Betty S. Pace, MD
Professor, Department of Molecular & Cell Biology
Director, Sickle Cell Disease Research Center
University of Texas at Dallas

SCDAA Chief Medical Officer

Dr. Betty S. Pace is currently a Professor in the Department of Molecular and Cell Biology and Director of the Sickle Cell Disease Research Center at the University of Texas at Dallas. Dr. Pace provides leadership for a large basic research and teaching laboratory focused on globin gene regulation and drug discovery for sickle cell disease. Dr. Pace received her M.D. degree from the Medical College of Wisconsin and completed a Pediatric Hematology/Oncology fellowship at the University of Colorado Health Sciences Center in 1990. After completing post doctoral training in Medical Genetics at the University of Washington she joined the faculty at the University of South Alabama in 1994. Most recently Dr. Pace was recruited to the University of Texas at Dallas in January 2003 where she currently serves as a valuable member of the faculty performing biomedical research, teaching and training undergraduate and graduate students.

For the past 10 years the Pace laboratory has studied the developmental regulation of hemoglobin gene expression. The goal of Dr. Pace’s research is to design novel treatment strategies for sickle cell disease. The approach chosen involves fetal hemoglobin induction, which blocks sickle hemoglobin polymerization and improves symptoms in the disease. Major contributions have been made to the field by the Pace lab towards drug discovery. Studies to understand the molecular mechanisms and transcription factors involved gamma gene regulation have also been completed. They demonstrated an important role for cell signaling pathways in transmitting the effects of drugs used to induce fetal hemoglobin. The p38 mitogen activated protein kinase pathway is the target of intense study. The Pace Laboratory recently expanded its efforts to functional genomics approaches, to identify epigenetic modifiers of gamma gene expression using genome wide association studies. This works promises to contribute to our knowledge of globin gene regulation during development and will serve as a rationale for future gene-based therapies for sickle cell disease.