The major basic science laboratory under the guidance of principal investigator, Yu-Ying He, PhD, is studying cell response to radiation and chemicals from external and internal sources that cause cancer.
Dr. He’s lab is currently exploring such topics as the role of autophagy and p62 in tumor initiation and progression, molecular control of DNA damage response, molecular control of DNA repair and extrinsic control of DNA repair and DNA damage response. Her research addresses the fundamental question of how cells respond to radiation and chemicals from internal or external sources to cause cancer, with a focus on skin cancer. She uses in vitro systems, clinically relevant animal models, genetically modified mouse models, and human patient samples to elucidate how intrinsic and extrinsic factors regulate DNA repair, DNA damage response, and cellular homeostasis in order to understand cancer susceptibility. Because skin is an epithelial tissue, the findings are relevant to cancers of other epithelial tissues, and the research has the potential to identify new targets and strategies to improve prevention and treatment for both skin and other epithelial cancers. Dr. He’s long-term goal is to identify previously unrecognized, therapeutically accessible molecular regulatory networks that predict susceptibility to skin cancer, and to improve our ability to prevent and treat it.
Melanoma is a leading cause of cancer death in the United States, and has an increasing incidence every year. Risk factors include family history, severe sunburns, chronic sun exposure, skin type, and presence of dysplastic, or medically unusual nevi. Melanocytes are pigment-producing cells most commonly found in the skin, but also present in the eyes and central nervous system. These cells can form benign nevi (moles) or malignant neoplasms (melanomas). The presence of multiple moderate and severe dysplastic nevi may confer an independent risk for development of melanoma. Dermatology investigators, including Christopher Shea, MD are determining in a current study funded by the Chicago Dermatology Society if the earliest biopsied clinically atypical melanocytic neoplasms in a patient’s history would show the most dysplasia on histopathology and therefore set a threshold for the present moles of the patient. This may preclude the need for additional biopsy, possibly minimizing healthcare costs and the morbidity of the patient.