My current research uses mixed methodology including implementation science frameworks, change management principles, and an adaptable collaboration blueprint where interventions and outcomes can be measured quantitatively using a developing database. My research aims to find optimal ways to promote collaboration between people from all different backgrounds, building psychological safety in teams, helping individuals communicate in language that all other team members can understand, and directing teams as they grow in flexibility of mind toward publishing groundbreaking papers and building multi-PI grants. I facilitate collaborations between Basic, Clinical, and Population Scientists as well as Community Partners with the aim to maximize the translational potential of Northwestern University’s cutting-edge cancer research. I run team building and goal setting workshops, facilitate complex discussions between researchers across specialties, and direct curriculum development and implementation aimed to guide our scholars to understand all that is involved in translational research.

When I was a basic researcher in the laboratory, I studied skin carcinogenesis and the biology of keratinocytes in response to environmental damage like exposure to ultraviolet (UV) light. I made several key contributions to understanding the process of skin carcinogenesis by studying how the p53 family of tumor suppressors is involved in transcriptional regulation and coordinating keratinocyte responses to DNA damaging agents. By delivering a nuclear-targeted DNA repair protein through the epidermis to increase the rate of repair of UV-induced DNA damage in basal keratinocytes, I demonstrated the feasibility of a potential clinical strategy for prevention of SCC. My laboratory focus from 2010-2019 was to understand how epithelial cells work to coordinate tissue-wide responses to environmental insults. I found that a protein involved in coordinating epidermal differentiation and maintenance of skin structure, called Desmoglein 1 (Dsg1), is reduced after ultraviolet (UVB) light exposure. We hypothesized that this regulator of skin structure and function may be acting as an environmental sensor and signaling transmitter for the skin after damage. In testing this hypothesis we uncovered a surprising new function for Dsg1 in regulating keratinocyte:melanocyte paracrine signaling which changes melanocyte behavior with regard to tanning response and hallmarks of early melanoma development. Building from this work, the laboratory is now pursuing the possibility that a Dsg1-deficient niche, as caused by UV exposure, may establish a permissive environment for melanoma growth and that restoring Dsg1 levels after skin damage may prevent or reduce the risk of developing melanoma. Today I work with global teams to continue to educate and grow the field of dermatology through writing and publishing with groups like the National Eczema Association, the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis, the Journal of Investigative Dermatology, multiple industry partners, and global health care practitioners.