Sally E Dickinson, PhD

Dr. Dickinson’s scientific training and current research are in the area of UV-induced skin carcinogenesis with a focus on molecular signaling pathways as targets for chemoprevention. Through this training, she has gained extensive experience with mouse models of non-melanoma skin cancer (NMSC), cell/molecular biology techniques and translational studies.

As a Research Assistant Professor of Pharmacology at the University of Arizona Cancer Center, she is currently the Co-PI of Project 1 of the Chemoprevention of Skin Cancer Program Project Grant (PPG).  Through this grant she is investigating the roles of MAP Kinases, PI3-Kinase, and mTOR/Akt signaling in the development of UV-induced NMSC. She is focused on exploring the use of specific inhibitors of these pathways as chemopreventive agents. They are currently investigating the activities of Rapamycin (an mTOR inhibitor), PHT-427 (a PDK1/Akt inhibitor) and the natural product sulforaphane (SFN, a Nrf2 inducer) in skin cancer prevention, the latter as an extension of her K07 Career Development award.  In fact, the PPG recently conducted a pilot clinical trial using topical SFN to examine its effects on epidermal signaling in the context of solar-simulated light. 

In addition, Dr. Dickinson is interested in examining the use of other natural products alone or in combination to boost our efficiency at topically preventing NMSC in the general population and in high-risk patients such as those subject to immunosuppression.

As PI on a Skin Cancer Institute Seed Grant, Dr. Dickinson hopes to pursue impactful cancer prevention research through our expansion into understanding the role of Toll-like Receptor 4 (TLR4) in UV-induced skin carcinogenesis. TLR4 directly regulates the innate immune response, which is often dysregulated in immunosuppressed patients, and thus may predispose the skin to the recurrent and life-threatening squamous cell carcinomas observed in this population. 

Read Dr. Dickinson's pharmacology faculty bio.