, there is a dearth of information on how acute inflammatory events alter the skin’s microenvironment in the long term and consequently its vulnerability to carcinogens. We found that even after skin inflammation has completely subsided, carcinogen exposure results in five times more tumors than in skin without a prior history of inflammation. Now, using a mouse model of squamous cell carcinoma coupled with high-resolution single-cell sequencing techniques, we will trace the evolution of tumor-forming cells and their microenvironment following resolution from a range of inflammatory attacks. These studies will uncover the factors that help provide a growth advantage to tumorigenic cells in inflammation-primed tissues and identify potential biomarkers for predicting cancer risk.
The Yun lab, at the Baylor College of Medicine, will decode the molecular connection between sugary drinks and the development of colorectal cancer (CRC). Sugary drinks are sweetened mainly with high-fructose corn syrup (HFCS), which consists of half glucose and half fructose. Initial work by my lab found that the chronic intake of a modest amount of HFCS that mimics one can of soda in humans directly increased the size and number of tumors in a mouse model of CRC. My group also found that HFCS increased the population of certain gut microbes and activated molecular pathways tied to CRC. Now we will tease out the tumorigenic effects of HFCS on CRC in mice harboring a human gut microbiome. Using this model, I will assess the impact of HFCS on the size, number, and grade of colon tumors formed. Additionally, I will analyze how HFCS alters the composition of gut microbes and their metabolism, and how these changes lead to CRC. Work from this study will untangle the complex relationship between diet and gut health and identify innovative biomarkers for the prevention and treatment of CRC.
