Katherine Hanlon (Award in Pain Recipient) earned a B.S. in biochemistry and molecular biophysics and a Ph.D. in pharmacology from the University of Arizona, where she worked with Todd Vanderah. She went on to complete a postdoctoral fellowship in tumor immunology at the Mount Sinai Medical Center with Joshua Brody and Peter Heeger. In addition to her work in the lab, Hanlon currently teaches Biochemistry and Principles of Pharmacology in the School of Pharmacy at Presbyterian College and directs the College’s Office of Research. Her primary research interests include macrophage-neuron communication in pain processing and the role of tumor-associated macrophages in cancer development. She also studies the mechanisms of dysregulation of cannabinoid receptor signaling in tumor and immune cells in metastatic disease.
Studies in the Hanlon lab are carried out using multiple in vitro and in vivo models, including leukocytes and neurons isolated from dorsal root ganglia, leukocytes and tumor cells isolated from murine mammary tumors, leukocytes harvested from post-surgical peritoneal adhesions, and human blood monocyte primary cultures. With the support of the Rita Allen Foundation and the American Pain Society, the lab is able to explore the communication that occurs between sensory neurons and macrophages (innate immune cells that are critical in injury response) in dorsal root ganglia (DRG). Macrophages in the DRG are a unique population of cells that bear some resemblance to brain microglia, but are functionally distinct and exhibit specific phenotype differences. In response to peripheral injury, DRG macrophages respond to activity in the ascending pain pathways and may alter pain perception. By evaluating the phenotype and function of this unique population, Hanlon hopes to isolate novel and exploitable mechanisms that may be used to develop non-opioid therapeutics for the treatment of persistent pain.