Hematopoiesis—the production of blood cells that occurs throughout a person’s lifetime—is regulated by proteins called transcription factors that regulate the expression of hematopoietic genes. Germ-line mutations in RUNX1, the gene coding for the transcription factor RUNX1, causes a familial platelet disorder predisposes people to develop blood cancer. So far, however, scientists haven’t identified the specific genes that RUNX1 controls. 

Kristy Stengel, Ph.D., has received a four-year, $2.6 million grant from the National Heart, Lung, and Blood Institute to identify which genes are regulated by RUNX1 and how RUNX1 controls them. Dr. Stengel’s lab recently developed a novel technology that uses a small molecule to rapidly remove RUNX1 proteins from cells within one-to-two hours of treatment; use of that technology suggests that RUNX1 collaborates with several other transcription factors and co-regulatory proteins to regulate hematopoietic gene networks. By incorporating the technology in a mouse model, Dr. Stengel hopes to determine how RUNX1 controls gene expression to promote normal blood development as well as the molecular mechanisms by which defective RUNX1 results in blood cancer.

Dr. Stengel is an assistant professor of cell biology at Einstein and a member of the Stem Cell & Cancer Biology Research (SCCB) Program at the National Cancer Institute-designated Montefiore Einstein Comprehensive Cancer Center. (1R01HL174948-01)